Table of contents :

• Prototheria
• Monotremata
• Ornithorhynchidae
• Ornithorhynchus
• Ornithorhynchus anatinus (a.k.a. duckbill or duck-billed platypus)


Other nontransmissible infections : Trypanosoma binneyi
• Metatheria
• Dasyuromorphia; Dasyuridae; Sarcophilus
• Sarcophilus harrisii (Tasmanian devil) : an epidemic of progressive and apparently transmissible neoplasia has been recorded in the wild since 1997 and has been especially apparent in the past 2 to 3 years. The tumors typically occur first in the mouth and facial areas, leading to speculation that the putative viral agent is spread directly by biting. Devils lead an aggressive lifestyle and fighting is common and savage, particularly among adult males in whom the disease incidence is the highest. Tumours are most commonly lymphomas or anaplastic round cell tumours, but considerable variation exists, hence the preference for the term "facial tumours" over more specifically descriptive terms. The disease is not limited to facial tumours, however, but is genuinely systemic. Draining lymph nodes and bone marrow are typically infiltrated with a clonal population of round cells with a high cytoplasmic/nuclear ratio and often a plasmacytoid appearance. Lymphocytes with a moderate or high mitotic index are commonly seen infiltrating other organs such as the liver, causing the appearance of hepatitis. Round cell tumours similar to those on the face occur later in other parts of the body. Other odd tumours seem to occur in association with this syndrome also, although there is no direct evidence that this is more than coincidence. In addition to facial tumours, one recent case had a functional adrenocortical tumour producing symptoms of Cushing's disease (overproduction of cortisone), whilst older reports describe examples of other seemingly unrelated neoplasms occurring in association with facial tumours in Tasmanian devils. First observed in the north east of the state, the disease has now been seen in many districts further south and west. Field studies have confirmed that it spread southward along the Freycinet Peninsular at a rate of 10-15 km/year, and westward about halfway across the state. In some areas, mortality rates have been as high as 80 to 90 per cent, with very few animals left over 12 months old. Animals of all ages and both sexes are affected with a greater incidence in adult males. Younger animals tend not to be affected so much, either due to reasons of susceptibility or because they tend not to fight, or possibly due to a lengthy incubation period for the disease. Devils might live up to 5 or 6 months or more following the development of clinical disease, but death seems to be the inevitable outcome. There is very little evidence of animals recovering from this disease. Death tends ultimately to result from starvation, as facial tumours invade and destroy facial bones and dental arcades, leaving hideously ulcerated and infected lesions on the face and in the mouth. Pathologists at the Animal Health Laboratory of the Tasmanian Department of Primary Industries, Water and Environment (DPIWE) have proposed a retroviral aetiology for this disease on the basis of a number of similarities with retroviral disease in other animals. The archetypal virus of the type-C group of cancer-causing retroviruses is feline leukemia virus (FeLV) that causes a range of syndromes in cats, including solid tumours of the lymphoma variety, leukemia of various types, and/or a chronic immunodeficiency syndrome over the longer term. Transmission is believed to be direct, mostly via fighting amongst male cats, which gives the disease a much greater incidence in adult males. Avian type-C retroviruses cause solid lymphomas or other round cell tumours of birds, and can also cause leukemic conditions. But the most interesting is a novel type-C retrovirus recently isolated from koalas (KoRV), another Australian marsupial, which is also associated with a syndrome including solid tumours of the lymphoma variety and leukemia^ref. When KoRV was first isolated it was tempting to speculate that FeLV might have made the evolutionary jump across the species barrier into koalas, given the extent of the problem of feral cat proliferation in the Australian bush. However, the work of Hangar et al at the University of Queensland found no genetic relationship between KoRV and FeLV. An additional candidate for a viral etiologic agent might be a polyomavirus. Under certain conditions murine polyomavirus infection induces a wide variety of tumours in its natural host; however, a marsupial polyomavirus has yet to be identifiedOther possible aetiologies include a herpesvirus and a non-viral aetiology. The one glaring flaw with the retrovirus hypothesis is that there is no precedent for the appearance of tumours at the initial