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Author Topic: Schwangerschaftstest rottet Frösche in Panama aus?  (Read 3132 times)

RubyCat

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Schwangerschaftstest rottet Frösche in Panama aus?
« on: June 22, 2013, 04:14:37 AM »

In den frühen Schwangerschaftstests wurden afrikanische Frösche benutzt, die zu diesem Zweck überallhin in in die Welt verschickt wurden. Ein Teil dieser Frösche war anscheinend mit einem Chytrid -Pilz verseucht.

Der auf diese Weise verbreitete Pilz fand woanders reichen Nährboden und breitete sich aus, wobei er die vorhandenen Froscharten zum Teil schnell auslöschte. So gibt es in Panama stellenweise keirne Frösche mehr. Panama, das ist ein Land, in dem es vor Fröschen nur so wimmelte.  Jetzt sind sie tot.

Wer Frösche retten will, sollte etwas tun. Ein Teil der Frösche kann in der Natur nicht mehr gerettet werden. Diese Arten können nur noch in Zoos überleben. Dafür wird dringend Hilfe benötigt, und das heißt: man braucht Geldspenden um das alles zu bezahlen. 

http://www.amphibianark.org hilft Frösche zu retten. Wir helfen http://www.amphibianark.org/  ,indem wir diesen Bericht weitergeben, denn wenn niemand etwas weiß, kann niemand etwas tun.

Helft auch Ihr! Helft den Fröschen!



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Bitte, helft http://www.amphibianark.org/ durch eine Spende!



Mehr über Chytrid-Pilze und Frösche:

http://www.amphibianark.org/the-crisis/chytrid-fungus/

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Chytrid Fungus

The Amphibian Chytrid Fungus and Chytridiomycosis

What is a “chytrid”? What is Bd?
Why is Bd Important?
What does Bd do? How does Bd kill amphibians?
Do all amphibians infected with Bd die?
Can populations with chytridiomycosis recover?
Where is Bd found? Where did Bd come from?
How does Bd spread?
What are the signs of chytridiomycosis?
How is chytridiomycosis diagnosed?
Can chytridiomycosis be treated?
How do I keep Bd and chytridiomycosis out of my amphibian collection?
Is Bd the greatest threat to amphibians?
Further reading
Literature cited

What is a “chytrid”? What is Bd?
 A “chytrid” is a type of fungus (Phylum Chytridiomycota) and there are approximately 1,000 different chytrid species that live exclusively in water or moist environments. The chytrids are among the oldest (most primitive) types of fungi and until very recently were considered members of the Kingdom Protista (and therefore thought to be more closely related to single celled organisms like protozoa). Most chytrids are saprobes meaning that they feed on dead and rotting organic matter. Other chytrids are parasites that live on plants or invertebrate animals. In 1999, a new species of chytrid was described that infects the skin of amphibians and was named Batrachochytrium dendrobatidis or “Bd” for short (Longcore et al., 1999). Although the name Batrachochytrium is hard for even many scientists to pronounce, it roughly translates to mean “frog chytrid”. Bd is unusual because it is the only chytrid that is a parasite of a vertebrate animal (amphibians specifically; Bd has not been observed to infect other vertebrates such as reptiles, birds or mammals).

Why is Bd Important?
Bd is a very important chytrid fungus because it appears to be capable of infecting most of the world’s approximately 6,000 amphibian species and many of those species develop the disease chytridiomycosis which is linked to devastating population declines and species extinctions (Berger et al., 1998; Skerratt et al., 2007; Fisher et al., 2009). In fact, infection with Bd has been called “the worst infectious disease ever recorded among vertebrates in terms of the number of species impacted, and it’s propensity to drive them to extinction (Gascon et al, 2007). Amphibian population declines due to chytridiomycosis can occur very rapidly— sometimes over a just a few weeks (Lips et al., 2006) and disproportionately eliminate species that are rare, specialized and endemic (e.g. those species that are most unique) (Smith et al., 2009). Because of these characteristics—rapid progression of population declines and loss of very important amphibian species—urgent mobilization of efforts to preserve amphibian species are required.

What is chytridiomycosis? How does Bd kill amphibians?
 Chytridiomycosis (“Mycosis” = disease caused by a fungus) is the disease that occurs when an amphibian is infected with large numbers of the Bd fungus. Infection with Bd occurs inside the cells of the outer skin layers that contain large amounts of a protein called “keratin”. Keratin is the material that makes the outside of the skin tough and resistant to injury and is also what hair, feathers and claws are made of. With chytridiomycosis, the skin becomes very thick due to a microscopic change in the skin that pathologists call “hyperplasia and hyperkeratosis”. These changes in the skin are deadly to amphibians because— unlike most other animals— amphibians “drink” water and absorb important salts (electrolytes) like sodium and potassium through the skin and not through the mouth. Abnormal electrolyte levels as the result of Bd-damaged skin cause the heart to stop beating and the death of the animal (Voyles et al., 2009). Other amphibians like the lungless salamanders, use the skin to breathe and skin changes due to chytridiomycosis could interfere with this function causing suffocation.

Do all amphibians infected with Bd Die?
 Not all amphibian species that are infected with Bd become sick or die. These species like the American bullfrog and the African clawed frog are said to be “resistant” to chytridiomycosis. Resistant species are a major concern because they are carriers of Bd (like a “Typhoid Mary”) that can move the fungus to new locations and expose new populations of amphibians that are “susceptible” or more likely to become sick with lethal chytridiomycosis.

The reason why some amphibian species are resistant to chytridiomycosis is an area of very active scientific research. If we can understand why some species are resistant, it might be possible to develop methods to control chytridiomycosis in amphibian populations that experience devastating population declines. Some of the mechanisms that could explain species resistance to chytridiomycosis are:
The presence on the skin of specific types of symbiotic bacteria that discourage the growth of Bd (Harris et al., 2009 a and b). Amphibians or amphibian populations that normally have large numbers of these bacteria in the skin might be more resistant to developing chytridiomycosis.
The production by the poison glands in amphibian skin of chemicals called “antimicrobial peptides” that discourage the growth of Bd. Specific types, combinations or amounts of antimicrobial peptides might help some species to be more resistant to chytridiomycosis.
Some amphibian species or populations may have genetic resistance to the development of chytridiomycosis by mechanisms that are not yet understood.

