Sonia M. Hernandez-Divers, DVM, PhD, DACZM
Warnell School of Forestry and Natural Resources & the Southeastern Cooperative Wildlife Disease Study at the College of Veterinary Medicine, University of Georgia, Athens, GA
This document is beyond covering all the of the diseases affecting wildlife in North America; however, I aim to highlight diseases of concern that may present to the small animal/exotics/wildlife practitioner, and particularly highlight disease issues that affect the overall health of wildlife populations, and the thought process involved in determining the outcome of wildlife patients.
Wildlife rehabilitation is one way that we, as humans, feel we can mitigate some of the anthropocentric damage on the environment; however, the effects of wildlife rehabilitation on populations of animals have not been adequately assessed. Lack of funding and other challenges have resulted in a paucity of studies that appropriately monitor animals after medical treatment and release. In some cases, wildlife rehabilitation efforts can results in the introduction or dissemination of diseases into wildlife populations (Porter, 1996). Several references have reviewed the biosafety, biosecurity and disease prevention measures needed to avoid such issues. Additionally, the effects of rehabilitating individual animals that might otherwise be "naturally removed" from a population (for example, as a consequence of weather) has not been investigated. Conversely, wildlife rehabilitation centers and clinics that offer medical treatment to wildlife can be a valuable resource in the early detection of disease outbreaks, and the first line of contact between the public and medical professionals (Sleeman, 2008). Whether you practice exotic, wildlife or zoological medicine, knowledge of the status of diseases in free-ranging animals is paramount. The general public will look to you, the zoological medicine professional, as a source for information on these diseases. Given that wildlife diseases are appearing in the news more commonly (either because they are emergent diseases or of zoonotic concern), the zoological medicine professional should stay abreast of these issues, not just to supply information when needed, to understand how to protect captive animal collections (i.e.: aviary and West Nile, rabies and zoo mammals), to design feral animal protocols, to design preventative medicine protocols for wildlife patients, but also to help in protecting wildlife population. Ultimately, maintaining a healthy free-ranging population is much more important than successfully rehabilitating any one individual patient. As wildlife medicine practitioners, we should be conscious of the potential risks of introducing disease agents into free-ranging populations, or creating situations in the wildlife clinic (overcrowding, mixing species, etc) that promote the infection of diseases to animals that might ultimately be released. The wildlife medicine practitioner should be specifically aware of disease details as they apply to the region in question, as wildlife disease management varies significantly by region. The scope of this lecture does not allow for a complete review of all wildlife diseases. This information, for example, can also be used to formulate a list of diseases for which a wildlife patient should be screened prior to release. The reader is directed to the most current and complete sources available, such as the NWHC, USGS Field Manual of Wildlife Diseases: Diseases of Birds (available free at http://www.nwhc.usgs.gov/publications/field_manual/), Infectious Diseases of Wild Mammals by Williams and Barker, Non-infectious diseases of Wildlife by Fairbrother, Locke and Hoff, Parasitic Diseases of Wild mammals by Samuel, Pybus and Kocan, Infectious Diseases of Wild Birds by Thomas, Hunter and Atkinson, and the Field Manual of Wildlife Diseases in the Southeastern United States by Davidson and Nettles. The information contained herein utilized a mixture of the above sources.
Diseases of Free Ranging Birds
There are many diseases of free-ranging birds worldwide. Their importance depends on the species and the region in question. In North America, we consider the following:
Bacterial Diseases: Avian Cholera, Avian Tuberculosis, Salmonellosis, Chlamydiosis, Mycoplasmosis.
Fungal Diseases: Aspergillosis, Candidiasis.
Viral Diseases: Duck Plague, Inclusion Body Disease of Cranes, Miscellaneous Herpesviruses of Birds, Avian Pox, Eastern Equine Encephalomyelitis, Newcastle Disease, Avian Influenza, Woodcock Reovirus.
Parasitic Diseases: Hemosporidiosis, Trichomoniasis, Intestinal Coccidiosis, Renal Coccidiosis, Sarcocystis.