site of infection, and it is somewhat inconsistent with the biology of retroviruses unless an acutely-transforming oncogene were involved, which would be extremely unusual. Cats also transmit FeLV by biting for example, but tumours occur at unrelated sites after many months following systemic proliferation of the virus. The only precedent for tumour induction at the site of "infection" that I am aware of would be the transmissible venereal tumour of dogs, which seems to have few parallels with the situation in devils. The veterinary and pathology group at DPIWE have established a minor research project consisting of a group of scientists and field workers keen to participate in working up the Tasmanian devil facial tumour syndrome and its aetiology, but the major limitation is the difficulty of obtaining research funding. Although still in the early stages of defining the disease, more extensive research will be required and external funds are being sought to assist in characterising this apparently devastating disease of our Tasmanian icon species. At this early stage we are focusing on attempts to obtain some virus either directly from plasma of infected animals by ultra-centrifugation, or indirectly from cell culture of peripheral blood monocytes from infected animals, as achieved by Hanger et al with respect to the koala retrovirus. Tasmanian devil facial tumour disease (DFTD) has now been recorded across the eastern half of Tasmania and as far west as Cradle Valley. In recent weeks, the disease has been confirmed at Fentonbury and Adamsfield in the south, and immediately north of Eaglehawk Neck on the Forestier Peninsula. So far, DFTD has only been recorded in wild Tasmanian devils. To December 2004, DFTD had been recorded over 65% of the State and is almost certainly present in a larger area. 30-50% the wild devil numbers in the State 10 years ago are likely to have been lost. The short and medium term effects of DFTD are severe; the long-term effects are not known at this stage. Assessment for DFTD is hampered by the lack of a pre-clinical test, meaning only devils with visible symptoms can be used for confirmation. Therefore, a very high proportion of a local population, and preferably a large absolute sample, must be physically examined to have confidence in a DFTD-free status; a laborious task. The results of TEM of tumour tissue for the presence of virus particles has so far been negative^ref. Neoplasms described 20 years earlier in 18 Tasmanian devils that were necropsied at the San Diego Zoo were mostly adenocarcinomas of the mammary, thyroid, and perianal glands^ref. They hadn't seen any cases that primarily involved the head or face, and none that were suspected to be of neuroendocrine origin. Is there any chance that this apparent oncovirus is transmitted on poorly sanitized live-traps? According to Animal Planet, there is a vigorous live-trapping program in Tasmania that catches individual Tasmanian devils several times a year for reproductive monitoring. As devils are intemperate by nature and tend to chew on the metal bars of their enclosure, trauma from escape attempts would seem a logical avenue to exposure to a virus of this type. The current best guess breaks all the rules of modern biology. Scientists suspect that the disease is caused by a cancer cell that itself moves from one animal to another when they bite one another. The real devil bears no resemblance to Taz, the Warner Brothers Looney Tunes cartoon character that roars and whirls like a dervish. A real devil is the size of a spaniel, with strong forelimbs, a huge head and a disappointing back end. Females have lustrous black coats with a purple hue, white stripes on their rump or below the neck, exceptionally long luxurious whiskers and narrow pointy faces. When they get excited, their ears turn blood red. Males have similar markings along with big boxy heads and heavily scarred faces and rumps. A devil can eat a quarter of its body weight in one feeding. Devils got their name from early European settlers who heard spine-chilling screams and thought that Satan was surely in the backyard. In March and April, males engage in vicious, blood-soaked combat. Females select big butch dudes, and allow themselves to be dragged by the scruff of the neck into a burrow. There they scream and fight for several days, mating many times for hours at a time. At the end of such bouts, the male thrusts his sperm into the female every 2 minutes. 