Other scientists study why some populations of amphibians succumb to chytridiomycosis while other populations of the same species persist. In addition to things like the presence of symbiotic bacteria or differences in skin peptide composition, some potential explanations include:
Environmental differences between populations such as temperature, humidity or water flow patterns. For instance, some of the most important amphibian population declines associated with chytridiomycosis have occurred at high elevation locations that have a cool temperature range (< 250C or 770F) that is most optimal for the growth of Bd.
Differences in virulence between different types or “strains” of the Bd fungus. The term virulence refers to the ability of the fungus to cause disease in amphibians. A type of Bd that is “highly virulent” easily makes amphibians sick, but another type of Bd that has “low virulence” makes fewer animals sick or results in less severe disease.

There is not a single explanation for why an amphibian population succumbs or does not succumb to chytridiomycosis and in most cases multiple factors are probably at work to result in a particular outcome.

Can amphibian populations with chytridiomycosis recover?
 Some amphibian populations experience devastating mass mortality events due to chytridiomycosis where most of the population succumbs to the disease, but a small number of animals remain or “persist” in the population. At this time it is unknown if these “persistent populations” might eventually recover and regain the numbers of animals they had prior to chytridiomycosis or if these populations will remain small or even eventually disappear.

Recent research has shown that a critical factor in determining if chytridiomycosis will cause extinction of an amphibian population is if the level of intensity of the infection with Bd crosses a certain threshold (Briggs et al., 2010; Vredenberg et al., 2010). What is very interesting about the “persistent” populations is that the remaining animals are still infected with Bd, but at a lower or less lethal intensity. Like the individual amphibian species that are resistant to chytridiomycosis (see above), understanding why persistent populations maintain low intensity infections with Bd is very important and could lead to methods to control the disease in wild populations.

Where is Bd found? Where did Bd come from?
 Since its discovery, Bd has been found in wild and captive amphibian populations on every amphibian-inhabited continent. It is actively spreading in South, Central, and western North America, as well as the Caribbean, Australia and Europe. Bd is also found in Africa, Asia, and eastern North America, but does not seem to be spreading in these locations. Bd is conspicuously absent from Madagascar, Borneo and New Guinea.

Scientists have questioned if Bd is a fungus that has always infected amphibians all over the world and has just now begun to cause disease— because of changes to the environment or suppression of amphibian immune systems—or if Bd has only recently been introduced to new populations of amphibians and causes disease in naïve populations that have not developed a natural resistance to Bd infection (Rachowicz et al., 2005). It is now well-documented for amphibian populations in Central America and the western United States that Bd was not present in the population until the beginning of declines due to chytridiomycosis (Lips et al., 2006; Vredenberg et al., 2010). In other words it appears that Bd was newly introduced to these locations and then caused the population declines.

So if Bd has only recently been introduced to new locations, where did it come from? There is genetic and historical evidence that Bd has been present for a long time in Africa (Soto-Azat et al., 2010; Weldon et al., 2004); Japan (Goka et al., 2009) and eastern North America (Garner et al., 2006) and all have been proposed as the possible site of origin. Although the exact origin of Bd has not yet been determined, it has become clear that global trade in amphibians for food, for use as laboratory animals, or for use as pets or display animals is responsible for movement of Bd to locations where it was not previously present (Weldon et al., 2004; Schloegel et al., 2009). This has led to international regulations under the World Organization for Animal Health to require that amphibians be free of Bd infection before international shipment (Schloegel et al, 2010).

How does Bd spread?
 Infection with Bd is transmitted by a form of the fungus called a “zoospore”. The zoospore has a very distinctive appearance with a single flagellum that helps the spore swim through water or moist environments. Zoospores require moisture and cool temperatures and can persist in moist environments for several months (Johnson and Speare, 2003), but do not tolerate conditions that are warm or dry for more than a few hours (Johnson and Speare, 2005). Therefore, the most common and successful ways that Bd zoospores spread from place to place are in water, moist or wet materials (including soil or equipment) or on the skin of infected amphibians. In fact, the most common way that Bd infection spreads between amphibians is from direct contact of an infected animal with an uninfected animal (e.g. during territorial or breeding encounters). In captivity, it is possible to house amphibians infected with Bd in enclosures next to enclosures with amphibians that are not infected with Bd and not transmit the infection as long as animals, water and wet materials and tools are not shared between the enclosures. Guidelines to reduce the transmission of Bd in captive environments are available (Pessier and Mendelson, 2010).

In the natural environment, it has been hypothesized that Bd can move on people’s boots or equipment or on birds and invertebrates that fly between watersheds (Johnson and Speare, 2005). Therefore, it is important that biologists and others take precautions to clean and disinfect their boots and equipment before moving from one location that has amphibians to another location in order to minimize the risk of spreading Bd (Phillot et al., 2010). Because many amphibians that are infected with Bd are resistant to the disease chytridiomycosis (see above), they can appear to be outwardly healthy but are still capable of spreading Bd from one location to another. This is important because these animals may act as a reservoir for transmitting Bd infection to other amphibians as part of natural movements between different watersheds. Amphibians can also move Bd to new locations as the result of trade in amphibians (see above) or potentially by the release of captive amphibians to the wild (See Amphibians in Classrooms).

What are the signs of chytridiomycosis?
 An amphibian that is sick with chytridiomycosis can have a wide variety of symptoms or “clinical signs”. Some of the most common signs are reddened or otherwise discolored skin, excessive shedding of skin, abnormal postures such as a preference for keeping the skin of the belly away from the ground, unnatural behaviors such as a nocturnal species that suddenly becomes active during the day, or seizures. Many of these signs are said to be “non-specific” and many different amphibian diseases have signs that overlap with those of chytridiomycosis. In addition, other cases of chytridiomycosis will not show any of these signs and amphibians will simply be found dead. For these reasons it is not possible to diagnose chytridiomycosis with the naked eye and laboratory testing is required (see How is Chytridiomycosis Diagnosed? below).