Toxins: Organophosphorus and Carbamate Pesticides, Chlorinated Hydrocarbon Insecticides, Polychlorinated Biphenyls, Oil, Lead, Selenium, Mercury, Cyanide, Salt, Barbiturates
Mycoplasma of House Finches
Source: an epizootic of conjunctivitis began in the Washington DC area in 1993-94, where many house finches (Carpodacus mexicanus) were found dead. The outbreak spread first North, then West and then southeast. By 1997, this disease could be found in the entire Eastern range of the house finch. Birds get infected in wintering grounds, and then take disease to breeding grounds (thus the spread N), the W spread was likely due to juvenile dispersal. Other species from which the same Mycoplasma has been isolated include American goldfinches, purple finches, pine grosbeak, evening grosbeak. Clinical signs: unilateral/bilateral conjunctivitis, swollen eyelids, discharges from eyes, lethargy, dyspnea, and acute death. Etiology: Mycoplasma gallisepticum. The MG strain of house finches is unique and not related to historical or current poultry isolates. Diagnosis: culture, isolation, PCR test. Treatment: treatment of individual free-ranging birds for release is very controversial. There are several protocols including Tylosin in the water, oral or parenteral enrofloxacin, with or without ocular ointments (Terramycin). However, it is the opinion of this author that birds with Mycoplasma conjunctivitis should not be treated and released as per evidence that birds after treatment can still test PCR positive for Mycoplasma (Wellehan, 2001). This is particularly true for house finches on the eastern portion of North America where these birds are considered an introduced invasive species. Mycoplasma conjunctivitis had a significant effect on the house finch population in the years immediately after the initial epizootic (caused significant declines, especially in high-density populations); however, it is currently thought to be evolving host-parasite relationship, where some populations are evolving resistance, or the organism is becoming less virulent. Some other passerine species, such as tufted titmice, appear to be asymptomatic carriers or have transient MG infections (Luttrell, 2007).
Avian salmonellosis is a common disease among birds of the order Passeriformes and is most often caused by Salmonella enterica serovar Typhimurium (syn. Salmonella typhimurium). Mortality is seen among passerines throughout North America and is often associated with congregations of birds at feed yards, grain fields, or backyard feeders. Mortality rates can be very high and fecal shedding is abundant. Diagnostic reports at the Southeastern Cooperative Wildlife Disease Study (SCWDS) indicate outbreaks are often limited to a subset of the species present and the species affected vary from one mortality event to another. Two recent reports have indicated that avian salmonellosis might be on the rise (Hall, 2004; Hernandez, 2009). Clinical signs: emaciation, fluffed appearance, indifference to human presence, lethargy, acute death, crop mass. Pathology: yellow, caseous nodules/plaques of the esophagus; Histopathology: fibrinopurulent esophagitis with intralesional bacteria. Diagnosis: histopathology and culture of the lesion, as well as liver to confirm Salmonella septicemia as cause of death. Concurrent infections with trichomoniasis are also seen. Treatment: typically songbirds birds die prior to presentation and efforts should be aimed at public education for prevention; however, antibiotics with a spectrum against Salmonella should be effective. It would be important to determine post-treatment shedding status prior to release because a carrier state can be encouraged with antibiotic therapy. Seasonality: the highest incidence of salmonellosis occurs during winter months which may be associated with concentration of birds at feeders, or concurrent physiologic stress. Prevention: during an epizootic, birds should be discouraged from congregating at feeders or water baths; these devices should be removed for 2-3 weeks and thoroughly cleaned with 10% bleach solutions (Doust, 2007). It is unknown if and how avian salmonellosis may be affecting songbird populations. To date, there have been no quantitative studies to demonstrate a population decline due to salmonellosis.