3 weeks later, the female gives birth to about 20 or 30 embryos that wiggle through a string of mucus that leads to her pouch, which has only 4 teats. The first to arrive lock on and survive. All others perish. By August the pouch gets crowded. When she hunts, the mother leaves her roly-poly little devils in a den. The young are weaned at 9 months, emerging from the den in the fall as goofy teenagers. Mom departs. After 6 years of scavenging, screeching and seeking mates, devils abruptly die. They are one of the few species in the world with so-called catastrophic mortality. How and why they die this way is not known. Tasmanians have always taken devils for granted. Few scientists ever bothered to study them. When the 1st animal with facial tumors was photographed, in 1996, people thought, eeew, that looks horrible, but it did not ring alarm bells. After 5 more years scientists realized the disease was widespread: later surveys show a devastating picture. Spread animal-to-animal, the disease is now endemic to 2/3 of the island, which is slightly smaller than West Virginia. The disease starts out as a raspberry-like lesion on the gums, palate or under the tongue. Within months, tumors erupt around the mouth, neck and face. A few weeks later, they explode, weeping and oozing, pushing out teeth, eyes or noses, and sometimes invading the rest of the body. Animals starve to death 3 to 6 months after the 1st signs of a tumor. A virus seemed likely to cause the disease, but so far every effort to identify a virus has come up empty-handed. A virus has not been ruled out, but scientists are now entertaining other hypotheses. Since Tasmania has widespread use of agricultural chemicals and pesticides, researchers are looking at 10 toxins to see if devil disease is associated with poisons that can cause tumors. But the leading theory is that devil facial tumor disease is caused by a transmissible tumor cell. It goes like this: About a decade ago, a random mutation occurred in a single animal in a type of cell involved in hormonal regulation. This devil developed tumors on or near its face. When another devil bit into the tumor, it was  infected with tumor cells. With time, tumor cells were passed around in the bloody fray of devil social life, spreading the disease. In this hypothesis, tumor cells alone are the infectious agent. In nature, this is not supposed to happen : healthy animals exposed to pathogens, including tumor cells, will normally mount an immune response to fight off the infection. But genetically speaking, devils are virtual clones. With scant variation in their DNA -- perhaps from a population bottleneck in the recent past -- they may have nearly identical immune systems. Hence they cannot fight off the tumor cells. Every tumor cell examined so far is the same in every animal, male and female, regardless of area of origin. The chromosomal rearrangements, presumably from the one random mutation, are identical. Another disease offered support for the idea that tumor cells could be infectious. That disorder, canine transmissible venereal tumor (TVT) disease, is passed among dogs during sex or when they lick and sniff infected tissue. The tumors are identical, suggesting that they are passed by contact. The big difference is that the disease is not fatal in dogs. They mount an immune response and get over it. Although TVT is self-curing in > 90%t of cases, it can, in odd cases, be very difficult to treat and even, on occasion, metastasize. This course of the disease is thought to be due to poor immunity in the patient. The tumor is very sensitive to irradiation. I wonder whether they have tried that with these tasmanian devils? DFTD is being investigated by a professional Australian team; the update of April 2005 can be accessed here. Researchers are growing devil tumor cells in petri dishes to explore their basic biology. Meanwhile, Dr. Mooney's team is trapping devils island-wide to determine the extent of the epidemic. They are also in the process of trapping 25 young animals from apparently disease-free areas as an insurance policy. The juvenile devils are being placed in urban and offshore sites to keep them apart from older, wild devils. If after a year or so they show no signs of disease, they will be bred to ensure survival of their species. We usually don't see the disease until after the animals turn 2 years old. It is possible they might get the disease from their mother's milk or contact with her saliva. On the other hand, they may have resistance to it. Veterinarians will watch the orphans for the next year or so to see what happens. The chromosomes in these tumours have undergone a complex rearrangement (13 instead of the normal 14 chromosomes) that is identical for every animal studied. In light of this remarkable finding and of the known fighting behaviour of the devils, we propose that the disease is transmitted by allograft, whereby an infectious cell line is passed directly between the animals through bites they inflict on one another. The low genetic diversity of the animals might reduce their immune response to the cancerous cell transferred during biting^ref


