This article is about the doomsday scenario. For the planet proposed by Zecharia Sitchin, see Nibiru (Sitchin). For the object from Babylonian mythology, see Nibiru (mythology). For similar ideas, see Astronomical objects proposed in religion, astrology and ufology. For other uses, see Nibiru.
Artist's conception of Nemesis, a hypothetical brown dwarf companion to the Sun often confused with Nibiru.Since 1995, an evolving cultural phenomenon has envisioned a disastrous collision or similar encounter between the Earth and a large planetary object, variously referred to as Nibiru, Planet X, or Wormwood, within the next few years. The idea was first proposed by Nancy Lieder, founder of the website ZetaTalk.[1] Lieder describes herself as a contactee with the ability to channel messages from extra-terrestrials called Zetas (from the Zeta Reticuli star system; see Betty and Barney Hill) through an implant in her brain. She states that she was chosen to warn mankind the object would sweep through the Solar System in May 2003 (later revised to around 2010), causing a pole shift that would destroy most of humanity. This idea has subsequently spread beyond Lieder's website and has been embraced by numerous internet doomsday groups, most of which tie the collision to the 2012 doomsday prediction. The idea that a planet-sized object could possibly collide with Earth in the near future is not supported by any scientific evidence and has been roundly rejected as pseudoscience by astronomers and planetary scientists.
Contents
[hide]
1 Origins
2 Names
3 Scientific criticism
4 Criticism by Sitchin
5 Public reaction
6 Film
7 References
8 External links
Origins
Pseudoscientific concepts
Claims
Earth's immanent collision with a giant planetoid
Related scientific disciplines
Astronomy, archaeology
Year proposed
1995
Original proponents
Nancy Leider
Subsequent proponents
Marshall Masters, Jaysen Rand, Burak Eldem, Mark Hazlewood, Pana Wave
The Nibiru collision idea originated with Nancy Lieder, a onetime employee of C2C Consulting in Foster City, California who now lives in Wisconsin.[2] She says that as a girl she was contacted by gray extraterrestrials called Zetas, who placed her on a table and examined her.[3] She also says she was implanted with a communications device in her twenties, which the Zetas use to channel themselves through her.[4] In 1995, she founded the website ZetaTalk as a repository for "the vast amount of information being relayed by the Zetas in answer to questions posed to their emissary, Nancy."[5] The site is written entirely in the Zetas' voice, with most sentences in the first person plural and Lieder referred to in the third person.
Lieder first came to notice on internet newsgroups during the build-up to Comet Hale-Bopp's 1997 perihelion.[1] She stated, speaking as the Zetas, that "The Hale-Bopp comet does not exist. It is a fraud, perpetrated by those who would have the teeming masses quiescent until it is too late. Hale-Bopp is nothing more than a distant star, and will draw no closer."[6] The event from which the masses were to be distracted was the imminent arrival of a large planetary object, "Planet X", which would soon pass by Earth and destroy civilisation.[1] After Hale-Bopp's perihelion revealed it as one of the brightest and longest-observed comets of the last century,[7] Lieder downplayed its impact, saying that the comet was neither as bright nor as large as had been predicted.[8] The first two sentences of her initial statement were subsequently removed from her site, though they can still be found in Google's archives.[6]
Lieder described Planet X as roughly 4 times the size of the Earth,[9] and said that its perigee would occur on May 27, 2003, resulting in the Earth's rotation ceasing for exactly 5.9 terrestrial days.[10] Then the Earth's pole would destabilise in a pole shift (a physical pole shift; i.e. the Earth's pole physically moving, not to be confused with a geomagnetic reversal) caused by magnetic attraction between the Earth's core and the magnetism of the passing planet, resulting in the core's magnetic disruption and subsequent displacement of the Earth's crust.[11]
After the 2003 date passed without incident, Lieder said that it was merely a "White Lie ... to fool the establishment,"[12] and said that to disclose the true date would give those in power enough time to declare martial law and trap people in cities during the shift, leading to their deaths.[13] She still insists that the Zetas tell her that Planet X is coming and that a more specific passage timeline will be forthcoming after Obama takes office,[14] possibly mid-2010.[15][16]
Lieder's Planet X idea first spread beyond her website in 2001, when Mark Hazlewood, a former member of the ZetaTalk community, took her ideas and published them in a book: Blindsided: Planet X Passes in 2003. Lieder would later accuse him of being a confidence trickster.[17] Hazlewood also still maintains that Planet X is due, and published a new book, Delicate Earth, in 2006.[18] Japanese cult the Pana Wave Laboratory, which famously blocked off roads and rivers with white cloths to protect itself from electromagnetic attacks, also warned that the world would end in May 2003 after the approach of a tenth planet.[19]
Today, several internet sites still proclaim that "Planet X" or "Nibiru" is en route to Earth, often citing its arrival year as 2012, which is the end of the current cycle (baktun) in the long count in the Mayan calendar. Authors such as Burak Eldem, Jaysen Rand and Marshall Masters have propagated 2012 as Nibiru's arrival date.[20][21][22] The whistleblowers' website projectcamelot.org says it in possession of an anonymous letter from a Norwegian politician that states "Planet X is coming" and describes a secret plan to construct a series of globe-spanning 2012 survival bases.[23]
Names
This object is most commonly referred to as Nibiru, a name derived from the works of ancient astronaut proponent Zecharia Sitchin. According to Sitchin's personal (and academically dismissed)[24] reading of Sumerian religious texts, a giant planet (Nibiru or Marduk) with a 3600-year orbit occasionally passes by Earth and allows its sentient inhabitants to interact with humanity. These beings, which Sitchin identifies with the Annunaki of Sumerian myth, would become humanity's first gods.[25] However, Sitchin disagrees that an apocalypse is immanent (see below), and it was Lieder who initially made the connection.[26] Another widely used name for the object is Wormwood, after a passage from the Book of Revelation that describes a star named Wormwood falling from the skies.[21]
This object has also been linked by name to a number of hypothetical and actual Solar System objects. Lieder originally referred to as "Planet X"; the same Planet X once searched for by astronomers to account for discrepancies in the orbits of Uranus and Neptune.[26] However, in 1992 astronomer Myles Standish showed that these discrepancies were illusory, and today astronomers accept that Planet X does not exist.[27][28] Others say it is identical with Nemesis,[29] the hypothetical brown or red dwarf companion to the Sun proposed by Richard A. Muller to explain a purported regularity in mass extinctions observed in the fossil record. In his hypothesis, now widely discounted by scientists,[30] Muller argued that, as the object passed through the cometary Oort cloud every few million years, its gravity would perturb the orbits of those distant objects, causing a swarm of comets to enter the inner Solar System, leading to a higher probability of a major impact which would trigger a mass extinction.[31] However, Nemesis, if it exists, would have an orbit thousands of times longer than that proposed for Nibiru, and would never itself come anywhere near Earth.[32] Still others refer to it as Eris;[33] however, Eris is a dwarf planet only slightly larger than Pluto[34] with a well-determined orbit that never takes it closer than 5.5 billion km from the Earth.[35] Astronomer Mike Brown, who discovered Eris, believes the confusion results from both the real Eris and the imaginary Nibiru having extremely elliptical orbits.[36]
Scientific criticism
V838 Mon, a star with an expanding gas shell passed off as "photographic evidence" of NibiruThe Nibiru collision idea fails on several basic scientific grounds. For instance, such an object so close to Earth would be easily visible to the naked eye (Jupiter and Saturn are both visible to the naked eye, and are dimmer than Nibiru would be at their distances), and would be creating noticeable effects in the orbits of the outer planets.[37] If this object's orbit were as described, it would only have lasted in the Solar System for a million years or so before Jupiter expelled it. Also, there is no way another object's magnetic field could have such an effect on Earth.[38] Lieder's assertions that the approach of Nibiru would cause the Earth's rotation to stop or its axis to shift violate the laws of physics; the energy required to do either would be enough to destroy the Earth completely.[39]
Many believers in the imminent approach of Planet X/Nibiru/Wormwood accuse NASA of deliberately covering up visual evidence of its existence.[40] One such accusation involves the IRAS infrared space observatory, launched in 1983. The satellite briefly made headlines due to an "unknown object" that was at first described as "possibly as large as the giant planet Jupiter and possibly so close to Earth that it would be part of this Solar System".[41] This newspaper article has been cited by proponents of the collision idea, beginning with Leider herself, as evidence for the existence of Nibiru.[42] However, further analysis revealed that of several unidentified objects, nine were distant galaxies and the tenth was "intergalactic cirrus"; none were found to be Solar System bodies.[43]
Another accusation frequently made by websites predicting the collision is that the US government built the South Pole Telescope to track Nibiru's trajectory, and that the object has been imaged optically.[44] However, the SPT is a radio telescope, and cannot take photographs. Its South Pole location was chosen due to the low-humidity environment, and there is no way an approaching object could be seen only from the South Pole.[45] The "picture" of Nibiru posted on Youtube was revealed to in fact be a Hubble image of the expanding gas shell around the star V838 Mon.[44]
Criticism by Sitchin
Zecharia Sitchin himself has criticized this doomsday scenario's association with his planet Nibiru. In 2007, partly in response to Lieder's proclamations, he published a book, The End of Days, which set the time for the last passing of Nibiru by Earth at roughly 600 BC, which would mean it would be unlikely to return in less than 1000 years.[46] In 2008, Sitchin gave a 2-hour lecture on his ideas, which denied any direct connection between his Nibiru and the supposed 2012 end date.[47]
Public reaction
Mike Brown now says that Nibiru is the most common pseudoscientific topic he is asked about.[38] David Morrison, an astrobiologist at NASA's Ames Research Center. says he receives 20-25 emails a week about the impending arrival of Nibiru; some frightened, others angry and naming him as part of the conspiracy to keep the truth of the impending apocalypse from the public.[40] "Planetary scientists are being driven to distraction by Nibiru," notes science writer Govert Schilling, "And it is not surprising; you devote so much time, energy and creativity to fascinating scientific research, and find yourself on the tracks of the most amazing and interesting things, and all the public at large is concerned about is some crackpot theory about clay tablets, god-astronauts and a planet that doesn't exist."[48] Morrison states that he hopes that the non-arrival of Nibiru could serve as a teaching moment for the public, instructing them on rational thought and baloney detection, but doubts that will happen.[40]
Film
A viral campaign for Sony Pictures' 2009 film 2012, directed by Roland Emmerich, which depicts the end of the world in that year, features a supposed warning from the "Institute for Human Continuity" that lists the arrival of Planet X as one of its doomsday scenarios.[49] Mike Brown attributes a spike in concerned emails and phone calls he received from the public to this site.[36]
References
^ a b c "Where do these ideas come from?". planet-x.150m.com. http://www.planet-x.150m.com/where.html. Retrieved on 2009-04-28.
^ "What Is Known About Nancy Lieder". Skeptical Mind. http://www.skepticalmind.com/nancy.html. Retrieved on 2009-04-28.
^ "first meeting". zetatalk.com. http://www.zetatalk.com/visitatn/v25.htm. Retrieved on 2009-04-28.
^ "Communications". zetatalk.com. http://zetatalk.com/transfor/t18.htm. Retrieved on 2009-04-28.
^ "ZetaTalk". zetatalk.com. http://zetatalk.com/. Retrieved on 2009-06-21.
^ a b "The Planet X Saga: Nancy Leider". badastronomy.com. http://www.badastronomy.com/bad/misc/planetx/lieder.html. Retrieved on 2009-04-28.
^ Kidger, M.R.; Hurst, G; James, N. (2004). "The Visual Light Curve Of C/1995 O1 (Hale-Bopp) From Discovery To Late 1997". Earth, Moon, and Planets 78 (1–3): 169–177. doi:10.1023/A:1006228113533. http://www.springerlink.com/content/h72381014307x661/.
^ "Hale Bopp". zetatalk.com. http://www.zetatalk.com/halebopp/hb000001.htm. Retrieved on 2009-04-28.
^ "Planet X: Distance, Speed, thus SIZE". zetatalk.com. http://www.zetatalk.com/usenet/use90652.htm. Retrieved on 2009-05-11.
^ "Pole Shift Date of May 27, 2003". zettalk.com. http://www.zetatalk.com/index/psdate1.htm. Retrieved on 2009-04-28.
^ "ZetaTalk: Pole Shift". zetatalk.com. http://www.zetatalk.com/poleshft/p21.htm. Retrieved on 2009-04-28.
^ "Pole Shift in 2003 Date". zetatalk. 2003. http://www.zetatalk.com/index/psdate.htm. Retrieved on 2009-04-12.
^ "ZetaTalk: White Lie". zetatalk.com. 2003. http://www.zetatalk.com/index/psdate2.htm. Retrieved on 2009-04-12.
^ "Zetatalk live chat". Godlike Productions. 2008. http://www.godlikeproductions.com/forum1/message606175/pg1. Retrieved on 2009-04-12.
^ "ZetaTalk: GodlikeProduction Live". zetatalk.com. 21 June 2008. http://zetatalk.com/index/zeta459.htm. Retrieved on 2009-04-12.
^ "ZetaTalk: GodlikeProduction Live". 2008. http://www.zetatalk.com/index/zeta463.htm. Retrieved on 2009-04-12.
^ "Mark Hazlewood Scam". Zetatalk. http://www.zetatalk.com/index/hazelwod.htm. Retrieved on 2009-04-12.
^ Mark Hazlewood (2006). "Planet X Inbound". planetxinbound.com. http://www.planetxinbound.com/index.htm. Retrieved on 2009-04-12.
^ Benjamin Dorman (2005). "Pana Wave The New Aum Shinrikyô or Another Moral Panic?". Caliber. doi:10.1525/nr.2005.8.3.83. http://caliber.ucpress.net/doi/abs/10.1525/nr.2005.8.3.83?cookieSet=1&journalCode=nr. Retrieved on 2009-05-09.
^ Burak Eldem. "About the Books". burakeldem.com. http://en.burakeldem.com/content/view/13/27/. Retrieved on 2009-04-12.
^ a b "The Return of Planet-X Forecast as our 2009/2012 cosmic timetable approaches". returnofplanet-x.com. http://www.returnofplanet-x.com/forecast.asp. Retrieved on 2009-05-05.
^ "Underground 2012 Survival Bases — Project Camelot Founders Bill Ryan and Kerry Cassidy". yowusa.com. 2007. http://www.yowusa.com/. Retrieved on 2008-02-13.
^ "Letter from "Norwegian politician"". Project Camelot. http://projectcamelot.org/norway.html. Retrieved on 2008-02-14.
^ Michael S. Heiser. "Stchin Is Wrong". http://www.sitchiniswrong.com/sitchinerrors.htm. Retrieved on 2009-06-27.
^ Zecharia Sithin (1976). The 12th Planet. Harper. pp. 120.
^ a b "Planet X". zetatalk.com. 1996. http://www.zetatalk.com/science/s58.htm. Retrieved on 2009-04-30.
^ Myles Standish (1992-07-16). "Planet X - No dynamical evidence in the optical observations". Astronomical Journal volume= 105 (5): 200-2006. http://adsbit.harvard.edu/cgi-bin/nph-iarticle_query?bibcode=1993AJ....105.2000S. Retrieved on 2009-04-30.
^ John Standage (2000). The Neptune File. Pengin. p. 168.
^ "2012 Warning". 2012warning.com. http://www.2012warning.com/nibiru.htm. Retrieved on 2009-05-04.
^ Robert Roy Britt (2001). "Nemesis: Does the Sun have a companion?". space.com. http://www.space.com/scienceastronomy/solarsystem/nemesis_010320-1.html. Retrieved on 2009-07-02.
^ J. G. Hills (1984-10-18). "Dynamical constraints on the mass and perihelion distance of Nemesis and the stability of its orbit". Nature (Nature Publishing Group) 311: 636–638. doi:10.1038/311636a0. http://www.nature.com/nature/journal/v311/n5987/abs/311636a0.html. Retrieved on 2008-03-25.
^ Ian O'Neill (2009). "Constraining the Orbits of Planet X and Nemesis". Universe Today. http://www.universetoday.com/2009/04/15/constraining-the-orbits-of-planet-x-and-nemesis/. Retrieved on 2009-05-04.
^ Cristian Negureanu (2007). "NASA AND PLANET ERIS/NIBIRU". UFO Digest. http://www.ufodigest.com/news/0707/eris-nibiru.html. Retrieved on 2009-04-12.
^ Mike Brown (2007). "Dysnomia, the moon of Eris". CalTech. http://www.gps.caltech.edu/~mbrown/planetlila/moon/index.html. Retrieved on 2007-06-14.
^ "JPL Small-Body Database Browser: 136199 Eris (2003 UB313)". 2008-10-04 last obs. http://ssd.jpl.nasa.gov/sbdb.cgi?sstr=Eris. Retrieved on 2009-01-21.
^ a b Mike Brown (2009). "Sony Pictures and the End of the World". Mike Brown's Planets. http://www.mikebrownsplanets.com/2009/06/sony-pictures-and-end-of-world.html. Retrieved on 2009-06-07.
^ Phil Plait (2003). "The Planet X Saga: Science". badastronomy.com. http://www.badastronomy.com/bad/misc/planetx/science.html#orbits. Retrieved on 2009-04-02. (this page relates to the initial supposed 2003 arrival, but holds just as well for 2012)
^ a b Mike Brown (2008). "I do not ♥ pseudo-science". Mike Brown's planets. http://www.mikebrownsplanets.com/2008/02/i-do-not-pseudo-science.html. Retrieved on 2009-04-12.
^ "It causes a pole shift? A what?". planet-x.150m.com. http://www.planet-x.150m.com/poleshift.html.
^ a b c David Morrison (2008). "Armageddon from Planet Nibiru in 2012? Not so fast". discovery.com. http://dsc.discovery.com/space/my-take/nibiru-armageddon-david-morrison.html. Retrieved on 2009-04-02.
^ Thomas O'Toole (1983-12-30). "Mystery Heavenly Body Discovered". Washington Post: p. A1. http://spider.ipac.caltech.edu/staff/tchester/iras/washington_post_mystery_object.html. Retrieved on 2008-01-28.
^ Phil Plait (2002). "The IRAS Incident". badastronomy.com. http://www.badastronomy.com/bad/misc/planetx/science.html. Retrieved on 2009-04-09.
^ J. R. Houck, D. P. Schneider, D. E. Danielson, et al. (1985). "Unidentified IRAS sources: Ultra-High Luminosity Galaxies". The Astrophysical Journal 290: 5–8. doi:10.1086/184431. http://adsabs.harvard.edu/cgi-bin/nph-bib_query?bibcode=1985ApJ...290L...5H&db_key=AST&high=3ccf23290006822. Retrieved on 2008-07-14.
^ a b David Morrison. "The Myth of Nibiru and the End of the World in 2012". Skepical Enquirer. http://www.csicop.org/si/2008-05/morrison.html. Retrieved on 2009-04-28.
^ David Morrison (2008). "Ask An Astrobiologist". NASA. http://astrobiology.nasa.gov/ask-an-astrobiologist/question/?id=4380. Retrieved on 2009-04-23.
^ Zacharia Sitchin (2007). The End of Days. William Morrow. pp. 401.
^ "Will the end come in 2012? publisher=Sitchin.com". http://www.sitchin.com/. Retrieved on 2009-06-23.
^ Govert Schilling. The Hunt For Planet X: New Worlds and the Fate of Pluto. Copernicus Books. pp. 111.
^ "IHC: Education/Awareness". Sony Pictures. 2009. http://www.instituteforhumancontinuity.org/?hs308=email#/initiatives/earth/education/planetX. Retrieved on 2009-06-08.
External links
ZetaTalk
History of ZetaTalk
Bad Astronomy on ZetaTalk's astronomical errors
Video of Lieder and Hazlewood
Jay Martell on Planet X/Nibiru
[hide]v • d • eUfology
Main areas of study Contactee · Crashes · Extraterrestrials · Sightings · Topics · SETI
Involvement Culture · Government personnel · Government responses · Organizations · Religions · Ufologists
Friday, July 3, 2009
extinction event from wiki
K-TTr-JP-TrLate DO-SMillions of years ago Marine extinction intensity through time. The blue graph shows the apparent percentage (not the absolute number) of marine animal genera becoming extinct during any given time interval. It does not represent all marine species, just those that are readily fossilized. The labels of the "Big Five" extinction events are clickable hyperlinks; see Extinction event for more details. (source and image info)An extinction event (also known as: mass extinction; extinction-level event, ELE) is a sharp decrease in the number of species in a relatively short period of time. Mass extinctions affect most major taxonomic groups present at the time — birds, mammals, reptiles, amphibians, fish, invertebrates and other simpler life forms. They may be caused by one or both of:
extinction of an unusually large number of species in a short period.
a sharp drop in the rate of speciation.[1]
Over 99% of species that ever lived are now extinct, but extinction occurs at an uneven rate. Based on the fossil record, the background rate of extinctions on Earth is about two to five taxonomic families of marine invertebrates and vertebrates every million years.[2] Marine fossils are mostly used to measure extinction rates because they are more plentiful and cover a longer time span than fossils of land organisms.
Since life began on earth, several major mass extinctions have significantly exceeded the background extinction rate. The most recent, the Cretaceous–Tertiary extinction event, occurred 65 million years ago, and has attracted more attention than all others as it marks the extinction of nearly all dinosaur species, which were the dominant animal class of the period. In the past 540 million years there have been five major events when over 50% of animal species died. There probably were mass extinctions in the Archean and Proterozoic Eons, but before the Phanerozoic there were no animals with hard body parts to leave a significant fossil record.
Estimates of the number of major mass extinctions in the last 540 million years range from as few as five to more than twenty. These differences stem from the threshold chosen for describing an extinction event as "major", and the data chosen to measure past diversity.
Contents
[hide]
1 Major extinction events
2 Minor events
3 Evolutionary importance
4 Apparent decreasing frequency
5 Causes
5.1 Looking for the causes of particular mass extinctions
5.2 Most widely supported explanations
5.2.1 Flood basalt events
5.2.2 Sea-level falls
5.2.3 Impact events
5.2.4 Sustained and significant global cooling
5.2.5 Sustained and significant global warming
5.2.6 Clathrate gun hypothesis
5.2.7 Anoxic events
5.2.8 Hydrogen sulfide emissions from the seas
5.2.9 Oceanic overturn
5.2.10 A nearby nova, supernova or gamma ray burst
5.2.11 Continental drift
5.2.12 Plate tectonics
5.2.13 Other hypotheses
6 Postulated extinction cycles
6.1 Hypothetical companion star to the sun
6.2 Galactic plane oscillations
6.3 Passage through galactic spiral arms
6.4 Geological instabilities
7 See also
8 References
8.1 Bibliography
8.2 Notes
9 External links
Major extinction events
The classical "Big Five" mass extinctions identified by Jack Sepkoski and David M. Raup in their 1982 paper are widely agreed upon as some of the most significant: End Ordovician, Late Devonian, End Permian, End Triassic, and End Cretaceous.[2][3] The Holocene extinction event is referred to as the Sixth Extinction.
These and a selection of other extinction events are outlined below. The articles about individual mass extinctions describe their effects in more detail and discuss theories about their causes.
Holocene extinction event - nearly 70% of biologists view the present era as part of a mass extinction event, possibly one of the fastest ever, according to a 1998 survey by the American Museum of Natural History.,[4] Some, such as E. O. Wilson of Harvard University, predict that humanity's destruction of the biosphere could cause the extinction of half of all species in the next 100 years. Research and conservation efforts, such as the IUCN's annual "Red List" of threatened species, all point to an ongoing period of enhanced extinction, though some offer much lower rates and hence longer time scales before the onset of catastrophic damage. The extinction of many megafauna near the end of the most recent ice age is also sometimes considered part of the Holocene extinction event.[5] Some paleontologists, however, question whether the available data support a comparison with mass extinctions in the past.[6]
Cretaceous–Tertiary extinction event - 65 Ma at the Cretaceous-Paleogene transition about 17% of all families and 50% of all genera went extinct.[7] (75% species). It ended the reign of dinosaurs and opened the way for mammals and birds to become the dominant land vertebrates. In the seas it reduced the percentage of sessile animals to about 33%. The K/T extinction was rather uneven — some groups of organisms became extinct, some suffered heavy losses and some appear to have been only minimally affected.
Triassic-Jurassic extinction event - 205 Ma at the Triassic-Jurassic transition about 20% of all marine families (55% genera) as well as most non-dinosaurian archosaurs, most therapsids, and the last of the large amphibians were eliminated. 23% of all families and 48% of all genera went extinct.[7]
Permian-Triassic extinction event - 251 Ma at the Permian-Triassic transition, Earth's largest extinction killed 53% of marine families, 84% of marine genera, about 96% of all marine species and an estimated 70% of land species (including plants, insects, and vertebrate animals). 57% of all families and 83% of all genera went extinct.[7] The "Great Dying" had enormous evolutionary significance: on land it ended the dominance of mammal-like reptiles, the recovery of vertebrates took 30 million years[8] but created the opportunity for archosaurs and then dinosaurs to become the dominant land vertebrates; in the seas the percentage of animals that were sessile dropped from 67% to 50%. The whole late Permian was a difficult time for at least marine life — even before the "Great Dying".
Late Devonian extinction 360-375 Ma near the Devonian-Carboniferous transition at the end of the Frasnian Age in the later part(s) of the Devonian Period. A prolonged series of extinctions eliminated about 70% of all species. This extinction event lasted perhaps as long as 20 MY, and there is evidence for a series of extinction pulses within this period. 19% of all families of life and 50% of all genera went extinct.[7]
Ordovician-Silurian extinction events 440-450 Ma at the Ordovician-Silurian transition two events occurred, and together are ranked by many scientists as the second largest of the five major extinctions in Earth's history in terms of percentage of genera that went extinct. 27% of all families and 57% of all genera became extinct.[7]
Cambrian-Ordovician extinction events - 488 Ma a series of mass extinctions at the Cambrian-Ordovician transition eliminated many brachiopods and conodonts and severely reduced the number of trilobite species.
The older the fossil record gets the more difficult it is to read it. This is because:
Older fossils are harder to find because they are usually buried at a considerable depth in the rock.
Dating fossils is difficult.
Productive fossil beds are researched more than unproductive ones, therefore leaving certain periods unresearched.
Prehistoric environmental disturbances can disturb the deposition process.
The preservation of fossils varies on land, but marine fossils tend to be better preserved than their sought after land-based cousins.[9]
It has been suggested that the apparent variations in marine biodiversity may actually be an artifact, with abundance estimates directly related to quantity of rock available for sampling from different time periods.[10] However, statistical analysis shows that this can only account for 50% of the observed pattern,[citation needed] and other evidence (such as fungal spikes)[clarification needed] provides reassurance that most widely accepted extinction events are indeed real. A quantification of the rock exposure of Western Europe does indicate that many of the minor events for which a biological explanation has been sought are most readily explained by sampling bias.[11]
Minor events
Minor extinction events include:[12]
Precambrian
End-Ediacaran extinction - circa 542 Ma
Cambrian Period
End Botomian - circa 517 Ma
Dresbachian
Silurian Period
Ireviken event
Mulde event
Lau event
End Silurian
Carboniferous Period
Middle Carboniferous
Jurassic Period
Toarcian turnover circa 183 Ma
End Jurassic
Cretaceous Period
Aptian extinction circa 117 Ma
Paleogene Period
Eocene-Oligocene extinction event
Neogene Period
Cat gap
Middle Miocene disruption circa 14.5 Ma
Quaternary Period (disputed)
Quaternary extinction event
Extinction events[hide]
view • talk • edit
Minor events↓End-Ediacaran?↓Lau event↓Toarcian turnover↓Aptian↓Middle Miocene
disruption↓Cambro-Ordovician↓Ordo-Silurian↓Late Devonian↓Permo-Triassic↓Triassic–Jurassic↓Cretaceous–Tertiary↓HoloceneMajor events Ediacaran Cambrian Ordovician Silurian Devonian Carboniferous Permian Triassic Jurassic Cretaceous Palæogene Neo-
gene Neoproterozoic Palæozoic Mesozoic Cenozoic | -600| -550| -500| -450| -400| -350| -300| -250| -200| -150| -100| -50| 0
Millions of years before present
Evolutionary importance
Mass extinctions have sometimes accelerated the evolution of life on earth. When dominance of particular ecological niches passes from one group of organisms to another, it is rarely because the new dominant group is "superior" to the old and usually because an extinction event eliminates the old dominant group and makes way for the new one.[13][14]
For example mammaliformes ("almost mammals") and then mammals existed throughout the reign of the dinosaurs, but could not compete for the large terrestrial vertebrate niches which dinosaurs monopolized. The end-Cretaceous mass extinction removed the non-avian dinosaurs and made it possible for mammals to expand into the large terrestrial vertebrate niches.
Another point of view put forward in the Escalation hypothesis predicts that species in ecological niches with more organism-to-organism conflict will be less likely to survive extinctions. This is because the very traits that keep a species numerous and viable under fairly static conditions become a burden once population levels fall among competing organisms during the dynamics of an extinction event.
Furthermore, many groups which survive mass extinctions do not recover in numbers or diversity, and many of these go into long-term decline, and these are often referred to as "Dead Clades Walking".[15] So analysing extinctions in terms of "what died and what survived" often fails to tell the full story.
Apparent decreasing frequency
All genera"Well-defined" generaTrend line"Big Five" mass extinctionsOther mass extinctionsMillion years agoThousands of generaPhanerozoic biodiversity as shown by the fossil recordThe gaps between mass extinctions appear to be becoming longer, while the average and background rates of extinction are decreasing. Mass extinctions are thought to result when a long-term stress is compounded by a short term shock.[16] Over the course of the Phanerozoic, individual taxa appear to be less likely to become extinct at any time,[17] which may reflect more robust food webs as well as less extinction-prone species and other factors such as continental distribution.[17] However the taxonomic susceptibility to extinction does not appear to make mass extinctions more or less probable.[17]
The idea that mass extinctions are becoming less frequent is rather speculative – from a statistical point of view a sample of about 10 extinction events is too small to be a reliable sign of any actual trend. But the average and background rates of extinction are based on hundreds of samples over a period of 550M years, so the apparent decrease in these rates is statistically significant and needs to be explained.
Both of these phenomena could be explained in one or more ways:[18]
Reasonably complete fossils are very rare, most extinct organisms are represented only by partial fossils, and complete fossils are rarest in the oldest rocks. So paleontologists have mistakenly assigned parts of the same organism to different genera which were often defined solely to accommodate these finds (an example is the story of Anomalocaris). The risk of this mistake is higher for older fossils because these are often unlike parts of any living organism. Many of the "superfluous" genera are represented by fragments which are not found again and the "superfluous" genera appear to become extinct very quickly.
Martin (1994, 1996) has argued that the oceans have become more hospitable to life over the last 500M years and less vulnerable to mass extinctions: dissolved oxygen became more widespread and penetrated to greater depths; the development of life on land reduced the run-off of nutrients and hence the risk of eutrophication and anoxic events; and marine ecosystems became more diversified so that food chains were less likely to be disrupted.[19][20]
Causes
There is still debate about the causes of all mass extinctions before the Holocene. In general, large extinctions may result when a biosphere under long-term stress undergoes a short-term shock.[21]
Looking for the causes of particular mass extinctions
A good theory for a particular mass extinction should: (i) explain all of the losses, not just focus on a few groups (such as dinosaurs); (ii) explain why particular groups of organisms died out and why others survived; (iii) provide mechanisms which are strong enough to cause a mass extinction but not a total extinction; (iv) be based on events or processes that can be shown to have happened, not just inferred from the extinction.
It may be necessary to consider combinations of causes. For example the marine aspect of the end-Cretaceous extinction appears to have been caused by several processes which partially overlapped in time and may have had different levels of significance in different parts of the world.[22]
Arens and West (2006) proposed a "press / pulse" model in which mass extinctions generally require two types of cause: long-term pressure on the eco-system ("press") and a sudden catastrophe ("pulse") towards the end of the period of pressure.[23] Their statistical analysis of marine extinction rates throughout the Phanerozoic suggested that neither long-term pressure alone nor a catastrophe alone was sufficient to cause a significant increase in the extinction rate.
Most widely supported explanations
Macleod (2001)[24] summarized the relationship between mass extinctions and events which are most often cited as causes of mass extinctions, using data from Courtillot et al. (1996),[25] Hallam (1992)[26] and Grieve et al. (1996):[27]
Flood basalt events: 11 occurrences, all associated with significant extinctions[28][29] But Wignall (2001) concluded that only 5 of the major extinctions coincided with flood basalt eruptions and that the main phase of extinctions started before the eruptions.[30]
Sea-level falls: 12, of which 7 were associated with significant extinctions.[29]
Asteroid impacts producing craters over 100km wide: one, associated with one mass extinction.
Asteroid impacts producing craters less than 100km wide: over 50, the great majority not associated with significant extinctions.
The most commonly suggested causes of mass extinctions are listed below.
Flood basalt events
The formation of large igneous provinces by flood basalt events could have:
produced dust and particulate aerosols which inhibited photosynthesis and thus caused food chains to collapse both on land and at sea
emitted sulfur oxides which were precipitated as acid rain and poisoned many organisms, contributing further to the collapse of food chains
emitted carbon dioxide and thus possibly causing sustained global warming once the dust and particulate aerosols dissipated.
Flood basalt events occur as pulses of activity punctuated by dormant periods. As a result they are likely to cause the climate to oscillate between cooling and warming, but with an overall trend towards warming as the carbon dioxide they emit can stay in the atmosphere for hundreds of years.
It is speculated that Massive volcanism caused or contributed to the End-Cretaceous, End-Permian, and End Triassic extinctions. [31] [32] [33]
Sea-level falls
These are often clearly marked by world-wide sequences of contemporaneous sediments which show all or part of a transition from sea-bed to tidal zone to beach to dry land - and where there is no evidence that the rocks in the relevant areas were raised by geological processes such as orogeny. Sea-level falls could reduce the continental shelf area (the most productive part of the oceans) sufficiently to cause a marine mass extinction, and could disrupt weather patterns enough to cause extinctions on land. But sea-level falls are very probably the result of other events, such as sustained global cooling or the sinking of the mid-ocean ridges.
Sea-level falls are associated with most of the mass extinctions, including all of the "Big Five" — End-Ordovician, Late Devonian, End-Permian, End-Triassic, and End-Cretaceous.
A study, published in the journal Nature (online June 15, 2008) established a relationship between the speed of mass extinction events and changes in sea level and sediment.[34] The study suggests changes in ocean environments related to sea level exert a driving influence on rates of extinction, and generally determine the composition of life in the oceans.[35]
Impact events
The impact of a sufficiently large asteroid or comet could have caused food chains to collapse both on land and at sea by producing dust and particulate aerosols and thus inhibiting photosynthesis. Impacts on sulfur-rich rocks could have emitted sulfur oxides precipitating as poisonous acid rain, contributing further to the collapse of food chains. Such impacts could also have caused megatsunamis and / or global forest fires, but evidence for these events has been difficult to find.[citation needed]
Only the Cretaceous–Tertiary extinction event is associated with strong evidence of such an impact, but that impact is easily the largest for which there is strong evidence.