How is chytridiomycosis diagnosed?
If animals are sick it is possible to diagnose chytridiomycosis by examining samples of the skin under a microscope and identifying the characteristic fungal organisms of Bd. These techniques require the assistance of an experienced biologist or veterinarian and are not good ways to detect amphibians that are carriers of Bd. Alternatively, non-invasive swabs of the skin can be obtained and analyzed by a technique called the polymerase chain reaction or “PCR” for short (Hyatt et al., 2007). PCR can detect very small amounts of Bd DNA in a sample and for this reason it is the test of choice for detecting animals that carry Bd infection and to survey wild and captive amphibian populations for the presence of Bd.

Check out a video clip that demonstrates the collection of samples for Bd PCR.

More information about sampling techniques (in English and in Spanish) can be found on the AmphibiaWeb site.

A complete discussion of different diagnostic methods for Bd can be found in Pessier and Mendelson, 2010.

Here is a list of laboratories that perform PCR for Bd:
Diagnostic Laboratory,
Wildlife Epidemiology
 Zoological Society of London (ZSL)
 Wellcome Building
 London NW1 4RY
 UK

Email: matthew.perkins@ioz.ac.uk   
Pisces Molecular
2200 Central Avenue, Suite F
 Boulder, CO 80301
 USA

Voice: 303-546-9300
 Fax: 303-546-9400
 Email: jwood@pisces-molecular.com

School of Biological Sciences
Center for Integrated Biotechnology
 Washington State University
 Pullman, WA 99164-4236
 USA

Andrew Storfer
 Associate Professor

Phone: (509) 335-7922
 Fax: (509) 335-3184
 Email: astorfer@wsu.edu   
Wildlife Disease Laboratories
 Institute for Conservation Research
 San Diego Zoo *

Dr. Allan Pessier
 Email: apessier@sandiegozoo.org
 619-231-1515, Ext 4510

* See details below

Center for Wildlife Disease
University of South Dakota
 Biology Department
 414 E. Clark Street
 Vermillion, SD 57069
 USA

Contact: Jake Kerby, Ph.D.
 Assistant Professor

Phone: (605) 677-6170
 Fax: (605) 677-6557
 Email: Jacob.Kerby@usd.edu   
The Swiss company Ecogenics (www.ecogenics.ch; info@ecogenics.ch) offers commercially a PCR-based test for the detection of chytrid fungus from amphibian tissue samples and non-invasive swabs. The test is the real-time PCR test developed by Boyle et al. (2005, Diseases of Aquatic Organisms 60: 141-148).

Please contact Ecogenics directly for pricing and further details. Establishment of the test by Ecogenics was financed by the Swiss federal office for the environment through a contract with KARCH.

Landesbetrieb Hessisches Landeslabor
 Schubertstraße 60 – Haus 13
 35392 Gießen
 Germany

Phone: 0641 – 4800 – 5219
 Fax : 0641 – 4800 – 5900
 Email: tobias.eisenberg (at) lhl.hessen.de
More information…   
Zoologix, Inc.
9811 Owensmouth Avenue, Suite 4
Chatsworth CA 91311
USA

Contact: Steven Lloyd, CEO

Phone 818-717-8880
Fax 818-717-8881
Email: slloyd@zoologix.com
www.zoologix.com



PCR requires a molecular biology laboratory that uses rigorous controls for positive and negative samples and that has carefully validated the PCR test. A disadvantage of PCR is that it is not able to distinguish between amphibians that are sick with chytridiomycosis and amphibians that are carriers of Bd, because both types of animals will test “positive” by PCR.

Can chytridiomycosis be treated?
 In captive amphibians, chytridiomycosis can be successfully treated with antifungal medications and by disinfection of contaminated enclosures (Pessier and Mendelson, 2010). A variety of different antifungal medications have been described for the treatment of chytridiomycosis, however, one of the most common methods was developed at the Smithsonian National Zoo and uses a series of baths in the drug itraconazole (Nichols and Lamirande, 2000). Itraconazole baths have been used successfully in rescue operations that capture wild amphibians from populations that are experiencing deaths to chytridiomycosis (Gagliardo et al., 2008). Other potential treatment methods include the use of elevated body temperature and paradoxically, the antibiotic chloramphenicol. Treatment is not always 100% successful and not all amphibians tolerate treatment very well, therefore chytridiomycosis should always be treated with the advice of a veterinarian.

Unfortunately, there are no good methods for the treatment of wild animals in the natural environment. It is very difficult or impossible to get enough of the antifungal medications into the environment to be able to successfully rid infected frogs of Bd. In the future it may be possible to treat some amphibians in the wild in order to reduce the intensity of infection to a less lethal level with the hope that animals could survive with a mild Bd infection (Briggs et al., 2010; Vrendenberg et al., 2010). Another promising area of research is looking at the possibility of introducing symbiotic bacteria that inhibit the growth of Bd into wild amphibian populations (Harris et al., 2009). So far, there is no evidence that a vaccine for chytridiomycosis could be effective for controlling the disease in wild populations (Stice and Briggs, 2010).

How can I keep Bd and chytridiomycosis out of my amphibian collection?
 Amphibians are commonly kept in captivity as pets, laboratory animals, education animals and for species conservation efforts. In these situations, prevention and control of Bd infection and chytridiomycosis have become very important for maintaining healthy captive populations. Methods that are helpful in this regard include:
Quarantine of new amphibians before they enter an established amphibian collection. New animals are kept separate from the established collection for a period of time (usually 60-90 days) to allow for observation for signs of disease and to perform laboratory testing for diseases such as Bd.
Testing or treating animals for Bd infection during the quarantine period.
Perform surveillance for Bd infection in your amphibian collection. This is done by regular necropsies (autopsies) of animals that die and by PCR testing of collection animals. Many amphibian collections have Bd infected frogs and don’t know it.
Develop “specific pathogen free” amphibian populations that are known to be free of Bd infection. If all captive raised amphibians can be certified as Bd-free it will simplify quarantine and amphibian shipment practices for everyone.
Practice good hygiene and barrier management between animal rooms and displays. Use separate equipment and disposable gloves between enclosures and dispose of wastes and waste water responsibly.