• Didelphimorphia, Didelphidae
• Caluromyinae
• Caluromys (woolly opossums)
• Caluromys philander : Leishmania mexicana amazonensis


• Didelphinae
• Didelphis spp. : Trypanosoma cruzi
• Didelphis marsupialis (southern opossum) : Leishmania guyanensis
• Marmosa
• Marmosa murina (murine mouse opossum) : Leishmania mexicana amazonensis


• Marmosa mitis : Leishmania mexicana amazonensis
• Marmosa fuscata : Leishmania mexicana amazonensis
• Metachirus
• Metachirus nudicaudatus (brown four-eyed opossum) : Leishmania mexicana amazonensis


Rickettsia felis, Rickettsia typhi
• Diprotodontia
• Macropodidae
• Macropus
• Macropus eugenii (a.k.a. tammar wallabies)

Outbreaks of toxoplasmosis in wild and captive marsupials, with high mortality, have been described in scientific literature for several decades. Affected animals may exhibit diarrhea, respiratory compromise, lethargy, weight loss, blindness, or neurological deficits. The susceptibility of Macropus eugenii has been demonstrated experimentally: 13 animals were dosed orally with 500, 1000, or 10 000 oocysts of Toxoplasma gondii, as part of a vaccination trial.
11 animals died of acute toxoplasmosis 9 to 15 days after challenge. The lesions were similar in all animals, consisting of foci of necrosis and inflammation in the intestines, lymphoid tissue, adrenal cortex, heart, skeletal muscle and brain, and severe generalised pulmonary congestion and edema^ref.
• Macropus giganteus (eastern gray kangaroo)

Other nontransmissible infections : Trypanosoma spp.

cutaneous leishmaniasis (CL) in 4 red kangaroos (Macropus rufus : an arid zone species and could be described as maladapted to the wet tropical region of the Darwin area) was reported on 18 Jun 2003 in a fauna park outside Darwin in the Northern Territory of Australia^ref. Detailed investigations have since confirmed that the infection is due to Leishmania parasites, but molecular characterisation of the parasites from skin lesions show that the parasite species is not L. major or L. tropica, causing CL in the Old World, nor L. donovani infantum (Old World visceral leishmaniasis), nor L. enriettii a parasite of laboratory guinea pigs in Brazil, and not L. mexicana causing CL in Central America. Nevertheless all infected kangaroos had detectable anti-Leishmania antibodies. The conclusion was that the parasites infecting kangaroos are probably a
new species of Leishmania. Although imported cases of CL have been recorded from soldiers returning from overseas and immigrants and also from dogs, leishmaniasis transmission in Australia has not previously been recorded. Worldwide vectors of leishmaniasis are phlebotomine sandflies, but until now Australia has been considered free of suitable vectors. Although recent importation of the parasite into Australia is possible, it is equally possible that the parasite has been endemic, yet undetected. Additional work is currently being conducted to characterize the phylogeny of the organism. There is the possibility of human transmission of leishmaniasis in Australia, especially as most forms of leishmaniasis infecting humans are zoonoses. The parasites infected the cells only at 33°C and not at the normal human body temperature of 37°C : but this did not necessarily rule out infection in humans, as human skin temperature could be less than 37°C. The Leishmania (Viannia) subgenus is restricted to South and Central America; hosts are South American edentates (sloths, armadillos) and marsupials, which have cooler core body temperatures than  placentals; and the temperature of optimum growth of amastigotes (the form found in mammals) is about 32°C, similar to the optimum infectivity of mouse macrophages at 33°C rather than 37°C found by Rose et al. At least one hypothesis suggests that marsupials dispersed from South America via Antarctica to Australia (Martin 1977, cited in Nowak 1991), which suggests a possible dispersal route for Leishmania from South America to Australia in marsupials
• Phascolarctidae
• Phascolarctos
• Phascolarctos cinereus (koala)