Avian Vacuolar Myelinopathy
Avian Vacuolar Myelinopathy was first observed in 1994-5 in bald eagles. It is a neurologic disease affecting primarily bald eagles and American coots in the SE USA. It is characterized by spongy degeneration of the white matter of the CNS, particularly around the optic tectum. Clinical signs: inability to fly, difficulty swimming/walking and other neurological signs; some birds recover. This disease is seasonal (late fall-early winter), is quick in onset (5 days post-exposure), and associated with specific geographic locations. Additional hosts: mallards, ring-necked duck, bufflehead, Canada goose, great horned owl, and killdeer. Etiology: it is suspected to be a natural toxin, produced by cyanobacteria associated with aquatic plants. Diagnosis: at this time no pre-mortem test is available; diagnosis is made by history of the location of the waterways associated with AVM, clinical signs and histopathology. At least regionally, AVM has impacted bald eagle populations significantly, particularly in areas where eagles are breeding near waterways associated with AVM, such as South Carolina. It is suspected, but not investigated, that coots are also on the decline due to AVM. Currently the only effort to manage AVM is to manage waterways to discourage the aquatic plants thought to be associated with this disease (Landsberg, 2007).
West Nile Virus
Etiology: West Nile (WN) virus has emerged in recent years in temperate regions of Europe and North America, presenting a threat to public, equine, and animal health. West Nile virus (WNV) is a flavivirus virus commonly found in Africa, West Asia, and the Middle East, and was introduced to New York, USA in 1999. It is closely related to St. Louis encephalitis virus found in the United States. It is spread by infected mosquitoes. The virus usually infects birds, but it can be spread to humans by mosquitoes that feed on infected birds and then bite humans. One of the species of mosquitos found to carry West Nile virus is the Culex species which survive through the winter, or "overwinter," in the adult stage. That the virus survived along with the mosquitoes was documented by the widespread transmission the summer of 2000. The continued expansion of West Nile virus in the United States indicates that it is permanently established in the Western Hemisphere. In the temperate zone of the world, West Nile encephalitis cases occur primarily in the late summer or early fall. In the southern climates where temperatures are milder, West Nile virus can be transmitted year round. Transmission: Mosquitoes obtain the virus by feeding on infected birds. The level of viremia in animals other than birds is too low to infect mosquitoes. Infected mosquitoes then transmit the virus to animals and humans through bites, and West Nile viral encephalitis develops in animals and humans when the virus multiplies and crosses the blood-brain barrier. Ticks infected with the virus have been found in Asia and Africa; however, there are no verified reports of ticks spreading the virus and their role in transmission has not been determined. West Nile virus has now spread throughout the continental USA, Canada, Caribbean and Latin America. Clinical signs: in highly susceptible species (crows, jays, black-billed magpies, grackles, ring-billed gulls, house finches and house sparrows) the disease causes various neurological signs (ataxia, tremors, abnormal head posture, circling, sternal recumbency, seizures, depression) and is accompanied by a high level of viremia. Several host species experience low viremias and no clinical disease (Galliformes), Passeriformes and Charadriiformes had higher viremias and are considered better reservoirs. Among birds of prey, owls (particularly northern breeding species) have been reported to experience high mortalities, whereas those of southern breeding species did not. Falconids and peregrine falcons were less susceptible than northern goshawks which were considered very susceptible. Diagnosis: serologic IFA tests for IgM antibody, ELISA, virus isolation, histopathology. Population impact: WNV affected local populations of crows initially, but sustained significant declines have not been documented; white pelicans experienced a significant decline in north central USA, particularly of nestlings in North Dakota; greater sage-grouse also experienced significant declines. Treatment is not successful. Management is aimed at mosquito control and is for the benefit of preventing disease in humans and domestic animals (McLean, 2007).