If Bd is identified in your amphibian collection: DON’T PANIC. Bd infection is common in captive amphibians and there are effective treatment methods available (see above). Use outbreaks of chytridiomycosis in collection as an opportunity to make your animals healthier by screening the collection for unsuspected carriers of Bd infection; treating infected animals and reviewing protocols for controlling the spread of infectious diseases in the collection.

Detailed methods for amphibian quarantine and the treatment and control of Bd infection can be found in Pessier and Mendelson, 2010.

Is Bd the greatest threat to amphibians?
 No. Habitat loss affects more amphibian species than any other threat by nearly a factor of 4. However, while habitat loss proceeds at a steady pace, Bd can often work quickly. The IUCN has called amphibian chytridiomycosis “the worst infectious disease ever recorded among vertebrates in terms of the number of species impacted, and its propensity to drive them to extinction.” And because the Amphibian Ark focuses on species facing threats that cannot currently be mitigated in the wild, such as Bd, we necessarily focus largely on this disease and leave the mitigable threats, such as habitat loss, to our ASA partners specializing in those areas.

Further reading

Developing a safe antifungal treatment protocol to eliminate Batrachochytrium dendrobatidis from amphibians – A. MARTEL, P. VAN ROOIJ, G. VERCAUTEREN, K. BAERT, L. VAN WAEYENBERGHE, P. DEBACKER, T. W. J. GARNER, T. WOELTJES, R. DUCATELLE, F. HAESEBROUCK & F. PASMANS

Field-Sampling Protocol for Batrachochytrium Dendrobatids From Living Amphibians, using Alcohol Preserved Swabs – Brem, Mendelson and Lips

Fisher, M.C., T. W. J. Garner, and S. F. Walker. 2009. Global emergence of Batrachochytrium dendrobatidis and amphibian chytridiomycosis in space, time, and host. Annual Review of Microbiology 63:291–310.

Kilpatrick A.M., C.J. Briggs, and P. Daszak. 2009. The ecology and impact of chytridiomycosis: an emerging disease of amphibians. Trends in Ecology & Evolution online.

Rosenblum, E. B., J. Voyles, T. J. Poorten, and J. E. Stajich. The deadly chytrid fungus: a story of an emerging pathogen. PLoS Pathogens 6: e1000550.

A guide to husbandry and biosecurity standards required for the safe and responsible management of ex situ populations of amphibians
These standards are based upon those reported in the proceedings of the CBSG/WAZA Amphibian Ex situ Conservation Planning Workshop, El Valle, Panama, 12-15th February 2006.

Citations
 Berger, L., R. Speare, P Dazsak, D.E. Green, A.A. Cunningham, C.L. Goggin, R. Slocombe, M.A. Ragan, A.D. Hyatt, K.R. McDonald, H.B. Hines, K.R. Lips, G. Marantelli and H. Parkes . 1998. Chytridiomycosis causes amphibian mortality associated with population declines in the rain forests of Australia and Central America. Proceedings of the National Academy of Sciences of the United States of America 95: 9031-9036.

Briggs, C.J., R.A. Knapp, V.T. Vrendenberg. 2010. Enzootic and epizootic dynamics of the chytrid fungal pathogen of amphibians. Proceedings of the National Academy of Sciences of the United States of America (in press)

Fisher, M.C., T.W.J. Garner, and S.F. Walker. 2009. Global emergence of Batrachochytrium dendrobatidis and amphibian chytridiomycosis in space, time, and host. Annual Review of Microbiology 63:291–310.

Gagliardo, R., P.Crump , E. Griffith,et al. 2008. The principles of rapid response for amphibian conservation using the programmes in Panama as an example, International Zoo Yearbook 42: 125-135.

Garner T.W.J., M. Perkins, P. Govindarajulu, D. Seglie, S.J. Walker, A.A. Cunningham, and M.C. Fisher. 2006. The emerging amphibian pathogen Batrachochytrium dendrobatidis globally infects introduced populations of the North American bullfrog, Rana catesbeiana. Biol. Letters 2:455-459.

Gascon C., J.P. Collins, R.D. Moore et al., editors: Amphibian Conservation Action Plan. IUCN/SSC Amphibian Specialist Group. Gland, Switzerland and Cambridge UK, 2007.

Goka K, J. Yokoyama, Y. Une, T. Kuroki, K. Suzuki, M. Nakahara, A. Kobayashi, S. Inaba, T. Mizutani, and A.D. Hyatt. 2009. Amphibian chytridiomycosis in Japan: distribution, haplotypes and possible route of entry into Japan. Molecular. Ecology. 18:4757-4774.

Harris R.N., R.M. Brucker, J.B. Walke et al. 2009a. Skin microbes on frogs prevent morbidity and mortality caused by a lethal skin fungus, ISME J 3: 818-824.

Harris, R.N., A. Lauer, M.A. Simon, J.L. Banning, and R.A. Alford. 2009b. Addition of antifungal skin bacteria to salamanders ameliorates the effects of chytridiomycosis. Diseases of Aquatic Organisms 83:11-16.

Hyatt, A.D., DG Boyle, Olsen V et al. 2007. Diagnostic assays and sampling protocols for the detection of Batrachochytrium dendrobatidis, Diseases of Aquatic Organisms 73: 175–192.

Johnson, M.L., R. Speare. 2003. Survival of Batrachochytrium dendrobatidis in water: Quarantine and disease control implications, Emerging Infectious Diseases 9: 922-925.

Johnson, M.L., R. Speare. 2005. Possible modes of dissemination of the amphibian chytrid Batrachochytrium dendrobatidis in the environment, Diseases of Aquatic Organisms 65:181-186.

Lips, K.R., F. Brem, R. Brenes, J.D. Reeve, R.A. Alford, J. Voyles, C. Carey, L. Livo, A.P. Pessier, and J.P. Collins. 2006. Emerging infectious disease and the loss of biodiversity in a Neotropical amphibian community. Proceedings of the National Academy of Sciences of the United States of America 103:3165-3170.