Sustained and significant global cooling
Sustained global cooling could kill many polar and temperate species and force others to migrate towards the equator; reduce the area available for tropical species; often make the Earth's climate more arid on average, mainly by locking up more of the planet's water in ice and snow. The glaciation cycles of the current ice age are believed to have had only a very mild impact on biodiversity, so the mere existence of a significant cooling is not sufficient on its own to explain a mass extinction.
It has been suggested that global cooling caused or contributed to the End-Ordovician, Permian-Triassic, Late Devonian extinctions, and possibly others. Sustained global cooling is distinguished from the temporary climatic effects of flood basalt events or impacts.
Sustained and significant global warming
This would have the opposite effects: expand the area available for tropical species; kill temperate species or force them to migrate towards the poles; possibly cause severe extinctions of polar species; often make the Earth's climate wetter on average, mainly by melting ice and snow and thus increasing the volume of the water cycle. It might also cause anoxic events in the oceans (see below).
Global warming as a cause of mass extinction is supported by several recent studies.[36]
The most dramatic example of sustained warming is the Paleocene-Eocene Thermal Maximum, which was associated with one of the smaller mass extinctions. It has also been suggested to have caused the Triassic-Jurassic extinction event, during which 20% of all marine families went extinct. Furthermore, the Permian–Triassic extinction event has been suggested to have been caused by warming. [37][38][39]
Clathrate gun hypothesis
Main article: Clathrate Gun Hypothesis
Clathrates are composites in which a lattice of one substance forms a cage round another. Methane clathrates (in which water molecules are the cage) form on continental shelves. These clathrates are likely to break up rapidly and release the methane if the temperature rises quickly or the pressure on them drops quickly — for example in response to sudden global warming or a sudden drop in sea level or even earthquakes. Methane is a much more powerful greenhouse gas than carbon dioxide, so a methane eruption ("clathrate gun") could cause rapid global warming or make it much more severe if the eruption was itself caused by global warming.
The most likely signature of such a methane eruption would be a sudden decrease in the ratio of carbon-13 to carbon-12 in sediments, since methane clathrates are low in carbon-13; but the change would have to be very large, as other events can also reduce the percentage of carbon-13.[40]
It has been suggested that "clathrate gun" methane eruptions were involved in the end-Permian extinction ("the Great Dying") and in the Paleocene-Eocene Thermal Maximum, which was associated with one of the smaller mass extinctions.
Anoxic events
Anoxic events are situations in which the upper and even the middle layers of the ocean become deficient or totally lacking in oxygen. Their causes are complex and controversial, but all known instances are associated with severe and sustained global warming, mostly caused by massive sustained volcanism.
It has been suggested that anoxic events caused or contributed to the late Devonian, Permian-Triassic and Triassic-Jurassic extinctions. On the other hand, there are widespread black shale beds from the mid-Cretaceous which indicate anoxic events but are not associated with mass extinctions.
Hydrogen sulfide emissions from the seas
Kump, Pavlov and Arthur (2005) have proposed that during the Permian-Triassic extinction event the warming also upset the oceanic balance between photosynthesising plankton and deep-water sulfate-reducing bacteria, causing massive emissions of hydrogen sulfide which poisoned life on both land and sea and severely weakened the ozone layer, exposing much of the life that still remained to fatal levels of UV radiation.[41][42][43]
Oceanic overturn
Oceanic overturn is a disruption of thermo-haline circulation which lets surface water (which is more saline than deep water because of evaporation) sink straight down, bringing anoxic deep water to the surface and therefore killing most of the oxygen-breathing organisms which inhabit the surface and middle depths. It may occur either at the beginning or the end of a glaciation, although an overturn at the start of a glaciation is more dangerous because the preceding warm period will have created a larger volume of anoxic water.[44]
Unlike other oceanic catastrophes such as regressions (sea-level falls) and anoxic events, overturns do not leave easily-identified "signatures" in rocks and are theoretical consequences of researchers' conclusions about other climatic and marine events.
It has been suggested that oceanic overturn caused or contributed to the late Devonian and Permian-Triassic extinctions.
A nearby nova, supernova or gamma ray burst
A nearby gamma ray burst (fewer than 6000 light years away) could sufficiently irradiate the surface of Earth to kill organisms living there and destroy the ozone layer in the process. From statistical arguments, approximately 1 gamma ray burst would be expected to occur close to Earth in the last 540 million years. A proposal that a supernova or gamma ray burst had caused a mass extinction would also have to be backed up by astronomical evidence of such an explosion at the right place and time.
It has been suggested that a supernova or gamma ray burst caused the End-Ordovician extinction.
Continental drift
Movement of the continents into some configurations can cause or contribute to extinctions in several ways: by initiating or ending ice ages; by changing ocean and wind currents and thus altering climate; by opening seaways or land bridges which expose previously isolated species to competition for which they are poorly-adapted (for example the extinction of most American marsupials after the creation of a land bridge between North and South America). Occasionally continental drift creates a super-continent which includes the vast majority of Earth's land area, which in addition to the effects listed above is likely to reduce the total area of continental shelf (the most species-rich part of the ocean) and produce a vast, arid continental interior which may have extreme seasonal variations.
It is widely thought that the creation of the super-continent Pangaea contributed to the End-Permian mass extinction. Pangaea was almost fully formed at the transition from mid-Permian to late-Permian, and the "Marine genus diversity" diagram at the top of this article shows a level of extinction starting at that time which might have qualified for inclusion in the "Big Five" if it were not overshadowed by the "Great Dying" at the end of the Permian.
Plate tectonics
Plate tectonics is the mechanism which drives many of the possible causes of mass extinctions, especially volcanism and continental drift. So it is implicated in many extinctions, but in each case it is necessary to specify which manifestations of plate tectonics were involved.
Other hypotheses
Many other hypotheses have been proposed, such as the spread of a new disease or simple out-competition following an especially successful biological innovation. But all have been rejected, usually for one of the following reasons: they require events or processes for which there is no evidence; they assume mechanisms which are contrary to the available evidence; they are based on other theories which have been rejected or superseded.
Postulated extinction cycles
It has been suggested by several sources that biodiversity and/or extinction events may be influenced by cyclic processes. The best-known hypothesis of extinction events by a cyclic process is the 26M to 30M year cycle in extinctions proposed by Raup and Sepkoski (1986).[45] More recently, Rohde and Muller (2005) have suggested that biodiversity fluctuates primarily on 62 ± 3 million year cycles.[46]
It is difficult to evaluate the validity of such claims except through reduction to statistical arguments about how plausible or implausible it is for the observed data to exhibit a particular pattern, as the causes of most extinction events are still too uncertain to attribute to them any specific cause let alone a recurring one. Much early work in this area also suffered from the poor accuracy of geological dating, where errors often exceed 10M years. However, improvements in radiometric dating have reduced the scale of uncertainty to at most 4M years — theoretically adequate for studying these processes.[verification needed]
While the statistics alone have been judged as sufficiently compelling to warrant publication, it is important to consider processes that might be responsible for a cyclic pattern of extinctions and future work may focus on trying to find evidence of such processes.
Hypothetical companion star to the sun
The physicist Richard A. Muller has produced a number of speculative hypotheses for the regularity of mass extinctions. One is that the extinction cycle could be caused by the orbit of a hypothetical companion star dubbed Nemesis that periodically disturbs the Oort cloud, sending storms of large asteroids and comets towards the Solar System.[47]
Galactic plane oscillations
Muller has also speculated the periodicity of mass extinctions may be related to the solar system's oscillation through the plane of our Milky Way galaxy as it rotates around the galactic centre, with a number of possible hypothesized effects including gravitationally-induced comet showers or periods of intense radiation as the solar system hits the galactic shock wave.[48][49]
Passage through galactic spiral arms
It has also been suggested that extinction events correlate to the passage of the solar system through the spiral arms of the Milky Way. The Earth passes through all four arms every 700 million years, and there is some evidence to suggest a cyclicity of extraterrestrial activity back to 2 billion years ago.[50]
Geological instabilities
Other hypotheses are that geological instabilities allow heat to periodically build up deep in the Earth, which is then released through mantle plumes, periods of major volcanism and active plate tectonics.[verification needed]
See also
Background extinction rate
Doomsday event
Elvis taxon
Endangered species
Impact event
Lazarus taxon
Middle Miocene disruption
Rare species
Signor-Lipps Effect
Snowball Earth
Timeline of extinctions
References
Bibliography
Cowen, R. (1999). "The History of Life". Blackwell Science. The chapter about extinctions is creproduced at [1]
Richard Leakey and Roger Lewin, 1996, The Sixth Extinction : Patterns of Life and the Future of Humankind, Anchor, ISBN 0-385-46809-1. Excerpt from this book: The Sixth Extinction
Wilson, E.O., 2002, The Future of Life, Vintage (pb), ISBN 0-679-76811-4
Raup, D., and J. Sepkoski (1986). "Periodic extinction of families and genera". Science 231 (4740): 833–836. doi:10.1126/science.11542060. PMID 11542060.
Rohde, R.A. & Muller, R.A. (2005). "Cycles in fossil diversity". Nature 434 (7030): 209–210. doi:10.1038/nature03339.
The Current Mass Extinction Event
Nemesis — Raup and Sepkoski
Richard A. Muller, 1988, Nemesis, Weidenfeld & Nicolson, ISBN 1-55584-173-2
Robert J. Sawyer, 2000, Calculating God, TOR, ISBN 0-812-58035-4
Ward, P.D., (2000) Rivers In Time: The Search for Clues to Earth's Mass Extinctions
Ward, P.D., (2007) Under a Green Sky: Global Warming, the Mass Extinctions of the Past, and What They Can Tell Us About Our Future (2007) ISBN 9780061137921 0061137928
Phil Berardelli, Of Cosmic Rays and Dangerous Days at ScienceNOW, August 1 2007.
Notes
^ Bambach, R.K.; Knoll, A.H.; Wang, S.C. (December 2004), "Origination, extinction, and mass depletions of marine diversity", Paleobiology 30 (4): 522–542, doi:10.1666/0094-8373(2004)030<0522:OEAMDO>2.0.CO;2, http://findarticles.com/p/articles/mi_qa4067/is_200410/ai_n9458414/pg_1
^ a b Raup, D. & Sepkoski, J. (1982). "Mass extinctions in the marine fossil record". Science 215: 1501–1503. doi:10.1126/science.215.4539.1501. PMID 17788674.
^ Morell, V., and Lanting, F., 1999. "The Sixth Extintion," National Geographic Magazine, February.
^ American Museum of Natural History. "National Survey Reveals Biodiversity Crisis - Scientific Experts Believe We are in the Midst of the Fastest Mass Extinction in Earth's History". URL accessed September 20, 2006.
^ Eldredge, Niles (June 2001). "The Sixth Extinction". ActionBioscience.org. http://www.actionbioscience.org/newfrontiers/eldredge2.html. Retrieved on 2006-03-17.
^ Regan, H.M.; Lupia, R; Drinnan, A.N.; Burgman, M.A. (2001), "The Currency and Tempo of Extinction", The American Naturalist (University of Chicago Press) 157: 1–10, doi:10.1086/317005
^ a b c d e "extinction". Math.ucr.edu. http://math.ucr.edu/home/baez/extinction. Retrieved on 2008-11-09.
^ Sahney S & Benton MJ (2008). "Recovery from the most profound mass extinction of all time". Proceedings of the Royal Society: Biological 275 (759).
^ Sole, R. V., and Newman, M., 2002. "Extinctions and Biodiversity in the Fossil Record - Volume Two, The earth system: biological and ecological dimensions of global environment change" pp. 297-391, Encyclopedia of Global Enviromental Change John Wilely & Sons.
^ Smith, A.; A. McGowan (2005). "Cyclicity in the fossil record mirrors rock outcrop area". Biology Letters 1 (4): 443–445. doi:10.1098/rsbl.2005.0345.
^ ANDREW B. SMITH, ALISTAIR J. McGOWAN (July 2007). "The Shape Of The Phanerozoic Marine Palaeodiversity Curve: How Much Can Be Predicted From The Sedimentary Rock Record Of Western Europe?". Palaeontology 50 (4): 765–774. doi:10.1111/j.1475-4983.2007.00693.x.
^ Partial list from Image:Extinction Intensity.png
^ Benton, M.J. (2004). "6. Reptiles Of The Triassic". Vertebrate Palaeontology. Blackwell. http://www.blackwellpublishing.com/book.asp?ref=0632056371.
^ Van Valkenburgh, B. (1999). "Major patterns in the history of carnivorous mammals". Annual Review of Earth and Planetary Sciences 26: 463–493. doi:10.1146/annurev.earth.27.1.463. http://arjournals.annualreviews.org/doi/abs/10.1146/annurev.earth.27.1.463.
^ Jablonski, D. (2002). "Survival without recovery after mass extinctions". PNAS 99 (12): 8139–8144. doi:10.1073/pnas.102163299. PMID 12060760.
^ Arens, Nan Crystal (2008). "Press-pulse: a general theory of mass extinction?". Paleobiology 34: 456. doi:10.1666/07034.1.
^ a b c Wang, Steve C. (2008). "Adjusting global extinction rates to account for taxonomic susceptibility". Paleobiology 34: 434. doi:10.1666/07060.1.
^ MacLeod, Norman (2001-01-06). "Extinction!". http://www.firstscience.com/home/articles/earth/extinction-page-3-1_1258.html.
^ Martin, R.E. (1995). "Cyclic and secular variation in microfossil biomineralization: clues to the biogeochemical evolution of Phanerozoic oceans". Global and Planetary Change 11 (1): 1. doi:10.1016/0921-8181(94)00011-2.
^ Martin, R.E. (1996). "Secular increase in nutrient levels through the Phanerozoic: Implications for productivity, biomass, and diversity of the marine biosphere". Palaios 11: 209–219. doi:10.2307/3515230.
^ Arens, Nan Crystal (2008). "Press-pulse: a general theory of mass extinction?". Paleobiology 34: 456. doi:10.1666/07034.1.
^ Marshall, C.R.; Ward, P.D. (1996). "Sudden and Gradual Molluscan Extinctions in the Latest Cretaceous of Western European Tethys". Science 274: 1360–1363. doi:10.1126/science.274.5291.1360. http://www.sciencemag.org/cgi/content/full/274/5291/1360?ijkey=ea611116afd7f95233c7b9b1451b6f16702ed11e.
^ Arens, N.C. and West, I.D. (2006). "Press/Pulse: A General Theory of Mass Extinction?"" 'GSA Conference paper' Abstract
^ MacLeod, N (2001-01-06). "Extinction!". http://www.firstscience.com/home/articles/earth/extinction-page-3-1_1258.html.
^ Courtillot, V., Jaeger, J-J., Yang, Z., Féraud, G., Hofmann, C. (1996). "The influence of continental flood basalts on mass extinctions: where do we stand?" in Ryder, G., Fastovsky, D., and Gartner, S, eds. "The Cretaceous-Tertiary event and other catastrophes in earth history". The Geological Society of America, Special Paper 307, 513-525.
^ Hallam, A. (1992). "Phanerozoic sea-level changes". New York; Columbia University Press.
^ Grieve, R., Rupert, J., Smith, J., Therriault, A. (1996). "The record of terrestrial impact cratering". GSA Today 5: 193-195
^ The earliest known flood basalt event is the one which produced the Siberian Traps and is associated with the end-Permian extinction.
^ a b Some of the extinctions associated with flood basalts and sea-level falls were significantly smaller than the "major" extinctions, but still much greater than the background extinction level.
^ Wignall, P.B. (2001), "Large igneous provinces and mass extinctions", Earth-Science Reviews vol. 53 issues 1-2 pp 1-33
^ http://park.org/Canada/Museum/extinction/cretcause.html Speculated Causes of the End-Cretaceous Extinction]
^ What was the Permian–Triassic Extinction Event?
^ What is the Triassic-Jurassic Extinction Event?
^ Peters, S.E. (2008/06/15/online). "Environmental determinants of extinction selectivity in the fossil record". Nature 454: 626. doi:10.1038/nature07032.
^ Newswise: Ebb and Flow of the Sea Drives World's Big Extinction Events Retrieved on June 15, 2008.
^ Mayhew, Peter J.; Gareth B. Jenkins, Timothy G. Benton (January 07, 2008). "A long-term association between global temperature and biodiversity, origination and extinction in the fossil record". Proceedings of the Royal Society B: Biological Sciences. 275 (1630): 47–53. doi:10.1098/rspb.2007.1302. http://journals.royalsociety.org/content/3x081w5n5358qj01. Retrieved on 2009-02-04.
^ Knoll, A. H.; Bambach, Canfield, Grotzinger (26 July 1996). "Fossil record supports evidence of impending mass extinction". Science 273: 452–457. doi:10.1126/science.273.5274.452. PMID 8662528. http://www.sciencemag.org/cgi/content/abstract/273/5274/452. Retrieved on 2009-02-04.
^ Ward, Peter D.; Jennifer Botha, Roger Buick, Michiel O. De Kock, Douglas H. Erwin, Geoffrey H. Garrison, Joseph L. Kirschvink, Roger Smith (4 February 2005). "Abrupt and Gradual Extinction Among Late Permian Land Vertebrates in the Karoo Basin, South Africa". Science 307 (5710): 709–714. doi:10.1126/science.1107068. http://www.sciencemag.org/cgi/content/full/307/5710/709. Retrieved on 2009-02-04.
^ Kiehl, Jeffrey T.; Christine A. Shields (September 2005). "Climate simulation of the latest Permian: Implications for mass extinction". Geology 33 (9): 757–760. doi:10.1130/G21654.1. http://geology.geoscienceworld.org/cgi/content/abstract/33/9/757. Retrieved on 2009-02-04.
^ Hecht, J (2002-03-26). "Methane prime suspect for greatest mass extinction". New Scientist. http://www.newscientist.com/article.ns?id=dn2088.
^ Berner, R.A., and Ward, P.D. (2004). "Positive Reinforcement, H2S, and the Permo-Triassic Extinction: Comment and Reply" describes possible positive feedback loops in the catastrophic release of hydrogen sulfide proposed by Kump, Pavlov and Arthur (2005).
^ Kump, L.R., Pavlov, A., and Arthur, M.A. (2005). "Massive release of hydrogen sulfide to the surface ocean and atmosphere during intervals of oceanic anoxia". Geology v. 33, p.397–400. Abstract. Summarised by Ward (2006).
^ Ward, P.D. (2006). "Impact from the Deep". Scientific American October 2006.
^ Wilde, P; Berry, W.B.N. (1984), "Destabilization of the oceanic density structure and its significance to marine "extinction" events", Palaeogeography, Palaeoclimatology, Palaeaecology 48: 143–162, doi:10.1016/0031-0182(84)90041-5, http://www.marscigrp.org/ppp84.html
^ Raup, D.M.; Sepkoski, J.J. (1984-02-01). "Periodicity of Extinctions in the Geologic Past". Proceedings of the National Academy of Sciences 81 (3): 801–805. doi:10.1073/pnas.81.3.801. PMID 6583680. http://www.pnas.org/cgi/content/abstract/81/3/801. Retrieved on 2007-07-13.
^ Rohde, R.A.; Muller, R.A. (2005). "Cycles in fossil diversity". Nature 434 (7030): 208–10. doi:10.1038/nature03339.
^ R. A. Muller. "Nemesis". Muller.lbl.gov. http://muller.lbl.gov/pages/lbl-nem.htm. Retrieved on 2007-05-19.
^ David Perlman (2005-03-10). "Mass extinction comes every 62 million years, UC physicists discover". http://sfgate.com/cgi-bin/article.cgi?f=/c/a/2005/03/10/MNGFIBN6PO1.DTL. Retrieved on 2007-07-09.
^ Christopher Mims (2007-07-26). "In 12 million years, we're dead". http://blog.sciam.com/index.php?title=in_12_million_years_we_re_dead&more=1&c=1&tb=1&pb=1. Retrieved on 2007-07-09.
^ Michael Gillmana ; Hilary Erenlera (2008). "The galactic cycle of extinction". Astrobiology 7. doi:10.1017/S1473550408004047.
External links
Calculate the effects of an Impact
The Current Mass Extinction Event
Species Alliance (nonprofit organization producing a documentary about Mass Extinction titled "Call of Life: Facing the Mass Extinction)
American Museum of Natural History official statement on the current mass extinction
Interstellar Dust Cloud-induced Extinction Theory
Extinction Level Event in short
The Extinction Website
Nasa's Near Earth Object Program
Fossils Suggest Chaotic Recovery from Mass Extinction — LiveScience.com
Sepkoski's Global Genus Database of Marine Animals — Calculate extinction rates for yourself!
Retrieved from "http://en.wikipedia.org/wiki/Extinction_event"
Categories: Biology | Extinction events | Graphical timelines | Planetary science
Hidden categories: All articles with unsourced statements | Articles with unsourced statements from July 2007 | All pages needing cleanup | Wikipedia articles needing clarification from March 2008 | Articles with unsourced statements from August 2008 | Wikipedia articles needing factual verification from July 2007 | All pages needing factual verification
extinction of an unusually large number of species in a short period.
a sharp drop in the rate of speciation.[1]
Over 99% of species that ever lived are now extinct, but extinction occurs at an uneven rate. Based on the fossil record, the background rate of extinctions on Earth is about two to five taxonomic families of marine invertebrates and vertebrates every million years.[2] Marine fossils are mostly used to measure extinction rates because they are more plentiful and cover a longer time span than fossils of land organisms.
Since life began on earth, several major mass extinctions have significantly exceeded the background extinction rate. The most recent, the Cretaceous–Tertiary extinction event, occurred 65 million years ago, and has attracted more attention than all others as it marks the extinction of nearly all dinosaur species, which were the dominant animal class of the period. In the past 540 million years there have been five major events when over 50% of animal species died. There probably were mass extinctions in the Archean and Proterozoic Eons, but before the Phanerozoic there were no animals with hard body parts to leave a significant fossil record.
Estimates of the number of major mass extinctions in the last 540 million years range from as few as five to more than twenty. These differences stem from the threshold chosen for describing an extinction event as "major", and the data chosen to measure past diversity.
Contents
[hide]
1 Major extinction events
2 Minor events
3 Evolutionary importance
4 Apparent decreasing frequency
5 Causes
5.1 Looking for the causes of particular mass extinctions
5.2 Most widely supported explanations
5.2.1 Flood basalt events
5.2.2 Sea-level falls
5.2.3 Impact events
5.2.4 Sustained and significant global cooling
5.2.5 Sustained and significant global warming
5.2.6 Clathrate gun hypothesis
5.2.7 Anoxic events
5.2.8 Hydrogen sulfide emissions from the seas
5.2.9 Oceanic overturn
5.2.10 A nearby nova, supernova or gamma ray burst
5.2.11 Continental drift
5.2.12 Plate tectonics
5.2.13 Other hypotheses
6 Postulated extinction cycles
6.1 Hypothetical companion star to the sun
6.2 Galactic plane oscillations
6.3 Passage through galactic spiral arms
6.4 Geological instabilities
7 See also
8 References
8.1 Bibliography
8.2 Notes
9 External links
Major extinction events
The classical "Big Five" mass extinctions identified by Jack Sepkoski and David M. Raup in their 1982 paper are widely agreed upon as some of the most significant: End Ordovician, Late Devonian, End Permian, End Triassic, and End Cretaceous.[2][3] The Holocene extinction event is referred to as the Sixth Extinction.
These and a selection of other extinction events are outlined below. The articles about individual mass extinctions describe their effects in more detail and discuss theories about their causes.
Holocene extinction event - nearly 70% of biologists view the present era as part of a mass extinction event, possibly one of the fastest ever, according to a 1998 survey by the American Museum of Natural History.,[4] Some, such as E. O. Wilson of Harvard University, predict that humanity's destruction of the biosphere could cause the extinction of half of all species in the next 100 years. Research and conservation efforts, such as the IUCN's annual "Red List" of threatened species, all point to an ongoing period of enhanced extinction, though some offer much lower rates and hence longer time scales before the onset of catastrophic damage. The extinction of many megafauna near the end of the most recent ice age is also sometimes considered part of the Holocene extinction event.[5] Some paleontologists, however, question whether the available data support a comparison with mass extinctions in the past.[6]
Cretaceous–Tertiary extinction event - 65 Ma at the Cretaceous-Paleogene transition about 17% of all families and 50% of all genera went extinct.[7] (75% species). It ended the reign of dinosaurs and opened the way for mammals and birds to become the dominant land vertebrates. In the seas it reduced the percentage of sessile animals to about 33%. The K/T extinction was rather uneven — some groups of organisms became extinct, some suffered heavy losses and some appear to have been only minimally affected.
Triassic-Jurassic extinction event - 205 Ma at the Triassic-Jurassic transition about 20% of all marine families (55% genera) as well as most non-dinosaurian archosaurs, most therapsids, and the last of the large amphibians were eliminated. 23% of all families and 48% of all genera went extinct.[7]
Permian-Triassic extinction event - 251 Ma at the Permian-Triassic transition, Earth's largest extinction killed 53% of marine families, 84% of marine genera, about 96% of all marine species and an estimated 70% of land species (including plants, insects, and vertebrate animals). 57% of all families and 83% of all genera went extinct.[7] The "Great Dying" had enormous evolutionary significance: on land it ended the dominance of mammal-like reptiles, the recovery of vertebrates took 30 million years[8] but created the opportunity for archosaurs and then dinosaurs to become the dominant land vertebrates; in the seas the percentage of animals that were sessile dropped from 67% to 50%. The whole late Permian was a difficult time for at least marine life — even before the "Great Dying".
Late Devonian extinction 360-375 Ma near the Devonian-Carboniferous transition at the end of the Frasnian Age in the later part(s) of the Devonian Period. A prolonged series of extinctions eliminated about 70% of all species. This extinction event lasted perhaps as long as 20 MY, and there is evidence for a series of extinction pulses within this period. 19% of all families of life and 50% of all genera went extinct.[7]
Ordovician-Silurian extinction events 440-450 Ma at the Ordovician-Silurian transition two events occurred, and together are ranked by many scientists as the second largest of the five major extinctions in Earth's history in terms of percentage of genera that went extinct. 27% of all families and 57% of all genera became extinct.[7]
Cambrian-Ordovician extinction events - 488 Ma a series of mass extinctions at the Cambrian-Ordovician transition eliminated many brachiopods and conodonts and severely reduced the number of trilobite species.
The older the fossil record gets the more difficult it is to read it. This is because:
Older fossils are harder to find because they are usually buried at a considerable depth in the rock.
Dating fossils is difficult.
Productive fossil beds are researched more than unproductive ones, therefore leaving certain periods unresearched.
Prehistoric environmental disturbances can disturb the deposition process.
The preservation of fossils varies on land, but marine fossils tend to be better preserved than their sought after land-based cousins.[9]
It has been suggested that the apparent variations in marine biodiversity may actually be an artifact, with abundance estimates directly related to quantity of rock available for sampling from different time periods.[10] However, statistical analysis shows that this can only account for 50% of the observed pattern,[citation needed] and other evidence (such as fungal spikes)[clarification needed] provides reassurance that most widely accepted extinction events are indeed real. A quantification of the rock exposure of Western Europe does indicate that many of the minor events for which a biological explanation has been sought are most readily explained by sampling bias.[11]
Minor events
Minor extinction events include:[12]
Precambrian
End-Ediacaran extinction - circa 542 Ma
Cambrian Period
End Botomian - circa 517 Ma
Dresbachian
Silurian Period
Ireviken event
Mulde event
Lau event
End Silurian
Carboniferous Period
Middle Carboniferous
Jurassic Period
Toarcian turnover circa 183 Ma
End Jurassic
Cretaceous Period
Aptian extinction circa 117 Ma
Paleogene Period
Eocene-Oligocene extinction event
Neogene Period
Cat gap
Middle Miocene disruption circa 14.5 Ma
Quaternary Period (disputed)
Quaternary extinction event
Extinction events[hide]
view • talk • edit
Minor events↓End-Ediacaran?↓Lau event↓Toarcian turnover↓Aptian↓Middle Miocene
disruption↓Cambro-Ordovician↓Ordo-Silurian↓Late Devonian↓Permo-Triassic↓Triassic–Jurassic↓Cretaceous–Tertiary↓HoloceneMajor events Ediacaran Cambrian Ordovician Silurian Devonian Carboniferous Permian Triassic Jurassic Cretaceous Palæogene Neo-
gene Neoproterozoic Palæozoic Mesozoic Cenozoic | -600| -550| -500| -450| -400| -350| -300| -250| -200| -150| -100| -50| 0
Millions of years before present
Evolutionary importance
Mass extinctions have sometimes accelerated the evolution of life on earth. When dominance of particular ecological niches passes from one group of organisms to another, it is rarely because the new dominant group is "superior" to the old and usually because an extinction event eliminates the old dominant group and makes way for the new one.[13][14]
For example mammaliformes ("almost mammals") and then mammals existed throughout the reign of the dinosaurs, but could not compete for the large terrestrial vertebrate niches which dinosaurs monopolized. The end-Cretaceous mass extinction removed the non-avian dinosaurs and made it possible for mammals to expand into the large terrestrial vertebrate niches.
Another point of view put forward in the Escalation hypothesis predicts that species in ecological niches with more organism-to-organism conflict will be less likely to survive extinctions. This is because the very traits that keep a species numerous and viable under fairly static conditions become a burden once population levels fall among competing organisms during the dynamics of an extinction event.
Furthermore, many groups which survive mass extinctions do not recover in numbers or diversity, and many of these go into long-term decline, and these are often referred to as "Dead Clades Walking".[15] So analysing extinctions in terms of "what died and what survived" often fails to tell the full story.
Apparent decreasing frequency
All genera"Well-defined" generaTrend line"Big Five" mass extinctionsOther mass extinctionsMillion years agoThousands of generaPhanerozoic biodiversity as shown by the fossil recordThe gaps between mass extinctions appear to be becoming longer, while the average and background rates of extinction are decreasing. Mass extinctions are thought to result when a long-term stress is compounded by a short term shock.[16] Over the course of the Phanerozoic, individual taxa appear to be less likely to become extinct at any time,[17] which may reflect more robust food webs as well as less extinction-prone species and other factors such as continental distribution.[17] However the taxonomic susceptibility to extinction does not appear to make mass extinctions more or less probable.[17]
The idea that mass extinctions are becoming less frequent is rather speculative – from a statistical point of view a sample of about 10 extinction events is too small to be a reliable sign of any actual trend. But the average and background rates of extinction are based on hundreds of samples over a period of 550M years, so the apparent decrease in these rates is statistically significant and needs to be explained.
Both of these phenomena could be explained in one or more ways:[18]
Reasonably complete fossils are very rare, most extinct organisms are represented only by partial fossils, and complete fossils are rarest in the oldest rocks. So paleontologists have mistakenly assigned parts of the same organism to different genera which were often defined solely to accommodate these finds (an example is the story of Anomalocaris). The risk of this mistake is higher for older fossils because these are often unlike parts of any living organism. Many of the "superfluous" genera are represented by fragments which are not found again and the "superfluous" genera appear to become extinct very quickly.
Martin (1994, 1996) has argued that the oceans have become more hospitable to life over the last 500M years and less vulnerable to mass extinctions: dissolved oxygen became more widespread and penetrated to greater depths; the development of life on land reduced the run-off of nutrients and hence the risk of eutrophication and anoxic events; and marine ecosystems became more diversified so that food chains were less likely to be disrupted.[19][20]
Causes
There is still debate about the causes of all mass extinctions before the Holocene. In general, large extinctions may result when a biosphere under long-term stress undergoes a short-term shock.[21]
Looking for the causes of particular mass extinctions
A good theory for a particular mass extinction should: (i) explain all of the losses, not just focus on a few groups (such as dinosaurs); (ii) explain why particular groups of organisms died out and why others survived; (iii) provide mechanisms which are strong enough to cause a mass extinction but not a total extinction; (iv) be based on events or processes that can be shown to have happened, not just inferred from the extinction.
It may be necessary to consider combinations of causes. For example the marine aspect of the end-Cretaceous extinction appears to have been caused by several processes which partially overlapped in time and may have had different levels of significance in different parts of the world.[22]
Arens and West (2006) proposed a "press / pulse" model in which mass extinctions generally require two types of cause: long-term pressure on the eco-system ("press") and a sudden catastrophe ("pulse") towards the end of the period of pressure.[23] Their statistical analysis of marine extinction rates throughout the Phanerozoic suggested that neither long-term pressure alone nor a catastrophe alone was sufficient to cause a significant increase in the extinction rate.
Most widely supported explanations
Macleod (2001)[24] summarized the relationship between mass extinctions and events which are most often cited as causes of mass extinctions, using data from Courtillot et al. (1996),[25] Hallam (1992)[26] and Grieve et al. (1996):[27]
Flood basalt events: 11 occurrences, all associated with significant extinctions[28][29] But Wignall (2001) concluded that only 5 of the major extinctions coincided with flood basalt eruptions and that the main phase of extinctions started before the eruptions.[30]
Sea-level falls: 12, of which 7 were associated with significant extinctions.[29]
Asteroid impacts producing craters over 100km wide: one, associated with one mass extinction.
Asteroid impacts producing craters less than 100km wide: over 50, the great majority not associated with significant extinctions.
The most commonly suggested causes of mass extinctions are listed below.
Flood basalt events
The formation of large igneous provinces by flood basalt events could have:
produced dust and particulate aerosols which inhibited photosynthesis and thus caused food chains to collapse both on land and at sea
emitted sulfur oxides which were precipitated as acid rain and poisoned many organisms, contributing further to the collapse of food chains
emitted carbon dioxide and thus possibly causing sustained global warming once the dust and particulate aerosols dissipated.
Flood basalt events occur as pulses of activity punctuated by dormant periods. As a result they are likely to cause the climate to oscillate between cooling and warming, but with an overall trend towards warming as the carbon dioxide they emit can stay in the atmosphere for hundreds of years.
It is speculated that Massive volcanism caused or contributed to the End-Cretaceous, End-Permian, and End Triassic extinctions. [31] [32] [33]
Sea-level falls
These are often clearly marked by world-wide sequences of contemporaneous sediments which show all or part of a transition from sea-bed to tidal zone to beach to dry land - and where there is no evidence that the rocks in the relevant areas were raised by geological processes such as orogeny. Sea-level falls could reduce the continental shelf area (the most productive part of the oceans) sufficiently to cause a marine mass extinction, and could disrupt weather patterns enough to cause extinctions on land. But sea-level falls are very probably the result of other events, such as sustained global cooling or the sinking of the mid-ocean ridges.
Sea-level falls are associated with most of the mass extinctions, including all of the "Big Five" — End-Ordovician, Late Devonian, End-Permian, End-Triassic, and End-Cretaceous.