Common Diseases of Free Ranging Mammals
White-tailed Deer (Odocoileus virginianus): Hemorrhagic Disease, Cutaneous Fibroma, Dermatophilosis, Brain abscesses, BVD, MCF, IBR, Rabies, Vesicular Stomatitis, Anthrax, Bovine tuberculosis, Chronic Wasting Disease; Parasitic diseases: Toxoplasmosis, Liver flukes (Fascioloides magna), Lungworm (Dictyocaulus viviparous), Stomach worm (Haemonchus contortus), Meningeal worm (Parelaphostrongylus tenuis), Arterial worm (Elaeophora schneideri), Abdominal worm (Setaria yehi), Larval tapeworm (Taenia hydatigena), Nasal bot (Cephenemyia), Ticks (several sp, depending on region), Mange: Demodex odocoilei. Black Bear (Ursus americanus): Rabies, Parasites: Roundworms (Baylisascaris transfuga), Canine heartworm, (Dirofilaria immitis), Trichinosis
Raccoon (Procyon lotor): Rabies, Canine distemper, Parvovirus enteritis (Raccoon parvovirus), Leptospirosis reservoir; Parasites: Spirometra, Ascarid (Baylisascaris procyonis), Subcutaneous worm (Dracunculus insignis), Stomach worms (Physaloptera rara, Gnathostoma procyonis), Trichinosis, Thorny-headed worm (Macracanthorhynchus ingens)
Skunk (Mephitis mephitis): Rabies, Canine Distemper, Infectious Canine Hepatitis, Leptospirosis-reservoir; Parasites: Ascarid roundworm (Baylisascaris columnaris)
Red Fox (Vulpes vulpes): Rabies, Canine Distemper, Infectious Canine Hepatitis (adenovirus), Leptospirosis; Parasites: Echinococcus (Echinococcus multilocularis)-definitive host, Canine heartworm, Subcutaneous worm (Dracunculus insignis), Sarcoptic mange (Sarcoptes scabiei),
Gray Fox (Urocyon cinereoargenteus): Canine distemper, Rabies, Leptospirosis-reservoir; Parasites: Canine heartworm (rare)
Coyote (Canis latrans): Canine distemper, Canine parvovirus, Rabies, Brucellosis; Parasites: Echinococcus, Canine heartworm
Bobcat (Felis rufus): Feline panleukopenia, Rabies; Parasites: Toxoplasmosis (Toxoplasma gondii)-definitive host, Cytauxzoonosis (Cytauxzoon felis)-reservoir, Spirometra-definitive host
Opossum (Didelphis virginianus): Leptospirosis-reservoir, Sarcocystis (Sarcocystis falcatula), Besnoitia infection (Besnoitia darlingi), Stomach worm (Physaloptera turgida)
River Otter (Lutra canadensis): Canine distemper; Parasites: Subcutaneous worm (Dracunculus lutrae)
Beaver (Castor Canadensis): Tularemia; Parasites: Giardia
Cottontail Rabbit (Sylvilagus floridanus): Shope's fibroma, Tularemia, Staphylococcosis; Parasites: Sarcosporidiosis (Sarcocystis leporum), Larval tapeworm (Taenia pisiformis), Ascarid roundworm (B. procyonis, columnaris)
Gray Squirrel (Sciurus carolinensis): Squirrel fibroma, Dermatophytoses; Parasites: Cutaneous warbles (Cuterebra)
Woodchuck (Marmota monax): Woodchuck hepatitis (hepadnavirus), Rabies; Parasites: Ascarid roundworms (B. procyonis, columnaris)
Armadillo (Dasypus novemcinctus): Leprosy (Mycobacterium leprae)
White-nose Syndrome of Bats
Background: bats found dead 2006-2007 in a few hibernation caves, New York, >8,000 bats dead; winter of 2007-2008 bats found dead in 18 additional caves and mines in NY, Massachusetts, Connecticut and Vermont. In some cases, 90-100% mortality rate. In 2008, mortality > half-million animals, by February 2009 WNS confirmed in New Jersey, Pennsylvania, and central West Virginia. By March 2009 it was confirmed in Virginia. Etiology: White nose syndrome is defined as a cutaneous fungal infection and phylogenetic analyses from ten fungal isolates provide evidence that it is caused by an inoperculate ascomycetes (Order Heliotiales), now called Geomyces destructans which is a terrestrial, saprophytic, psychrophilic fungus (5-10°C; 40-50°F), that prefers high levels of humidity (>90%), yet has distinct morphologic characteristics from other