Longcore, J.E., A.P. Pessier and D.K. Nichols. 1999. Batrachochytrium dendrobatidis gen. et sp. nov., a chytrid pathogenic to amphibians. Mycologia 91:219-227.

Pessier, A.P. and J.R. Mendelson (eds.). 2010. A Manual for Control of Infectious Diseases in Amphibian Survival Assurance Colonies and Reintroduction Programs. IUCN/SSC Conservation Breeding Specialist Group: Apple Valley, MN.

Phillott A.D., R. Speare, H.B. Hines,L.F. Skerratt, E. Meyer, K.R. McDonald, S.D. Cashins, D. Mendez, L. Berger. 2010. Minimising exposure of amphibians to pathogens during field studies. Diseases of Aquatic Organisms (in press)

Murray, K.A., L.F. Skerratt, R. Speare, and H. McCallum. 2009. Impact and dynamics of disease in species threatened by the amphibian chytrid fungus, Batrachochytrium dendrobatidis. Conservation Biology:23:1242-52.

Nichols, D.K. and E.W. Lamirande. 2000. Treatment of cutaneous chytridiomycosis in blue-and-yellow poison dart frogs (Dendrobates tinctorius). In: R. Speare (ed.), Proceedings: Getting the Jump on Amphibian Disease, Cairns, James Cook University: 51. www.amphibians.org/wp-content/uploads/2012/05/Froglog46.pdf

Rachowicz, L.J., J. Hero, R.A. Alford, J.W. Taylor, J.A.T. Morgan, V.T. Vrendenberg, J.P. Collins, & C.J. Briggs. 2005. The novel and endemic pathogen hypotheses: Competing explanations for the origin of emerging infectious diseases of wildlife. Conservation Biology 19: 1441-1448.

Schloegel, L.M., A.M. Picco, A.M. Kilpatrick, A.J. Davies, A.D. Hyatt, and P. Daszak. 2009. Magnitude of the US trade in amphibians and the presence of Batrachochytrium dendrobatidis and Ranavirus infection in imported North American bullfrogs (Rana catesbeiana). Biological Conservation 142:1420-1426.

Schloegel, L.M., P. Daszak, A.A. Cunningham, R. Speare, B. Hill. 2010. Two amphibian diseases, chytridiomycosis and ranaviral disease are now globally notifiable to World Organization for Animal Health (OIE): an assessment. Diseases of Aquatic Organisms (in press)

Skerratt, L.F., L. Berger, R. Speare, S. Cashins, K.R. Mcdonald, A. Phillott, H.Hines, and N. Kenyon. 2007. Spread of chytridiomycosis has caused the rapid global decline and extinction of frogs. EcoHealth 4:125-134.

Smith, K.G., K.R. Lips, and J.M. Chase. 2009 Selecting for extinction: nonrandom disease-associated extinction homogenizes amphibian biotas. Ecology Letters 12:1069-1078

Soto-Azat, C., B.T. Clarke, J.C. Poynton, and A.C. Cunningham. 2010. Widespread historical presence of Batrachochytrium dendrobatidis in African pipid frogs. Diversity and Distributions 16:126-131.

Stice, M.J., C.J. Briggs. 2010. Immununization is ineffective against preventing infection and mortality due to the amphibian chytrid fungus Batrachochytrium dendrobatidis. Journal of Wildlife Diseases 46: 70-77.

Voyles, J., S. Young, L. Berger, C. Campbell, W.F. Voyles, A. Dinudom, D. Cook, R. Webb, R.A. Alford, L.F. Skerratt, and R. Speare. 2009. Pathogenesis of chytridiomycosis, a cause of catastrophic amphibian declines. Science 326:582-585.

Vrendenberg, V.T., Knapp, R.A., Tunstall, T., Briggs, C. 2010. Dynamics of an emerging disease drive large-scale amphibian population extinctions. Proceedings of the National Academy of Sciences of the United States of America (in press)

Weldon, C., L.H. du Preez, A.D. Hyatt, R. Muller, and R. Speare. 2004 Origin of the amphibian chytrid fungus. Emerging Infectious Diseases 10:2100-2105. http://www.cdc.gov/NCIDOD/eid/vol10no12/03-0804.htm

* Testing for amphibian infectious diseases (chytrid fungus and ranavirus) available from the San Diego Zoo
The Wildlife Disease Laboratories of the Institute for Conservation Research at the San Diego Zoo are pleased to be able to offer low-cost testing for the amphibian chytrid fungus (Batrachochytrium dendrobatidis) and Ranaviruses. The testing is subsidized by an Institute of Museum and Library Services (IMLS) National Leadership grant “Infectious Disease Control and Bioresource Banking for the Amphibian Extinction Crisis” awarded to the Zoological Society of San Diego and Zoo Atlanta.

The goal of the subsidized testing is to encourage widespread surveillance of zoo collections for these potentially population-limiting infectious diseases. Hopefully, these efforts will facilitate eradication of chytrid fungal infections from established zoo collections and enable the collection of data of the occurrence and prevalence of these diseases that is needed to make use of disease risk assessment tools for reintroduction programs.

The laboratory is also able to provide assistance in working up outbreaks of infectious diseases in captive collections (especially molecular diagnostic testing) working together with your facility veterinarian and pathologist.

Available Tests:
 Real-Time (Taqman) PCR for Amphibian Chytrid Fungus
 Conventional PCR for Ranavirus

Tests are US $20 each for Bd and $25 each for Ranavirus, for zoos and aquariums.

Questions can be addressed to:
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 619-231-1515, Ext 4510

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[*/quote*]

RubyCat

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Re: Schwangerschaftstest rottet Frösche in Panama aus?
« Reply #1 on: June 22, 2013, 04:29:54 AM »

Die Frösche sind Teil unserer Umwelt. Jeder von ihnen spielt eine wichtige Rolle. sterben die Frösche, sterben andere Arten, und so sterben auch wir.