A study, published in the journal Nature (online June 15, 2008) established a relationship between the speed of mass extinction events and changes in sea level and sediment.[34] The study suggests changes in ocean environments related to sea level exert a driving influence on rates of extinction, and generally determine the composition of life in the oceans.[35]
Impact events
The impact of a sufficiently large asteroid or comet could have caused food chains to collapse both on land and at sea by producing dust and particulate aerosols and thus inhibiting photosynthesis. Impacts on sulfur-rich rocks could have emitted sulfur oxides precipitating as poisonous acid rain, contributing further to the collapse of food chains. Such impacts could also have caused megatsunamis and / or global forest fires, but evidence for these events has been difficult to find.[citation needed]
Only the Cretaceous–Tertiary extinction event is associated with strong evidence of such an impact, but that impact is easily the largest for which there is strong evidence.
Sustained and significant global cooling
Sustained global cooling could kill many polar and temperate species and force others to migrate towards the equator; reduce the area available for tropical species; often make the Earth's climate more arid on average, mainly by locking up more of the planet's water in ice and snow. The glaciation cycles of the current ice age are believed to have had only a very mild impact on biodiversity, so the mere existence of a significant cooling is not sufficient on its own to explain a mass extinction.
It has been suggested that global cooling caused or contributed to the End-Ordovician, Permian-Triassic, Late Devonian extinctions, and possibly others. Sustained global cooling is distinguished from the temporary climatic effects of flood basalt events or impacts.
Sustained and significant global warming
This would have the opposite effects: expand the area available for tropical species; kill temperate species or force them to migrate towards the poles; possibly cause severe extinctions of polar species; often make the Earth's climate wetter on average, mainly by melting ice and snow and thus increasing the volume of the water cycle. It might also cause anoxic events in the oceans (see below).
Global warming as a cause of mass extinction is supported by several recent studies.[36]
The most dramatic example of sustained warming is the Paleocene-Eocene Thermal Maximum, which was associated with one of the smaller mass extinctions. It has also been suggested to have caused the Triassic-Jurassic extinction event, during which 20% of all marine families went extinct. Furthermore, the Permian–Triassic extinction event has been suggested to have been caused by warming. [37][38][39]
Clathrate gun hypothesis
Main article: Clathrate Gun Hypothesis
Clathrates are composites in which a lattice of one substance forms a cage round another. Methane clathrates (in which water molecules are the cage) form on continental shelves. These clathrates are likely to break up rapidly and release the methane if the temperature rises quickly or the pressure on them drops quickly — for example in response to sudden global warming or a sudden drop in sea level or even earthquakes. Methane is a much more powerful greenhouse gas than carbon dioxide, so a methane eruption ("clathrate gun") could cause rapid global warming or make it much more severe if the eruption was itself caused by global warming.
The most likely signature of such a methane eruption would be a sudden decrease in the ratio of carbon-13 to carbon-12 in sediments, since methane clathrates are low in carbon-13; but the change would have to be very large, as other events can also reduce the percentage of carbon-13.[40]
It has been suggested that "clathrate gun" methane eruptions were involved in the end-Permian extinction ("the Great Dying") and in the Paleocene-Eocene Thermal Maximum, which was associated with one of the smaller mass extinctions.
Anoxic events
Anoxic events are situations in which the upper and even the middle layers of the ocean become deficient or totally lacking in oxygen. Their causes are complex and controversial, but all known instances are associated with severe and sustained global warming, mostly caused by massive sustained volcanism.
It has been suggested that anoxic events caused or contributed to the late Devonian, Permian-Triassic and Triassic-Jurassic extinctions. On the other hand, there are widespread black shale beds from the mid-Cretaceous which indicate anoxic events but are not associated with mass extinctions.
Hydrogen sulfide emissions from the seas
Kump, Pavlov and Arthur (2005) have proposed that during the Permian-Triassic extinction event the warming also upset the oceanic balance between photosynthesising plankton and deep-water sulfate-reducing bacteria, causing massive emissions of hydrogen sulfide which poisoned life on both land and sea and severely weakened the ozone layer, exposing much of the life that still remained to fatal levels of UV radiation.[41][42][43]
Oceanic overturn
Oceanic overturn is a disruption of thermo-haline circulation which lets surface water (which is more saline than deep water because of evaporation) sink straight down, bringing anoxic deep water to the surface and therefore killing most of the oxygen-breathing organisms which inhabit the surface and middle depths. It may occur either at the beginning or the end of a glaciation, although an overturn at the start of a glaciation is more dangerous because the preceding warm period will have created a larger volume of anoxic water.[44]
Unlike other oceanic catastrophes such as regressions (sea-level falls) and anoxic events, overturns do not leave easily-identified "signatures" in rocks and are theoretical consequences of researchers' conclusions about other climatic and marine events.
It has been suggested that oceanic overturn caused or contributed to the late Devonian and Permian-Triassic extinctions.
A nearby nova, supernova or gamma ray burst
A nearby gamma ray burst (fewer than 6000 light years away) could sufficiently irradiate the surface of Earth to kill organisms living there and destroy the ozone layer in the process. From statistical arguments, approximately 1 gamma ray burst would be expected to occur close to Earth in the last 540 million years. A proposal that a supernova or gamma ray burst had caused a mass extinction would also have to be backed up by astronomical evidence of such an explosion at the right place and time.
It has been suggested that a supernova or gamma ray burst caused the End-Ordovician extinction.
Continental drift
Movement of the continents into some configurations can cause or contribute to extinctions in several ways: by initiating or ending ice ages; by changing ocean and wind currents and thus altering climate; by opening seaways or land bridges which expose previously isolated species to competition for which they are poorly-adapted (for example the extinction of most American marsupials after the creation of a land bridge between North and South America). Occasionally continental drift creates a super-continent which includes the vast majority of Earth's land area, which in addition to the effects listed above is likely to reduce the total area of continental shelf (the most species-rich part of the ocean) and produce a vast, arid continental interior which may have extreme seasonal variations.
It is widely thought that the creation of the super-continent Pangaea contributed to the End-Permian mass extinction. Pangaea was almost fully formed at the transition from mid-Permian to late-Permian, and the "Marine genus diversity" diagram at the top of this article shows a level of extinction starting at that time which might have qualified for inclusion in the "Big Five" if it were not overshadowed by the "Great Dying" at the end of the Permian.
Plate tectonics
Plate tectonics is the mechanism which drives many of the possible causes of mass extinctions, especially volcanism and continental drift. So it is implicated in many extinctions, but in each case it is necessary to specify which manifestations of plate tectonics were involved.
Other hypotheses
Many other hypotheses have been proposed, such as the spread of a new disease or simple out-competition following an especially successful biological innovation. But all have been rejected, usually for one of the following reasons: they require events or processes for which there is no evidence; they assume mechanisms which are contrary to the available evidence; they are based on other theories which have been rejected or superseded.
Postulated extinction cycles
It has been suggested by several sources that biodiversity and/or extinction events may be influenced by cyclic processes. The best-known hypothesis of extinction events by a cyclic process is the 26M to 30M year cycle in extinctions proposed by Raup and Sepkoski (1986).[45] More recently, Rohde and Muller (2005) have suggested that biodiversity fluctuates primarily on 62 ± 3 million year cycles.[46]
It is difficult to evaluate the validity of such claims except through reduction to statistical arguments about how plausible or implausible it is for the observed data to exhibit a particular pattern, as the causes of most extinction events are still too uncertain to attribute to them any specific cause let alone a recurring one. Much early work in this area also suffered from the poor accuracy of geological dating, where errors often exceed 10M years. However, improvements in radiometric dating have reduced the scale of uncertainty to at most 4M years — theoretically adequate for studying these processes.[verification needed]
While the statistics alone have been judged as sufficiently compelling to warrant publication, it is important to consider processes that might be responsible for a cyclic pattern of extinctions and future work may focus on trying to find evidence of such processes.
Hypothetical companion star to the sun
The physicist Richard A. Muller has produced a number of speculative hypotheses for the regularity of mass extinctions. One is that the extinction cycle could be caused by the orbit of a hypothetical companion star dubbed Nemesis that periodically disturbs the Oort cloud, sending storms of large asteroids and comets towards the Solar System.[47]
Galactic plane oscillations
Muller has also speculated the periodicity of mass extinctions may be related to the solar system's oscillation through the plane of our Milky Way galaxy as it rotates around the galactic centre, with a number of possible hypothesized effects including gravitationally-induced comet showers or periods of intense radiation as the solar system hits the galactic shock wave.[48][49]
Passage through galactic spiral arms
It has also been suggested that extinction events correlate to the passage of the solar system through the spiral arms of the Milky Way. The Earth passes through all four arms every 700 million years, and there is some evidence to suggest a cyclicity of extraterrestrial activity back to 2 billion years ago.[50]
Geological instabilities
Other hypotheses are that geological instabilities allow heat to periodically build up deep in the Earth, which is then released through mantle plumes, periods of major volcanism and active plate tectonics.[verification needed]
See also
Background extinction rate
Doomsday event
Elvis taxon
Endangered species
Impact event
Lazarus taxon
Middle Miocene disruption
Rare species
Signor-Lipps Effect
Snowball Earth
Timeline of extinctions
References
Bibliography
Cowen, R. (1999). "The History of Life". Blackwell Science. The chapter about extinctions is creproduced at [1]
Richard Leakey and Roger Lewin, 1996, The Sixth Extinction : Patterns of Life and the Future of Humankind, Anchor, ISBN 0-385-46809-1. Excerpt from this book: The Sixth Extinction
Wilson, E.O., 2002, The Future of Life, Vintage (pb), ISBN 0-679-76811-4
Raup, D., and J. Sepkoski (1986). "Periodic extinction of families and genera". Science 231 (4740): 833–836. doi:10.1126/science.11542060. PMID 11542060.
Rohde, R.A. & Muller, R.A. (2005). "Cycles in fossil diversity". Nature 434 (7030): 209–210. doi:10.1038/nature03339.
The Current Mass Extinction Event
Nemesis — Raup and Sepkoski
Richard A. Muller, 1988, Nemesis, Weidenfeld & Nicolson, ISBN 1-55584-173-2
Robert J. Sawyer, 2000, Calculating God, TOR, ISBN 0-812-58035-4
Ward, P.D., (2000) Rivers In Time: The Search for Clues to Earth's Mass Extinctions
Ward, P.D., (2007) Under a Green Sky: Global Warming, the Mass Extinctions of the Past, and What They Can Tell Us About Our Future (2007) ISBN 9780061137921 0061137928
Phil Berardelli, Of Cosmic Rays and Dangerous Days at ScienceNOW, August 1 2007.
Notes
^ Bambach, R.K.; Knoll, A.H.; Wang, S.C. (December 2004), "Origination, extinction, and mass depletions of marine diversity", Paleobiology 30 (4): 522–542, doi:10.1666/0094-8373(2004)030<0522:OEAMDO>2.0.CO;2, http://findarticles.com/p/articles/mi_qa4067/is_200410/ai_n9458414/pg_1
^ a b Raup, D. & Sepkoski, J. (1982). "Mass extinctions in the marine fossil record". Science 215: 1501–1503. doi:10.1126/science.215.4539.1501. PMID 17788674.
^ Morell, V., and Lanting, F., 1999. "The Sixth Extintion," National Geographic Magazine, February.
^ American Museum of Natural History. "National Survey Reveals Biodiversity Crisis - Scientific Experts Believe We are in the Midst of the Fastest Mass Extinction in Earth's History". URL accessed September 20, 2006.
^ Eldredge, Niles (June 2001). "The Sixth Extinction". ActionBioscience.org. http://www.actionbioscience.org/newfrontiers/eldredge2.html. Retrieved on 2006-03-17.
^ Regan, H.M.; Lupia, R; Drinnan, A.N.; Burgman, M.A. (2001), "The Currency and Tempo of Extinction", The American Naturalist (University of Chicago Press) 157: 1–10, doi:10.1086/317005
^ a b c d e "extinction". Math.ucr.edu. http://math.ucr.edu/home/baez/extinction. Retrieved on 2008-11-09.
^ Sahney S & Benton MJ (2008). "Recovery from the most profound mass extinction of all time". Proceedings of the Royal Society: Biological 275 (759).
^ Sole, R. V., and Newman, M., 2002. "Extinctions and Biodiversity in the Fossil Record - Volume Two, The earth system: biological and ecological dimensions of global environment change" pp. 297-391, Encyclopedia of Global Enviromental Change John Wilely & Sons.
^ Smith, A.; A. McGowan (2005). "Cyclicity in the fossil record mirrors rock outcrop area". Biology Letters 1 (4): 443–445. doi:10.1098/rsbl.2005.0345.
^ ANDREW B. SMITH, ALISTAIR J. McGOWAN (July 2007). "The Shape Of The Phanerozoic Marine Palaeodiversity Curve: How Much Can Be Predicted From The Sedimentary Rock Record Of Western Europe?". Palaeontology 50 (4): 765–774. doi:10.1111/j.1475-4983.2007.00693.x.
^ Partial list from Image:Extinction Intensity.png
^ Benton, M.J. (2004). "6. Reptiles Of The Triassic". Vertebrate Palaeontology. Blackwell. http://www.blackwellpublishing.com/book.asp?ref=0632056371.
^ Van Valkenburgh, B. (1999). "Major patterns in the history of carnivorous mammals". Annual Review of Earth and Planetary Sciences 26: 463–493. doi:10.1146/annurev.earth.27.1.463. http://arjournals.annualreviews.org/doi/abs/10.1146/annurev.earth.27.1.463.
^ Jablonski, D. (2002). "Survival without recovery after mass extinctions". PNAS 99 (12): 8139–8144. doi:10.1073/pnas.102163299. PMID 12060760.
^ Arens, Nan Crystal (2008). "Press-pulse: a general theory of mass extinction?". Paleobiology 34: 456. doi:10.1666/07034.1.
^ a b c Wang, Steve C. (2008). "Adjusting global extinction rates to account for taxonomic susceptibility". Paleobiology 34: 434. doi:10.1666/07060.1.
^ MacLeod, Norman (2001-01-06). "Extinction!". http://www.firstscience.com/home/articles/earth/extinction-page-3-1_1258.html.
^ Martin, R.E. (1995). "Cyclic and secular variation in microfossil biomineralization: clues to the biogeochemical evolution of Phanerozoic oceans". Global and Planetary Change 11 (1): 1. doi:10.1016/0921-8181(94)00011-2.
^ Martin, R.E. (1996). "Secular increase in nutrient levels through the Phanerozoic: Implications for productivity, biomass, and diversity of the marine biosphere". Palaios 11: 209–219. doi:10.2307/3515230.
^ Arens, Nan Crystal (2008). "Press-pulse: a general theory of mass extinction?". Paleobiology 34: 456. doi:10.1666/07034.1.
^ Marshall, C.R.; Ward, P.D. (1996). "Sudden and Gradual Molluscan Extinctions in the Latest Cretaceous of Western European Tethys". Science 274: 1360–1363. doi:10.1126/science.274.5291.1360. http://www.sciencemag.org/cgi/content/full/274/5291/1360?ijkey=ea611116afd7f95233c7b9b1451b6f16702ed11e.
^ Arens, N.C. and West, I.D. (2006). "Press/Pulse: A General Theory of Mass Extinction?"" 'GSA Conference paper' Abstract
^ MacLeod, N (2001-01-06). "Extinction!". http://www.firstscience.com/home/articles/earth/extinction-page-3-1_1258.html.
^ Courtillot, V., Jaeger, J-J., Yang, Z., Féraud, G., Hofmann, C. (1996). "The influence of continental flood basalts on mass extinctions: where do we stand?" in Ryder, G., Fastovsky, D., and Gartner, S, eds. "The Cretaceous-Tertiary event and other catastrophes in earth history". The Geological Society of America, Special Paper 307, 513-525.
^ Hallam, A. (1992). "Phanerozoic sea-level changes". New York; Columbia University Press.
^ Grieve, R., Rupert, J., Smith, J., Therriault, A. (1996). "The record of terrestrial impact cratering". GSA Today 5: 193-195
^ The earliest known flood basalt event is the one which produced the Siberian Traps and is associated with the end-Permian extinction.
^ a b Some of the extinctions associated with flood basalts and sea-level falls were significantly smaller than the "major" extinctions, but still much greater than the background extinction level.
^ Wignall, P.B. (2001), "Large igneous provinces and mass extinctions", Earth-Science Reviews vol. 53 issues 1-2 pp 1-33
^ http://park.org/Canada/Museum/extinction/cretcause.html Speculated Causes of the End-Cretaceous Extinction]
^ What was the Permian–Triassic Extinction Event?
^ What is the Triassic-Jurassic Extinction Event?
^ Peters, S.E. (2008/06/15/online). "Environmental determinants of extinction selectivity in the fossil record". Nature 454: 626. doi:10.1038/nature07032.
^ Newswise: Ebb and Flow of the Sea Drives World's Big Extinction Events Retrieved on June 15, 2008.
^ Mayhew, Peter J.; Gareth B. Jenkins, Timothy G. Benton (January 07, 2008). "A long-term association between global temperature and biodiversity, origination and extinction in the fossil record". Proceedings of the Royal Society B: Biological Sciences. 275 (1630): 47–53. doi:10.1098/rspb.2007.1302. http://journals.royalsociety.org/content/3x081w5n5358qj01. Retrieved on 2009-02-04.
^ Knoll, A. H.; Bambach, Canfield, Grotzinger (26 July 1996). "Fossil record supports evidence of impending mass extinction". Science 273: 452–457. doi:10.1126/science.273.5274.452. PMID 8662528. http://www.sciencemag.org/cgi/content/abstract/273/5274/452. Retrieved on 2009-02-04.
^ Ward, Peter D.; Jennifer Botha, Roger Buick, Michiel O. De Kock, Douglas H. Erwin, Geoffrey H. Garrison, Joseph L. Kirschvink, Roger Smith (4 February 2005). "Abrupt and Gradual Extinction Among Late Permian Land Vertebrates in the Karoo Basin, South Africa". Science 307 (5710): 709–714. doi:10.1126/science.1107068. http://www.sciencemag.org/cgi/content/full/307/5710/709. Retrieved on 2009-02-04.
^ Kiehl, Jeffrey T.; Christine A. Shields (September 2005). "Climate simulation of the latest Permian: Implications for mass extinction". Geology 33 (9): 757–760. doi:10.1130/G21654.1. http://geology.geoscienceworld.org/cgi/content/abstract/33/9/757. Retrieved on 2009-02-04.
^ Hecht, J (2002-03-26). "Methane prime suspect for greatest mass extinction". New Scientist. http://www.newscientist.com/article.ns?id=dn2088.
^ Berner, R.A., and Ward, P.D. (2004). "Positive Reinforcement, H2S, and the Permo-Triassic Extinction: Comment and Reply" describes possible positive feedback loops in the catastrophic release of hydrogen sulfide proposed by Kump, Pavlov and Arthur (2005).
^ Kump, L.R., Pavlov, A., and Arthur, M.A. (2005). "Massive release of hydrogen sulfide to the surface ocean and atmosphere during intervals of oceanic anoxia". Geology v. 33, p.397–400. Abstract. Summarised by Ward (2006).
^ Ward, P.D. (2006). "Impact from the Deep". Scientific American October 2006.
^ Wilde, P; Berry, W.B.N. (1984), "Destabilization of the oceanic density structure and its significance to marine "extinction" events", Palaeogeography, Palaeoclimatology, Palaeaecology 48: 143–162, doi:10.1016/0031-0182(84)90041-5, http://www.marscigrp.org/ppp84.html
^ Raup, D.M.; Sepkoski, J.J. (1984-02-01). "Periodicity of Extinctions in the Geologic Past". Proceedings of the National Academy of Sciences 81 (3): 801–805. doi:10.1073/pnas.81.3.801. PMID 6583680. http://www.pnas.org/cgi/content/abstract/81/3/801. Retrieved on 2007-07-13.
^ Rohde, R.A.; Muller, R.A. (2005). "Cycles in fossil diversity". Nature 434 (7030): 208–10. doi:10.1038/nature03339.
^ R. A. Muller. "Nemesis". Muller.lbl.gov. http://muller.lbl.gov/pages/lbl-nem.htm. Retrieved on 2007-05-19.
^ David Perlman (2005-03-10). "Mass extinction comes every 62 million years, UC physicists discover". http://sfgate.com/cgi-bin/article.cgi?f=/c/a/2005/03/10/MNGFIBN6PO1.DTL. Retrieved on 2007-07-09.
^ Christopher Mims (2007-07-26). "In 12 million years, we're dead". http://blog.sciam.com/index.php?title=in_12_million_years_we_re_dead&more=1&c=1&tb=1&pb=1. Retrieved on 2007-07-09.
^ Michael Gillmana ; Hilary Erenlera (2008). "The galactic cycle of extinction". Astrobiology 7. doi:10.1017/S1473550408004047.
External links
Calculate the effects of an Impact
The Current Mass Extinction Event
Species Alliance (nonprofit organization producing a documentary about Mass Extinction titled "Call of Life: Facing the Mass Extinction)
American Museum of Natural History official statement on the current mass extinction
Interstellar Dust Cloud-induced Extinction Theory
Extinction Level Event in short
The Extinction Website
Nasa's Near Earth Object Program
Fossils Suggest Chaotic Recovery from Mass Extinction — LiveScience.com
Sepkoski's Global Genus Database of Marine Animals — Calculate extinction rates for yourself!
Retrieved from "http://en.wikipedia.org/wiki/Extinction_event"
Categories: Biology | Extinction events | Graphical timelines | Planetary science
Hidden categories: All articles with unsourced statements | Articles with unsourced statements from July 2007 | All pages needing cleanup | Wikipedia articles needing clarification from March 2008 | Articles with unsourced statements from August 2008 | Wikipedia articles needing factual verification from July 2007 | All pages needing factual verification
nemesis (star)
from wikipedia
You can support Wikipedia by making a tax-deductible donation.Nemesis (star)
From Wikipedia, the free encyclopedia
Jump to: navigation, search
For other uses, see Nemesis.
Artist's conception of Nemesis as a red dwarf seen from a nearby debris field with the Sun visible in the center.Nemesis is a hypothetical red dwarf or brown dwarf star, orbiting the Sun at a distance of about 50,000 to 100,000 AU, somewhat beyond the Oort cloud. This star was originally postulated to exist as part of a hypothesis to explain a perceived cycle of mass extinctions in the geological record.
Contents
[hide]
1 Claimed periodicity of mass extinctions
2 Development of the Nemesis hypotheses
3 Looking for Nemesis
4 Other hypotheses
5 Literary references
6 See also
7 References
8 External links
Claimed periodicity of mass extinctions
In 1984 paleontologists David Raup and Jack Sepkoski published a paper claiming that they had identified a statistical periodicity in extinction rates over the last 250 million years using various forms of time series analysis.[1] They focused on the extinction intensity of fossil families of marine vertebrates, invertebrates, and protozoans, identifying 12 extinction events over the time period in question. The average time interval between extinction events was determined as 26 million years. At the time, two of the identified extinction events (Cretaceous-Tertiary and Late Eocene) could be shown to coincide with large impact events. Although Raup and Sepkoski could not identify the cause of their supposed periodicity, they suggested that there might be a non-terrestrial connection. The challenge to propose a mechanism was quickly addressed by several teams of astronomers.
Development of the Nemesis hypotheses
Two teams of astronomers, Whitmire and Jackson, and Davis, Hut, and Muller, independently published similar hypotheses to explain Raup and Sepkoski's extinction periodicity in the same issue of the journal Nature.[2][3] This hypothesis proposes that the sun may have an as yet undetected companion star in a highly elliptical orbit that periodically disturbs comets in the Oort cloud, causing a large increase in the number of comets visiting the inner solar system with a consequential increase in impact events on Earth. This became known as the Nemesis (or, more colorfully, Death Star) hypothesis.
If it does exist, the exact nature of Nemesis is uncertain. Richard A. Muller suggests that the most likely object is a red dwarf with magnitude between 7 and 12,[4] while Daniel P. Whitmire and Albert A. Jackson argue for a brown dwarf. If a red dwarf, it would undoubtedly already exist in star catalogs, but its true nature would only be detectable by measuring its parallax; due to orbiting the Sun it would have a very low proper motion and would escape detection by proper motion surveys that have found stars like the 9th magnitude Barnard's star.
The last major extinction event was about 5 million years ago, so Muller posits that Nemesis is likely 1-1.5 light years away at present, and even has ideas of what area of the sky it might be in (supported by Yarris, 1987), near Hydra, based on a hypothetical orbit derived from original apogees of a number of atypical long-period comets that describe an orbital arc meeting the specifications of Muller's hypothesis.
Looking for Nemesis
If Nemesis exists, it may be detected by the planned Pan-STARRS or LSST astronomical surveys, or similar future projects. If Nemesis is a brown dwarf, as proposed by Dr. Dan Whitmire and Albert A. Jackson IV, then the upcoming WISE mission (scheduled for November 2009) should easily find it.
Other hypotheses
Matese and Whitman have suggested that the supposed extinction periodicity might be caused by the solar system oscillating across the galactic plane of the Milky Way. These oscillations may lead to gravitational disturbances in the Oort cloud with the same proposed consequences as the orbit of "Nemesis". However, the period of oscillation is not well-constrained observationally, and may differ from the needed 26 million years by as much as 40%.
Literary references
Certain parallels may be drawn between Nemesis and the red star from Anne McCaffrey's Pern books series. Both disturb the Oort cloud and both bring destruction down upon their respective planets.
Larry Niven and Jerry Pournelle also describe such a mechanism in the novel Lucifer's Hammer. Niven commented in his short story collection N-Space that had they named the conceptual dark companion in Lucifer's Hammer, the name "Nemesis" would have been used.
Isaac Asimov's novel Nemesis deals with the repercussions of a future colony being established around a star named Nemesis as a way of escaping an oppressive Earth. While the star in the book is on a course that will take it through the solar system, it is not in orbit around the sun as is the theorized Nemesis.
Piers Anthony makes several 'matter-of-fact' comments on the existence of the Nemesis star, stating it to be a companion star of the Sun, in his Bio of a Space Tyrant series.
Matthew Reilly's novel The Six Sacred Stones deals with a dark companion to the sun that will end all life on the planet unless it is stopped by the accumulation of several artifacts from around the world.
In the Japanese Sailor Moon metaseries by Naoko Takeuchi, the members of the Black Moon Clan, the antagonists of the second major story arc, come from Nemesis.
See also
Brown dwarf
Extinction events
Red dwarf
Stellar classification
Nibiru collision
References
^ Raup, D.M.; Sepkoski, J.J. (1984-02-01). "Periodicity of Extinctions in the Geologic Past". Proceedings of the National Academy of Sciences 81 (3): 801–805. doi:10.1073/pnas.81.3.801. PMID 6583680. http://www.pnas.org/cgi/reprint/81/3/801.pdf. Retrieved on 2007-04-30.
^ Whitmire, D.P.; Jackson, A.A. (1984). "Are periodic mass extinctions driven by a distant solar companion?". Nature 308 (5961): 713–715. doi:10.1038/308713a0.
^ Davis, M.; Hut, P., Muller, R.A. (1984). "Extinction of species by periodic comet showers". Nature 308 (5961): 715–717. doi:10.1038/308715a0.
^ http://muller.lbl.gov/pages/lbl-nem.htm Muller.lbl.gov Retrieved on 05-19-07
External links
Richard A. Muller, Nemesis (Weidenfeld and Nichoson, 1988, OP)
Richard A. Muller, Measurement of the lunar impact record for the past 3.5 billion years, and implications for the Nemesis theory, Geological Society of America Special Paper 356, pp 659-665 (2002).I
Undergraduate lecture by Richard A. Muller where he describes Nemesis Theory
Documentary on Nemesis and Planet X
Robert Roy Britt, Nemesis: Does the Sun Have a 'Companion'?, Space.com, 3 April 2001.
You can support Wikipedia by making a tax-deductible donation.Nemesis (star)
From Wikipedia, the free encyclopedia
Jump to: navigation, search
For other uses, see Nemesis.
Artist's conception of Nemesis as a red dwarf seen from a nearby debris field with the Sun visible in the center.Nemesis is a hypothetical red dwarf or brown dwarf star, orbiting the Sun at a distance of about 50,000 to 100,000 AU, somewhat beyond the Oort cloud. This star was originally postulated to exist as part of a hypothesis to explain a perceived cycle of mass extinctions in the geological record.
Contents
[hide]
1 Claimed periodicity of mass extinctions
2 Development of the Nemesis hypotheses
3 Looking for Nemesis
4 Other hypotheses
5 Literary references
6 See also
7 References
8 External links
Claimed periodicity of mass extinctions
In 1984 paleontologists David Raup and Jack Sepkoski published a paper claiming that they had identified a statistical periodicity in extinction rates over the last 250 million years using various forms of time series analysis.[1] They focused on the extinction intensity of fossil families of marine vertebrates, invertebrates, and protozoans, identifying 12 extinction events over the time period in question. The average time interval between extinction events was determined as 26 million years. At the time, two of the identified extinction events (Cretaceous-Tertiary and Late Eocene) could be shown to coincide with large impact events. Although Raup and Sepkoski could not identify the cause of their supposed periodicity, they suggested that there might be a non-terrestrial connection. The challenge to propose a mechanism was quickly addressed by several teams of astronomers.
Development of the Nemesis hypotheses
Two teams of astronomers, Whitmire and Jackson, and Davis, Hut, and Muller, independently published similar hypotheses to explain Raup and Sepkoski's extinction periodicity in the same issue of the journal Nature.[2][3] This hypothesis proposes that the sun may have an as yet undetected companion star in a highly elliptical orbit that periodically disturbs comets in the Oort cloud, causing a large increase in the number of comets visiting the inner solar system with a consequential increase in impact events on Earth. This became known as the Nemesis (or, more colorfully, Death Star) hypothesis.
If it does exist, the exact nature of Nemesis is uncertain. Richard A. Muller suggests that the most likely object is a red dwarf with magnitude between 7 and 12,[4] while Daniel P. Whitmire and Albert A. Jackson argue for a brown dwarf. If a red dwarf, it would undoubtedly already exist in star catalogs, but its true nature would only be detectable by measuring its parallax; due to orbiting the Sun it would have a very low proper motion and would escape detection by proper motion surveys that have found stars like the 9th magnitude Barnard's star.
The last major extinction event was about 5 million years ago, so Muller posits that Nemesis is likely 1-1.5 light years away at present, and even has ideas of what area of the sky it might be in (supported by Yarris, 1987), near Hydra, based on a hypothetical orbit derived from original apogees of a number of atypical long-period comets that describe an orbital arc meeting the specifications of Muller's hypothesis.
Looking for Nemesis
If Nemesis exists, it may be detected by the planned Pan-STARRS or LSST astronomical surveys, or similar future projects. If Nemesis is a brown dwarf, as proposed by Dr. Dan Whitmire and Albert A. Jackson IV, then the upcoming WISE mission (scheduled for November 2009) should easily find it.
Other hypotheses
Matese and Whitman have suggested that the supposed extinction periodicity might be caused by the solar system oscillating across the galactic plane of the Milky Way. These oscillations may lead to gravitational disturbances in the Oort cloud with the same proposed consequences as the orbit of "Nemesis". However, the period of oscillation is not well-constrained observationally, and may differ from the needed 26 million years by as much as 40%.
Literary references
Certain parallels may be drawn between Nemesis and the red star from Anne McCaffrey's Pern books series. Both disturb the Oort cloud and both bring destruction down upon their respective planets.
Larry Niven and Jerry Pournelle also describe such a mechanism in the novel Lucifer's Hammer. Niven commented in his short story collection N-Space that had they named the conceptual dark companion in Lucifer's Hammer, the name "Nemesis" would have been used.
Isaac Asimov's novel Nemesis deals with the repercussions of a future colony being established around a star named Nemesis as a way of escaping an oppressive Earth. While the star in the book is on a course that will take it through the solar system, it is not in orbit around the sun as is the theorized Nemesis.
Piers Anthony makes several 'matter-of-fact' comments on the existence of the Nemesis star, stating it to be a companion star of the Sun, in his Bio of a Space Tyrant series.
Matthew Reilly's novel The Six Sacred Stones deals with a dark companion to the sun that will end all life on the planet unless it is stopped by the accumulation of several artifacts from around the world.
In the Japanese Sailor Moon metaseries by Naoko Takeuchi, the members of the Black Moon Clan, the antagonists of the second major story arc, come from Nemesis.
See also
Brown dwarf
Extinction events
Red dwarf
Stellar classification
Nibiru collision
References
^ Raup, D.M.; Sepkoski, J.J. (1984-02-01). "Periodicity of Extinctions in the Geologic Past". Proceedings of the National Academy of Sciences 81 (3): 801–805. doi:10.1073/pnas.81.3.801. PMID 6583680. http://www.pnas.org/cgi/reprint/81/3/801.pdf. Retrieved on 2007-04-30.
^ Whitmire, D.P.; Jackson, A.A. (1984). "Are periodic mass extinctions driven by a distant solar companion?". Nature 308 (5961): 713–715. doi:10.1038/308713a0.
^ Davis, M.; Hut, P., Muller, R.A. (1984). "Extinction of species by periodic comet showers". Nature 308 (5961): 715–717. doi:10.1038/308715a0.
^ http://muller.lbl.gov/pages/lbl-nem.htm Muller.lbl.gov Retrieved on 05-19-07
External links
Richard A. Muller, Nemesis (Weidenfeld and Nichoson, 1988, OP)
Richard A. Muller, Measurement of the lunar impact record for the past 3.5 billion years, and implications for the Nemesis theory, Geological Society of America Special Paper 356, pp 659-665 (2002).I
Undergraduate lecture by Richard A. Muller where he describes Nemesis Theory
Documentary on Nemesis and Planet X
Robert Roy Britt, Nemesis: Does the Sun Have a 'Companion'?, Space.com, 3 April 2001.
Sunday, December 7, 2008
Sky burial
Sky burial
From Wikipedia, the free encyclopedia
Jump to: navigation, search
This article is about the Tibetan practice. For the Xinran Xue novel, see Sky Burial.
Drigung Monastery, Tibetan monastery famous for performing sky burials.
Sky burial site, Yerpa Valley
Sky burial or ritual dissection was once a common funerary practice in Tibet wherein a human corpse is cut into small pieces and placed on a mountaintop, exposing it to the elements or the mahabhuta and animals – especially to birds of prey. In Tibetan the practice is known as jhator (Tibetan: བྱ་གཏོར་; Wylie: bya gtor), which literally means, "giving alms to the birds."
The majority of Tibetans adhere to Buddhism, which teaches reincarnation. There is no need to preserve the body, as it is now an empty vessel. Birds may eat it, or nature may let it decompose. So the function of the sky burial is simply the disposal of the remains. In much of Tibet the ground is too hard and rocky to dig a grave, and with fuel and timber scarce, a sky burial is often more practical than cremation.
Additionally, since no fuel, land, or topsoil is consumed, this way of burial is arguably more ecologically friendly than cremation or interment.