Geomyces sp. (i.e.: single, curved conidia as opposed to clavate, arthroconidia). Clinical signs: Fungal growth is sometimes obvious on hairless skin (face, muzzle), depleted body fat stores and poor body condition and dehydration. Bats can also present with NO fungal growth but abnormal behavior, such as gathering at cave entrance, flying during the day, leaving hibernacula prematurely. Pathogenesis: Fungal hyphae replace hair follicles and associated sebaceous and sweat glands, breaching the basement membrane and invading regional tissue; hyphae also erode the epidermis of ears and wings. At this point, evidence points towards emaciation and starvation as the ultimate cause of death. Concentrations of chlorinated hydrocarbon contaminants, pyrethroids and heavy metals are not markedly elevated, nor have there been any other known bacterial or viral pathogens have been identified. Diagnosis: High mortality in cave coupled with bats dead at entrance of caves in winter, aforementioned clinical signs, scarring on wings, histopathology, PCR and ultimately fungus isolation. Treatment with antifungals is currently being investigated by the National Wildlife Health Center, at this point all efforts are on surveillance, cave closures and the investigation of decontamination procedures to limit the transmission to new caves. Significance for populations: major population declines documented in NY, but it is important to note that 45 bat species in USA, half are hibernating bats. It is speculated that this is an introduced disease, perhaps from Europe, since there are reports of bats with fungi from the past several years, and historical literature (1983) in Germany. Fungal growth apparent at the end of winter, and fuzz disappears when the bats are taken out of the hibernacula or groom it off. No mass mortalities have been reported in Europe.
Chronic Wasting Disease-USA
For current updates of CWD, the reader is directed to the National Wildlife Health Center CWD website: http://www.nwhc.usgs.gov/disease_information/chronic_wasting_disease/index.jsp:
Background: Transmissible Spongiform Encephalopathies that have been described: Scrapie-sheep/goats, Kuru, Creutzfeldt-Jacob-humans, BSE-cattle, domestic cats, wild mammals-UK and France, BSE associated with variant of CJD in humans in 1996, Scrapie-like dz in moufflon in UK.
Etiology: TSE's-caused by prions (proteinaceous agents without nucleic acid); protease-resistance forms PrPres of cellular proteins (PrPc) coded for and normally synthesized in CNS and lymphoid tissue-humans, PrPc can mutate and convert to PrPres -familial disease, or acquired. Familiar form not described in animals. CWD was 1st recognized in 1967 in captive mule deer (O. hemionus) in captive research facilities in Colorado. In 1978 it was recognized it as spongiform encephalopathy by histo-path of CNS, then recognized it as CWD in Wyoming and soon after in Rocky Mt elk in same facilities. Some deer/elk in zoos were dx with CWD during that time also. In wild herds, it can sometimes be found in up to 30 percent of animals; in captivity nearly entire herds can be affected. In 1981 it was found CWD in free-ranging elk in Colorado; then in Wyoming (elk), then in mule deer and WTD in Colorado and Wyoming. The current distribution is fourteen states in the U.S. and in two Canadian provinces, predominantly in the West, both in the wild and on commercial farms: captive and free-ranging cervids in SE Wyoming, North, Central and NE Colorado and other game farms. Hosts: 3 sp of cervidae=mule deer, WTD, RM elk; others not susceptible, even when exposed. Experimentally disease has been caused in lab mice, sq. monkey, mink, ferret, goat by intracranial inoculation.