Die staatlichen CDC (Centers for Disease Control and Prevention) in den USA haben sich des Themas angenommen. Es ist kein esoterisches Hobby, sondern ernsthafte Grundlagenforschung zum Überleben! Auch deutsche Labors sind an der Forschung beteiligt,

Rettet die Natur!

http://wwwnc.cdc.gov/eid/article/10/12/03-0804_article.htm

[*quote*]
EID Journal
Volume 10, Number 12—December 2004
Research
Origin of the Amphibian Chytrid Fungus

Article Contents
Materials and Methods
Results
Discussion
Acknowledgments
References
Figure 1
Figure 2
Figure 3
Table 1
Table 2
Suggested Citation
Ché Weldon* , Louis H. du Preez*, Alex D. Hyatt†, Reinhold Muller‡, and Rick Speare‡
Author affiliations: *North-West University, Potchefstroom, South Africa; †CSIRO, Geelong, Australia; ‡James Cook University, Townsville, Australia

Suggested citation for this article

Abstract

The sudden appearance of chytridiomycosis, the cause of amphibian deaths and population declines in several continents, suggests that its etiologic agent, the amphibian chytrid Batrachochytrium dendrobatidis, was introduced into the affected regions. However, the origin of this virulent pathogen is unknown. A survey was conducted of 697 archived specimens of 3 species of Xenopus collected from 1879 to 1999 in southern Africa in which the histologic features of the interdigital webbing were analyzed. The earliest case of chytridiomycosis found was in a Xenopus laevis frog in 1938, and overall prevalence was 2.7%. The prevalence showed no significant differences between species, regions, season, or time period. Chytridiomycosis was a stable endemic infection in southern Africa for 23 years before any positive specimen was found outside Africa. We propose that Africa is the origin of the amphibian chytrid and that the international trade in X. laevis that began in the mid-1930s was the means of dissemination.


One of the biggest threats facing amphibian species and population survival worldwide is the disease chytridiomycosis, caused by the chytrid fungus, Batrachochytrium dendrobatidis (1,2). Chytridiomycosis was proposed as the cause of death in frog populations in the rain forests of Australia and Panama and was associated with the decline of frog populations in Ecuador, Venezuela, New Zealand, and Spain (3–6). Evidence for a countrywide decline in frog populations in South Africa is lacking (7), and local declines of several species have been ascribed to two main threats, habitat destruction and pollution (8). Chytridiomycosis is known in South Africa from infections in X. laevis, Afrana fuscigula, and Strongylopus grayii (9–11). Through surveys of extant and archived specimens, Batrachochytrium has been found in every continent that has amphibians, except Asia (6,9,12,13). Since B. dendrobatidis has been recognized as an emerging pathogen, whose spread is facilitated by the international and intranational movement of amphibians (1), identifying its origin will be useful.

Some emerging infectious diseases arise when pathogens localized that have been localized to a single host or small geographic region go beyond previous boundaries (14). If B. dendrobatidis emerged in this fashion, we hypothesize that the source would meet the following criteria: 1) the hosts would show minimal or no apparent clinical effects, 2) the site would be the place of the earliest known global occurrence, 3) the date of this occurrence would precede any amphibian declines in pristine areas (i.e., late 1970s), 4) the prevalence in the source host or hosts would be stable over time, 5) no geographic spreading pattern would be observed over time in the region, 6) a feasible means of global dissemination of Batrachochytrium from the region of origin would be identified, and 7) B. dendrobatidis would show a greater genetic variation in the host region than in more recently invaded regions.

B. dendrobatidis is common in African frogs from Ghana, Kenya, South Africa, and Western Africa (12,15) and declines in frog populations are poorly documented in Africa (7,16). These factors, combined with the global trade in X. laevis and X. tropicalis, prompted us to investigate the likelihood that Africa was the origin of Batrachochytrium and that the trade in Xenopus spp. played a key role in its global dissemination. Within the Xenopus genus, X. laevis is distributed over the greatest area in sub-Saharan Africa. X. laevis occupies most bodies of water in savannah habitats from the Cape of Good Hope to Nigeria and Sudan (17,18).

We report the earliest case of the amphibian chytrid found in any amphibian and present epidemiologic evidence to support the hypothesis that B. dendrobatidis originated in Africa. In this article, chytridiomycosis refers to infection of amphibians by B. dendrobatidis.
Materials and Methods

A retrospective survey was conducted on archived specimens of the genus Xenopus housed in five southern Africa institutions, Bayworld (Port Elizabeth), Natal Museum (Pietermaritzburg), National Museum (Bloemfontein), South African Museum (Cape Town), and Transvaal Museum (Pretoria). Specimens in these museums had been collected for archiving by a large number of persons for various purposes and had not been selected for a systematic survey of amphibian disease. Specimens were collected mainly from South Africa, Lesotho, and Swaziland. A piece (3 x 3 mm) of the interdigital webbing was removed from one hind foot of each specimen of X. gilli, X. muelleri, and X. laevis. Tissue was prepared for histologic examination with routine techniques (19). Sections were cut at 6 μm and stained with hematoxylin and eosin. Chytridiomycosis was diagnosed by using described criteria (20). Sections from the two specimens diagnosed as having chytridiomycosis with hematoxylin and eosin before 1971 (one collected in 1938, the other in 1943) were confirmed with the more specific immunoperoxidase test (21) to increase the confidence of the diagnosis. Measurements of sporangia were performed with a calibrated eyepiece and expressed as mean ± standard deviation (SD). Histologic slides were examined “blind,” without reference to dates that the frogs were collected, to decrease any opportunity for bias in diagnosis.

Exact versions of chi-square tests were used to analyze bivariate associations between chytridiomycosis prevalence and host species, region in South Africa (southwestern, eastern, and central), and season. Bivariate time trends of prevalences were analyzed by exact chi-square tests for trend. Multivariate logistic regression models were applied to assess potential confounding effect of species, region, and season on the time trend of chytridiomycosis prevalence. Confidence intervals (CI) were calculated by using exact binomial probabilities. Longitudinal and latitudinal historical patterns of spread were analyzed with linear regression models.
Results

Figure 1


Figure 1. Micrographs of immunoperoxidase stained sections through the interdigital webbing of Xenopus gilli, showing the morphologic features and size of zoosporangia consistent with Batrachochytrium dendrobatidis. A) Arrow a indicates localized hyperplastic epidermal...