Contents
[hide]
* 1 History and development
* 2 Purpose and meaning
* 3 Iconography
* 4 Setting
* 5 Procedure
o 5.1 Participants
o 5.2 Disassembling the body
o 5.3 Vultures
* 6 References
* 7 External links
[edit] History and development
The Tibetan sky-burial practices appear to have evolved out of practical considerations:[1][2][3] a) most of the Tibet is above the tree line, and the scarcity of timber makes cremation economically unfeasible; b) subsurface interment is equally difficult since the active layer is not more than a few centimeters deep, with solid rock or permafrost beneath it. The customs are first recorded in an indigenous 12th century Buddhist treatise known colloquially as the Book of the Dead. Tibetan tantricism appears to have influenced the procedure.[4][5] in that it is designed to destroy all the major bones, which would prevent them being taken for use as tantric ritual implements such as kapalas (skullcups), thigh-bone trumpets, and the like.
[edit] Purpose and meaning
As the name implies, jhator is considered an act of generosity: the deceased and his/her surviving relatives are providing food to sustain living beings. Generosity and compassion for all beings are important virtues or paramita in Buddhism. Although some observers have suggested that jhator is also meant to unite the deceased person with the sky or sacred realm, this does not seem consistent with most of the knowledgeable commentary and eyewitness reports, which indicate that Tibetans believe that at this point life has completely left the body and the body contains nothing more than simple flesh.
The government of the People's Republic of China, which has controlled Tibet since 1950, prohibited the practice (which it considered barbaric) in the 1960s but started to allow it again in the 1980s.[6] Non-Tibetans are usually not permitted to observe it, and direct photography is considered unethical, offensive and is generally forbidden.
A jhator was filmed, with permission from the family, for the documentary Secret Towers of the Himalayas which aired on the Science Channel in Fall 2008. The camera work was deliberately careful to never show the body itself, while documenting the procedure, birds, and tools.
[edit] Iconography
The tradition and custom of the jhator forded Traditional Tibetan medicine and thangka iconography with a particular insight into the interior workings of the human body. Pieces of the human skeleton were employed in ritual tools such as the skullcup, thigh-bone trumpet, etc.
[edit] Setting
A traditional jhator is performed in specified locations in Tibet (and surrounding areas traditionally occupied by Tibetans). Drigung Monastery is one of the three most important jhator sites.
The procedure takes place on a large flat rock long used for the purpose. The charnel ground (durtro) is always higher than its surroundings. It may be very simple, consisting only of the flat rock, or it may be more elaborate, incorporating temples and stupa (chorten in Tibetan).
Relatives may remain nearby during the jhator, possibly in a place where they cannot see it directly. The jhator usually takes place at dawn.
The full jhator procedure (as described below) is elaborate and expensive. Those who cannot afford it simply place their deceased on a high rock where the body decomposes or is eaten by birds and animals.
[edit] Procedure
Accounts from observers vary. The following description is assembled from multiple accounts by observers from the U.S. and Europe. References appear at the end.
[edit] Participants
Prior to the procedure, monks may chant mantra around the body and burn juniper incense – although ceremonial activities often take place on the preceding day.
The work of disassembling of the body may be done by a monk, or, more commonly, by rogyapas ("body-breakers").
All the eyewitness accounts remarked on the fact that the rogyapas did not perform their task with gravity or ceremony, but rather talked and laughed as during any other type of physical labor. According to Buddhist teaching, this makes it easier for the soul of the deceased to move on from the uncertain plane between life and death onto the next life.
[edit] Disassembling the body
In one account, the leading rogyapa cut off the limbs and hacked the body to pieces, handing each part to his assistants, who used rocks to pound the flesh and bones together to a pulp, which they mixed with tsampa (barley flour with tea and yak butter or milk) before the vultures were summoned to eat.
In several accounts, the flesh was stripped from the bones and given to vultures without further preparation; the bones then were broken up with sledgehammers, and usually mixed with tsampa before being given to the vultures. Many rogyapa first feed the bones and cartilage to the vultures, keeping the best flesh until last. After having had their fill of good quality meat, the birds usually fly away - leaving the bones and less favored bits.
In another account, vultures were given the whole body. When only the bones remained, they were broken up with mallets, ground with tsampa, and given to crows and hawks that had waited until the vultures had departed.
Sometimes the internal organs were removed and processed separately, but they too were consumed by birds. The hair is removed from the head and may be simply thrown away; at Drigung it seems at least some hair is kept in a room of the monastery.
None of the eyewitness accounts specifies what kind of knife is used in the jhator. One source states that it is a "ritual flaying knife" or trigu (Sanskrit kartika), but another source expresses skepticism, noting that the trigu is considered a woman's tool (rogyapas seem to be exclusively male).
[edit] Vultures
The species of vulture involved is apparently the "Eurasian Griffon" or "Old World vulture," Order Falconiformes, Family Accipitridae, scientific name Gyps fulvus.
In places where there are several jhator offerings each day, the birds sometimes had to be coaxed to eat, which in one case was accomplished by a ritual dance. It is considered a bad omen if the vultures will not eat, or if even a small portion of the body is left after the birds fly away.
In places where fewer bodies are processed, the vultures were more eager and sometimes had to be fended off with sticks during the initial preparations.
[edit] References
1. ^ Wylie, Turrell V. (1965), "Mortuary Customs at Sa-Skya, Tibet", Harvard Journal of Asiatic Studies 25: 229-242 , p. 232.
2. ^ Martin, Daniel Preston (1996), "On the Cultural Ecology of Sky Burial on the Himalayan Plateau", East and West 46 (3-4): 353-370 , pp. 360-365.
3. ^ Joyce, Kelly A.; Williamson, John B. (2003), "Body recycling", in Bryant, Clifton D., Handbook of Death & Dying, 2, Thousand Oaks: Sage, p. 815, ISBN 0-7619-2514-7 .
4. ^ Ramachandra Rao, Saligrama Krishna (1977), Tibetan Tantrik Tradition, New Delhi: Arnold Heinemann, p. 5, OCLC 5942361
.
5. ^ cf. Wylie, Turrell V. (1964), "Ro-langs: the Tibetan zombie", History of Religions 4 (1): 69-80 ,
6. ^ Faison, Seth (July 3, 1999), "Lirong Journal; Tibetans, and Vultures, Keep Ancient Burial Rite"
, New York Times, nytimes.com .
Eyewitness accounts:
* Eyewitness account
, Niema Ash, 1980s
* Eyewitness account
, Pamela Logan, 1997
* Eyewitness account
, Mondo Secter, 1999 - This page also includes references and links to other eyewitness accounts and to a 1986 documentary film that shows a jhator
* Description of Drigung site
, Keith Dowman, orig. pub. 1988
[edit] External links
* Tibet's Sky Burials
* Tibetan Sky Burial
* Entry on jhator in Dakini Yogini Central
Retrieved from "http://en.wikipedia.org/wiki/Sky_burial"
Categories: Death customs | Tibetan culture | Tibetan Buddhist practices
Views
From Wikipedia, the free encyclopedia
Jump to: navigation, search
This article is about the Tibetan practice. For the Xinran Xue novel, see Sky Burial.
Drigung Monastery, Tibetan monastery famous for performing sky burials.
Sky burial site, Yerpa Valley
Sky burial or ritual dissection was once a common funerary practice in Tibet wherein a human corpse is cut into small pieces and placed on a mountaintop, exposing it to the elements or the mahabhuta and animals – especially to birds of prey. In Tibetan the practice is known as jhator (Tibetan: བྱ་གཏོར་; Wylie: bya gtor), which literally means, "giving alms to the birds."
The majority of Tibetans adhere to Buddhism, which teaches reincarnation. There is no need to preserve the body, as it is now an empty vessel. Birds may eat it, or nature may let it decompose. So the function of the sky burial is simply the disposal of the remains. In much of Tibet the ground is too hard and rocky to dig a grave, and with fuel and timber scarce, a sky burial is often more practical than cremation.
Additionally, since no fuel, land, or topsoil is consumed, this way of burial is arguably more ecologically friendly than cremation or interment.
Contents
[hide]
* 1 History and development
* 2 Purpose and meaning
* 3 Iconography
* 4 Setting
* 5 Procedure
o 5.1 Participants
o 5.2 Disassembling the body
o 5.3 Vultures
* 6 References
* 7 External links
[edit] History and development
The Tibetan sky-burial practices appear to have evolved out of practical considerations:[1][2][3] a) most of the Tibet is above the tree line, and the scarcity of timber makes cremation economically unfeasible; b) subsurface interment is equally difficult since the active layer is not more than a few centimeters deep, with solid rock or permafrost beneath it. The customs are first recorded in an indigenous 12th century Buddhist treatise known colloquially as the Book of the Dead. Tibetan tantricism appears to have influenced the procedure.[4][5] in that it is designed to destroy all the major bones, which would prevent them being taken for use as tantric ritual implements such as kapalas (skullcups), thigh-bone trumpets, and the like.
[edit] Purpose and meaning
As the name implies, jhator is considered an act of generosity: the deceased and his/her surviving relatives are providing food to sustain living beings. Generosity and compassion for all beings are important virtues or paramita in Buddhism. Although some observers have suggested that jhator is also meant to unite the deceased person with the sky or sacred realm, this does not seem consistent with most of the knowledgeable commentary and eyewitness reports, which indicate that Tibetans believe that at this point life has completely left the body and the body contains nothing more than simple flesh.
The government of the People's Republic of China, which has controlled Tibet since 1950, prohibited the practice (which it considered barbaric) in the 1960s but started to allow it again in the 1980s.[6] Non-Tibetans are usually not permitted to observe it, and direct photography is considered unethical, offensive and is generally forbidden.
A jhator was filmed, with permission from the family, for the documentary Secret Towers of the Himalayas which aired on the Science Channel in Fall 2008. The camera work was deliberately careful to never show the body itself, while documenting the procedure, birds, and tools.
[edit] Iconography
The tradition and custom of the jhator forded Traditional Tibetan medicine and thangka iconography with a particular insight into the interior workings of the human body. Pieces of the human skeleton were employed in ritual tools such as the skullcup, thigh-bone trumpet, etc.
[edit] Setting
A traditional jhator is performed in specified locations in Tibet (and surrounding areas traditionally occupied by Tibetans). Drigung Monastery is one of the three most important jhator sites.
The procedure takes place on a large flat rock long used for the purpose. The charnel ground (durtro) is always higher than its surroundings. It may be very simple, consisting only of the flat rock, or it may be more elaborate, incorporating temples and stupa (chorten in Tibetan).
Relatives may remain nearby during the jhator, possibly in a place where they cannot see it directly. The jhator usually takes place at dawn.
The full jhator procedure (as described below) is elaborate and expensive. Those who cannot afford it simply place their deceased on a high rock where the body decomposes or is eaten by birds and animals.
[edit] Procedure
Accounts from observers vary. The following description is assembled from multiple accounts by observers from the U.S. and Europe. References appear at the end.
[edit] Participants
Prior to the procedure, monks may chant mantra around the body and burn juniper incense – although ceremonial activities often take place on the preceding day.
The work of disassembling of the body may be done by a monk, or, more commonly, by rogyapas ("body-breakers").
All the eyewitness accounts remarked on the fact that the rogyapas did not perform their task with gravity or ceremony, but rather talked and laughed as during any other type of physical labor. According to Buddhist teaching, this makes it easier for the soul of the deceased to move on from the uncertain plane between life and death onto the next life.
[edit] Disassembling the body
In one account, the leading rogyapa cut off the limbs and hacked the body to pieces, handing each part to his assistants, who used rocks to pound the flesh and bones together to a pulp, which they mixed with tsampa (barley flour with tea and yak butter or milk) before the vultures were summoned to eat.
In several accounts, the flesh was stripped from the bones and given to vultures without further preparation; the bones then were broken up with sledgehammers, and usually mixed with tsampa before being given to the vultures. Many rogyapa first feed the bones and cartilage to the vultures, keeping the best flesh until last. After having had their fill of good quality meat, the birds usually fly away - leaving the bones and less favored bits.
In another account, vultures were given the whole body. When only the bones remained, they were broken up with mallets, ground with tsampa, and given to crows and hawks that had waited until the vultures had departed.
Sometimes the internal organs were removed and processed separately, but they too were consumed by birds. The hair is removed from the head and may be simply thrown away; at Drigung it seems at least some hair is kept in a room of the monastery.
None of the eyewitness accounts specifies what kind of knife is used in the jhator. One source states that it is a "ritual flaying knife" or trigu (Sanskrit kartika), but another source expresses skepticism, noting that the trigu is considered a woman's tool (rogyapas seem to be exclusively male).
[edit] Vultures
The species of vulture involved is apparently the "Eurasian Griffon" or "Old World vulture," Order Falconiformes, Family Accipitridae, scientific name Gyps fulvus.
In places where there are several jhator offerings each day, the birds sometimes had to be coaxed to eat, which in one case was accomplished by a ritual dance. It is considered a bad omen if the vultures will not eat, or if even a small portion of the body is left after the birds fly away.
In places where fewer bodies are processed, the vultures were more eager and sometimes had to be fended off with sticks during the initial preparations.
[edit] References
1. ^ Wylie, Turrell V. (1965), "Mortuary Customs at Sa-Skya, Tibet", Harvard Journal of Asiatic Studies 25: 229-242 , p. 232.
2. ^ Martin, Daniel Preston (1996), "On the Cultural Ecology of Sky Burial on the Himalayan Plateau", East and West 46 (3-4): 353-370 , pp. 360-365.
3. ^ Joyce, Kelly A.; Williamson, John B. (2003), "Body recycling", in Bryant, Clifton D., Handbook of Death & Dying, 2, Thousand Oaks: Sage, p. 815, ISBN 0-7619-2514-7 .
4. ^ Ramachandra Rao, Saligrama Krishna (1977), Tibetan Tantrik Tradition, New Delhi: Arnold Heinemann, p. 5, OCLC 5942361
.
5. ^ cf. Wylie, Turrell V. (1964), "Ro-langs: the Tibetan zombie", History of Religions 4 (1): 69-80 ,
6. ^ Faison, Seth (July 3, 1999), "Lirong Journal; Tibetans, and Vultures, Keep Ancient Burial Rite"
, New York Times, nytimes.com .
Eyewitness accounts:
* Eyewitness account
, Niema Ash, 1980s
* Eyewitness account
, Pamela Logan, 1997
* Eyewitness account
, Mondo Secter, 1999 - This page also includes references and links to other eyewitness accounts and to a 1986 documentary film that shows a jhator
* Description of Drigung site
, Keith Dowman, orig. pub. 1988
[edit] External links
* Tibet's Sky Burials
* Tibetan Sky Burial
* Entry on jhator in Dakini Yogini Central
Retrieved from "http://en.wikipedia.org/wiki/Sky_burial"
Categories: Death customs | Tibetan culture | Tibetan Buddhist practices
Views
Leprosy
Leprosy
From Wikipedia, the free encyclopedia
Jump to: navigation, search
For the malady found in the Hebrew Bible, see Tzaraath. For the album by the band Death, see Leprosy (album).
Leprosy (Hansen's Disease )
Classification and external resources
A 24-year-old man infected with leprosy.
ICD-10 A30.
ICD-9 030
OMIM 246300
DiseasesDB 8478
MedlinePlus 001347
eMedicine med/1281
derm/223
neuro/187
MeSH C01.252.410.040.552.386
Leprosy (from the Greek lepi (λέπι), meaning scales on a fish), or Hansen's disease, is a chronic disease caused by the bacteria Mycobacterium leprae and Mycobacterium lepromatosis.[1][2] Leprosy is primarily a granulomatous disease of the peripheral nerves and mucosa of the upper respiratory tract; skin lesions are the primary external symptom.[3] Left untreated, leprosy can be progressive, causing permanent damage to the skin, nerves, limbs and eyes. Contrary to popular belief, leprosy does not actually cause body parts to simply fall off.[4]
Historically, leprosy has affected mankind since at least 600 BC, and was well-recognized in the civilizations of ancient China, Egypt and India.[5] In 1995, the World Health Organization (WHO) estimated that between two and three million people were permanently disabled because of leprosy.[6] Although the forced quarantine or segregation of patients is unnecessary—and can be considered unethical—a few leper colonies still remain around the world, in countries such as India, Japan, Egypt, Nepal and Vietnam. It is now commonly believed that many of the people who were segregated into these communities were presumed to have leprosy, when they actually had syphilis. Leprosy is not highly infectious, as approximately 95% of people are immune and sufferers are no longer infectious after only a couple of days on treatment. They would not have spread leprosy through a community; whereas syphilis, which has similar symptoms, is more contagious. One of the first signs of leprosy is the unexpected loss of eyelashes.
The age-old social stigma associated with the advanced form of leprosy lingers in many areas, and remains a major obstacle to self-reporting and early treatment. Effective treatment for leprosy appeared in the late 1930s with the introduction of dapsone and its derivatives. However, leprosy bacilli resistant to dapsone gradually evolved and became widespread, and it was not until the introduction of multidrug therapy (MDT) in the early 1980s that the disease could be diagnosed and treated successfully within the community.[citation needed]
Contents
[hide]
* 1 Characteristics
* 2 Classification
* 3 Cause
* 4 Pathophysiology
* 5 Treatment
* 6 Prevention
* 7 Epidemiology
o 7.1 Risk groups
o 7.2 Disease burden
o 7.3 Global situation
* 8 History
* 9 Famous lepers
* 10 References
* 11 See also
* 12 Further reading
* 13 External links
[edit] Characteristics
Cutaneous leprosy lesions on a patient's thigh.
The clinical symptoms of leprosy vary but primarily affect the skin, nerves, and mucous membranes.[7] Patients with this chronic infectious disease are classified as having paucibacillary Hansen's disease (tuberculoid leprosy), multibacillary Hansen's disease (lepromatous leprosy), or borderline leprosy.
[edit] Classification
There is some confusion over classification because the WHO (World Health Organization) replaced an older, more complicated classification system with a simpler system that identifies two subtypes of leprosy: paucibacillary and multibacillary. The older system included six categories: Indeterminate Leprosy, Borderline Tuberculoid Leprosy, Midborderline Leprosy, Borderline Lepromatous Leprosy, Lepromatous Leprosy, and Tuberculoid Leprosy.
Paucibacillary leprosy encompasses indeterminate, tuberculoid, and borderline tuberculoid leprosy. It is characterized by one or more hypopigmented skin macules and anaesthetic patches, where skin sensations are lost because of damaged peripheral nerves that have been attacked by the human host's immune cells.
Multibacillary leprosy includes midborderline, borderline lepromatous, and lepromatous leprosy. It is associated with symmetric skin lesions, nodules, plaques, thickened dermis, and frequent involvement of the nasal mucosa resulting in nasal congestion and epistaxis (nose bleeds) but typically detectable nerve damage is late.
Borderline leprosy is of intermediate severity and is the most common form. Skin lesions resemble tuberculoid leprosy but are more numerous and irregular; large patches may affect a whole limb, and peripheral nerve involvement with weakness and loss of sensation is common. This type is unstable and may become more like lepromatous leprosy or may undergo a reversal reaction, becoming more like the tuberculoid form.
[edit] Cause
Mycobacterium leprae, one of the causative agents of leprosy. As acid-fast bacteria, M. leprae appear red when a Ziehl-Neelsen stain is used.
Main article: Mycobacterium leprae
Mycobacterium leprae and Mycobacterium lepromatosis are the causative agents of leprosy. M. lepromatosis is only the causitive agent in diffuse lepromatous leprosy, which can be lethal.[3][2]
An intracellular, acid-fast bacterium, M. leprae is aerobic and rod-shaped, and is surrounded by the waxy cell membrane coating characteristic of Mycobacterium species.[8]
Due to extensive loss of genes necessary for independent growth, M. leprae and M. lepromatosis are unculturable in the laboratory, a factor which leads to difficulty in definitively identifying the organism under a strict interpretation of Koch's postulates.[9][2] The use of non-culture-based techniques such as molecular genetics has allowed for alternative establishment of causation.
[edit] Pathophysiology
The exact mechanism of transmission of leprosy is not known: prolonged close contact and transmission by nasal droplet have both been proposed, and, while the latter fits the pattern of disease, both remain unproven.[10] The only other animals besides humans known to contract leprosy are the armadillo, chimpanzee, sooty mangabey, and cynomolgus macaque.[11] The bacterium can also be grown in the laboratory by injection into the footpads of mice.[12] There is evidence that not all people who are infected with M. leprae develop leprosy, and genetic factors have long been thought to play a role, due to the observation of clustering of leprosy around certain families, and the failure to understand why certain individuals develop lepromatous leprosy while others develop other types of leprosy.[13] It is estimated that due to genetic factors, only 5 percent of the population is susceptible to leprosy.[14] This is mostly because the body is naturally immune to the bacteria, and those persons who do become infected are experiencing a severe allergic reaction to the disease. However, the role of genetic factors is not entirely clear in determining this clinical expression. In addition, malnutrition and prolonged exposure to infected persons may play a role in development of the overt disease.
The incubation period for the bacteria can last anywhere from two to ten years.
The most widely held belief is that the disease is transmitted by contact between infected persons and healthy persons.[15] In general, closeness of contact is related to the dose of infection, which in turn is related to the occurrence of disease. Of the various situations that promote close contact, contact within the household is the only one that is easily identified, although the actual incidence among contacts and the relative risk for them appear to vary considerably in different studies. In incidence studies, infection rates for contacts of lepromatous leprosy have varied from 6.2 per 1000 per year in Cebu, Philippines[16] to 55.8 per 1000 per year in a part of Southern India.[17]
Two exit routes of M. leprae from the human body often described are the skin and the nasal mucosa, although their relative importance is not clear. It is true that lepromatous cases show large numbers of organisms deep down in the dermis. However, whether they reach the skin surface in sufficient numbers is doubtful. Although there are reports of acid-fast bacilli being found in the desquamating epithelium (sloughing of superficial layer of skin) of the skin, Weddell et al had reported in 1963 that they could not find any acid-fast bacilli in the epidermis, even after examining a very large number of specimens from patients and contacts.[18] In a recent study, Job et al found fairly large numbers of M. leprae in the superficial keratin layer of the skin of lepromatous leprosy patients, suggesting that the organism could exit along with the sebaceous secretions.[19]
The importance of the nasal mucosa was recognized as early as 1898 by Schäffer, particularly that of the ulcerated mucosa.[20] The quantity of bacilli from nasal mucosal lesions in lepromatous leprosy was demonstrated by Shepard as large, with counts ranging from 10,000 to 10,000,000.[21] Pedley reported that the majority of lepromatous patients showed leprosy bacilli in their nasal secretions as collected through blowing the nose.[22] Davey and Rees indicated that nasal secretions from lepromatous patients could yield as much as 10 million viable organisms per day.[23]
The entry route of M. leprae into the human body is also not definitely known. The two seriously considered are the skin and the upper respiratory tract. While older research dealt with the skin route, recent research has increasingly favored the respiratory route. Rees and McDougall succeeded in the experimental transmission of leprosy through aerosols containing M. leprae in immune-suppressed mice, suggesting a similar possibility in humans.[24] Successful results have also been reported on experiments with nude mice when M. leprae were introduced into the nasal cavity by topical application.[25] In summary, entry through the respiratory route appears the most probable route, although other routes, particularly broken skin, cannot be ruled out. The CDC notes the following assertion about the transmission of the disease: "Although the mode of transmission of Hansen's disease remains uncertain, most investigators think that M. leprae is usually spread from person to person in respiratory droplets."[26]
In leprosy both the reference points for measuring the incubation period and the times of infection and onset of disease are difficult to define; the former because of the lack of adequate immunological tools and the latter because of the disease's slow onset. Even so, several investigators have attempted to measure the incubation period for leprosy. The minimum incubation period reported is as short as a few weeks and this is based on the very occasional occurrence of leprosy among young infants.[27] The maximum incubation period reported is as long as 30 years, or over, as observed among war veterans known to have been exposed for short periods in endemic areas but otherwise living in non-endemic areas. It is generally agreed that the average incubation period is between 3 and 5 years.
[edit] Treatment
MDT patient packs and blisters
Until the development of dapsone, rifampicin, and clofazimine in the 1940s, there was no effective cure for leprosy. However, dapsone is only weakly bactericidal against M. leprae and it was considered necessary for patients to take the drug indefinitely. Moreover, when dapsone was used alone, the M. leprae population quickly evolved antibiotic resistance; by the 1960s, the world's only known anti-leprosy drug became virtually useless.
The search for more effective anti-leprosy drugs than dapsone led to the use of clofazimine and rifampicin in the 1960s and 1970s.[28] Later, Indian scientist Shantaram Yawalkar and his colleagues formulated a combined therapy using rifampicin and dapsone, intended to mitigate bacterial resistance.[29] Multidrug therapy (MDT) and combining all three drugs was first recommended by a WHO Expert Committee in 1981. These three anti-leprosy drugs are still used in the standard MDT regimens. None of them are used alone because of the risk of developing resistance.
Because this treatment is quite expensive, it was not quickly adopted in most endemic countries. In 1985 leprosy was still considered a public health problem in 122 countries. The 44th World Health Assembly (WHA), held in Geneva in 1991 passed a resolution to eliminate leprosy as a public health problem by the year 2000 — defined as reducing the global prevalence of the disease to less than 1 case per 100,000. At the Assembly, the World Health Organization (WHO) was given the mandate to develop an elimination strategy by its member states, based on increasing the geographical coverage of MDT and patients’ accessibility to the treatment.
The WHO Study Group's report on the Chemotherapy of Leprosy in 1993 recommended two types of standard MDT regimen be adopted.[30] The first was a 24-month treatment for multibacillary (MB or lepromatous) cases using rifampicin, clofazimine, and dapsone. The second was a six-month treatment for paucibacillary (PB or tuberculoid) cases, using rifampicin and dapsone. At the First International Conference on the Elimination of Leprosy as a Public Health Problem, held in Hanoi the next year, the global strategy was endorsed and funds provided to WHO for the procurement and supply of MDT to all endemic countries.
MDT anti-leprosy drugs: standard regimens
Between 1995 and 1999, WHO, with the aid of the Nippon Foundation (Chairman Yōhei Sasakawa, World Health Organization Goodwill Ambassador for Leprosy Elimination), supplied all endemic countries with free MDT in blister packs, channelled through Ministries of Health. This free provision was extended in 2000 with a donation by the MDT manufacturer Novartis, which will run until at least the end of 2010. At the national level, non-government organizations (NGOs) affiliated to the national programme will continue to be provided with an appropriate free supply of this WHO supplied MDT by the government.
MDT remains highly effective and patients are no longer infectious after the first monthly dose.[5] It is safe and easy to use under field conditions due to its presentation in calendar blister packs.[5] Relapse rates remain low, and there is no known resistance to the combined drugs.[5] The Seventh WHO Expert Committee on Leprosy,[31] reporting in 1997, concluded that the MB duration of treatment—then standing at 24 months—could safely be shortened to 12 months "without significantly compromising its efficacy."
Persistent obstacles to the elimination of the disease include improving detection, educating patients and the population about its cause, and fighting social taboos about a disease for which patients have historically been considered "unclean" or "cursed by God" as outcasts. Where taboos are strong, patients may be forced to hide their condition (and avoid seeking treatment) to avoid discrimination. The lack of awareness about Hansen's disease can lead people to falsely believe that the disease is highly contagious and incurable.
The ALERT hospital and research facility in Ethiopia provides training to medical personnel from around the world in the treatment of leprosy, as well as treating many local patients. Surgical techniques, such as for the restoration of control of movement of thumbs, have been developed there.
[edit] Prevention
A single dose of rifampicin is able to reduce the rate of leprosy in contacts by 57% to 75%.[32][33]
BCG is able to offer a variable amount of protection against leprosy as well as against tuberculosis.[34][35]
[edit] Epidemiology
World distribution of leprosy, 2003.
Worldwide, two to three million people are estimated to be permanently disabled because of Leprosy.[6] India has the greatest number of cases, with Brazil second and Burma third.
In 1999, the world incidence of Hansen's disease was estimated to be 640,000. In 2000, 738,284 cases were identified. In 1999, 108 cases occurred in the United States. In 2000, the World Health Organization (WHO) listed 91 countries in which Hansen's disease is endemic. India, Myanmar and Nepal contained 70% of cases. In 2002, 763,917 new cases were detected worldwide, and in that year the WHO listed Brazil, Madagascar, Mozambique, Tanzania and Nepal as having 90% of Hansen's disease cases.
According to recent figures from the WHO, new cases detected worldwide have decreased by approximately 107,000 cases (or 21%) from 2003 to 2004. This decreasing trend has been consistent for the past three years. In addition, the global registered prevalence of HD was 286,063 cases; 407,791 new cases were detected during 2004.
In the United States, Hansen's disease is tracked by the Centers for Disease Control and Prevention (CDC), with a total of 92 cases being reported in 2002.[36] Although the number of cases worldwide continues to fall, pockets of high prevalence continue in certain areas such as Brazil, South Asia (India, Nepal), some parts of Africa (Tanzania, Madagascar, Mozambique) and the western Pacific.
[edit] Risk groups
At highest risk are those living in endemic areas with poor conditions such as inadequate bedding, contaminated water and insufficient diet, or other diseases (such as HIV) that compromise immune function. Recent research suggests that there is a defect in cell-mediated immunity that causes susceptibility to the disease. Less than ten percent of the world's population is actually capable of acquiring the disease[citation needed]. The region of DNA responsible for this variability is also involved in Parkinson disease[citation needed], giving rise to current speculation that the two disorders may be linked in some way at the biochemical level. In addition, men are twice as likely to contract leprosy as women. According to The Leprosy Mission Canada, most people – about 95% of the population – are naturally immune.
[edit] Disease burden
Although annual incidence—the number of new leprosy cases occurring each year—is important as a measure of transmission, it is difficult to measure in leprosy due to its long incubation period, delays in diagnosis after onset of the disease and the lack of laboratory tools to detect leprosy in its very early stages. - - Instead, the registered prevalence is used. Registered prevalence is a useful proxy indicator of the disease burden as it reflects the number of active leprosy cases diagnosed with the disease and receiving treatment with MDT at a given point in time. The prevalence rate is defined as the number of cases registered for MDT treatment among the population in which the cases have occurred, again at a given point in time.[37]
New case detection is another indicator of the disease that is usually reported by countries on an annual basis. It includes cases diagnosed with onset of disease in the year in question (true incidence) and a large proportion of cases with onset in previous years (termed a backlog prevalence of undetected cases). The new case detection rate (NCDR) is defined by the number of newly detected cases, previously untreated, during a year divided by the population in which the cases have occurred.
Endemic countries also report the number of new cases with established disabilities at the time of detection, as an indicator of the backlog prevalence. However, determination of the time of onset of the disease is generally unreliable, is very labor-intensive and is seldom done in recording these statistics.
[edit] Global situation
Table 1: Prevalence at beginning of 2006, and trends in new case detection 2001-2005, excluding Europe
Region Registered prevalence
(rate/1,000,000 pop.)
New case detection during the year
Start of 2006 2001 2002 2003 2004 2005
Africa 40,830 (0.56) 39,612 48,248 47,006 46,918 42,814
Americas 32,904 (0.39) 42,830 39,939 52,435 52,662 41,780
South-East Asia 133,422 (0.81) 668,658 520,632 405,147 298,603 201,635
Eastern Mediterranean 4,024 (0.09) 4,758 4,665 3,940 3,392 3,133
Western Pacific 8,646 (0.05) 7,404 7,154 6,190 6,216 7,137
Totals NA 763,262 620,638 514,718 407,791 296,499
Table 2: Prevalence and detection, countries still to reach elimination
Countries Registered prevalence
(rate/10,000 pop.)
New case detection
(rate/100,000 pop.)
Start of 2004 Start of 2005 Start of 2006 During 2003 During 2004 During 2005
Brazil 79,908 (4.6) 30,693 (1.7) 27,313 (1.5) 49,206 (28.6) 49,384 (26.9) 38,410 (20.6)
Mozambique 6,810 (3.4) 4,692 (2.4) 4,889 (2.5) 5,907 (29.4) 4,266 (22.0) 5,371 (27.1)
Nepal 7,549 (3.1) 4,699 (1.8) 4,921 (1.8) 8,046 (32.9) 6,958 (26.2) 6,150 (22.7)
Tanzania 5,420 (1.6) 4,777 (1.3) 4,190 (1.1) 5,279 (15.4) 5,190 (13.8) 4,237 (11.1)
Totals NA NA NA NA NA NA
As reported to WHO by 115 countries and territories in 2006, and published in the Weekly Epidemiological Record the global registered prevalence of leprosy at the beginning of the year was 219,826 cases.[38] New case detection during the previous year (2005 - the last year for which full country information is available) was 296,499. The reason for the annual detection being higher than the prevalence at the end of the year can be explained by the fact that a proportion of new cases complete their treatment within the year and therefore no longer remain on the registers. The global detection of new cases continues to show a sharp decline, falling by 110,000 cases (27%) during 2005 compared with the previous year.
Table 1 shows that global annual detection has been declining since 2001. The African region reported an 8.7% decline in the number of new cases compared with 2004. The comparable figure for the Americas was 20.1%, for South-East Asia 32% and for the Eastern Mediterranean it was 7.6%. The Western Pacific area, however, showed a 14.8% increase during the same period.
Table 2 shows the leprosy situation in the four major countries which have yet to achieve the goal of elimination at the national level. It should be noted that: a) Elimination is defined as a prevalence of less than 1 case per 10,000 population; b) Madagascar reached elimination at the national level in September 2006; c) Nepal detection reported from mid-November 2004 to mid-November 2005; and d) D.R. Congo officially reported to WHO in 2008 that it had reached elimination by the end of 2007, at the national level.