Transmission: likely, lateral. Studies have shown that the disease can be transmitted orally - deer experimentally fed infected brain tissue become sick - but the animals are not carnivores, nor cannibalistic. NOT from rendered infected meat (like BSE); lateral transmission supported by epidemiology; potential maternal transmission; prob. transmitted from mule deer elk; prion found in alimentary lymph nodes in other TSE's, and recent evidence of fecal shedding, which is likely responsible for rapid spread in wild populations. Prion is very resistant in environment; concentration of cervids at feeders increases transmission
Incubation: Unknown, youngest animal affected 17 mos (at least that long)
Prevalence: in endemic areas (based on examination of hunter killed brains) 1-8%
Clinical Signs: decreased body wt; changes in behavior (might be very subtle); pacing; not associating with herd; depression (but aroused with stimuli); animals eat less; PU/PD; inc. salivation; incoordination; post ataxia; head tremors; aspiration pneumonia.
Clinical Course: days-yrs (3-4 mos average)
Pathogenesis: animal ingests PrPres, which is found in retropharyngeal and ileocecal lymph nodes, tonsils and Peyer's patches; PrPres accumulates in parasympathetic vagal nucleus of medulla oblongata. Clinical path: low urine specific gravity and other non-specific sings; Pathology: gross lesions: no real lxs; poor body condition, excessive water in rumen; sand/gravel in forestomachs, aspiration pneumonia; typical lesion of TSE's in parasympathetic vagal nucleus in the dorsal portion of the medulla oblongata at the obex, hypothalamus and thalamus; plaques with PrPres found with H&E stain in WTD and mule deer, but not necc. elk; plaques surrounded by vacuolization; stain well with immunohistochemistry stains.
Diagnosis: histopath-spongiform lesions on brain in sheep, dx scrapie by finding PrPres in lymph nodes, tonsils premortem.
Differential diagnoses: brain abscesses, encephalitis/meningitis, peritonitis, starvation, pneumonia; arthritis, etc. Immunity: no known immune response to TSE's has been reported previously and it is unknown if certain genotypes confer resistance or have an increased susceptibility to CWD.
Treatment: no treatment is available; quarantine and depopulate attempts to eradicate CWD from captive facility failed-contaminated environment is to blame. Decreasing population size might help; discouraging supplemental feeding (now banned).
Management: cannot move deer from endemic areas; surveillance is expensive; impact on populations is truly unknown, but suspected to affect them negatively. Many states have both passive and active CWD surveillance programs and if receiving cervids in your clinic, you should contact your state agency to discuss whether they are testing.
Diseases of Free Ranging Herpetofauna
Herpetofauna are declining in drastic numbers. Although most of the attention has been focused on the global decline of amphibians, reptiles are also suffering at the population level due to disease. Diseases of importance are: Tortoise mycoplasmosis, Sea Turtle Fibropapillomatosis, Shell Diseases of turtles and tortoises, aural abscesses of turtles, Chytridiomycosis, Iridoviruses of amphibians, ranaviruses, and leg deformities of amphibians.
Tortoise and Turtle Mycoplasmosis
Etiology: Mycoplasma agassizii. Background: Desert tortoise (Gopherus agassizii): dramatic declines of desert tortoises from SW USA and CA in the past 20 years; G. agassizii listed as threatened; mycoplasmosis considered a factor in the species decline; Gopher tortoise (G. polyphemus): first documented in 1989 in Florida; Box turtle (Terrapene carolina carolina): a novel type of Mycoplasma closely related to M. pulmonis or M. agassizii is thought to be the etiologic agent.
Clinical signs for all tortoises: Mucopurulent discharge from nares and eyes, palpebral edema, conjunctivitis, eyes recessed into the orbits, dullness to skin and scutes; infection is usually chronic, often subclinical; intermittent/cyclical disease expression exists; carrier state exists
Diagnosis: culture, PCR, serology (ELISA); Pathology: mild to severe inflammation of upper respiratory tract, hyperplasia and dysplasia of mucous membranes, often isolate secondary gram negative bacteria
Treatment: Clarithromycin 15 mg/kg po every 2-3 days (drug appears to accumulate), readily penetrates intracellularly, accumulates in respiratory lining cells and secretions; liver metabolism yields an active 14-OH-Clarithromycin, increasing antibiotic efficacy
Management: A chronically infected status may occur with this disease, therefore infected animals should not be returned to the wild; decision tree analysis can be used to determine the best solution for disposition of animals (Jacobson, 2004). A recent review challenged the view that M. agassizii causes consistent levels of morbidity and/or mortality across the Mojave Desert in desert tortoises. Instead, the authors proposed that upper respiratory disease in tortoise might be more accurately as a "context-dependent" disease and recommended abandoning policies to euthanize tortoises that test positive for an immune response to M. agassizii (Sandmeier, 2009).