Zoosporangia with a diameter (mean ± SD) of 5.2 ± 0.72 μm (maximum 6 μm) were seen in the stratum corneum of the digital webbing of infected frogs (Figure 1). Most sporangia were empty spherical structures, but occasional sporangia were observed with developing stages, septa, or discharge papillae. The structures stained brown (indicating positivity) in the immunoperoxidase test with the specific anti-Batrachochytrium antibody (Figure 1). Lesions usually associated with chytridiomycosis, including hyperplasia of the epidermis and hyperkeratosis of the stratum corneum, were mild and localized to areas of infection.

Figure 2


Figure 2. Historical time-trend of chytridiomycosis prevalence in southern Africa. No significant change was shown in the prevalence over time (p = 0.22, 95% confidence interval).

Overall, chytridiomycosis prevalence from the survey was 2.7% (19 positives out of 697 specimens) and did not differ significantly across species (p = 0.7; Table 1). The earliest date for a chytridiomycosis-positive specimen was 1938 in an X. laevis collected from the Western Cape coastal lowland. This specimen is housed in the South African Museum, Cape Town (SAMZR 18927). The next earliest positive specimen detected was an X. gilli from 1943 (specimen number NMB 112, National Museum, Bloemfontein). The distribution of dates specimens were collected was greatly skewed to the latter half of the 20th century (Table 2). The breakdown for the time interval 1871–1940 is presented in order (decade, number of frogs infected/number of frogs examined) as follows: 1871–1880, 0/1; 1881–1890, 0/0; 1891–1900, 0/6; 1901–1910, 0/6; 1911–1920, 0/4; 1921–1930, 0/2; 1931–1940, 1/37. No statistically significant change of chytridiomycosis prevalence occurred over the decades since the 1940s (p = 0.36), or when the broader interval of pre-1971 is used as the baseline for the calculations (p = 0.22; Figure 2). No evidence for any trend in prevalence over time could be found using multivariate modeling where the odds ratios for the time intervals were adjusted for the potential confounders of species, season, and region. The multivariate odds ratios in these models were not significant and very similar to the bivariate findings, which indicate no confounding effects. The prevalence of chytridiomycosis in South Africa showed no significant change over time after 1940. No significant change of the geographic distribution of chytridiomycosis was detected after 1973. By 1973 the distribution of chytridiomycosis, as proved by positive specimens, covered already the area from 27° to 34° latitude and 18.25° to 32.5° longitude. This finding implies that positive specimens were detected from all regions of southern Africa by 1973. Infected frogs were found in 5 of the 9 provinces in South Africa, including the Western Cape (5 of 171), Northern Cape (2 of 22), Free State (6 of 141), Kwazulu-Natal (3 of 152), and Eastern Cape (1 of 137), as well as in Swaziland (2 of 42). Prevalence of B. dendrobatidis did not differ (p = 0.24) between the designated three broader regions with prevalences of 3.0% in the southwest, 3.8% in the central region, and 1.5% in the eastern region. Overall, the seasons (wet versus dry) when the specimens were collected were not significantly associated with prevalence (p = 0.22). Only in the eastern region, was a significantly higher prevalence found in the wet season than the dry season.
Discussion

Figure 3


Figure 3. Time bar indicating when chytridiomycosis first appeared in the major centers of occurrence in relation to each other. Following a 23-year interruption in occurrences after the Xenopus laevis infection in 1938,...

Our study has extended the date for the earliest case of chytridiomycosis in wild amphibians by 23 years. The next earliest case outside South Africa was found in Rana clamitans from Saint-Pierre-de-Wakefield, Québec, Canada, in 1961 (22). After the case in Canada, the earliest cases from other countries follow sequentially over a period of 38 years from 1961 to 1999 (Figure 3).

X. laevis in the wild does not show clinical signs, nor has it experienced any sudden die-offs. Moreover, only subclinical chytrid infections have been observed among captive colonies of X. laevis (26,27). A frog of a related species, X. tropicalis, died in captivity from chytridiomycosis, it was suspected of having contracted the fungus from X. laevis (27). An ideal host for transmission of chytridiomycosis through international translocation would be a species of amphibian that does not become diseased or die from the infection; hence, X. laevis could take on the role of a natural carrier.

The sudden appearance of chytridiomycosis can best be explained by the hypothesis that B. dendrobatidis was recently introduced into new regions and subsequently infected novel host species (1). Dispersal of B. dendrobatidis between countries is most likely by the global transportation of amphibians (1,2,23,28,29). The World Organization for Animal Health has recently placed amphibian chytridiomycosis on the Wildlife Diseases List in recognition of this risk. If Africa is the source of B. dendrobatidis, a feasible route of dissemination by infected amphibians needs to be identified. Some members of the family Pipidae have been exported, in particular Hymenochirus curtipes and X. laevis, to North America and Europe (30).

In terms of a most likely candidate for spread from Africa, the number of frogs and geographic dissemination favor X. laevis. Soon after discovery of the pregnancy assay for humans in 1934 (30), enormous quantities of the species were caught in the wild in southern Africa and exported around the world. The pregnancy assay is based on the principle that ovulation in X. laevis is induced by injection with urine from pregnant women because of high levels of gonadotropic hormones in the urine (31,32). X. laevis was selected as the most suitable amphibian for investigating the mechanism of the mating reflex because of the relative ease with which the animal can be maintained in captivity (33). For 34 years, the trade in X. laevis in South Africa was controlled by the then Cape of Good Hope Inland Fisheries Department (Western Cape Nature Conservation Board) at the Jonkershoek Fish Hatchery. As an indication of the numbers involved in this trade, 10,866 frogs were distributed in 1949, of which 3,803 (35%) were exported, and of the 20,942 frogs distributed in 1970, a total of 4,950 (24%) were shipped abroad (34,35). After the introduction of nonbiologic pregnancy tests, X. laevis became important as a model for the scientific study of immunity and later embryology and molecular biology. X. laevis could have carried the disease globally, particularly if the prevalence was similar to that seen in wild-caught X. laevis today. In the importing country, escaped frogs, the water they lived in (36), or both, could have come into contact with local amphibian species, and subsequent transmission of the disease could have followed. The establishment of feral populations of X. laevis in Ascension Island, the United Kingdom, the United States, and Chile in 1944, 1962, the 1960s, and 1985 (37), respectively, show that transmission could have become ongoing if these feral populations were infected.