[edit] History
The Oxford Illustrated Companion to Medicine holds that the mention of leprosy, as well as ritualistic cures for it, were already described in the Hindu religious book Atharva-veda.[39] Writing in the Encyclopedia Britannica 2008, Kearns & Nash state that the first mention of leprosy is described in the Indian medical treatise Sushruta Samhita (6th century BC).[40] The Cambridge Encyclopedia of Human Paleopathology (1998) holds that: "The Sushruta Samhita from India describes the condition quite well and even offers therapeutic suggestions as early as about 600 BC"[41] The surgeon Sushruta flourished in the Indian city of Kashi by the 6th century BC,[42] and the medical treatise Sushruta Samhita—attributed to him—made its appearance during the 1st millennium BC.[40] The earliest surviving excavated written material which contains the works of Sushruta is the Bower Manuscript—dated to the 4th century AD, almost a millennium after the original work.[43]
In regards to ancient China, Katrina C. D. McLeod and Robin D. S. Yates identify the State of Qin's Feng zhen shi 封診式 (Models for sealing and investigating), dated 266-246 BC, as offering the earliest known unambiguous description of the symptoms of low-resistance leprosy, even though it was termed then under li 癘, a general Chinese word for skin disorder.[44] This 3rd century BC Chinese text on bamboo slip, found in an excavation of 1975 at Shuihudi, Yunmeng, Hubei province, not only described the destruction of the "pillar of the nose", but also the "swelling of the eyebrows, loss of hair, absorption of nasal cartilage, affliction of knees and elbows, difficult and hoarse respiration, as well as anaesthesia."[44]
In the West, the earliest known description of leprosy there was made by the Roman encyclopedist Aulus Cornelius Celsus (25 BC – 37 AD) in his De Medicina; he called leprosy "elephantiasis".[44] The Roman author Pliny the Elder (23–79 AD) mentioned the same disease.[44] Although "sara't" of Leviticus (Old Testament) is translated as "lepra" in the 5th century AD Vulgate, the original term sara't found in Leviticus was not the elephantiasis described by Celsus and Pliny; in fact, sara't was used to describe a disease which could affect houses and clothing.[44] Katrina C. D. McLeod and Robin D. S. Yates state that sara't "denotes a condition of ritual impurity or a temporary form of skin disease."[44] In the Muslim world, the Persian polymath Avicenna (c. 980–1037) was the first outside of China to describe the destruction of the nasal septum in those suffering from leprosy.[44]
Numerous leprosaria, or leper hospitals, sprang up in the Middle Ages; Matthew Paris estimated that in the early thirteenth century there were 19,000 across Europe.[45] The first recorded Leper colony was in Harbledown. These institutions were run along monastic lines and, while lepers were encouraged to live in these monastic-type establishments, this was for their own health as well as quarantine. Indeed, some medieval sources indicate belief that those suffering from leprosy were considered to be going through Purgatory on Earth, and for this reason their suffering was considered holier than the ordinary person's. More frequently, lepers were seen to exist in a place between life and death: they were still alive, yet many chose or were forced to ritually separate themselves from mundane existence.[46]
Radegund was noted for washing the feet of lepers. Orderic Vitalis writes of a monk, Ralf, who was so overcome by the plight of lepers that he prayed to catch leprosy himself (which he eventually did). The leper would carry a clapper and bell to warn of his approach, and this was as much to attract attention for charity as to warn people that a diseased person was near.
G. H. A. Hansen, discoverer of M. leprae
Mycobacterium leprae, the causative agent of leprosy, was discovered by G. H. Armauer Hansen in Norway in 1873, making it the first bacterium to be identified as causing disease in humans.[47][48] He worked at St. Jørgens Hospital in Bergen, founded early in the fifteenth century. St. Jørgens is today a museum, Lepramuseet, probably the best preserved leprosy hospital in Northern Europe.[49]
Historically, individuals with Hansen's disease have been known as lepers, however, this term is falling into disuse as a result of the diminishing number of leprosy patients and the pejorative connotations of the term. The term most widely accepted among professionals is "people affected by Hansen's disease."
Historically, the term Tzaraath from the Hebrew Bible was, erroneously, commonly translated as leprosy, although the symptoms of Tzaraath were not entirely consistent with leprosy and rather referred to a variety of disorders other than Hansen's disease.[50]
In particular, tinea capitis (fungal scalp infection) and related infections on other body parts caused by the dermatophyte fungus Trichophyton violaceum are abundant throughout the Middle East and North Africa today and might also have been common in biblical times. Similarly, the related agent of the disfiguring skin disease favus, Trichophyton schoenleinii, appears to have been common throughout Eurasia and Africa before the advent of modern medicine. Persons with severe favus and similar fungal diseases (and potentially also with severe psoriasis and other diseases not caused by microorganisms) tended to be classed as having leprosy as late as the 17th century in Europe.[51] This is clearly shown in the painting Governors of the Home for Lepers at Haarlem 1667 by Jan de Bray (Frans Hals Museum, Haarlem, the Netherlands), where a young Dutchman with a vivid scalp infection, almost certainly caused by a fungus, is shown being cared for by three officials of a charitable home intended for leprosy sufferers. The use of the word "leprosy" before the mid-19th century, when microscopic examination of skin for medical diagnosis was first developed, can seldom be correlated reliably with Hansen's disease as we understand it today.
The word "leprosy" derives from the ancient Greek words lepros, a scale, and lepein, to peel.[52] The word came into the English language via Latin and Old French. The first attested English use is in the Ancrene Wisse, a 13th-century manual for nuns ("Moyseses hond..bisemde o þe spitel uuel & þuhte lepruse." The Middle English Dictionary, s.v., "leprous"). A roughly contemporaneous use is attested in the Anglo-Norman Dialogues of Saint Gregory, "Esmondez i sont li lieprous" (Anglo-Norman Dictionary, s.v., "leprus").
[edit] Famous lepers
* Blessed Damien of Moloka'i was a Roman Catholic missionary who became a leper when he spent the rest of his life serving in the leper colony at Moloka'i.
* King Baldwin IV of Jerusalem.
* Possibly Robert I de Brus, King of Scots.
* Vietnamese poet Han Mac Tu
* Otani Yoshitsugu, a Japanese Daimyo.
[edit] References
1. ^ Sasaki S, Takeshita F, Okuda K, Ishii N (2001). "Mycobacterium leprae and leprosy: a compendium
". Microbiol Immunol 45 (11): 729–36. PMID 11791665
, http://www.jstage.jst.go.jp/article/mandi/45/11/729/_pdf
.
2. ^ a b c http://www.sciencedaily.com/releases/2008/11/081124141047.htm
3. ^ a b Kenneth J. Ryan, C. George Ray, editors. (2004). Ryan KJ, Ray CG. ed.. Sherris Medical Microbiology (4th ed. ed.), McGraw Hill. pp. 451–3. ISBN 0838585299. OCLC 52358530 61405904
.
4. ^ "Lifting the stigma of leprosy: a new vaccine offers hope against an ancient disease
". Time 119 (19): 87. May 1982. PMID 10255067
, http://www.time.com/time/magazine/article/0,9171,925377,00.html
.
5. ^ a b c d "Leprosy
". WHO. Retrieved on 2007-08-22.
6. ^ a b WHO (1995). "Leprosy disabilities: magnitude of the problem". Weekly Epidemiological Record 70 (38): 269–75. PMID 7577430
.
7. ^ Naafs B, Silva E, Vilani-Moreno F, Marcos E, Nogueira M, Opromolla D (2001). "Factors influencing the development of leprosy: an overview". Int J Lepr Other Mycobact Dis 69 (1): 26–33. PMID 11480313
.
8. ^ McMurray DN (1996). Mycobacteria and Nocardia. in: Baron's Medical Microbiology (Baron S et al, eds.)
(4th ed. ed.), Univ of Texas Medical Branch. ISBN 0-9631172-1-1. OCLC 33838234
, http://www.ncbi.nlm.nih.gov/books/bv.fcgi?rid=mmed.section.1833
.
9. ^ Bhattacharya S, Vijayalakshmi N, Parija SC (2002). "Uncultivable bacteria: Implications and recent trends towards identification
". Indian journal of medical microbiology 20 (4): 174–7. PMID 17657065
, http://www.ijmm.org/article.asp?issn=0255-0857;year=2002;volume=20;issue=4;spage=174;epage=177;aulast=Bhattacharya
.
10. ^ Reich CV (1987). "Leprosy: cause, transmission, and a new theory of pathogenesis". Rev. Infect. Dis. 9 (3): 590–4. PMID 3299638
.
11. ^ Rojas-Espinosa O, Løvik M (2001). "Mycobacterium leprae and Mycobacterium lepraemurium infections in domestic and wild animals". Rev. - Off. Int. Epizoot. 20 (1): 219–51. PMID 11288514
.
12. ^ Hastings RC, Gillis TP, Krahenbuhl JL, Franzblau SG (1988). "Leprosy
". Clin. Microbiol. Rev. 1 (3): 330–48. PMID 3058299
, http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=3058299
.
13. ^ Alcaïs A, Mira M, Casanova JL, Schurr E, Abel L (2005). "Genetic dissection of immunity in leprosy". Curr. Opin. Immunol. 17 (1): 44–8. doi:10.1016/j.coi.2004.11.006
. PMID 15653309
.
14. ^ "AR Dept of Health debunks leprosy fears
" (2008-02-08). Retrieved on 2008-04-08.
15. ^ Kaur H, Van Brakel W (2002). "Dehabilitation of leprosy-affected people—a study on leprosy-affected beggars". Leprosy review 73 (4): 346–55. PMID 12549842
.
16. ^ Doull JA, Guinto RA, Rodriguez RS, et al. (1942). "The incidence of leprosy in Cordova and Talisay, Cebu, Philippines". International Journal of Leprosy 10: 107–131.
17. ^ Noordeen S, Neelan P (1978). "Extended studies on chemoprophylaxis against leprosy". Indian J Med Res 67: 515–27. PMID 355134
.
18. ^ Weddell G, Palmer E (1963). "The pathogenesis of leprosy. An experimental approach". Leprosy Review 34: 57–61. PMID 13999438
.
19. ^ Job C, Jayakumar J, Aschhoff M (1999). ""Large numbers" of Mycobacterium leprae are discharged from the intact skin of lepromatous patients; a preliminary report". Int J Lepr Other Mycobact Dis 67 (2): 164–7. PMID 10472371
.
20. ^ Arch Dermato Syphilis 1898; 44:159–174
21. ^ Shepard C (1960). "Acid-fast bacilli in nasal excretions in leprosy, and results of inoculation of mice". Am J Hyg 71: 147–57. PMID 14445823
.
22. ^ Pedley J (1973). "The nasal mucus in leprosy". Lepr Rev 44 (1): 33–5. PMID 4584261
.
23. ^ Davey T, Rees R (1974). "The nasal dicharge in leprosy: clinical and bacteriological aspects". Lepr Rev 45 (2): 121–34. PMID 4608620
.
24. ^ Rees R, McDougall A (1977). "Airborne infection with Mycobacterium leprae in mice". J Med Microbiol 10 (1): 63–8. PMID 320339
.
25. ^ Chehl S, Job C, Hastings R (1985). "Transmission of leprosy in nude mice". Am J Trop Med Hyg 34 (6): 1161–6. PMID 3914846
.
26. ^ CDC Disease Info hansens_t
Hansen's Disease (Leprosy)
27. ^ Montestruc E, Berdonneau R (1954). "2 New cases of leprosy in infants in Martinique" (in French). Bull Soc Pathol Exot Filiales 47 (6): 781–3. PMID 14378912
.
28. ^ Rees RJ, Pearson JM, Waters MF (1970). "Experimental and clinical studies on rifampicin in treatment of leprosy". Br Med J 688 (1): 89–92. PMID 4903972
.
29. ^ Yawalkar SJ, McDougall AC, Languillon J, Ghosh S, Hajra SK, Opromolla DV, Tonello CJ (1982). "Once-monthly rifampicin plus daily dapsone in initial treatment of lepromatous leprosy". Lancet 8283 (1): 1199–1202. doi:10.1016/S0140-6736(82)92334-0
. PMID 6122970
.
30. ^ "Chemotherapy of Leprosy
". WHO Technical Report Series 847. WHO (1994). Retrieved on 2007-03-24.
31. ^ "Seventh WHO Expert Committee on Leprosy
". WHO Technical Report Series 874. WHO (1998). Retrieved on 2007-03-24.
32. ^ Moet FJ, Pahan D, Oskam L, Richardus JH (2008). "Effectiveness of single dose rifampicin in preventing leprosy in close contacts of patients with newly diagnosed leprosy: cluster randomised controlled trial". BMJ 336: 761. doi:10.1136/bmj.39500.885752.BE
. PMID 18332051
.
33. ^ Bakker MI, Hatta M, Kwenang A, et al. (2005). "Prevention of leprosy using rifampicin as chemoprophylaxis
". Am J Trop Med Hyg 72: 443–8. PMID 15827283
, http://www.ajtmh.org/cgi/content/abstract/72/4/443?ijkey=4b15a78b876fd990dfd877ee89b22399c026501c&keytype2=tf_ipsecsha
.
34. ^ Fine PE, Smith PG (1996). "Vaccination against leprosy—the view from 1996". Lepr Rev 67 (4): 249–52. PMID 9033195
.
35. ^ Karonga prevention trial group (1996). "Randomized controlled trial of single BCG, repeated BCG, or combined BCG and killed Mycobacterium leprae vaccine for prevention of leprosy and tuberculosis in Malawi". Lancet 348: 17–24. doi:10.1016/S0140-6736(96)02166-6
. PMID 8691924
.
36. ^ CDC Leprosy Fact Sheet
.
37. ^ "Epidemiology of leprosy in relation to control. Report of a WHO Study Group". World Health Organ Tech Rep Ser (Geneva: World Health Organization) 716: 1–60. 1985. ISBN 9241207167. OCLC 12095109
. PMID 3925646
.
38. ^ "Global leprosy situation, 2006
" (PDF). Weekly Epidemiological Record 81 (32): 309–16. August 2006. PMID 16903018
, http://www.who.int/lep/resources/wer8132.pdf
.
39. ^ Lock etc., page 420
40. ^ a b Kearns & Nash (2008)
41. ^ Aufderheide, A. C.; Rodriguez-Martin, C. & Langsjoen, O. (1998). The Cambridge Encyclopedia of Human Paleopathology. Cambridge University Press. ISBN 0521552036. Page 148.
42. ^ Dwivedi & Dwivedi (2007)
43. ^ Kutumbian, P. (2005). Ancient Indian Medicine. Orient Longman. ISBN 8125015213. pages XXXII-XXXIII.
44. ^ a b c d e f g McLeod, Katrina C. D. and Robin D. S. Yates (June 1981). "Forms of Ch'in Law: An Annotated Translation of The Feng-chen shih". Harvard Journal of Asiatic Studies 41 (1): 111–63. Pages 152–3 & footnote 147. doi:10.2307/2719003
.
45. ^ "Leprosy". Catholic Encyclopedia. (1913). New York: Robert Appleton Company.
46. ^ Brody, Saul Nathaniel (1974). The Disease of the Soul: Leprosy in Medieval Literature. Ithaca: Cornell Press.
47. ^ Hansen GHA (1874). "Undersøgelser Angående Spedalskhedens Årsager (Investigations concerning the etiology of leprosy)" (in Norwegian). Norsk Mag. Laegervidenskaben 4: 1–88.
48. ^ Irgens L (2002). "The discovery of the leprosy bacillus". Tidsskr nor Laegeforen 122 (7): 708–9. PMID 11998735
.
49. ^ Bymuseet i Bergen
50. ^ Artscroll Tanakh, Leviticus 13:59, 1996
51. ^ Kane J, Summerbell RC, Sigler L, Krajden S, Land G (1997). Laboratory Handbook of Dermatophytes: A clinical guide and laboratory manual of dermatophytes and other filamentous fungi from skin, hair and nails, Star Publishers (Belmont, CA). ISBN 0898631572. OCLC 37116438
.
52. ^ Barnhart RK (1995). Barnhart Concise Dictionary of Etymology. New York: Harper Collins. ISBN 0062700847. OCLC 221898877 223496345 231655185 30399281
.
[edit] See also
* Dwivedi, Girish & Dwivedi, Shridhar (2007). History of Medicine: Sushruta – the Clinician – Teacher par Excellence
. National Informatics Centre (Government of India).
* Dunea, George; Lock, Stephen; Last, John M. (2001). The Oxford illustrated companion to medicine. Oxford [Oxfordshire]: Oxford University Press. ISBN 0-19-262950-6. OCLC 150308752 180030517 213488544 244006190 43342122 46678589 58460632 59406536 69646604
.
* Kearns, Susannah C.J. & Nash, June E. (2008). Leprosy. Encyclopedia Britannica.
[edit] Further reading
* Bargès A (1993). "Ségrégation antilépreuse et comportements adaptatifs à Bamako (Mali)
" (PDF). Ecologie humaine 11 (2): 7–20, http://halshs.archives-ouvertes.fr/docs/00/25/89/20/PDF/Environnmement_africain_et_maladie-Barges1993.pdf
.
* Bargès A (1996). "Entre conformismes et changements, le monde de la lèpre au Mali
" (PDF). Paris, Editions Karthala: 280–313, http://halshs.archives-ouvertes.fr/docs/00/26/60/96/PDF/Le_monde_la_lepre_1996(1993).pdf
.
* Clark E (1994). "Social Welfare and Mutual Aid in the Medieval Countryside
". The Journal of British Studies 33 (4): 394–6, http://links.jstor.org/sici?sici=0021-9371(199410)33%3A4%3C381%3ASWAMAI%3E2.0.CO%3B2-L
.
* Icon Health Publications (2004). Leprosy: A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References, San Diego: Icon Health Publications. ISBN 0-597-84006-7. OCLC 162128079 191036288
.
* Demaitre L (2007). Leprosy in Premodern Medicine: A Malady of the Whole Body. Baltimore, Maryland: The Johns Hopkins University Press. ISBN 978-0-8018-8613-3. OCLC 238882127 70921424
.
* Rawcliffe C (2001). "Learning to Love the Leper: aspects of institutional Charity in Anglo Norman England". Anglo Norman Studies 23: 233–52.
* Rawcliffe C (2006). Leprosy in Medieval England. Ipswich: Boydell Press. ISBN 1843832739. OCLC 70765638
.
* Talarigo J (2004). The Pearl Diver: (fiction) young woman with leprosy is exiled to leprosy colony in Japan, 1929, Doubleday. ISBN 1-4025-8661-2. OCLC 55066644
.
* Tayman J (2006). The Colony: The Harrowing True Story of the Exiles of Molokai, Simon & Schuster. ISBN 0-7432-3300.
* Brennert A (2003). Moloka'i:(fiction) young woman with leprosy is exiled to leprosy colony in Hawaii, 1891, St. Martin's Press. ISBN 0-312-30435-8. OCLC 123959155 56695775
.
[edit] External links
Sister project Wikimedia Commons has media related to: Leprosy
* Leprosy and Human Rights
- event held at Woodrow Wilson International Center for Scholars, March 2008
* National Hansen's Disease Programs (NHDP), U.S. Health Resources and Services Administration
* Hansen's Disease (Leprosy)
- Centers for Disease Control and Prevention
* World Health Organization (WHO) leprosy website
* Hope in a Modern-Day Leper Colony
Article from a leper colony in India
* American Leprosy Missions
* Rinaldi A (December 2005). "The global campaign to eliminate leprosy
". PLoS Med. 2 (12): e341. doi:10.1371/journal.pmed.0020341
. PMID 16363908
.
* LEPRA - Health in Action
UK Based organisation founded in 1924 to treat leprosy and related diseases of poverty.
History of leprosy
* "History of Leprosy, Urban Environment and French Colonization in West Africa
" (PDF).
* "Anthropology and History of leprosy
" (Histoire & Anthropologie, 15 (1995) 115-122).
* ILA Global Project on the History of Leprosy
* National Hansen's Disease Museum
* BBC News: Slave trade key to leprosy spread
* "Interview with author John Tayman (The Colony)
" (MP3 audio: runtime = 00:23:20, 10.7 mb). IT Conversations Tech Nation (2006-02-07). Retrieved on 2007-03-22.
Research
* Pathology Images of Leprosy and Other Granulomatous diseases
Yale Rosen, M.D.
* INFOLEP Leprosy Information Services
* Leprosy Review
* "Medical anthropology, Leprosy and Health Care in French speaking West-Africa
" (PDF).
* "Anthropologie, lèpre et santé publique
".
* "Gender and Leprosy
".
* Photographs of leprosy patients
: type leprosy in the diagnosis space for some photographs and then type leproma for another photograph.
[show]
v • d • e
Diseases of the skin and appendages by morphology
Growths
Epidermal
verruca, clavus, seborrheic keratosis, acrochordon, molluscum contagiosum, actinic keratosis, squamous cell carcinoma, basal cell carcinoma, merkel cell carcinoma, nevus sebaceous, trichoepithelioma
Pigmented
ephelis, lentigo, melasma, nevus, malignant melanoma
Dermal and subcutaneous
epidermal inclusion cyst, hemangioma, dermatofibroma, keloid, lipoma, neurofibroma, xanthoma, Kaposi's sarcoma, infantile digital fibromatosis, granular cell tumor, leiomyoma, lymphangioma circumscriptum, myxoid cyst
Rashes
With epidermal involvement
Eczematous
essential dermatitis, contact dermatitis, atopic dermatitis, seborrheic dermatitis, stasis dermatitis, lichen simplex chronicus, Darier's disease, glucagonoma syndrome, langerhans cell histiocytosis, lichen sclerosus, pemphigus foliaceus, Wiskott-Aldrich syndrome, Zinc deficiency
Scaling
psoriasis, tinea corporis, tinea cruris, tinea pedis, tinea manuum, tinea faciale, pityriasis rosea, secondary syphillis, mycosis fungoides, systemic lupus erythematosus, pityriasis rubra pilaris, parapsoriasis, icthyosis
Blistering
herpes simplex, herpes zoster, varicella, bullous impetigo, acute contact dermatitis, pemphigus vulgaris, bullous pemphigoid, dermatitis herpetiformis, porphyria cutanea tarda, epidermolysis bullosa simplex
Papular
scabies, insect bite reactions, lichen planus, miliaria, keratosis pilaris, lichen spinulosus, transient acantholytic dermatosis, lichen nitidus, pityriasis lichenoides et varioliformis acuta
Pustular
acne vulgaris, acne rosacea, folliculitis, impetigo, candidiasis, gonococcemia, dermatophyte, coccidioidomycosis, subcorneal pustular dermatosis
Hypopigmented
tinea versicolor, vitiligo, pityriasis alba, postinflammatory hypopigmentation, tuberous sclerosis, idiopathic guttate hypomelanosis, leprosy, hypopigmented mycosis fungoides
Without epidermal involvement
Red
Blanchable Erythema
Generalized
drug eruptions, viral exanthems, toxic erythema, systemic lupus erythematosus
Localized
cellulitis, abscess, furuncle, erythema nodosum, carcinoid syndrome, carcinoma erysipeloides, fixed drug eruption
Specialized
urticaria, erythema multiforme, erythema migrans, erythema gyratum repens, erythema annulare centrifugum, erythema ab igne
Nonblanchable Purpura
Macular
thrombocytopenic purpura, actinic purpura
Papular
disseminated intravascular coagulation, vasculitis
Indurated
scleroderma/morphea, granuloma annulare, lichen sclerosis et atrophicus, necrobiosis lipoidica
Miscellaneous
Ulcers
Hair disorders
telogen effluvium, androgenic alopecia, trichotillomania, alopecia areata, systemic lupus erythematosus, tinea capitis, loose anagen syndrome, lichen planopilaris, folliculitis decalvans, acne keloidalis nuchae
Nail disorders
onychomycosis, psoriasis, paronychia, ingrown nail
Mucous membrane disorders
aphthous stomatitis, oral candidiasis, lichen planus, leukoplakia, pemphigus vulgaris, mucous membrane pemphigoid, cicatricial pemphigoid, herpesvirus, coxsackievirus, syphilis, systemic histoplasmosis, squamous cell carcinoma
[show]
v • d • e
Infectious diseases · Bacterial diseases: G+ (primarily A00-A79, 001-041,080-109)
Firmicutes/
(low-G+C)
Clostridium
(ob. anaerobic)
spore-forming: motile (Pseudomembranous colitis, Botulism, Tetanus) · nonmotile (Gas gangrene)
non-spore forming: Peptostreptococcus
Bacilli
(class)
Coccus
Strep (Cat-)
Alpha hemolytic
optochin susceptible: S. pneumoniae (Pneumococcal infection)
optochin resistant: S. viridans (S. mutans)
Beta hemolytic
A, bacitracin susceptible: S. pyogenes (Scarlet fever, Erysipelas, Rheumatic fever, Streptococcal pharyngitis)
B, bacitracin resistant: S. agalactiae
Gamma hemolytic
D: Enterococcus faecalis · Streptococcus bovis
Staph (Cat+)
Cg+ S. aureus (Staphylococcal scalded skin syndrome, Toxic shock syndrome)
Cg- novobiocin susceptible (S. epidermidis) · novobiocin resistant (S. saprophyticus)
Bacillus (shape)
Bacillus (Anthrax, Bacillus cereus) · Listeria (Listeriosis)
Actinobacteria/
(high-G+C)
Actinomycineae
Actinomycosis/Actinomycetoma (Whipple's disease) · Propionibacterium acnes
Corynebacterineae
Mycobacteriaceae
M. tuberculosis/bovis
Tuberculosis: Ghon focus/Ghon's complex · Pott disease · brain (Meningitis, Rich focus) · cutaneous (Scrofula, Bazin disease, Lupus vulgaris, Prosector's wart) · Miliary
M. leprae
Leprosy
Nontuberculous
R1: Mycobacterium kansasii
R3: Mycobacterium avium complex (MAA, MAP, MAI, Lady Windermere syndrome) · Mycobacterium ulcerans (Buruli ulcer)
Corynebacteriaceae
Corynebacterium (Diphtheria, Erythrasma)
Nocardiaceae
Nocardia (Nocardiosis, Maduromycosis)
[show]
v • d • e
Antimycobacterials (J04)
Tuberculosis/
tuberculosis treatment
Aminosalicylic acid
Calcium aminosalicylate · Sodium aminosalicylate
Antibiotics
rifamycins (Rifampicin, Rifabutin, Rifapentine)
aminoglycosides (Amikacin, Capreomycin, Kanamycin, Streptomycin)
alanine analogue (Cycloserine)
Hydrazides
Isoniazid
Thiocarbamides
Ethionamide · Protionamide · Tiocarlide
Others
Ethambutol · Morinamide · Pyrazinamide · Terizidone
Leprosy/
leprostatic agents
rifamycin (Rifampicin)
antifolates (Dapsone, Aldesulfone sodium)
other (Clofazimine)
Retrieved from "http://en.wikipedia.org/wiki/Leprosy"
Categories: Leprosy | Bacterial skin diseases | Infectious skin diseases | Bacterial diseases | Tropical diseases | Neglected diseases
Hidden categories: All articles with unsourced statements | Articles with unsourced statements since November 2007 | Articles with unsourced statements since January 2008 | Articles with unsourced statements since July 2008
Views
From Wikipedia, the free encyclopedia
Jump to: navigation, search
For the malady found in the Hebrew Bible, see Tzaraath. For the album by the band Death, see Leprosy (album).
Leprosy (Hansen's Disease )
Classification and external resources
A 24-year-old man infected with leprosy.
ICD-10 A30.
ICD-9 030
OMIM 246300
DiseasesDB 8478
MedlinePlus 001347
eMedicine med/1281
derm/223
neuro/187
MeSH C01.252.410.040.552.386
Leprosy (from the Greek lepi (λέπι), meaning scales on a fish), or Hansen's disease, is a chronic disease caused by the bacteria Mycobacterium leprae and Mycobacterium lepromatosis.[1][2] Leprosy is primarily a granulomatous disease of the peripheral nerves and mucosa of the upper respiratory tract; skin lesions are the primary external symptom.[3] Left untreated, leprosy can be progressive, causing permanent damage to the skin, nerves, limbs and eyes. Contrary to popular belief, leprosy does not actually cause body parts to simply fall off.[4]
Historically, leprosy has affected mankind since at least 600 BC, and was well-recognized in the civilizations of ancient China, Egypt and India.[5] In 1995, the World Health Organization (WHO) estimated that between two and three million people were permanently disabled because of leprosy.[6] Although the forced quarantine or segregation of patients is unnecessary—and can be considered unethical—a few leper colonies still remain around the world, in countries such as India, Japan, Egypt, Nepal and Vietnam. It is now commonly believed that many of the people who were segregated into these communities were presumed to have leprosy, when they actually had syphilis. Leprosy is not highly infectious, as approximately 95% of people are immune and sufferers are no longer infectious after only a couple of days on treatment. They would not have spread leprosy through a community; whereas syphilis, which has similar symptoms, is more contagious. One of the first signs of leprosy is the unexpected loss of eyelashes.
The age-old social stigma associated with the advanced form of leprosy lingers in many areas, and remains a major obstacle to self-reporting and early treatment. Effective treatment for leprosy appeared in the late 1930s with the introduction of dapsone and its derivatives. However, leprosy bacilli resistant to dapsone gradually evolved and became widespread, and it was not until the introduction of multidrug therapy (MDT) in the early 1980s that the disease could be diagnosed and treated successfully within the community.[citation needed]
Contents
[hide]
* 1 Characteristics
* 2 Classification
* 3 Cause
* 4 Pathophysiology
* 5 Treatment
* 6 Prevention
* 7 Epidemiology
o 7.1 Risk groups
o 7.2 Disease burden
o 7.3 Global situation
* 8 History
* 9 Famous lepers
* 10 References
* 11 See also
* 12 Further reading
* 13 External links
[edit] Characteristics
Cutaneous leprosy lesions on a patient's thigh.
The clinical symptoms of leprosy vary but primarily affect the skin, nerves, and mucous membranes.[7] Patients with this chronic infectious disease are classified as having paucibacillary Hansen's disease (tuberculoid leprosy), multibacillary Hansen's disease (lepromatous leprosy), or borderline leprosy.
[edit] Classification
There is some confusion over classification because the WHO (World Health Organization) replaced an older, more complicated classification system with a simpler system that identifies two subtypes of leprosy: paucibacillary and multibacillary. The older system included six categories: Indeterminate Leprosy, Borderline Tuberculoid Leprosy, Midborderline Leprosy, Borderline Lepromatous Leprosy, Lepromatous Leprosy, and Tuberculoid Leprosy.
Paucibacillary leprosy encompasses indeterminate, tuberculoid, and borderline tuberculoid leprosy. It is characterized by one or more hypopigmented skin macules and anaesthetic patches, where skin sensations are lost because of damaged peripheral nerves that have been attacked by the human host's immune cells.
Multibacillary leprosy includes midborderline, borderline lepromatous, and lepromatous leprosy. It is associated with symmetric skin lesions, nodules, plaques, thickened dermis, and frequent involvement of the nasal mucosa resulting in nasal congestion and epistaxis (nose bleeds) but typically detectable nerve damage is late.
Borderline leprosy is of intermediate severity and is the most common form. Skin lesions resemble tuberculoid leprosy but are more numerous and irregular; large patches may affect a whole limb, and peripheral nerve involvement with weakness and loss of sensation is common. This type is unstable and may become more like lepromatous leprosy or may undergo a reversal reaction, becoming more like the tuberculoid form.
[edit] Cause
Mycobacterium leprae, one of the causative agents of leprosy. As acid-fast bacteria, M. leprae appear red when a Ziehl-Neelsen stain is used.
Main article: Mycobacterium leprae
Mycobacterium leprae and Mycobacterium lepromatosis are the causative agents of leprosy. M. lepromatosis is only the causitive agent in diffuse lepromatous leprosy, which can be lethal.[3][2]
An intracellular, acid-fast bacterium, M. leprae is aerobic and rod-shaped, and is surrounded by the waxy cell membrane coating characteristic of Mycobacterium species.[8]
Due to extensive loss of genes necessary for independent growth, M. leprae and M. lepromatosis are unculturable in the laboratory, a factor which leads to difficulty in definitively identifying the organism under a strict interpretation of Koch's postulates.[9][2] The use of non-culture-based techniques such as molecular genetics has allowed for alternative establishment of causation.
[edit] Pathophysiology
The exact mechanism of transmission of leprosy is not known: prolonged close contact and transmission by nasal droplet have both been proposed, and, while the latter fits the pattern of disease, both remain unproven.[10] The only other animals besides humans known to contract leprosy are the armadillo, chimpanzee, sooty mangabey, and cynomolgus macaque.[11] The bacterium can also be grown in the laboratory by injection into the footpads of mice.[12] There is evidence that not all people who are infected with M. leprae develop leprosy, and genetic factors have long been thought to play a role, due to the observation of clustering of leprosy around certain families, and the failure to understand why certain individuals develop lepromatous leprosy while others develop other types of leprosy.[13] It is estimated that due to genetic factors, only 5 percent of the population is susceptible to leprosy.[14] This is mostly because the body is naturally immune to the bacteria, and those persons who do become infected are experiencing a severe allergic reaction to the disease. However, the role of genetic factors is not entirely clear in determining this clinical expression. In addition, malnutrition and prolonged exposure to infected persons may play a role in development of the overt disease.
The incubation period for the bacteria can last anywhere from two to ten years.
The most widely held belief is that the disease is transmitted by contact between infected persons and healthy persons.[15] In general, closeness of contact is related to the dose of infection, which in turn is related to the occurrence of disease. Of the various situations that promote close contact, contact within the household is the only one that is easily identified, although the actual incidence among contacts and the relative risk for them appear to vary considerably in different studies. In incidence studies, infection rates for contacts of lepromatous leprosy have varied from 6.2 per 1000 per year in Cebu, Philippines[16] to 55.8 per 1000 per year in a part of Southern India.[17]
Two exit routes of M. leprae from the human body often described are the skin and the nasal mucosa, although their relative importance is not clear. It is true that lepromatous cases show large numbers of organisms deep down in the dermis. However, whether they reach the skin surface in sufficient numbers is doubtful. Although there are reports of acid-fast bacilli being found in the desquamating epithelium (sloughing of superficial layer of skin) of the skin, Weddell et al had reported in 1963 that they could not find any acid-fast bacilli in the epidermis, even after examining a very large number of specimens from patients and contacts.[18] In a recent study, Job et al found fairly large numbers of M. leprae in the superficial keratin layer of the skin of lepromatous leprosy patients, suggesting that the organism could exit along with the sebaceous secretions.[19]
The importance of the nasal mucosa was recognized as early as 1898 by Schäffer, particularly that of the ulcerated mucosa.[20] The quantity of bacilli from nasal mucosal lesions in lepromatous leprosy was demonstrated by Shepard as large, with counts ranging from 10,000 to 10,000,000.[21] Pedley reported that the majority of lepromatous patients showed leprosy bacilli in their nasal secretions as collected through blowing the nose.[22] Davey and Rees indicated that nasal secretions from lepromatous patients could yield as much as 10 million viable organisms per day.[23]
The entry route of M. leprae into the human body is also not definitely known. The two seriously considered are the skin and the upper respiratory tract. While older research dealt with the skin route, recent research has increasingly favored the respiratory route. Rees and McDougall succeeded in the experimental transmission of leprosy through aerosols containing M. leprae in immune-suppressed mice, suggesting a similar possibility in humans.[24] Successful results have also been reported on experiments with nude mice when M. leprae were introduced into the nasal cavity by topical application.[25] In summary, entry through the respiratory route appears the most probable route, although other routes, particularly broken skin, cannot be ruled out. The CDC notes the following assertion about the transmission of the disease: "Although the mode of transmission of Hansen's disease remains uncertain, most investigators think that M. leprae is usually spread from person to person in respiratory droplets."[26]
In leprosy both the reference points for measuring the incubation period and the times of infection and onset of disease are difficult to define; the former because of the lack of adequate immunological tools and the latter because of the disease's slow onset. Even so, several investigators have attempted to measure the incubation period for leprosy. The minimum incubation period reported is as short as a few weeks and this is based on the very occasional occurrence of leprosy among young infants.[27] The maximum incubation period reported is as long as 30 years, or over, as observed among war veterans known to have been exposed for short periods in endemic areas but otherwise living in non-endemic areas. It is generally agreed that the average incubation period is between 3 and 5 years.