Other nontransmissible infections : koala retrovirus (KoRV) is an endogenous retrovirus, morphologically similar to mammalian C-type retroviruses. KoRV was detected initially by electron microscopy in mitogen-stimulated peripheral blood mononuclear cell cultures from numerous koalas and in lymphoma tissue from others. Viral mRNA, viral genomic RNA, and reverse transcriptase activity were present in koala serum and cell culture supernatants. Sequences analysis of these RNAs and Southern blot analysis of koala tissue genomic DNA using labelled KoRV probes demonstrated banding consistent with an endogenous retrovirus. Complete (and truncated) proviruses were detected in DNA of both clinically normal koalas and those with hematopoietic disease. KoRV-related viruses were not detected in other marsupials, and phylogenetic analysis showed that KoRV clustered with gibbon ape leukemia virus. The close similarity between gibbon ape leukemia virus and KoRV indicated unexpectedly that these viruses are closely related and that cross-species transmission may have occurred in the recent past. Gibbon  leukemia virus is a replication competent member of the genus Gammaretrovirus, which includes both exogenous viruses (like murine leukemia virus) and endogenous viruses like KoRV. < 1% of humans die of leukemia or lymphoma. However, up to 70% of captive koalas, and 3-5% of wild koalas, die of cancer. It remains to be established whether this difference is determined by genetic divergence or by environmental factors^ref
• Vombatidae
• Vombatus
• Vombatus ursinus (a.k.a. common or coarse-haired wombat)

Other nontransmissible infections : Trypanosoma spp.

• Eutheria
• Insectivora
• Erinaceidae (hedgehogs) : Mycobacterium leprae, Leptospira interrogans serovar icterohaemorrhagiae, foot-and-mouth disease virus (FMDV)


• Edentata
• Bradypodidae
• Bradypus
• Bradypus infuscatus : Leishmania panamensis
• Dasypodidae
• Dasypus spp. : Trypanosoma cruzi


•  Megalonychidae
• Choloepus spp. : Leishmania guyanensis
• Choloepus hoffmanni : Leishmania panamensis


• Myrmecophagidae
• Tamandua spp. : Trypanosoma cruzi, Trypanosoma rangeli
• Tamandua tetradactyla : Leishmania guyanensis


• Hyracoidea
• Procaviidae
• Heterohyrax
• Heterohyrax brucei (yellow-spotted hyrax) : Leishmania aethiopica


• Procavia
• Procavia capensis : Leishmania aethiopica


• Proboscidea
• Elephantidae (elephants)

Bacillus anthracis is not a new phenomenon in south eastern Bangladesh, as there are published reports from the 1960s : the area is home to 400 wild elephants, including 100 believed to have migrated from forests in Burma and India. While elephants graze, they are also subject to infections via tabanids and blowflies. They can get infected either as a result of their feeding near villages or near wildlife cases, though primary cases are seen in the Etosha National Park. So it is possible that this forest case is not primary and follows upon cases in other species yet to be found. Elephants respond well to treatment if caught in time, which can of course be difficult when they are wild. They respond well to vaccination with darted Sterne vaccine, if there is the desire. We have had reports of elephant anthrax in India. In Namibia it has been reported in elephants in the Etosha National Park for about 80 years, initially in working elephants. Burning a dead elephant is a major undertaking.
• Rodentia
• Chiroptera
• Carnivora
• Lagomorpha
• Cetartiodactyla
• Perissodactyla
• Primates

struck / hemorrhagic enterotoxemia / Romney Marsh disease : a usually fatal enterotoxemia of calves, lambs, and piglets, caused by Clostridium perfringens serotype C, occurring chiefly in the winter and spring and characterized by hemorrhagic enteritis and peritonitis

• chorioptic acariasis, itch, or mange : mange caused by infestation with Chorioptes spp.; it usually occurs on the posterior body of cattle or horses, from the udder and perineum to the hind legs
• demodectic acariasis or mange / follicular mange / demodicosis : mange caused by infestation with Demodex spp., characterized by folliculitis with pustule formation, usually on the head, neck, or shoulders; it is common in dogs (red mange) and cattle and occurs sporadically in other species
• notoedric mange : infestation of the ears, head, or neck of a cat by a Notoedres spp.; it is intensely irritating and serious cases can be fatal.
• otodectic mange : mange in the ear region from infestation by Otodectes spp.
• psoroptic mange : infestation by Psoroptes spp.. Psoroptes cuniculi infests the ears of rabbits and goats, sometimes causing secondary infections of the inner ear or central nervous system. Psoroptes ovis causes sheep scab, the most common type of mange in sheep, as well as scabies in cattle and horses. Psoroptes equi infests sheltered areas on horses, such as those covered by hair.
• sarcoptic mange : Sarcoptes scabiei in animals other than humans.
• Knemidokoptes spp.

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