Although we have demonstrated that B. dendrobatidis was in southern Africa since 1938, our studies provide no indication regarding whether this region was the original source within Africa. B. dendrobatidis has been found in wild frogs in Kenya and in frogs (X. tropicalis and X. laevis) wild-caught in Western Africa and detected after importation into the United States (12,26,27,38), which indicates that B. dendrobatidis is widely disseminated in Africa. Xenopus consists of 17 species that are found in sub-Saharan Africa, with a varying degree of sympatry between species (17). The overlap in the distribution and, in some cases, the sharing of habitats could facilitate transmission of B. dendrobatidis between these species. This finding would imply that chytridiomycosis could have originated elsewhere in Africa and spread within multiple host-region combinations. More detailed historical studies of archived African amphibians may indicate whether B. dendrobatidis was originally present in a small area of Africa from which it emerged to occupy large areas of the continent. Until the deficit in distribution data and comparative genetic studies is remedied, locating the source of the origin of B. dendrobatidis within Africa remains speculative. The relationship appears to have coevolved within an anuran host, and the opportunity to disseminate across the globe existed for B. dendrobatidis in southern Africa.

If X. laevis did carry B. dendrobatidis out of Africa as we propose, other amphibian species subsequently could have distributed it between and within countries. The American bullfrog, Rana catesbeiana, has been proposed as an important vector, mainly through international trade as a food item, but also within countries as populations established for the food trade escape and spread (29). The earliest current record for the occurrence of chytridiomycosis in R. catesbeiana is 1978 in South Carolina (38), 40 years after the first record in southern Africa, but details on the intensity of the search for chytridiomycosis in archived bullfrogs are not available. The transmission of chytridiomycosis globally may involve a series of key steps: 1) occurrence of B. dendrobatidis in an amphibian vector in southern Africa that is relatively resistant to disease (X. laevis), 2) sudden rise in 1935 of export trade in this vector because of technologic advances (Xenopus pregnancy test), 3) escape of the pathogen from the exported Xenopus to establish new foci in other countries (possibly expedited in some countries by establishment of feral populations of X. laevis), 4) transmission into other vector amphibians (food and pet trade), and 5) further transmission to other countries along different trade routes in key amphibian vectors that move in high numbers and become established in commercial populations and closely interact with wild frogs, which likely leads to feral populations (food frogs R. catesbeiana). Spread through native amphibian populations with epidemic disease in some species could have occurred at any point after B. dendrobatidis entered a naïve native species.

We have provided epidemiologic evidence that Africa is the origin of the amphibian chytrid fungus. Support for six of the seven criteria proposed for the source of B. dendrobatidis has been demonstrated: 1) the major host (X. laevis) shows minimal or no apparent clinical effects, 2) site of the earliest global occurrence (1938), 3) this date precedes any amphibian declines in pristine areas, 4) the prevalence in the source host or hosts (Xenopus spp.) has been stable over time, 5) no geographic spreading pattern could be observed over time, and 6) a feasible means of global dissemination exists via the international trade in wild-caught X. laevis, which commenced in 1935 and continues today. Criterion 7, greater genetic diversity of B. dendrobatidis at the source, has not been investigated. A low level of genetic variation was shown for 35 strains of B. dendrobatidis and suggested that B. dendrobatidis was a recently emerged clone (39). The strains had been collected in North America, Australia, Panama, and Africa from wild and captive amphibians. Three strains isolated from captive X. tropicalis in United States had been imported from Ghana. Although these showed no significant differences from the U.S. strains (39), their assignment to Africa assumes no cross-infection had occurred within the importing facility. Future work on the genetic diversity of B. dendrobatidis in Africa compared with strains from regions outside Africa will add weight to the hypothesis if greater genetic diversity is found in African strains.

Mr. Weldon is a Ph.D. candidate and research assistant at the School of Environmental Sciences and Development, North-West University, South Africa. His research interests include the role of disease in amphibian declines, the effect of pesticides on amphibian biology, and the captive husbandry of Xenopus.
Acknowledgments

We thank Bayworld (Port Elizabeth), Natal Museum (Pietermaritzburg), National Museum (Bloemfontein), South African Museum (Cape Town), and Transvaal Museum (Pretoria) for making the material available.

This work was supported by the National Research Foundation (South Africa) and the Declining Amphibian Populations Task Force.
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Figures
Figure 1. Micrographs of immunoperoxidase stained sections through the interdigital webbing of Xenopus gilli, showing the morphologic features and size of zoosporangia consistent with Batrachochytrium dendrobatidis. A) Arrow a indicates localized...
Figure 2. Historical time-trend of chytridiomycosis prevalence in southern Africa. No significant change was shown in the prevalence over time (p = 0.22, 95% confidence interval).
Figure 3. Time bar indicating when chytridiomycosis first appeared in the major centers of occurrence in relation to each other. Following a 23-year interruption in occurrences after the Xenopus laevis infection...
Tables
Table 1. Prevalence of chytridiomycosis in archived Xenopus spp. from southern Africaa
Table 2. Prevalence of chytridiomycosis in archived Xenopus, by time intervalsa

Suggested citation for this article: Weldon C, du Preez LH, Hyatt AD, Muller R, Speare R. Origin of the amphibian chytrid fungus. Emerg Infect Dis [serial on the Internet]. 2004 Dec [date cited]. Available from http://wwwnc.cdc.gov/eid/article/10/12/03-0804.htm

DOI: 10.3201/eid1012.030804

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Table of Contents – Volume 10, Number 12—December 2004
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Page created: April 14, 2011
Page last updated: April 14, 2011
Page last reviewed: April 14, 2011
Content source: Centers for Disease Control and Prevention
National Center for Emerging and Zoonotic Infectious Diseases (NCEZID)
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Re: Schwangerschaftstest rottet Frösche in Panama aus?
« Reply #2 on: February 15, 2024, 02:31:38 PM »

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