[edit] Treatment
MDT patient packs and blisters
Until the development of dapsone, rifampicin, and clofazimine in the 1940s, there was no effective cure for leprosy. However, dapsone is only weakly bactericidal against M. leprae and it was considered necessary for patients to take the drug indefinitely. Moreover, when dapsone was used alone, the M. leprae population quickly evolved antibiotic resistance; by the 1960s, the world's only known anti-leprosy drug became virtually useless.
The search for more effective anti-leprosy drugs than dapsone led to the use of clofazimine and rifampicin in the 1960s and 1970s.[28] Later, Indian scientist Shantaram Yawalkar and his colleagues formulated a combined therapy using rifampicin and dapsone, intended to mitigate bacterial resistance.[29] Multidrug therapy (MDT) and combining all three drugs was first recommended by a WHO Expert Committee in 1981. These three anti-leprosy drugs are still used in the standard MDT regimens. None of them are used alone because of the risk of developing resistance.
Because this treatment is quite expensive, it was not quickly adopted in most endemic countries. In 1985 leprosy was still considered a public health problem in 122 countries. The 44th World Health Assembly (WHA), held in Geneva in 1991 passed a resolution to eliminate leprosy as a public health problem by the year 2000 — defined as reducing the global prevalence of the disease to less than 1 case per 100,000. At the Assembly, the World Health Organization (WHO) was given the mandate to develop an elimination strategy by its member states, based on increasing the geographical coverage of MDT and patients’ accessibility to the treatment.
The WHO Study Group's report on the Chemotherapy of Leprosy in 1993 recommended two types of standard MDT regimen be adopted.[30] The first was a 24-month treatment for multibacillary (MB or lepromatous) cases using rifampicin, clofazimine, and dapsone. The second was a six-month treatment for paucibacillary (PB or tuberculoid) cases, using rifampicin and dapsone. At the First International Conference on the Elimination of Leprosy as a Public Health Problem, held in Hanoi the next year, the global strategy was endorsed and funds provided to WHO for the procurement and supply of MDT to all endemic countries.
MDT anti-leprosy drugs: standard regimens
Between 1995 and 1999, WHO, with the aid of the Nippon Foundation (Chairman Yōhei Sasakawa, World Health Organization Goodwill Ambassador for Leprosy Elimination), supplied all endemic countries with free MDT in blister packs, channelled through Ministries of Health. This free provision was extended in 2000 with a donation by the MDT manufacturer Novartis, which will run until at least the end of 2010. At the national level, non-government organizations (NGOs) affiliated to the national programme will continue to be provided with an appropriate free supply of this WHO supplied MDT by the government.
MDT remains highly effective and patients are no longer infectious after the first monthly dose.[5] It is safe and easy to use under field conditions due to its presentation in calendar blister packs.[5] Relapse rates remain low, and there is no known resistance to the combined drugs.[5] The Seventh WHO Expert Committee on Leprosy,[31] reporting in 1997, concluded that the MB duration of treatment—then standing at 24 months—could safely be shortened to 12 months "without significantly compromising its efficacy."
Persistent obstacles to the elimination of the disease include improving detection, educating patients and the population about its cause, and fighting social taboos about a disease for which patients have historically been considered "unclean" or "cursed by God" as outcasts. Where taboos are strong, patients may be forced to hide their condition (and avoid seeking treatment) to avoid discrimination. The lack of awareness about Hansen's disease can lead people to falsely believe that the disease is highly contagious and incurable.
The ALERT hospital and research facility in Ethiopia provides training to medical personnel from around the world in the treatment of leprosy, as well as treating many local patients. Surgical techniques, such as for the restoration of control of movement of thumbs, have been developed there.
[edit] Prevention
A single dose of rifampicin is able to reduce the rate of leprosy in contacts by 57% to 75%.[32][33]
BCG is able to offer a variable amount of protection against leprosy as well as against tuberculosis.[34][35]
[edit] Epidemiology
World distribution of leprosy, 2003.
Worldwide, two to three million people are estimated to be permanently disabled because of Leprosy.[6] India has the greatest number of cases, with Brazil second and Burma third.
In 1999, the world incidence of Hansen's disease was estimated to be 640,000. In 2000, 738,284 cases were identified. In 1999, 108 cases occurred in the United States. In 2000, the World Health Organization (WHO) listed 91 countries in which Hansen's disease is endemic. India, Myanmar and Nepal contained 70% of cases. In 2002, 763,917 new cases were detected worldwide, and in that year the WHO listed Brazil, Madagascar, Mozambique, Tanzania and Nepal as having 90% of Hansen's disease cases.
According to recent figures from the WHO, new cases detected worldwide have decreased by approximately 107,000 cases (or 21%) from 2003 to 2004. This decreasing trend has been consistent for the past three years. In addition, the global registered prevalence of HD was 286,063 cases; 407,791 new cases were detected during 2004.
In the United States, Hansen's disease is tracked by the Centers for Disease Control and Prevention (CDC), with a total of 92 cases being reported in 2002.[36] Although the number of cases worldwide continues to fall, pockets of high prevalence continue in certain areas such as Brazil, South Asia (India, Nepal), some parts of Africa (Tanzania, Madagascar, Mozambique) and the western Pacific.
[edit] Risk groups
At highest risk are those living in endemic areas with poor conditions such as inadequate bedding, contaminated water and insufficient diet, or other diseases (such as HIV) that compromise immune function. Recent research suggests that there is a defect in cell-mediated immunity that causes susceptibility to the disease. Less than ten percent of the world's population is actually capable of acquiring the disease[citation needed]. The region of DNA responsible for this variability is also involved in Parkinson disease[citation needed], giving rise to current speculation that the two disorders may be linked in some way at the biochemical level. In addition, men are twice as likely to contract leprosy as women. According to The Leprosy Mission Canada, most people – about 95% of the population – are naturally immune.
[edit] Disease burden
Although annual incidence—the number of new leprosy cases occurring each year—is important as a measure of transmission, it is difficult to measure in leprosy due to its long incubation period, delays in diagnosis after onset of the disease and the lack of laboratory tools to detect leprosy in its very early stages. - - Instead, the registered prevalence is used. Registered prevalence is a useful proxy indicator of the disease burden as it reflects the number of active leprosy cases diagnosed with the disease and receiving treatment with MDT at a given point in time. The prevalence rate is defined as the number of cases registered for MDT treatment among the population in which the cases have occurred, again at a given point in time.[37]
New case detection is another indicator of the disease that is usually reported by countries on an annual basis. It includes cases diagnosed with onset of disease in the year in question (true incidence) and a large proportion of cases with onset in previous years (termed a backlog prevalence of undetected cases). The new case detection rate (NCDR) is defined by the number of newly detected cases, previously untreated, during a year divided by the population in which the cases have occurred.
Endemic countries also report the number of new cases with established disabilities at the time of detection, as an indicator of the backlog prevalence. However, determination of the time of onset of the disease is generally unreliable, is very labor-intensive and is seldom done in recording these statistics.
[edit] Global situation
Table 1: Prevalence at beginning of 2006, and trends in new case detection 2001-2005, excluding Europe
Region Registered prevalence
(rate/1,000,000 pop.)
New case detection during the year
Start of 2006 2001 2002 2003 2004 2005
Africa 40,830 (0.56) 39,612 48,248 47,006 46,918 42,814
Americas 32,904 (0.39) 42,830 39,939 52,435 52,662 41,780
South-East Asia 133,422 (0.81) 668,658 520,632 405,147 298,603 201,635
Eastern Mediterranean 4,024 (0.09) 4,758 4,665 3,940 3,392 3,133
Western Pacific 8,646 (0.05) 7,404 7,154 6,190 6,216 7,137
Totals NA 763,262 620,638 514,718 407,791 296,499
Table 2: Prevalence and detection, countries still to reach elimination
Countries Registered prevalence
(rate/10,000 pop.)
New case detection
(rate/100,000 pop.)
Start of 2004 Start of 2005 Start of 2006 During 2003 During 2004 During 2005
Brazil 79,908 (4.6) 30,693 (1.7) 27,313 (1.5) 49,206 (28.6) 49,384 (26.9) 38,410 (20.6)
Mozambique 6,810 (3.4) 4,692 (2.4) 4,889 (2.5) 5,907 (29.4) 4,266 (22.0) 5,371 (27.1)
Nepal 7,549 (3.1) 4,699 (1.8) 4,921 (1.8) 8,046 (32.9) 6,958 (26.2) 6,150 (22.7)
Tanzania 5,420 (1.6) 4,777 (1.3) 4,190 (1.1) 5,279 (15.4) 5,190 (13.8) 4,237 (11.1)
Totals NA NA NA NA NA NA
As reported to WHO by 115 countries and territories in 2006, and published in the Weekly Epidemiological Record the global registered prevalence of leprosy at the beginning of the year was 219,826 cases.[38] New case detection during the previous year (2005 - the last year for which full country information is available) was 296,499. The reason for the annual detection being higher than the prevalence at the end of the year can be explained by the fact that a proportion of new cases complete their treatment within the year and therefore no longer remain on the registers. The global detection of new cases continues to show a sharp decline, falling by 110,000 cases (27%) during 2005 compared with the previous year.
Table 1 shows that global annual detection has been declining since 2001. The African region reported an 8.7% decline in the number of new cases compared with 2004. The comparable figure for the Americas was 20.1%, for South-East Asia 32% and for the Eastern Mediterranean it was 7.6%. The Western Pacific area, however, showed a 14.8% increase during the same period.
Table 2 shows the leprosy situation in the four major countries which have yet to achieve the goal of elimination at the national level. It should be noted that: a) Elimination is defined as a prevalence of less than 1 case per 10,000 population; b) Madagascar reached elimination at the national level in September 2006; c) Nepal detection reported from mid-November 2004 to mid-November 2005; and d) D.R. Congo officially reported to WHO in 2008 that it had reached elimination by the end of 2007, at the national level.
[edit] History
The Oxford Illustrated Companion to Medicine holds that the mention of leprosy, as well as ritualistic cures for it, were already described in the Hindu religious book Atharva-veda.[39] Writing in the Encyclopedia Britannica 2008, Kearns & Nash state that the first mention of leprosy is described in the Indian medical treatise Sushruta Samhita (6th century BC).[40] The Cambridge Encyclopedia of Human Paleopathology (1998) holds that: "The Sushruta Samhita from India describes the condition quite well and even offers therapeutic suggestions as early as about 600 BC"[41] The surgeon Sushruta flourished in the Indian city of Kashi by the 6th century BC,[42] and the medical treatise Sushruta Samhita—attributed to him—made its appearance during the 1st millennium BC.[40] The earliest surviving excavated written material which contains the works of Sushruta is the Bower Manuscript—dated to the 4th century AD, almost a millennium after the original work.[43]
In regards to ancient China, Katrina C. D. McLeod and Robin D. S. Yates identify the State of Qin's Feng zhen shi 封診式 (Models for sealing and investigating), dated 266-246 BC, as offering the earliest known unambiguous description of the symptoms of low-resistance leprosy, even though it was termed then under li 癘, a general Chinese word for skin disorder.[44] This 3rd century BC Chinese text on bamboo slip, found in an excavation of 1975 at Shuihudi, Yunmeng, Hubei province, not only described the destruction of the "pillar of the nose", but also the "swelling of the eyebrows, loss of hair, absorption of nasal cartilage, affliction of knees and elbows, difficult and hoarse respiration, as well as anaesthesia."[44]
In the West, the earliest known description of leprosy there was made by the Roman encyclopedist Aulus Cornelius Celsus (25 BC – 37 AD) in his De Medicina; he called leprosy "elephantiasis".[44] The Roman author Pliny the Elder (23–79 AD) mentioned the same disease.[44] Although "sara't" of Leviticus (Old Testament) is translated as "lepra" in the 5th century AD Vulgate, the original term sara't found in Leviticus was not the elephantiasis described by Celsus and Pliny; in fact, sara't was used to describe a disease which could affect houses and clothing.[44] Katrina C. D. McLeod and Robin D. S. Yates state that sara't "denotes a condition of ritual impurity or a temporary form of skin disease."[44] In the Muslim world, the Persian polymath Avicenna (c. 980–1037) was the first outside of China to describe the destruction of the nasal septum in those suffering from leprosy.[44]
Numerous leprosaria, or leper hospitals, sprang up in the Middle Ages; Matthew Paris estimated that in the early thirteenth century there were 19,000 across Europe.[45] The first recorded Leper colony was in Harbledown. These institutions were run along monastic lines and, while lepers were encouraged to live in these monastic-type establishments, this was for their own health as well as quarantine. Indeed, some medieval sources indicate belief that those suffering from leprosy were considered to be going through Purgatory on Earth, and for this reason their suffering was considered holier than the ordinary person's. More frequently, lepers were seen to exist in a place between life and death: they were still alive, yet many chose or were forced to ritually separate themselves from mundane existence.[46]
Radegund was noted for washing the feet of lepers. Orderic Vitalis writes of a monk, Ralf, who was so overcome by the plight of lepers that he prayed to catch leprosy himself (which he eventually did). The leper would carry a clapper and bell to warn of his approach, and this was as much to attract attention for charity as to warn people that a diseased person was near.
G. H. A. Hansen, discoverer of M. leprae
Mycobacterium leprae, the causative agent of leprosy, was discovered by G. H. Armauer Hansen in Norway in 1873, making it the first bacterium to be identified as causing disease in humans.[47][48] He worked at St. Jørgens Hospital in Bergen, founded early in the fifteenth century. St. Jørgens is today a museum, Lepramuseet, probably the best preserved leprosy hospital in Northern Europe.[49]
Historically, individuals with Hansen's disease have been known as lepers, however, this term is falling into disuse as a result of the diminishing number of leprosy patients and the pejorative connotations of the term. The term most widely accepted among professionals is "people affected by Hansen's disease."
Historically, the term Tzaraath from the Hebrew Bible was, erroneously, commonly translated as leprosy, although the symptoms of Tzaraath were not entirely consistent with leprosy and rather referred to a variety of disorders other than Hansen's disease.[50]
In particular, tinea capitis (fungal scalp infection) and related infections on other body parts caused by the dermatophyte fungus Trichophyton violaceum are abundant throughout the Middle East and North Africa today and might also have been common in biblical times. Similarly, the related agent of the disfiguring skin disease favus, Trichophyton schoenleinii, appears to have been common throughout Eurasia and Africa before the advent of modern medicine. Persons with severe favus and similar fungal diseases (and potentially also with severe psoriasis and other diseases not caused by microorganisms) tended to be classed as having leprosy as late as the 17th century in Europe.[51] This is clearly shown in the painting Governors of the Home for Lepers at Haarlem 1667 by Jan de Bray (Frans Hals Museum, Haarlem, the Netherlands), where a young Dutchman with a vivid scalp infection, almost certainly caused by a fungus, is shown being cared for by three officials of a charitable home intended for leprosy sufferers. The use of the word "leprosy" before the mid-19th century, when microscopic examination of skin for medical diagnosis was first developed, can seldom be correlated reliably with Hansen's disease as we understand it today.
The word "leprosy" derives from the ancient Greek words lepros, a scale, and lepein, to peel.[52] The word came into the English language via Latin and Old French. The first attested English use is in the Ancrene Wisse, a 13th-century manual for nuns ("Moyseses hond..bisemde o þe spitel uuel & þuhte lepruse." The Middle English Dictionary, s.v., "leprous"). A roughly contemporaneous use is attested in the Anglo-Norman Dialogues of Saint Gregory, "Esmondez i sont li lieprous" (Anglo-Norman Dictionary, s.v., "leprus").
[edit] Famous lepers
* Blessed Damien of Moloka'i was a Roman Catholic missionary who became a leper when he spent the rest of his life serving in the leper colony at Moloka'i.
* King Baldwin IV of Jerusalem.
* Possibly Robert I de Brus, King of Scots.
* Vietnamese poet Han Mac Tu
* Otani Yoshitsugu, a Japanese Daimyo.
[edit] References
1. ^ Sasaki S, Takeshita F, Okuda K, Ishii N (2001). "Mycobacterium leprae and leprosy: a compendium
". Microbiol Immunol 45 (11): 729–36. PMID 11791665
, http://www.jstage.jst.go.jp/article/mandi/45/11/729/_pdf
.
2. ^ a b c http://www.sciencedaily.com/releases/2008/11/081124141047.htm
3. ^ a b Kenneth J. Ryan, C. George Ray, editors. (2004). Ryan KJ, Ray CG. ed.. Sherris Medical Microbiology (4th ed. ed.), McGraw Hill. pp. 451–3. ISBN 0838585299. OCLC 52358530 61405904
.
4. ^ "Lifting the stigma of leprosy: a new vaccine offers hope against an ancient disease
". Time 119 (19): 87. May 1982. PMID 10255067
, http://www.time.com/time/magazine/article/0,9171,925377,00.html
.
5. ^ a b c d "Leprosy
". WHO. Retrieved on 2007-08-22.
6. ^ a b WHO (1995). "Leprosy disabilities: magnitude of the problem". Weekly Epidemiological Record 70 (38): 269–75. PMID 7577430
.
7. ^ Naafs B, Silva E, Vilani-Moreno F, Marcos E, Nogueira M, Opromolla D (2001). "Factors influencing the development of leprosy: an overview". Int J Lepr Other Mycobact Dis 69 (1): 26–33. PMID 11480313
.
8. ^ McMurray DN (1996). Mycobacteria and Nocardia. in: Baron's Medical Microbiology (Baron S et al, eds.)
(4th ed. ed.), Univ of Texas Medical Branch. ISBN 0-9631172-1-1. OCLC 33838234
, http://www.ncbi.nlm.nih.gov/books/bv.fcgi?rid=mmed.section.1833
.
9. ^ Bhattacharya S, Vijayalakshmi N, Parija SC (2002). "Uncultivable bacteria: Implications and recent trends towards identification
". Indian journal of medical microbiology 20 (4): 174–7. PMID 17657065
, http://www.ijmm.org/article.asp?issn=0255-0857;year=2002;volume=20;issue=4;spage=174;epage=177;aulast=Bhattacharya
.
10. ^ Reich CV (1987). "Leprosy: cause, transmission, and a new theory of pathogenesis". Rev. Infect. Dis. 9 (3): 590–4. PMID 3299638
.
11. ^ Rojas-Espinosa O, Løvik M (2001). "Mycobacterium leprae and Mycobacterium lepraemurium infections in domestic and wild animals". Rev. - Off. Int. Epizoot. 20 (1): 219–51. PMID 11288514
.
12. ^ Hastings RC, Gillis TP, Krahenbuhl JL, Franzblau SG (1988). "Leprosy
". Clin. Microbiol. Rev. 1 (3): 330–48. PMID 3058299
, http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=3058299
.
13. ^ Alcaïs A, Mira M, Casanova JL, Schurr E, Abel L (2005). "Genetic dissection of immunity in leprosy". Curr. Opin. Immunol. 17 (1): 44–8. doi:10.1016/j.coi.2004.11.006
. PMID 15653309
.
14. ^ "AR Dept of Health debunks leprosy fears
" (2008-02-08). Retrieved on 2008-04-08.
15. ^ Kaur H, Van Brakel W (2002). "Dehabilitation of leprosy-affected people—a study on leprosy-affected beggars". Leprosy review 73 (4): 346–55. PMID 12549842
.
16. ^ Doull JA, Guinto RA, Rodriguez RS, et al. (1942). "The incidence of leprosy in Cordova and Talisay, Cebu, Philippines". International Journal of Leprosy 10: 107–131.
17. ^ Noordeen S, Neelan P (1978). "Extended studies on chemoprophylaxis against leprosy". Indian J Med Res 67: 515–27. PMID 355134
.
18. ^ Weddell G, Palmer E (1963). "The pathogenesis of leprosy. An experimental approach". Leprosy Review 34: 57–61. PMID 13999438
.
19. ^ Job C, Jayakumar J, Aschhoff M (1999). ""Large numbers" of Mycobacterium leprae are discharged from the intact skin of lepromatous patients; a preliminary report". Int J Lepr Other Mycobact Dis 67 (2): 164–7. PMID 10472371
.
20. ^ Arch Dermato Syphilis 1898; 44:159–174
21. ^ Shepard C (1960). "Acid-fast bacilli in nasal excretions in leprosy, and results of inoculation of mice". Am J Hyg 71: 147–57. PMID 14445823
.
22. ^ Pedley J (1973). "The nasal mucus in leprosy". Lepr Rev 44 (1): 33–5. PMID 4584261
.
23. ^ Davey T, Rees R (1974). "The nasal dicharge in leprosy: clinical and bacteriological aspects". Lepr Rev 45 (2): 121–34. PMID 4608620
.
24. ^ Rees R, McDougall A (1977). "Airborne infection with Mycobacterium leprae in mice". J Med Microbiol 10 (1): 63–8. PMID 320339
.
25. ^ Chehl S, Job C, Hastings R (1985). "Transmission of leprosy in nude mice". Am J Trop Med Hyg 34 (6): 1161–6. PMID 3914846
.
26. ^ CDC Disease Info hansens_t
Hansen's Disease (Leprosy)
27. ^ Montestruc E, Berdonneau R (1954). "2 New cases of leprosy in infants in Martinique" (in French). Bull Soc Pathol Exot Filiales 47 (6): 781–3. PMID 14378912
.
28. ^ Rees RJ, Pearson JM, Waters MF (1970). "Experimental and clinical studies on rifampicin in treatment of leprosy". Br Med J 688 (1): 89–92. PMID 4903972
.
29. ^ Yawalkar SJ, McDougall AC, Languillon J, Ghosh S, Hajra SK, Opromolla DV, Tonello CJ (1982). "Once-monthly rifampicin plus daily dapsone in initial treatment of lepromatous leprosy". Lancet 8283 (1): 1199–1202. doi:10.1016/S0140-6736(82)92334-0
. PMID 6122970
.
30. ^ "Chemotherapy of Leprosy
". WHO Technical Report Series 847. WHO (1994). Retrieved on 2007-03-24.
31. ^ "Seventh WHO Expert Committee on Leprosy
". WHO Technical Report Series 874. WHO (1998). Retrieved on 2007-03-24.
32. ^ Moet FJ, Pahan D, Oskam L, Richardus JH (2008). "Effectiveness of single dose rifampicin in preventing leprosy in close contacts of patients with newly diagnosed leprosy: cluster randomised controlled trial". BMJ 336: 761. doi:10.1136/bmj.39500.885752.BE
. PMID 18332051
.
33. ^ Bakker MI, Hatta M, Kwenang A, et al. (2005). "Prevention of leprosy using rifampicin as chemoprophylaxis
". Am J Trop Med Hyg 72: 443–8. PMID 15827283
, http://www.ajtmh.org/cgi/content/abstract/72/4/443?ijkey=4b15a78b876fd990dfd877ee89b22399c026501c&keytype2=tf_ipsecsha
.
34. ^ Fine PE, Smith PG (1996). "Vaccination against leprosy—the view from 1996". Lepr Rev 67 (4): 249–52. PMID 9033195
.
35. ^ Karonga prevention trial group (1996). "Randomized controlled trial of single BCG, repeated BCG, or combined BCG and killed Mycobacterium leprae vaccine for prevention of leprosy and tuberculosis in Malawi". Lancet 348: 17–24. doi:10.1016/S0140-6736(96)02166-6
. PMID 8691924
.
36. ^ CDC Leprosy Fact Sheet
.
37. ^ "Epidemiology of leprosy in relation to control. Report of a WHO Study Group". World Health Organ Tech Rep Ser (Geneva: World Health Organization) 716: 1–60. 1985. ISBN 9241207167. OCLC 12095109
. PMID 3925646
.
38. ^ "Global leprosy situation, 2006
" (PDF). Weekly Epidemiological Record 81 (32): 309–16. August 2006. PMID 16903018
, http://www.who.int/lep/resources/wer8132.pdf
.
39. ^ Lock etc., page 420
40. ^ a b Kearns & Nash (2008)
41. ^ Aufderheide, A. C.; Rodriguez-Martin, C. & Langsjoen, O. (1998). The Cambridge Encyclopedia of Human Paleopathology. Cambridge University Press. ISBN 0521552036. Page 148.
42. ^ Dwivedi & Dwivedi (2007)
43. ^ Kutumbian, P. (2005). Ancient Indian Medicine. Orient Longman. ISBN 8125015213. pages XXXII-XXXIII.
44. ^ a b c d e f g McLeod, Katrina C. D. and Robin D. S. Yates (June 1981). "Forms of Ch'in Law: An Annotated Translation of The Feng-chen shih". Harvard Journal of Asiatic Studies 41 (1): 111–63. Pages 152–3 & footnote 147. doi:10.2307/2719003
.
45. ^ "Leprosy". Catholic Encyclopedia. (1913). New York: Robert Appleton Company.
46. ^ Brody, Saul Nathaniel (1974). The Disease of the Soul: Leprosy in Medieval Literature. Ithaca: Cornell Press.
47. ^ Hansen GHA (1874). "Undersøgelser Angående Spedalskhedens Årsager (Investigations concerning the etiology of leprosy)" (in Norwegian). Norsk Mag. Laegervidenskaben 4: 1–88.
48. ^ Irgens L (2002). "The discovery of the leprosy bacillus". Tidsskr nor Laegeforen 122 (7): 708–9. PMID 11998735
.
49. ^ Bymuseet i Bergen
50. ^ Artscroll Tanakh, Leviticus 13:59, 1996
51. ^ Kane J, Summerbell RC, Sigler L, Krajden S, Land G (1997). Laboratory Handbook of Dermatophytes: A clinical guide and laboratory manual of dermatophytes and other filamentous fungi from skin, hair and nails, Star Publishers (Belmont, CA). ISBN 0898631572. OCLC 37116438
.
52. ^ Barnhart RK (1995). Barnhart Concise Dictionary of Etymology. New York: Harper Collins. ISBN 0062700847. OCLC 221898877 223496345 231655185 30399281
.
[edit] See also
* Dwivedi, Girish & Dwivedi, Shridhar (2007). History of Medicine: Sushruta – the Clinician – Teacher par Excellence
. National Informatics Centre (Government of India).
* Dunea, George; Lock, Stephen; Last, John M. (2001). The Oxford illustrated companion to medicine. Oxford [Oxfordshire]: Oxford University Press. ISBN 0-19-262950-6. OCLC 150308752 180030517 213488544 244006190 43342122 46678589 58460632 59406536 69646604
.
* Kearns, Susannah C.J. & Nash, June E. (2008). Leprosy. Encyclopedia Britannica.
[edit] Further reading
* Bargès A (1993). "Ségrégation antilépreuse et comportements adaptatifs à Bamako (Mali)
" (PDF). Ecologie humaine 11 (2): 7–20, http://halshs.archives-ouvertes.fr/docs/00/25/89/20/PDF/Environnmement_africain_et_maladie-Barges1993.pdf
.
* Bargès A (1996). "Entre conformismes et changements, le monde de la lèpre au Mali
" (PDF). Paris, Editions Karthala: 280–313, http://halshs.archives-ouvertes.fr/docs/00/26/60/96/PDF/Le_monde_la_lepre_1996(1993).pdf
.
* Clark E (1994). "Social Welfare and Mutual Aid in the Medieval Countryside
". The Journal of British Studies 33 (4): 394–6, http://links.jstor.org/sici?sici=0021-9371(199410)33%3A4%3C381%3ASWAMAI%3E2.0.CO%3B2-L
.
* Icon Health Publications (2004). Leprosy: A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References, San Diego: Icon Health Publications. ISBN 0-597-84006-7. OCLC 162128079 191036288
.
* Demaitre L (2007). Leprosy in Premodern Medicine: A Malady of the Whole Body. Baltimore, Maryland: The Johns Hopkins University Press. ISBN 978-0-8018-8613-3. OCLC 238882127 70921424
.
* Rawcliffe C (2001). "Learning to Love the Leper: aspects of institutional Charity in Anglo Norman England". Anglo Norman Studies 23: 233–52.
* Rawcliffe C (2006). Leprosy in Medieval England. Ipswich: Boydell Press. ISBN 1843832739. OCLC 70765638
.
* Talarigo J (2004). The Pearl Diver: (fiction) young woman with leprosy is exiled to leprosy colony in Japan, 1929, Doubleday. ISBN 1-4025-8661-2. OCLC 55066644
.
* Tayman J (2006). The Colony: The Harrowing True Story of the Exiles of Molokai, Simon & Schuster. ISBN 0-7432-3300.
* Brennert A (2003). Moloka'i:(fiction) young woman with leprosy is exiled to leprosy colony in Hawaii, 1891, St. Martin's Press. ISBN 0-312-30435-8. OCLC 123959155 56695775
.
[edit] External links
Sister project Wikimedia Commons has media related to: Leprosy
* Leprosy and Human Rights
- event held at Woodrow Wilson International Center for Scholars, March 2008
* National Hansen's Disease Programs (NHDP), U.S. Health Resources and Services Administration
* Hansen's Disease (Leprosy)
- Centers for Disease Control and Prevention
* World Health Organization (WHO) leprosy website
* Hope in a Modern-Day Leper Colony
Article from a leper colony in India
* American Leprosy Missions
* Rinaldi A (December 2005). "The global campaign to eliminate leprosy
". PLoS Med. 2 (12): e341. doi:10.1371/journal.pmed.0020341
. PMID 16363908
.
* LEPRA - Health in Action
UK Based organisation founded in 1924 to treat leprosy and related diseases of poverty.
History of leprosy
* "History of Leprosy, Urban Environment and French Colonization in West Africa
" (PDF).
* "Anthropology and History of leprosy
" (Histoire & Anthropologie, 15 (1995) 115-122).
* ILA Global Project on the History of Leprosy
* National Hansen's Disease Museum
* BBC News: Slave trade key to leprosy spread
* "Interview with author John Tayman (The Colony)
" (MP3 audio: runtime = 00:23:20, 10.7 mb). IT Conversations Tech Nation (2006-02-07). Retrieved on 2007-03-22.
Research
* Pathology Images of Leprosy and Other Granulomatous diseases
Yale Rosen, M.D.
* INFOLEP Leprosy Information Services
* Leprosy Review
* "Medical anthropology, Leprosy and Health Care in French speaking West-Africa
" (PDF).
* "Anthropologie, lèpre et santé publique
".
* "Gender and Leprosy
".
* Photographs of leprosy patients
: type leprosy in the diagnosis space for some photographs and then type leproma for another photograph.
[show]
v • d • e
Diseases of the skin and appendages by morphology
Growths
Epidermal
verruca, clavus, seborrheic keratosis, acrochordon, molluscum contagiosum, actinic keratosis, squamous cell carcinoma, basal cell carcinoma, merkel cell carcinoma, nevus sebaceous, trichoepithelioma
Pigmented
ephelis, lentigo, melasma, nevus, malignant melanoma
Dermal and subcutaneous
epidermal inclusion cyst, hemangioma, dermatofibroma, keloid, lipoma, neurofibroma, xanthoma, Kaposi's sarcoma, infantile digital fibromatosis, granular cell tumor, leiomyoma, lymphangioma circumscriptum, myxoid cyst
Rashes
With epidermal involvement
Eczematous
essential dermatitis, contact dermatitis, atopic dermatitis, seborrheic dermatitis, stasis dermatitis, lichen simplex chronicus, Darier's disease, glucagonoma syndrome, langerhans cell histiocytosis, lichen sclerosus, pemphigus foliaceus, Wiskott-Aldrich syndrome, Zinc deficiency
Scaling
psoriasis, tinea corporis, tinea cruris, tinea pedis, tinea manuum, tinea faciale, pityriasis rosea, secondary syphillis, mycosis fungoides, systemic lupus erythematosus, pityriasis rubra pilaris, parapsoriasis, icthyosis
Blistering
herpes simplex, herpes zoster, varicella, bullous impetigo, acute contact dermatitis, pemphigus vulgaris, bullous pemphigoid, dermatitis herpetiformis, porphyria cutanea tarda, epidermolysis bullosa simplex
Papular
scabies, insect bite reactions, lichen planus, miliaria, keratosis pilaris, lichen spinulosus, transient acantholytic dermatosis, lichen nitidus, pityriasis lichenoides et varioliformis acuta
Pustular
acne vulgaris, acne rosacea, folliculitis, impetigo, candidiasis, gonococcemia, dermatophyte, coccidioidomycosis, subcorneal pustular dermatosis
Hypopigmented
tinea versicolor, vitiligo, pityriasis alba, postinflammatory hypopigmentation, tuberous sclerosis, idiopathic guttate hypomelanosis, leprosy, hypopigmented mycosis fungoides
Without epidermal involvement
Red
Blanchable Erythema
Generalized
drug eruptions, viral exanthems, toxic erythema, systemic lupus erythematosus
Localized
cellulitis, abscess, furuncle, erythema nodosum, carcinoid syndrome, carcinoma erysipeloides, fixed drug eruption
Specialized
urticaria, erythema multiforme, erythema migrans, erythema gyratum repens, erythema annulare centrifugum, erythema ab igne
Nonblanchable Purpura
Macular
thrombocytopenic purpura, actinic purpura
Papular
disseminated intravascular coagulation, vasculitis
Indurated
scleroderma/morphea, granuloma annulare, lichen sclerosis et atrophicus, necrobiosis lipoidica
Miscellaneous
Ulcers
Hair disorders
telogen effluvium, androgenic alopecia, trichotillomania, alopecia areata, systemic lupus erythematosus, tinea capitis, loose anagen syndrome, lichen planopilaris, folliculitis decalvans, acne keloidalis nuchae
Nail disorders
onychomycosis, psoriasis, paronychia, ingrown nail
Mucous membrane disorders
aphthous stomatitis, oral candidiasis, lichen planus, leukoplakia, pemphigus vulgaris, mucous membrane pemphigoid, cicatricial pemphigoid, herpesvirus, coxsackievirus, syphilis, systemic histoplasmosis, squamous cell carcinoma
[show]
v • d • e
Infectious diseases · Bacterial diseases: G+ (primarily A00-A79, 001-041,080-109)
Firmicutes/
(low-G+C)
Clostridium
(ob. anaerobic)
spore-forming: motile (Pseudomembranous colitis, Botulism, Tetanus) · nonmotile (Gas gangrene)
non-spore forming: Peptostreptococcus
Bacilli
(class)
Coccus
Strep (Cat-)
Alpha hemolytic
optochin susceptible: S. pneumoniae (Pneumococcal infection)
optochin resistant: S. viridans (S. mutans)
Beta hemolytic
A, bacitracin susceptible: S. pyogenes (Scarlet fever, Erysipelas, Rheumatic fever, Streptococcal pharyngitis)
B, bacitracin resistant: S. agalactiae
Gamma hemolytic
D: Enterococcus faecalis · Streptococcus bovis
Staph (Cat+)
Cg+ S. aureus (Staphylococcal scalded skin syndrome, Toxic shock syndrome)
Cg- novobiocin susceptible (S. epidermidis) · novobiocin resistant (S. saprophyticus)
Bacillus (shape)
Bacillus (Anthrax, Bacillus cereus) · Listeria (Listeriosis)
Actinobacteria/
(high-G+C)
Actinomycineae
Actinomycosis/Actinomycetoma (Whipple's disease) · Propionibacterium acnes
Corynebacterineae
Mycobacteriaceae
M. tuberculosis/bovis
Tuberculosis: Ghon focus/Ghon's complex · Pott disease · brain (Meningitis, Rich focus) · cutaneous (Scrofula, Bazin disease, Lupus vulgaris, Prosector's wart) · Miliary
M. leprae
Leprosy
Nontuberculous
R1: Mycobacterium kansasii
R3: Mycobacterium avium complex (MAA, MAP, MAI, Lady Windermere syndrome) · Mycobacterium ulcerans (Buruli ulcer)
Corynebacteriaceae
Corynebacterium (Diphtheria, Erythrasma)
Nocardiaceae
Nocardia (Nocardiosis, Maduromycosis)
[show]
v • d • e
Antimycobacterials (J04)
Tuberculosis/
tuberculosis treatment
Aminosalicylic acid
Calcium aminosalicylate · Sodium aminosalicylate
Antibiotics
rifamycins (Rifampicin, Rifabutin, Rifapentine)
aminoglycosides (Amikacin, Capreomycin, Kanamycin, Streptomycin)
alanine analogue (Cycloserine)
Hydrazides
Isoniazid
Thiocarbamides
Ethionamide · Protionamide · Tiocarlide
Others
Ethambutol · Morinamide · Pyrazinamide · Terizidone
Leprosy/
leprostatic agents
rifamycin (Rifampicin)
antifolates (Dapsone, Aldesulfone sodium)
other (Clofazimine)
Retrieved from "http://en.wikipedia.org/wiki/Leprosy"
Categories: Leprosy | Bacterial skin diseases | Infectious skin diseases | Bacterial diseases | Tropical diseases | Neglected diseases
Hidden categories: All articles with unsourced statements | Articles with unsourced statements since November 2007 | Articles with unsourced statements since January 2008 | Articles with unsourced statements since July 2008
Views
Biological pest control
Biological pest control
From Wikipedia, the free encyclopedia
Jump to: navigation, search
Ladybird larva eating Wooly Apple Aphids (Eriosoma lanigerum)
Biological control of pests in agriculture is a method of controlling pests (including insects, mites, weeds and plant diseases) that relies on predation, parasitism, herbivory, or other natural mechanisms. It can be an important component of integrated pest management (IPM) programs.
Contents
[hide]
* 1 Overview
* 2 Conservation
o 2.1 Effects of biological control on biodiversity
+ 2.1.1 Effects on native biodiversity
+ 2.1.2 Effects on invasive species
+ 2.1.3 Effects on future
+ 2.1.4 Economic effects
* 3 Classical biological control
* 4 Augmentation
* 5 Examples of predators
* 6 Parasitoid insects
* 7 Biological control with micro-organisms
o 7.1 Bacteria and biological control
o 7.2 Fungi and biological control
* 8 Plants to regulate insect pests
* 9 Plants to regulate plants
* 10 Directly introducing biological controls
* 11 Economics of biological pest control
* 12 Negative results of biological pest control
* 13 References
* 14 See also
* 15 External links and references
[edit] Overview
Diagram illustrating the natural enemies of cabbage pests
Biological Control is defined as the reduction of pest populations by natural enemies and typically involves an active human role. Natural enemies of insect pests, also known as biological control agents, include predators, parasitoids, and pathogens. Biological control agents of plant diseases are most often referred to as antagonists. Biological control agents of weeds include herbivores and plant pathogens. Predators, such as lady beetles and lacewings, are mainly free-living species that consume a large number of prey during their lifetime. Parasitoids are species whose immature stage develops on or within a single insect host, ultimately killing the host. Most have a very narrow host range. Many species of wasps and some flies are parasitoids. Pathogens are disease-causing organisms including bacteria, fungi, and viruses. They kill or debilitate their host and are relatively specific to certain insect groups. There are three basic types of biological control strategies; conservation, classical biological control, and augmentation. These are discussed in more detail below.
[edit] Conservation
The conservation of natural enemies is probably the most important and readily available biological control practice available to homeowners and gardeners. Natural enemies occur in all areas, from the backyard garden to the commercial field. They are adapted to the local environment and to the target pest, and their conservation is generally simple and cost-effective. Lacewings, lady beetles, hover fly larvae, and parasitized aphid mummies are almost always present in aphid colonies. Fungus-infected adult flies are often common following periods of high humidity. These naturally occurring biological controls are often susceptible to the same pesticides used to target their hosts. Preventing the accidental eradication of natural enemies is termed simple conservation.
[edit] Effects of biological control on biodiversity
[edit] Effects on native biodiversity
The cane toad, Bufo marinus
Biological control can potentially have positive and negative effects on biodiversity. Most of the time a biological control is introduced to an area to protect a native species from an invasive or exotic species that has moved into its area. The control is introduced to lessen the competition among native and invasive species. However, the introduced control does not always target only the intended species. It can also target native species.[citation needed]
When introducing a biological control to a new area, a primary concern is the host- or prey-specificity of the control agent. Generalist feeders (control agents that are not restricted to a single species or a small range of species) often make poor biological control agents, and may become invasive species themselves. For this reason, potential biological control agents should be subject to extensive testing and quarantine before release into any new environment. If a species is introduced and attacks a native species, the biodiversity in that area can decrease dramatically. When one native species is removed from an area, it may have filled an essential niche, When this niche is absent it will directly affect the entire ecosystem.[citation needed] Because they tend to be generalist feeders, vertebrate animals seldom make good biological control agents, and many of the classic cases of "biocontrol gone awry" involve vertebrates. For example, the cane toad (Bufo marinus) was introduced as a biological control and had significant negative impact on biodiversity. The cane toad was intentionally introduced to Australia to control the cane beetle. When introduced, the cane toad thrived very well and did not only feed on cane beetles but other insects as well. The cane toad soon spread very rapidly, thus taking over native habitat. The introduction of the cane toad also brought foreign disease to native reptiles. This drastically reduced the population of native toads and frogs. “The cane toad also exudes and can squirt poison from the parotid glands on their shoulders when threatened or handled. This toxin contains a cocktail of chemicals that can kill animals that eat it. Freshwater crocodiles, goannas, tiger snakes, dingos and northern quolls have all died after eating cane toads, as have pet dogs (Cane toad,2003) ”. This goes to show a small but deadly organism can alter the native biodiversity in an ecosystem in a very expedient manner. A pyramid effect can take place if native species are reduced or eradicated. The domino effect keeps on going and can potentially exude on other bordering ecosystems until an equilibrium is reached.
A second example of a biological control agent that subsequently crossed over to native species is the Rhinocyllus conicus. The seed feeding weevil was introduced to North America to control exotic thistles (Musk and Canadian). However, the weevil did not target only the exotic thistles, it also targeted native thistles that are essential to various native insects. The native insects rely solely on native thistles and do not adapt to other plant species. Therefore, they cannot survive. Biological controls do not always have negative impacts on biodiversity (Corry 2000). Successful biological control reduces the density of the target species over several years, thus providing the potential for native species to re-establish. In addition, regeneration and reestablishment programs can aid to the recovery of native species. Native species can be affected in a positive way as well. To develop or find a biological control that exerts control only on the targeted species is a very lengthy process of research and experiments. In the late 1800’s, the citrus industry was in great fear when the cottony cushion scale was discovered. This organism could cause a great deal of economic loss to the industry. However, a biological control was introduced. The vedalia beetle and a parasitoid fly were introduced to control the pest. Within a few years time, the cottony cushion scale was controlled by the natural enemies and the citrus industry suffered little financial loss. Many exotic or invasive species can suppress the development of native species. The introduction of an effective biological control that reduces the population of the invasive species allows the rejuvenation of the native species. Biological controls can reduce competition for biotic and abiotic factors which can result in the re-establishment of the once over ran native species.[citation needed]
[edit] Effects on invasive species
The invasive species Alternanthera philoxeroides (alligator weed) was successfully controlled in Florida (U.S.) by the introduction of Agasicles hygrophila (alligator weed flea beetle)
Invasive species are closely associated with biological controls because the environment in which they are invasive most likely does not contain their natural enemies. If invasive species are not controlled, biodiversity may be at great threat in the affected area. An example of an invasive species is the alligator weed.[1] This plant was introduced to the United States from South America. This aquatic weed spreads very rapidly and causes many problems in lakes and rivers. The weed takes root in shallow water causing major problems such as navigation, irrigation, and flood control. The alligator weed flea beetle and two other biological controls were released in Florida. Because of their success, Florida banned the use of herbicides to control alligator weed three years after the controls were introduced (Cofrancesco 2007). Biological controls for invasive species also can have a negative impact on biodiversity.
The cane toad, as mentioned previously, is a great example of trying to control an invasive species. The cane toad was introduced to eradicate an invasive species. However, it became invasive, thus altering the biodiversity. The introduction of the cane toad could have potentially caused more of a disturbance in biodiversity than the targeted species did.
[edit] Effects on future
With further research and more scientific experiments, biological control could potentially play a huge role in the future of pest prevention. Biological control is being used among society today; however, it could someday reduce the use of many pesticides and herbicides. Since biological control could potentially have a large economic value, if found to be successful, research and job fields would increase continually. By increasing awareness of biological controls among more people, new successful biological controls could be discovered in the future. This could eliminate the overuse of chemicals. Biodiversity would increase because untargeted species that are exterminated with chemicals would no longer occur.[citation needed]
[edit] Economic effects
Therefore, biological control is heavily analyzed by the amount of economic gain that directly comes from biological control. Many of the known economics of biological control are related directly to agriculture practices. Since agriculture has a huge impact on biodiversity this could potentially increase the biodiversity among agricultural practices. In order for agriculture to keep up with the growing population, many inputs are increased resulting in the loss of un-harmful species. Biological control use has been very minimal in agriculture. Less than 1% of global pest control sales of $30 billion involve biological methods (Griffiths 2007:in press). Very few case studies on the cost-benefit analysis of biological control have been done however a few have taken place. A Critical evaluation of augmentative biological control has found four case studies. In one case, “the releases of a parasitoid Gryon pennsylvanicum Ashmead to control the true bug Anasa tristis DeGeer on pumpkins produced lower net benefit (in dollars) than applications of esfenvalerate (pesticide); 18% lower in one year and 120% lower in the next. In 1 year of the study, a combination of augmentative releases and use of a resistant pumpkin variety produced greater net benefit than pesticide alone, but not pesticide combined with the resistant variety (Olson et al. 1996) ”. Another case study found that “calculated that releases of T. nubilale were considerably less cost-effective than pesticide applications used to control ECB on feed corn and fresh-market sweet corn. Pesticide applications produced 87% and 45% more net benefit (in dollars) than augmentation for feed corn and fresh market corn, respectively. In seed corn, however, Trichogramma releases produced essentially equivalent net benefits to pesticide treatments. In a third cost-benefit analysis of augmentation, Lundgren et al. (2002) showed that Trichogramma brassicae Bezdenko releases produced considerably less net benefit (94%; measured in cabbage head production) than methomyl treatments (Andow 1997). In two other studies, “biological control releases were about two times the cost of pesticide applications; this was true for releases of a parasitoid, Choetospila elegans Westwood, used to control a stored product pest, Rhyzopertha dominica (F.) (Flinn et al.,1996) and releases of green lacewings, Chrysoperla carnea Stephens to control leafhoppers in grapes (Daane et al., 1996). Finally Prokrym et al. (1992) suggested that Trichogramma releases were about six times as expensive as pesticide treatments for O. nubilalis in sweet corn,” (Collier 2003). These case studies offer us some idea of how economical biological control can be. These show that biological control is less cost effective than chemical applications and in result raises a flag that more research needs to be done. With progression in research, we can use more controls at a cheaper cost and increase the amount of biodiversity in areas because of the minimal use of chemicals that cannot target a specific species of pest.
[edit] Classical biological control
Classical biological control is the introduction of natural enemies to a new locale where they did not originate or do not occur naturally. This is usually done by government authorities. In many instances the complex of natural enemies associated with an insect pest may be inadequate. This is especially evident when an insect pest is accidentally introduced into a new geographic area without its associated natural enemies. These introduced pests are referred to as exotic pests and comprise about 40% of the insect pests in the United States. Examples of introduced vegetable pests include the European corn borer (Ostrinia nubilalis), one of the most destructive insects in North America. To obtain the needed natural enemies, scientists turned to classical biological control. This is the practice of importing, and releasing for establishment, natural enemies to control an introduced (exotic) pest, although it is also practiced against native insect pests. The first step in the process is to determine the origin of the introduced pest and then collect appropriate natural enemies associated with the pest or closely related species. The natural enemy is then passed through a rigorous quarantine process, to ensure that no unwanted organisms (such as hyperparasitoids) are introduced, then they are mass produced, and released. Follow-up studies are conducted to determine if the natural enemy becomes successfully established at the site of release, and to assess the long-term benefit of its presence.
There are many examples of successful classical biological control programs. One of the earliest successes was in controlling Icerya purchasi, the cottony cushion scale, a pest that was devastating the California citrus industry in the late 1800s. A predatory insect Rodolia cardinalis (the Vedalia Beetle), and a parasitoid fly were introduced from Australia. Within a few years the cottony cushion scale was completely controlled by these introduced natural enemies.
Damage from Hypera postica Gyllenhal, the alfalfa weevil, a serious introduced pest of forage, was substantially reduced by the introduction of several natural enemies. About 20 years after their introduction, the population of weevils, in the alfalfa area treated for alfalfa weevil in the Northeastern United States, was reduced by 75 percent. A small wasp, Trichogramma ostriniae, was introduced from China to help control the European corn borer making it a recent example of a long history of classical biological control efforts for this major pest. Many classical biological control programs for insect pests and weeds are under way across the United States and Canada. The population of Levuana irridescens (the Levuana moth), a serious coconut pest in Fiji was brought under control by a classical biological control program in the 1920s.
Classical biological control is long lasting and inexpensive. Other than the initial costs of collection, importation, and rearing, little expense is incurred. When a natural enemy is successfully established it rarely requires additional input and it continues to kill the pest with no direct help from humans and at no cost. Unfortunately, classical biological control does not always work. It is usually most effective against exotic pests and less so against native insect pests. The reasons for failure are not often known, but may include the release of too few individuals, poor adaptation of the natural enemy to environmental conditions at the release location, and lack of synchrony between the life cycle of the natural enemy and host pest.
[edit] Augmentation
This third type of biological control involves the supplemental release of natural enemies. Relatively few natural enemies may be released at a critical time of the season (inoculative release) or literally millions may be released (inundative release). Additionally, the cropping system may be modified to favor or augment the natural enemies. This latter practice is frequently referred to as habitat manipulation.
An example of inoculative release occurs in greenhouse production of several crops. Periodic releases of the parasitoid, Encarsia formosa, are used to control greenhouse whitefly, and the predaceous mite, Phytoseiulus persimilis, is used for control of the two-spotted spider mite.
Lady beetles, lacewings, or parasitoids such as those from the genus Trichogramma are frequently released in large numbers (inundative release). Recommended release rates for Trichogramma in vegetable or field crops range from 5,000 to 200,000 per acre per week depending on level of pest infestation. Similarly, entomopathogenic nematodes are released at rates of millions and even billions per acre for control of certain soil-dwelling insect pests.
A turnaround flowerpot, filled with straw to attract Dermaptera-species
Habitat or environmental manipulation is another form of augmentation. This tactic involves altering the cropping system to augment or enhance the effectiveness of a natural enemy. Many adult parasitoids and predators benefit from sources of nectar and the protection provided by refuges such as hedgerows, cover crops, and weedy borders. Also, the provisioning of natural shelters in the form of wooden caskets, boxes or (turnaround) flowerpots is a form of this. For example, the stimulation of the natural predator Dermaptera is done in gardens by hanging up turnaround flowerpots with straw or wood wool.
Mixed plantings and the provision of flowering borders can increase the diversity of habitats and provide shelter and alternative food sources. They are easily incorporated into home gardens and even small-scale commercial plantings, but are more difficult to accommodate in large-scale crop production. There may also be some conflict with pest control for the large producer because of the difficulty of targeting the pest species and the use of refuges by the pest insects as well as natural enemies.
Examples of habitat manipulation include growing flowering plants (pollen and nectar sources) near crops to attract and maintain populations of natural enemies. For example, hover fly adults can be attracted to umbelliferous plants in bloom.
Biological control experts in California have demonstrated that planting prune trees in grape vineyards provides an improved overwintering habitat or refuge for a key grape pest parasitoid. The prune trees harbor an alternate host for the parasitoid, which could previously overwinter only at great distances from most vineyards. Caution should be used with this tactic because some plants attractive to natural enemies may also be hosts for certain plant diseases, especially plant viruses that could be vectored by insect pests to the crop. Although the tactic appears to hold much promise, only a few examples have been adequately researched and developed.
[edit] Examples of predators
Lacewings are available from biocontrol dealers.
Ladybugs, and in particular their larvae which are active between May and July in the northern hemisphere, are voracious predators of aphids such as greenfly and blackfly, and will also consume mites, scale insects and small caterpillars. The ladybug is a very familiar beetle with various colored markings, whilst its larvae are initially small and spidery, growing up to 17 mm long. The larvae have a tapering segmented grey/black body with orange/yellow markings and ferocious mouthparts. They can be encouraged by cultivating a patch of nettles in the garden and by leaving hollow stems and some plant debris over winter so that they can hibernate.
Hoverflies resemble slightly darker bees or wasps and they have characteristic hovering, darting flight patterns. There are over 100 species of hoverfly whose larvae principally feed upon greenfly, one larva devouring up to fifty a day, or 1000 in its lifetime. They also eat fruit tree spider mites and small caterpillars. Adults feed on nectar and pollen, which they require for egg production. Eggs are minute (1 mm), pale yellow white and laid singly near greenfly colonies. Larvae are 8-17 mm long, disguised to resemble bird droppings, they are legless and have no distinct head. Semi-transparent in a range of colours from green, white, brown and black.
Predatory Polistes wasp looking for bollworms or other caterpillars on a cotton plant
Hoverflies can be encouraged by growing attractant flowers such as the poached egg plant (Limnanthes douglasii), marigolds or phacelia throughout the growing season.
Dragonflies are important predators of mosquitoes, both in the water, where the dragonfly naiads eat mosquito larvae, and in the air, where adult dragonflies capture and eat adult mosquitoes. Community-wide mosquito control programs that spray adult mosquitoes also kill dragonflies, thus removing an important biocontrol agent, and can actually increase mosquito populations in the long term.
Other useful garden predators include lacewings, pirate bugs, rove and ground beetles, aphid midge, centipedes, predatory mites, as well as larger fauna such as frogs, toads, lizards, hedgehogs, slow-worms and birds. Cats and rat terriers kill field mice, rats, June bugs, and birds. Dogs chase away many types of pest animals. Dachshunds are bred specifically to fit inside tunnels underground to kill badgers.
* Phytoseiulus persimilis (against spider mites)
* Amblyseius californicus (against spider mites)
* Amblyseius cucumeris (against spider mites)[2]
* Typhlodromips swirskii (against spider mites, thrips, and white flies)
* Feltiella acarisuga (against spider mites)
* Stethorus punctillum (against spider mites)
* Macrolophus caluginosus (against spider mites)
* Encarsia formosa (against white flies)
* Eretmocerus spp. (against white flies)[3]
[edit] Parasitoid insects
Most insect parasitoids are wasps or flies. Parasitiods comprise a diverse range of insects that lay their egg on or in the body of an insect host, which is then used as a food for developing larvae. Parasitic wasps take much longer than predators to consume their victims, for if the larvae were to eat too fast they would run out of food before they became adults. Such parasites are very useful in the organic garden, for they are very efficient hunters, always at work searching for pest invaders. As adults they require high energy fuel as they fly from place to place, and feed upon nectar, pollen and sap, therefore planting plenty of flowering plants, particularly buckwheat, umbellifers, and composites will encourage their presence.
Four of the most important groups are:
* Ichneumonid wasps: (5-10 mm). Prey mainly on caterpillars of butterflies and moths.
* Braconid wasps: Tiny wasps (up to 5 mm) attack caterpillars and a wide range of other insects including greenfly. A common parasite of the cabbage white caterpillar- seen as clusters of sulphur yellow cocoons bursting from collapsed caterpillar skin.
* Chalcid wasps: Among the smallest of insects (<3 mm). Parasitize eggs/larvae of greenfly, whitefly, cabbage caterpillars, scale insects and Strawberry Tortrix Moth (Acleris comariana).
* Tachinid flies: Parasitize a wide range of insects including caterpillars, adult and larval beetles, true bugs, and others.
[edit] Biological control with micro-organisms
Various microbial insect diseases occur naturally, but may also be used as biological pesticides. When naturally occurring, these outbreaks are density dependent in that they generally only occur as insect populations become denser.
[edit] Bacteria and biological control
Bacteria used for biological control infect insects via their digestive tracts, so insects with sucking mouth parts like aphids and scale insects are difficult to control with bacterial biological control.[4] Bacillus thuringiensis is the most widely applied species of bacteria used for biological control, with at least four sub-species used to control Lepidopteran (moth, butterfly), Coleopteran (beetle) and Dipteran (true flies) insect pests.
[edit] Fungi and biological control
Fungi that cause disease in insects are known as entomopathogenic fungi, including at least fourteen species of entomophthoraceous fungi attack aphids.[5] Species in the genus Trichoderma are used to manage some soilborne plant pathogens.
[edit] Plants to regulate insect pests
Further information: List of pest-regulating plants
Further information: List_of_repellent_plants
See also: Ecologic pesticides and herbicides
Choosing a diverse range of plants for the garden can help to regulate pests in a variety of ways, including;
* Masking the crop plants from pests, depending on the proximity of the companion or intercrop.
* Producing olfactory inhibitors, odors that confuse and deter pests.
* Acting as trap plants by providing an alluring food that entices pests away from crops.
* Serving as nursery plants, providing breeding grounds for beneficial insects.
* Providing an alternative habitat, usually in a form of a shelterbelt, hedgerow, or beetle bank where beneficial insects can live and reproduce. Nectar-rich plants that bloom for long periods are especially good, as many beneficials are nectivorous during the adult stage, but parasitic or predatory as larvae. A good example of this is the soldier beetle which is frequently found on flowers as an adult, but whose larvae eat aphids, caterpillars, grasshopper eggs, and other beetles.
[edit] Plants to regulate plants
The legume vine Mucuna pruriens is used in the countries of Benin and Vietnam as a biological control for problematic Imperata cylindrica grass.[6] Mucuna pruriens is said not to be invasive outside its cultivated area.[6]
[edit] Directly introducing biological controls
Diagram illustrating the life cycles of Greenhouse whitefly and its parasitoid wasp Encarsia formosa
Most of the biological controls listed above depend on providing incentives in order to 'naturally' attract beneficial insects to the garden. However there are occasions when biological controls can be directly introduced. Common biocontrol agents include parasitoids, predators, pathogens or weed feeders. This is particularly appropriate in situations such as the greenhouse, a largely artificial environment, and are usually purchased by mail order.
Some biocontrol agents that can be introduced include;
* Encarsia formosa. This is a small predatory chalcid wasp which is parasitical on whitefly, a sap-feeding insect which can cause wilting and black sooty moulds. It is most effective when dealing with low level infestations, giving protection over a long period of time. The wasp lays its eggs in young whitefly 'scales', turning them black as the parasite larvae pupates. It should be introduced as soon as possible after the first adult whitefly are seen. Should be used in conjunction with insecticidal soap.
* Red spider mite, another pest found in the greenhouse, can be controlled with the predatory mite Phytoseilus persimilis. This is slightly larger than its prey and has an orange body. It develops from egg to adult twice as fast as the red spider mite and once established quickly overcomes infestation.
* A fairly recent development in the control of slugs is the introduction of 'Nemaslug', a microscopic nematode (Phasmarhabditis hermaphrodita) which will seek out and parasitize slugs, reproducing inside them and killing them. The nematode is applied by watering onto moist soil, and gives protection for up to six weeks in optimum conditions, though is mainly effective with small and young slugs under the soil surface.
* A bacterial biological control which can be introduced in order to control butterfly caterpillars is Bacillus thuringiensis. This available in sachets of dried spores which are mixed with water and sprayed onto vulnerable plants such as brassicas and fruit trees. The bacterial disease will kill the caterpillars, but leave other insects unharmed. There are strains of Bt that are effective against other insect larvae. Bt israelensis is effective against mosquito larvae and some midges.
The European Rabbit (Oryctolagus cuniculus) is seen as a major pest in Australia
* A viral biological control which can be introduced in order to control the overpopulation of European rabbit in Australia is the rabbit haemorrhagic disease virus that causes the rabbit haemorrhagic disease.
* A biological control being developed for use in the treatment of plant disease is the fungus Trichoderma viride. This has been used against Dutch Elm disease, and to treat the spread of fungal and bacterial growth on tree wounds. It may also have potential as a means of combating silver leaf disease.
* The parasitoid Gonatocerus ashmeadi (Hymenoptera: Mymaridae) has been introduced to control the glassy-winged sharpshooter Homalodisca vitripennis (Hemipterae: Cicadellidae) in French Polynesia and has successfully controlled ~95% of the pest density[7]
[edit] Economics of biological pest control
Biological control proves to be very successful economically, and even when the method has been less successful, it still produces a benefit-to-cost ratio of 11:1. One study has estimated that a successful biocontrol program returns £32 in benefits for each £1 invested in developing and implementing the program, i.e., a 32:1 benefit-to-cost ratio. The same study had shown that an average chemical pesticide program only returned profits in the ratio of 13:1.[citation needed]
[edit] Negative results of biological pest control
In some cases, biological pest control can have unforeseen negative results that could outweigh all benefits. For example, when the mongoose was introduced to Hawaii in order to control the rat population, it preyed on the endemic birds of Hawaii, especially their eggs, more often than it ate the rats.
Cane toads (Bufo marinus) were introduced to Australia in the 1930s in a failed attempt to control the cane beetle, a pest of sugar cane crops. 102 toads were obtained from Hawaii and bred in captivity to increase their numbers until they were released into the sugar cane fields of the tropic north in 1935. It was later discovered that the toads can't jump very high so they did not eat the cane beetles which stayed up on the upper stalks of the cane plants. The toads soon became very numerous and out-competed native species and became very harmful to the Australian environment, including being very toxic to would-be predators such as native snakes. [1]
[edit] References
This article needs additional citations for verification. Please help improve this article by adding reliable references. Unsourced material may be challenged and removed. (September 2007)
1. ^ "Alternanthera philoxeroides information from NPGS/GRIN
". www.ars-grin.gov. Retrieved on 2008-08-09.
2. ^ Spider mites and their natural enemies
3. ^ White flies and their natural enemies
4. ^ L.A. Swan. 1964. Beneficial Insects. 1st ed. page 249.
5. ^ I.M. Hall & P.H. Dunn, Entomophthorous Fungi Parasitic on the Spotted Alfalfa Aphid, Hilgardia, Sept 1957.
6. ^ a b "Factsheet - Mucuna pruriens
". www.tropicalforages.info. Retrieved on 2008-05-21.
7. ^ Hoddle M.S., Grandgirard J., Petit J., Roderick G.K., Davies N. (2006). "Glassy-winged sharpshooter Ko'ed - First round - in French Polynesia". Biocontrol News and Information 27 (3): 47N–62N.
Biological control
* Wiedenmann, R. 2000. Introduction to Biological Control. Midwest Institute for Biological Control. Illinois. Available from http://www.inhs.uiuc.edu/research/biocontrol
Building organic pest-free gardens
* The Time Saving Garden
by David and Charles PLC/Reader's Digest, ISBN 13: 9780276442452
Effects on native biodiversity
* Pereira, M.J. et al. (1998) Conservation of natural vegetation in Azores Islands. Bol. Mus. Munic. Funchal 5, 299–305
* Weeden, C.R., A. M. Shelton, and M. P. Hoffman. Biological Control: A Guide to Natural Enemies in North America. Available from [2]
(accessed December 2007)
* Cane toad: a case study. 2003. Available from [3]
(accessed December 2007)
* Humphrey, J. and Hyatt. 2004. CSIRO Australian Animal Health Laboratory. Biological Control of the Cane Toad Bufo marinus in Australia
* Cory, J. and Myers, J. 2000. Direct and indirect ecological effects of biological control. Trends in Ecology & Evolution. 15, 4, 137-139.
* Johnson, M. 2000. Nature and Scope of Biological Control. Biological Control of Pest. 675
Effects on invasive species
* Cofrancesco, A. 2007. U.S. National Management Plan: An Action Plant for the Nation- Control and Management. Army Corps of Engineers. Available from [4]
* Lass, D. and Miller, R. 1995. BioScience. 45, 10. 680.
Effects on the future
* Cooksey D. 2002. Biological Control in Pest Management Systems of Plants.
Western Regional Committee, Riverside, CA.
Economic effects
* Griffiths, G.J.K. 2007. Efficacy and economics of shelter habitats for conservation. Biological Control: in press. doi:10.1016/j.biocontrol.2007.09.002
* Collier T. and Steenwyka, R. 2003. A critical evaluation of augmentative biological control. Economics of augmentation: 31, 245-256.
[edit] See also
* Insectary plants
* Integrated Pest Management
* Japanese beetle (article includes information on biological control methods)
* Organic farming
* Biological pesticide
* Sterile insect technique
* Mating disruption
[edit] External links and references
* Biological Control: A Guide to Natural Enemies in North America
* Beyond Pesticides
- Provides information on pesticides and alternatives to their use.
* Grow'Em Organic Pest Control
- organic pest control solutions available to small- and large-scale gardeners, described in detail
* Construction of a ecological garden and implementation of natural pest control
* 2 other pdf-files about the construction of a ecological garden and implementation of natural pest control
* Education movies about biological pest control of white flies, aphids and spider mites in greenhouses
* Association of Natural Biocontrol Producers (ANBP)
Trade association of biological pest control industry.
* Successful biocontrol of the GWSS in French Polynesia
* R. James Cook (September 1993). "Making Greater Use of Introduced Microorganisms for Biological Control of Plant Pathogens
". Annual Review of Phytopathology 31: 53–80. doi:10.1146/annurev.py.31.090193.000413
, http://arjournals.annualreviews.org/doi/abs/10.1146/annurev.py.31.090193.000413
.
* U.S. Congress, Office of Technology Assessment. "Biologically based technologies for pest control
" (PDF). US Government Printing Office, Washington, DC.
* Felix Wäckers, Paul van Rijn and Jan Bruin. "Plant-Provided Food for Carnivorous Insects - a protective mutualism and its applications.". Cambridge University Press, UK, 2005.
* Alternative Methods of Mole Cricket Control
at the University of Florida
Retrieved from "http://en.wikipedia.org/wiki/Biological_pest_control"
Categories: Gardening | Organic gardening | Biological pest control
Hidden categories: All articles with unsourced statements | Articles with unsourced statements since December 2007 | Articles with unsourced statements since February 2007 | Articles needing additional references from September 2007
Views
From Wikipedia, the free encyclopedia
Jump to: navigation, search
Ladybird larva eating Wooly Apple Aphids (Eriosoma lanigerum)
Biological control of pests in agriculture is a method of controlling pests (including insects, mites, weeds and plant diseases) that relies on predation, parasitism, herbivory, or other natural mechanisms. It can be an important component of integrated pest management (IPM) programs.
Contents
[hide]
* 1 Overview
* 2 Conservation
o 2.1 Effects of biological control on biodiversity
+ 2.1.1 Effects on native biodiversity
+ 2.1.2 Effects on invasive species
+ 2.1.3 Effects on future
+ 2.1.4 Economic effects
* 3 Classical biological control
* 4 Augmentation
* 5 Examples of predators
* 6 Parasitoid insects
* 7 Biological control with micro-organisms
o 7.1 Bacteria and biological control
o 7.2 Fungi and biological control
* 8 Plants to regulate insect pests
* 9 Plants to regulate plants
* 10 Directly introducing biological controls
* 11 Economics of biological pest control
* 12 Negative results of biological pest control
* 13 References
* 14 See also
* 15 External links and references
[edit] Overview
Diagram illustrating the natural enemies of cabbage pests
Biological Control is defined as the reduction of pest populations by natural enemies and typically involves an active human role. Natural enemies of insect pests, also known as biological control agents, include predators, parasitoids, and pathogens. Biological control agents of plant diseases are most often referred to as antagonists. Biological control agents of weeds include herbivores and plant pathogens. Predators, such as lady beetles and lacewings, are mainly free-living species that consume a large number of prey during their lifetime. Parasitoids are species whose immature stage develops on or within a single insect host, ultimately killing the host. Most have a very narrow host range. Many species of wasps and some flies are parasitoids. Pathogens are disease-causing organisms including bacteria, fungi, and viruses. They kill or debilitate their host and are relatively specific to certain insect groups. There are three basic types of biological control strategies; conservation, classical biological control, and augmentation. These are discussed in more detail below.
[edit] Conservation
The conservation of natural enemies is probably the most important and readily available biological control practice available to homeowners and gardeners. Natural enemies occur in all areas, from the backyard garden to the commercial field. They are adapted to the local environment and to the target pest, and their conservation is generally simple and cost-effective. Lacewings, lady beetles, hover fly larvae, and parasitized aphid mummies are almost always present in aphid colonies. Fungus-infected adult flies are often common following periods of high humidity. These naturally occurring biological controls are often susceptible to the same pesticides used to target their hosts. Preventing the accidental eradication of natural enemies is termed simple conservation.
[edit] Effects of biological control on biodiversity
[edit] Effects on native biodiversity
The cane toad, Bufo marinus
Biological control can potentially have positive and negative effects on biodiversity. Most of the time a biological control is introduced to an area to protect a native species from an invasive or exotic species that has moved into its area. The control is introduced to lessen the competition among native and invasive species. However, the introduced control does not always target only the intended species. It can also target native species.[citation needed]
When introducing a biological control to a new area, a primary concern is the host- or prey-specificity of the control agent. Generalist feeders (control agents that are not restricted to a single species or a small range of species) often make poor biological control agents, and may become invasive species themselves. For this reason, potential biological control agents should be subject to extensive testing and quarantine before release into any new environment. If a species is introduced and attacks a native species, the biodiversity in that area can decrease dramatically. When one native species is removed from an area, it may have filled an essential niche, When this niche is absent it will directly affect the entire ecosystem.[citation needed] Because they tend to be generalist feeders, vertebrate animals seldom make good biological control agents, and many of the classic cases of "biocontrol gone awry" involve vertebrates. For example, the cane toad (Bufo marinus) was introduced as a biological control and had significant negative impact on biodiversity. The cane toad was intentionally introduced to Australia to control the cane beetle. When introduced, the cane toad thrived very well and did not only feed on cane beetles but other insects as well. The cane toad soon spread very rapidly, thus taking over native habitat. The introduction of the cane toad also brought foreign disease to native reptiles. This drastically reduced the population of native toads and frogs. “The cane toad also exudes and can squirt poison from the parotid glands on their shoulders when threatened or handled. This toxin contains a cocktail of chemicals that can kill animals that eat it. Freshwater crocodiles, goannas, tiger snakes, dingos and northern quolls have all died after eating cane toads, as have pet dogs (Cane toad,2003) ”. This goes to show a small but deadly organism can alter the native biodiversity in an ecosystem in a very expedient manner. A pyramid effect can take place if native species are reduced or eradicated. The domino effect keeps on going and can potentially exude on other bordering ecosystems until an equilibrium is reached.
A second example of a biological control agent that subsequently crossed over to native species is the Rhinocyllus conicus. The seed feeding weevil was introduced to North America to control exotic thistles (Musk and Canadian). However, the weevil did not target only the exotic thistles, it also targeted native thistles that are essential to various native insects. The native insects rely solely on native thistles and do not adapt to other plant species. Therefore, they cannot survive. Biological controls do not always have negative impacts on biodiversity (Corry 2000). Successful biological control reduces the density of the target species over several years, thus providing the potential for native species to re-establish. In addition, regeneration and reestablishment programs can aid to the recovery of native species. Native species can be affected in a positive way as well. To develop or find a biological control that exerts control only on the targeted species is a very lengthy process of research and experiments. In the late 1800’s, the citrus industry was in great fear when the cottony cushion scale was discovered. This organism could cause a great deal of economic loss to the industry. However, a biological control was introduced. The vedalia beetle and a parasitoid fly were introduced to control the pest. Within a few years time, the cottony cushion scale was controlled by the natural enemies and the citrus industry suffered little financial loss. Many exotic or invasive species can suppress the development of native species. The introduction of an effective biological control that reduces the population of the invasive species allows the rejuvenation of the native species. Biological controls can reduce competition for biotic and abiotic factors which can result in the re-establishment of the once over ran native species.[citation needed]
[edit] Effects on invasive species
The invasive species Alternanthera philoxeroides (alligator weed) was successfully controlled in Florida (U.S.) by the introduction of Agasicles hygrophila (alligator weed flea beetle)
Invasive species are closely associated with biological controls because the environment in which they are invasive most likely does not contain their natural enemies. If invasive species are not controlled, biodiversity may be at great threat in the affected area. An example of an invasive species is the alligator weed.[1] This plant was introduced to the United States from South America. This aquatic weed spreads very rapidly and causes many problems in lakes and rivers. The weed takes root in shallow water causing major problems such as navigation, irrigation, and flood control. The alligator weed flea beetle and two other biological controls were released in Florida. Because of their success, Florida banned the use of herbicides to control alligator weed three years after the controls were introduced (Cofrancesco 2007). Biological controls for invasive species also can have a negative impact on biodiversity.
The cane toad, as mentioned previously, is a great example of trying to control an invasive species. The cane toad was introduced to eradicate an invasive species. However, it became invasive, thus altering the biodiversity. The introduction of the cane toad could have potentially caused more of a disturbance in biodiversity than the targeted species did.
[edit] Effects on future
With further research and more scientific experiments, biological control could potentially play a huge role in the future of pest prevention. Biological control is being used among society today; however, it could someday reduce the use of many pesticides and herbicides. Since biological control could potentially have a large economic value, if found to be successful, research and job fields would increase continually. By increasing awareness of biological controls among more people, new successful biological controls could be discovered in the future. This could eliminate the overuse of chemicals. Biodiversity would increase because untargeted species that are exterminated with chemicals would no longer occur.[citation needed]
[edit] Economic effects
Therefore, biological control is heavily analyzed by the amount of economic gain that directly comes from biological control. Many of the known economics of biological control are related directly to agriculture practices. Since agriculture has a huge impact on biodiversity this could potentially increase the biodiversity among agricultural practices. In order for agriculture to keep up with the growing population, many inputs are increased resulting in the loss of un-harmful species. Biological control use has been very minimal in agriculture. Less than 1% of global pest control sales of $30 billion involve biological methods (Griffiths 2007:in press). Very few case studies on the cost-benefit analysis of biological control have been done however a few have taken place. A Critical evaluation of augmentative biological control has found four case studies. In one case, “the releases of a parasitoid Gryon pennsylvanicum Ashmead to control the true bug Anasa tristis DeGeer on pumpkins produced lower net benefit (in dollars) than applications of esfenvalerate (pesticide); 18% lower in one year and 120% lower in the next. In 1 year of the study, a combination of augmentative releases and use of a resistant pumpkin variety produced greater net benefit than pesticide alone, but not pesticide combined with the resistant variety (Olson et al. 1996) ”. Another case study found that “calculated that releases of T. nubilale were considerably less cost-effective than pesticide applications used to control ECB on feed corn and fresh-market sweet corn. Pesticide applications produced 87% and 45% more net benefit (in dollars) than augmentation for feed corn and fresh market corn, respectively. In seed corn, however, Trichogramma releases produced essentially equivalent net benefits to pesticide treatments. In a third cost-benefit analysis of augmentation, Lundgren et al. (2002) showed that Trichogramma brassicae Bezdenko releases produced considerably less net benefit (94%; measured in cabbage head production) than methomyl treatments (Andow 1997). In two other studies, “biological control releases were about two times the cost of pesticide applications; this was true for releases of a parasitoid, Choetospila elegans Westwood, used to control a stored product pest, Rhyzopertha dominica (F.) (Flinn et al.,1996) and releases of green lacewings, Chrysoperla carnea Stephens to control leafhoppers in grapes (Daane et al., 1996). Finally Prokrym et al. (1992) suggested that Trichogramma releases were about six times as expensive as pesticide treatments for O. nubilalis in sweet corn,” (Collier 2003). These case studies offer us some idea of how economical biological control can be. These show that biological control is less cost effective than chemical applications and in result raises a flag that more research needs to be done. With progression in research, we can use more controls at a cheaper cost and increase the amount of biodiversity in areas because of the minimal use of chemicals that cannot target a specific species of pest.
[edit] Classical biological control
Classical biological control is the introduction of natural enemies to a new locale where they did not originate or do not occur naturally. This is usually done by government authorities. In many instances the complex of natural enemies associated with an insect pest may be inadequate. This is especially evident when an insect pest is accidentally introduced into a new geographic area without its associated natural enemies. These introduced pests are referred to as exotic pests and comprise about 40% of the insect pests in the United States. Examples of introduced vegetable pests include the European corn borer (Ostrinia nubilalis), one of the most destructive insects in North America. To obtain the needed natural enemies, scientists turned to classical biological control. This is the practice of importing, and releasing for establishment, natural enemies to control an introduced (exotic) pest, although it is also practiced against native insect pests. The first step in the process is to determine the origin of the introduced pest and then collect appropriate natural enemies associated with the pest or closely related species. The natural enemy is then passed through a rigorous quarantine process, to ensure that no unwanted organisms (such as hyperparasitoids) are introduced, then they are mass produced, and released. Follow-up studies are conducted to determine if the natural enemy becomes successfully established at the site of release, and to assess the long-term benefit of its presence.
There are many examples of successful classical biological control programs. One of the earliest successes was in controlling Icerya purchasi, the cottony cushion scale, a pest that was devastating the California citrus industry in the late 1800s. A predatory insect Rodolia cardinalis (the Vedalia Beetle), and a parasitoid fly were introduced from Australia. Within a few years the cottony cushion scale was completely controlled by these introduced natural enemies.
Damage from Hypera postica Gyllenhal, the alfalfa weevil, a serious introduced pest of forage, was substantially reduced by the introduction of several natural enemies. About 20 years after their introduction, the population of weevils, in the alfalfa area treated for alfalfa weevil in the Northeastern United States, was reduced by 75 percent. A small wasp, Trichogramma ostriniae, was introduced from China to help control the European corn borer making it a recent example of a long history of classical biological control efforts for this major pest. Many classical biological control programs for insect pests and weeds are under way across the United States and Canada. The population of Levuana irridescens (the Levuana moth), a serious coconut pest in Fiji was brought under control by a classical biological control program in the 1920s.
Classical biological control is long lasting and inexpensive. Other than the initial costs of collection, importation, and rearing, little expense is incurred. When a natural enemy is successfully established it rarely requires additional input and it continues to kill the pest with no direct help from humans and at no cost. Unfortunately, classical biological control does not always work. It is usually most effective against exotic pests and less so against native insect pests. The reasons for failure are not often known, but may include the release of too few individuals, poor adaptation of the natural enemy to environmental conditions at the release location, and lack of synchrony between the life cycle of the natural enemy and host pest.
[edit] Augmentation
This third type of biological control involves the supplemental release of natural enemies. Relatively few natural enemies may be released at a critical time of the season (inoculative release) or literally millions may be released (inundative release). Additionally, the cropping system may be modified to favor or augment the natural enemies. This latter practice is frequently referred to as habitat manipulation.
An example of inoculative release occurs in greenhouse production of several crops. Periodic releases of the parasitoid, Encarsia formosa, are used to control greenhouse whitefly, and the predaceous mite, Phytoseiulus persimilis, is used for control of the two-spotted spider mite.
Lady beetles, lacewings, or parasitoids such as those from the genus Trichogramma are frequently released in large numbers (inundative release). Recommended release rates for Trichogramma in vegetable or field crops range from 5,000 to 200,000 per acre per week depending on level of pest infestation. Similarly, entomopathogenic nematodes are released at rates of millions and even billions per acre for control of certain soil-dwelling insect pests.
A turnaround flowerpot, filled with straw to attract Dermaptera-species
Habitat or environmental manipulation is another form of augmentation. This tactic involves altering the cropping system to augment or enhance the effectiveness of a natural enemy. Many adult parasitoids and predators benefit from sources of nectar and the protection provided by refuges such as hedgerows, cover crops, and weedy borders. Also, the provisioning of natural shelters in the form of wooden caskets, boxes or (turnaround) flowerpots is a form of this. For example, the stimulation of the natural predator Dermaptera is done in gardens by hanging up turnaround flowerpots with straw or wood wool.
Mixed plantings and the provision of flowering borders can increase the diversity of habitats and provide shelter and alternative food sources. They are easily incorporated into home gardens and even small-scale commercial plantings, but are more difficult to accommodate in large-scale crop production. There may also be some conflict with pest control for the large producer because of the difficulty of targeting the pest species and the use of refuges by the pest insects as well as natural enemies.
Examples of habitat manipulation include growing flowering plants (pollen and nectar sources) near crops to attract and maintain populations of natural enemies. For example, hover fly adults can be attracted to umbelliferous plants in bloom.
Biological control experts in California have demonstrated that planting prune trees in grape vineyards provides an improved overwintering habitat or refuge for a key grape pest parasitoid. The prune trees harbor an alternate host for the parasitoid, which could previously overwinter only at great distances from most vineyards. Caution should be used with this tactic because some plants attractive to natural enemies may also be hosts for certain plant diseases, especially plant viruses that could be vectored by insect pests to the crop. Although the tactic appears to hold much promise, only a few examples have been adequately researched and developed.
[edit] Examples of predators
Lacewings are available from biocontrol dealers.
Ladybugs, and in particular their larvae which are active between May and July in the northern hemisphere, are voracious predators of aphids such as greenfly and blackfly, and will also consume mites, scale insects and small caterpillars. The ladybug is a very familiar beetle with various colored markings, whilst its larvae are initially small and spidery, growing up to 17 mm long. The larvae have a tapering segmented grey/black body with orange/yellow markings and ferocious mouthparts. They can be encouraged by cultivating a patch of nettles in the garden and by leaving hollow stems and some plant debris over winter so that they can hibernate.
Hoverflies resemble slightly darker bees or wasps and they have characteristic hovering, darting flight patterns. There are over 100 species of hoverfly whose larvae principally feed upon greenfly, one larva devouring up to fifty a day, or 1000 in its lifetime. They also eat fruit tree spider mites and small caterpillars. Adults feed on nectar and pollen, which they require for egg production. Eggs are minute (1 mm), pale yellow white and laid singly near greenfly colonies. Larvae are 8-17 mm long, disguised to resemble bird droppings, they are legless and have no distinct head. Semi-transparent in a range of colours from green, white, brown and black.
Predatory Polistes wasp looking for bollworms or other caterpillars on a cotton plant
Hoverflies can be encouraged by growing attractant flowers such as the poached egg plant (Limnanthes douglasii), marigolds or phacelia throughout the growing season.
Dragonflies are important predators of mosquitoes, both in the water, where the dragonfly naiads eat mosquito larvae, and in the air, where adult dragonflies capture and eat adult mosquitoes. Community-wide mosquito control programs that spray adult mosquitoes also kill dragonflies, thus removing an important biocontrol agent, and can actually increase mosquito populations in the long term.
Other useful garden predators include lacewings, pirate bugs, rove and ground beetles, aphid midge, centipedes, predatory mites, as well as larger fauna such as frogs, toads, lizards, hedgehogs, slow-worms and birds. Cats and rat terriers kill field mice, rats, June bugs, and birds. Dogs chase away many types of pest animals. Dachshunds are bred specifically to fit inside tunnels underground to kill badgers.
* Phytoseiulus persimilis (against spider mites)
* Amblyseius californicus (against spider mites)
* Amblyseius cucumeris (against spider mites)[2]
* Typhlodromips swirskii (against spider mites, thrips, and white flies)
* Feltiella acarisuga (against spider mites)
* Stethorus punctillum (against spider mites)
* Macrolophus caluginosus (against spider mites)
* Encarsia formosa (against white flies)
* Eretmocerus spp. (against white flies)[3]
[edit] Parasitoid insects
Most insect parasitoids are wasps or flies. Parasitiods comprise a diverse range of insects that lay their egg on or in the body of an insect host, which is then used as a food for developing larvae. Parasitic wasps take much longer than predators to consume their victims, for if the larvae were to eat too fast they would run out of food before they became adults. Such parasites are very useful in the organic garden, for they are very efficient hunters, always at work searching for pest invaders. As adults they require high energy fuel as they fly from place to place, and feed upon nectar, pollen and sap, therefore planting plenty of flowering plants, particularly buckwheat, umbellifers, and composites will encourage their presence.
Four of the most important groups are:
* Ichneumonid wasps: (5-10 mm). Prey mainly on caterpillars of butterflies and moths.
* Braconid wasps: Tiny wasps (up to 5 mm) attack caterpillars and a wide range of other insects including greenfly. A common parasite of the cabbage white caterpillar- seen as clusters of sulphur yellow cocoons bursting from collapsed caterpillar skin.
* Chalcid wasps: Among the smallest of insects (<3 mm). Parasitize eggs/larvae of greenfly, whitefly, cabbage caterpillars, scale insects and Strawberry Tortrix Moth (Acleris comariana).
* Tachinid flies: Parasitize a wide range of insects including caterpillars, adult and larval beetles, true bugs, and others.
[edit] Biological control with micro-organisms
Various microbial insect diseases occur naturally, but may also be used as biological pesticides. When naturally occurring, these outbreaks are density dependent in that they generally only occur as insect populations become denser.
[edit] Bacteria and biological control
Bacteria used for biological control infect insects via their digestive tracts, so insects with sucking mouth parts like aphids and scale insects are difficult to control with bacterial biological control.[4] Bacillus thuringiensis is the most widely applied species of bacteria used for biological control, with at least four sub-species used to control Lepidopteran (moth, butterfly), Coleopteran (beetle) and Dipteran (true flies) insect pests.
[edit] Fungi and biological control
Fungi that cause disease in insects are known as entomopathogenic fungi, including at least fourteen species of entomophthoraceous fungi attack aphids.[5] Species in the genus Trichoderma are used to manage some soilborne plant pathogens.
[edit] Plants to regulate insect pests
Further information: List of pest-regulating plants
Further information: List_of_repellent_plants
See also: Ecologic pesticides and herbicides
Choosing a diverse range of plants for the garden can help to regulate pests in a variety of ways, including;
* Masking the crop plants from pests, depending on the proximity of the companion or intercrop.
* Producing olfactory inhibitors, odors that confuse and deter pests.
* Acting as trap plants by providing an alluring food that entices pests away from crops.
* Serving as nursery plants, providing breeding grounds for beneficial insects.
* Providing an alternative habitat, usually in a form of a shelterbelt, hedgerow, or beetle bank where beneficial insects can live and reproduce. Nectar-rich plants that bloom for long periods are especially good, as many beneficials are nectivorous during the adult stage, but parasitic or predatory as larvae. A good example of this is the soldier beetle which is frequently found on flowers as an adult, but whose larvae eat aphids, caterpillars, grasshopper eggs, and other beetles.
[edit] Plants to regulate plants
The legume vine Mucuna pruriens is used in the countries of Benin and Vietnam as a biological control for problematic Imperata cylindrica grass.[6] Mucuna pruriens is said not to be invasive outside its cultivated area.[6]
[edit] Directly introducing biological controls
Diagram illustrating the life cycles of Greenhouse whitefly and its parasitoid wasp Encarsia formosa
Most of the biological controls listed above depend on providing incentives in order to 'naturally' attract beneficial insects to the garden. However there are occasions when biological controls can be directly introduced. Common biocontrol agents include parasitoids, predators, pathogens or weed feeders. This is particularly appropriate in situations such as the greenhouse, a largely artificial environment, and are usually purchased by mail order.
Some biocontrol agents that can be introduced include;
* Encarsia formosa. This is a small predatory chalcid wasp which is parasitical on whitefly, a sap-feeding insect which can cause wilting and black sooty moulds. It is most effective when dealing with low level infestations, giving protection over a long period of time. The wasp lays its eggs in young whitefly 'scales', turning them black as the parasite larvae pupates. It should be introduced as soon as possible after the first adult whitefly are seen. Should be used in conjunction with insecticidal soap.
* Red spider mite, another pest found in the greenhouse, can be controlled with the predatory mite Phytoseilus persimilis. This is slightly larger than its prey and has an orange body. It develops from egg to adult twice as fast as the red spider mite and once established quickly overcomes infestation.
* A fairly recent development in the control of slugs is the introduction of 'Nemaslug', a microscopic nematode (Phasmarhabditis hermaphrodita) which will seek out and parasitize slugs, reproducing inside them and killing them. The nematode is applied by watering onto moist soil, and gives protection for up to six weeks in optimum conditions, though is mainly effective with small and young slugs under the soil surface.
* A bacterial biological control which can be introduced in order to control butterfly caterpillars is Bacillus thuringiensis. This available in sachets of dried spores which are mixed with water and sprayed onto vulnerable plants such as brassicas and fruit trees. The bacterial disease will kill the caterpillars, but leave other insects unharmed. There are strains of Bt that are effective against other insect larvae. Bt israelensis is effective against mosquito larvae and some midges.
The European Rabbit (Oryctolagus cuniculus) is seen as a major pest in Australia
* A viral biological control which can be introduced in order to control the overpopulation of European rabbit in Australia is the rabbit haemorrhagic disease virus that causes the rabbit haemorrhagic disease.
* A biological control being developed for use in the treatment of plant disease is the fungus Trichoderma viride. This has been used against Dutch Elm disease, and to treat the spread of fungal and bacterial growth on tree wounds. It may also have potential as a means of combating silver leaf disease.
* The parasitoid Gonatocerus ashmeadi (Hymenoptera: Mymaridae) has been introduced to control the glassy-winged sharpshooter Homalodisca vitripennis (Hemipterae: Cicadellidae) in French Polynesia and has successfully controlled ~95% of the pest density[7]
[edit] Economics of biological pest control
Biological control proves to be very successful economically, and even when the method has been less successful, it still produces a benefit-to-cost ratio of 11:1. One study has estimated that a successful biocontrol program returns £32 in benefits for each £1 invested in developing and implementing the program, i.e., a 32:1 benefit-to-cost ratio. The same study had shown that an average chemical pesticide program only returned profits in the ratio of 13:1.[citation needed]
[edit] Negative results of biological pest control
In some cases, biological pest control can have unforeseen negative results that could outweigh all benefits. For example, when the mongoose was introduced to Hawaii in order to control the rat population, it preyed on the endemic birds of Hawaii, especially their eggs, more often than it ate the rats.
Cane toads (Bufo marinus) were introduced to Australia in the 1930s in a failed attempt to control the cane beetle, a pest of sugar cane crops. 102 toads were obtained from Hawaii and bred in captivity to increase their numbers until they were released into the sugar cane fields of the tropic north in 1935. It was later discovered that the toads can't jump very high so they did not eat the cane beetles which stayed up on the upper stalks of the cane plants. The toads soon became very numerous and out-competed native species and became very harmful to the Australian environment, including being very toxic to would-be predators such as native snakes. [1]
[edit] References
This article needs additional citations for verification. Please help improve this article by adding reliable references. Unsourced material may be challenged and removed. (September 2007)
1. ^ "Alternanthera philoxeroides information from NPGS/GRIN
". www.ars-grin.gov. Retrieved on 2008-08-09.
2. ^ Spider mites and their natural enemies
3. ^ White flies and their natural enemies
4. ^ L.A. Swan. 1964. Beneficial Insects. 1st ed. page 249.
5. ^ I.M. Hall & P.H. Dunn, Entomophthorous Fungi Parasitic on the Spotted Alfalfa Aphid, Hilgardia, Sept 1957.
6. ^ a b "Factsheet - Mucuna pruriens
". www.tropicalforages.info. Retrieved on 2008-05-21.
7. ^ Hoddle M.S., Grandgirard J., Petit J., Roderick G.K., Davies N. (2006). "Glassy-winged sharpshooter Ko'ed - First round - in French Polynesia". Biocontrol News and Information 27 (3): 47N–62N.
Biological control
* Wiedenmann, R. 2000. Introduction to Biological Control. Midwest Institute for Biological Control. Illinois. Available from http://www.inhs.uiuc.edu/research/biocontrol
Building organic pest-free gardens
* The Time Saving Garden
by David and Charles PLC/Reader's Digest, ISBN 13: 9780276442452
Effects on native biodiversity
* Pereira, M.J. et al. (1998) Conservation of natural vegetation in Azores Islands. Bol. Mus. Munic. Funchal 5, 299–305
* Weeden, C.R., A. M. Shelton, and M. P. Hoffman. Biological Control: A Guide to Natural Enemies in North America. Available from [2]
(accessed December 2007)
* Cane toad: a case study. 2003. Available from [3]
(accessed December 2007)
* Humphrey, J. and Hyatt. 2004. CSIRO Australian Animal Health Laboratory. Biological Control of the Cane Toad Bufo marinus in Australia
* Cory, J. and Myers, J. 2000. Direct and indirect ecological effects of biological control. Trends in Ecology & Evolution. 15, 4, 137-139.
* Johnson, M. 2000. Nature and Scope of Biological Control. Biological Control of Pest. 675
Effects on invasive species
* Cofrancesco, A. 2007. U.S. National Management Plan: An Action Plant for the Nation- Control and Management. Army Corps of Engineers. Available from [4]
* Lass, D. and Miller, R. 1995. BioScience. 45, 10. 680.
Effects on the future
* Cooksey D. 2002. Biological Control in Pest Management Systems of Plants.
Western Regional Committee, Riverside, CA.
Economic effects
* Griffiths, G.J.K. 2007. Efficacy and economics of shelter habitats for conservation. Biological Control: in press. doi:10.1016/j.biocontrol.2007.09.002
* Collier T. and Steenwyka, R. 2003. A critical evaluation of augmentative biological control. Economics of augmentation: 31, 245-256.
[edit] See also
* Insectary plants
* Integrated Pest Management
* Japanese beetle (article includes information on biological control methods)
* Organic farming
* Biological pesticide
* Sterile insect technique
* Mating disruption
[edit] External links and references
* Biological Control: A Guide to Natural Enemies in North America
* Beyond Pesticides
- Provides information on pesticides and alternatives to their use.
* Grow'Em Organic Pest Control
- organic pest control solutions available to small- and large-scale gardeners, described in detail
* Construction of a ecological garden and implementation of natural pest control
* 2 other pdf-files about the construction of a ecological garden and implementation of natural pest control
* Education movies about biological pest control of white flies, aphids and spider mites in greenhouses
* Association of Natural Biocontrol Producers (ANBP)
Trade association of biological pest control industry.
* Successful biocontrol of the GWSS in French Polynesia
* R. James Cook (September 1993). "Making Greater Use of Introduced Microorganisms for Biological Control of Plant Pathogens
". Annual Review of Phytopathology 31: 53–80. doi:10.1146/annurev.py.31.090193.000413
, http://arjournals.annualreviews.org/doi/abs/10.1146/annurev.py.31.090193.000413
.
* U.S. Congress, Office of Technology Assessment. "Biologically based technologies for pest control
" (PDF). US Government Printing Office, Washington, DC.
* Felix Wäckers, Paul van Rijn and Jan Bruin. "Plant-Provided Food for Carnivorous Insects - a protective mutualism and its applications.". Cambridge University Press, UK, 2005.
* Alternative Methods of Mole Cricket Control
at the University of Florida
Retrieved from "http://en.wikipedia.org/wiki/Biological_pest_control"
Categories: Gardening | Organic gardening | Biological pest control
Hidden categories: All articles with unsourced statements | Articles with unsourced statements since December 2007 | Articles with unsourced statements since February 2007 | Articles needing additional references from September 2007
Views
Pathogen
Pathogen
From Wikipedia, the free encyclopedia
Jump to: navigation, search
A pathogen (from Greek πάθος pathos "suffering, passion", and γἰγνομαι (γεν-) gignomai (gen-) "I give birth to"), infectious agent, or (more commonly) germ, is a biological agent that causes disease or illness to its host.[1] The term pathogen is derived from the Greek "that which produces suffering." There are several substrates and pathways whereby pathogens can invade a host; the principal pathways have different episodic time frames, but soil contamination has the longest or most persistent potential for harboring a pathogen.
The body contains many natural defenses against some of the common pathogens (such as Pneumocystis) in the form of the human immune system and by some "helpful" bacteria present in the human body's normal flora. However, if the immune system or "good" bacteria is damaged in any way (such as by chemotherapy, human immunodeficiency virus (HIV), or antibiotics being taken to kill other pathogens), pathogenic bacteria that were being held at bay can proliferate and cause harm to the host. Such cases are called opportunistic infections.
Some pathogens (such as the bacterium Yersinia pestis, which may have caused the Black Plague, the Variola virus, and the Malaria protozoa) have been responsible for massive numbers of casualties and have had numerous effects on afflicted groups. Of particular note in modern times is HIV, which is known to have infected several million humans globally, along with Severe Acute Respiratory Syndrome (SARS) and the Influenza virus. Today, while many medical advances have been made to safeguard against infection by pathogens, through the use of vaccination, antibiotics, and fungicide, pathogens continue to threaten human life. Social advances such as food safety, hygiene, and water treatment have reduced the threat from some pathogens.
Not all pathogens are negative. In entomology, pathogens are one of the "Three P's" (predators, pathogens, and parasitoids) that serve as natural or introduced biological controls to suppress arthropod pest populations.
Contents
[hide]
* 1 Types of pathogens
o 1.1 Pathogenic bacteria
o 1.2 Pathogenic viruses
* 2 Pathogen strength
* 3 Transmission of pathogens
* 4 Examples of pathogens
o 4.1 Major human pathogens
* 5 References
[edit] Types of pathogens
Below is a list of different types of notable pathogens as categorized by their structural characteristics, and some of their known and predicted effects on infected host.
[edit] Pathogenic bacteria
Main article: Pathogenic bacteria
Although the vast majority of bacteria are harmless or beneficial, a few pathogenic bacteria can cause infectious diseases. The most common bacterial disease is tuberculosis, caused by the bacterium Mycobacterium tuberculosis, which effect about 2 million people mostly in sub-Saharan Africa. Pathogenic bacteria contribute to other globally important diseases, such as pneumonia, which can be caused by bacteria such as Streptococcus and Pseudomonas, and foodborne illnesses, which can be caused by bacteria such as Shigella, Campylobacter and Salmonella. Pathogenic bacteria also cause infections such as tetanus, typhoid fever, diphtheria, syphilis and leprosy. Bacteria can often be killed by antibiotics.
[edit] Pathogenic viruses
Further information: Table of clinically important viruses
Pathogenic viruses are mainly those of the families of: Adenoviridae, Picornaviridae, Herpesviridae, Hepadnaviridae, Flaviviridae, Retroviridae, Orthomyxoviridae, Paramyxoviridae, Papovaviridae, Rhabdoviridae, Togaviridae. Some notable pathogenic viruses cause: smallpox, influenza, mumps, measles, chickenpox and rubella. Ebola is another pathogenic virus.
[edit] Pathogen strength
A new theory regarding pathogens states that the longer a pathogen can survive outside of the body, the more dangerous it can be to a potential host. For example, the smallpox virus (variola virus) can survive outside the human body for approximately 885 days. It is also one of the most deadly pathogenic viruses, as it kills 1 in 10 of the people it infects. The tuberculosis bacterium kills 1 in 5 of the people it infects, but only survives 244 days outside of its host. The Ebola virus has devastating results, 9 out of 10 people will die from it.
In countries that have higher sanitation standards, pathogens cannot survive for as long outside of the body. This is seen as encouragement to mutations to the pathogen which would make it less deadly, as such mutations would allow the pathogen to survive in the host for longer periods of time.
[edit] Transmission of pathogens
Main article: Transmission (medicine)
One of the primary pathways by which food or water become contaminated is from the release of untreated sewage into a drinking water supply or onto cropland, with the result that people who eat or drink contaminated sources become infected. In developing countries most sewage is discharged into the environment or on cropland as of August 12 1985; even in developed countries there are periodic system failures resulting in a sanitary sewer overflow.
There should be more information on this page regarding the transmission of pathogens.
[edit] Examples of pathogens
[edit] Major human pathogens
* Mycobacterium tuberculosis
* Mycobacterium leprae
* Yersinia pestis
* Rickettsia prowazekii
* Bartonella spp.
* Spanish influenza virus
[edit] References
1. ^ http://www.medterms.com/script/main/art
.
Retrieved from "http://en.wikipedia.org/wiki/Pathogen"
Category: Microbiology
Views
From Wikipedia, the free encyclopedia
Jump to: navigation, search
A pathogen (from Greek πάθος pathos "suffering, passion", and γἰγνομαι (γεν-) gignomai (gen-) "I give birth to"), infectious agent, or (more commonly) germ, is a biological agent that causes disease or illness to its host.[1] The term pathogen is derived from the Greek "that which produces suffering." There are several substrates and pathways whereby pathogens can invade a host; the principal pathways have different episodic time frames, but soil contamination has the longest or most persistent potential for harboring a pathogen.
The body contains many natural defenses against some of the common pathogens (such as Pneumocystis) in the form of the human immune system and by some "helpful" bacteria present in the human body's normal flora. However, if the immune system or "good" bacteria is damaged in any way (such as by chemotherapy, human immunodeficiency virus (HIV), or antibiotics being taken to kill other pathogens), pathogenic bacteria that were being held at bay can proliferate and cause harm to the host. Such cases are called opportunistic infections.
Some pathogens (such as the bacterium Yersinia pestis, which may have caused the Black Plague, the Variola virus, and the Malaria protozoa) have been responsible for massive numbers of casualties and have had numerous effects on afflicted groups. Of particular note in modern times is HIV, which is known to have infected several million humans globally, along with Severe Acute Respiratory Syndrome (SARS) and the Influenza virus. Today, while many medical advances have been made to safeguard against infection by pathogens, through the use of vaccination, antibiotics, and fungicide, pathogens continue to threaten human life. Social advances such as food safety, hygiene, and water treatment have reduced the threat from some pathogens.
Not all pathogens are negative. In entomology, pathogens are one of the "Three P's" (predators, pathogens, and parasitoids) that serve as natural or introduced biological controls to suppress arthropod pest populations.
Contents
[hide]
* 1 Types of pathogens
o 1.1 Pathogenic bacteria
o 1.2 Pathogenic viruses
* 2 Pathogen strength
* 3 Transmission of pathogens
* 4 Examples of pathogens
o 4.1 Major human pathogens
* 5 References
[edit] Types of pathogens
Below is a list of different types of notable pathogens as categorized by their structural characteristics, and some of their known and predicted effects on infected host.
[edit] Pathogenic bacteria
Main article: Pathogenic bacteria
Although the vast majority of bacteria are harmless or beneficial, a few pathogenic bacteria can cause infectious diseases. The most common bacterial disease is tuberculosis, caused by the bacterium Mycobacterium tuberculosis, which effect about 2 million people mostly in sub-Saharan Africa. Pathogenic bacteria contribute to other globally important diseases, such as pneumonia, which can be caused by bacteria such as Streptococcus and Pseudomonas, and foodborne illnesses, which can be caused by bacteria such as Shigella, Campylobacter and Salmonella. Pathogenic bacteria also cause infections such as tetanus, typhoid fever, diphtheria, syphilis and leprosy. Bacteria can often be killed by antibiotics.
[edit] Pathogenic viruses
Further information: Table of clinically important viruses
Pathogenic viruses are mainly those of the families of: Adenoviridae, Picornaviridae, Herpesviridae, Hepadnaviridae, Flaviviridae, Retroviridae, Orthomyxoviridae, Paramyxoviridae, Papovaviridae, Rhabdoviridae, Togaviridae. Some notable pathogenic viruses cause: smallpox, influenza, mumps, measles, chickenpox and rubella. Ebola is another pathogenic virus.
[edit] Pathogen strength
A new theory regarding pathogens states that the longer a pathogen can survive outside of the body, the more dangerous it can be to a potential host. For example, the smallpox virus (variola virus) can survive outside the human body for approximately 885 days. It is also one of the most deadly pathogenic viruses, as it kills 1 in 10 of the people it infects. The tuberculosis bacterium kills 1 in 5 of the people it infects, but only survives 244 days outside of its host. The Ebola virus has devastating results, 9 out of 10 people will die from it.
In countries that have higher sanitation standards, pathogens cannot survive for as long outside of the body. This is seen as encouragement to mutations to the pathogen which would make it less deadly, as such mutations would allow the pathogen to survive in the host for longer periods of time.
[edit] Transmission of pathogens
Main article: Transmission (medicine)
One of the primary pathways by which food or water become contaminated is from the release of untreated sewage into a drinking water supply or onto cropland, with the result that people who eat or drink contaminated sources become infected. In developing countries most sewage is discharged into the environment or on cropland as of August 12 1985; even in developed countries there are periodic system failures resulting in a sanitary sewer overflow.
There should be more information on this page regarding the transmission of pathogens.
[edit] Examples of pathogens
[edit] Major human pathogens
* Mycobacterium tuberculosis
* Mycobacterium leprae
* Yersinia pestis
* Rickettsia prowazekii
* Bartonella spp.
* Spanish influenza virus
[edit] References
1. ^ http://www.medterms.com/script/main/art
.
Retrieved from "http://en.wikipedia.org/wiki/Pathogen"
Category: Microbiology
Views
Subscribe to:
Posts (Atom)