Sea Turtle Fibropapillomatosis
Background: Described in free-ranging green sea turtles (Chelonia mydas), worldwide, but especially high prevalence in Florida (31-62%) and Hawaii populations (49-91%); Has also been reported in other sea turtles such as loggerheads (Caretta caretta) and olive ridleys (Lepidochelys olivacea); Hosts: In Hawaii FP is found in green turtles that associate with coastal pastures of algae and sea-grass; FP affects immature turtles more severely; prevalence can reach >50% in some aggregations
Clinical signs: Number and size of tumors vary; range from gray to black and can grow up to 10 cm in diameter; cutaneous FPs are seen on the skin, especially front flippers, neck, periocular tissues, cornea, plastron and carapace; internal tumors most likely found in lung, liver, kidneys and GI tract; Turtles with FP are immunosuppressed, (Increased het/lymph ratio and decreased eos/mono ratio with increasing tumor score); lower PCV, TP, alpha and gamma globulins; lower mononuclear cell proliferation but immunosuppression not a prerequisite for development of FP; Biochemical changes present: Increased ALP and lower lactate in FP turtles; can use to predict infection. There are differences between wild and captive animals: wild animals had higher corticosterone, lactate, triglyceride, glucose, calcium than captive turtles, wild turtles had lower uric acid.
Etiology: Concensus is that this disease is caused by a herpesvirus, although it may be multifactorial and associated with coastal pollutants. Other etiologic agents have been suggested such as spirorchid trematodes, as their ova are often present in fibrotic portion of FPs in Hawaii or intravascular trematodes (Learedius sp., Carrettacola sp., Haplotrema spp.) which use snails and annelids as intermediate host and their cercariae shed and penetrate mucous membranes. The adult trematodes inhabit the heart, visceral and mesenteric vessels, the eggs are shed in feces and urine and can cause lymphoplasmacytic endarteritis, but no association between antibody reactivity to spirorchids and FP status.
Pathology: marked hyperplasia of epidermis, vacuolation of cytoplasm and ballooning degeneration of epidermal cells, dermis consists of proliferating fibroblasts, eosinophilic intranuclear inclusions, EM demonstrates presence of herpesvirus.
Treatment: involves surgical removal but turtles with visceral nodules have a poor prognosis.
Management: Affected animals should be maintained isolated and separate from non-infected animals. The release of sea turtles with fibropapillomas is controversial.
Background: first described in 1998 from adult amphibians collected at sites of mass death in Australia and Panama; also found in captive-bred poison dart frogs; now been discovered in captive and wild amphibians from SW USA, Colorado, Ecuador
Clinical signs: Abnormal posture, lethargy and loss of righting reflex, excessive shedding of skin, mild thickening and discoloration of skin of legs and ventrum, epidermal ulcerations and hemorrhage
Pathology: Microscopic exam of shed skin reveals the presence of the chytrids (Batrachochytrium dendrobatidis); epidermal hyperkeratosis, hyperplasia, and hypertrophy associated with low to moderate number of chytrids in keratin; experimentally transmitted to Dendrobates sp.
Pathogenesis: Most chytrids live off decaying organic matter, some parasitize other fungi, plants and invertebrates; none have been reported in be pathogenic to vertebrates until recently; emergence is characteristic of an introduced virulent pathogen dispersing through an naïve population.
Emergence: Introduced infected cane toads may be the source in Australia; fungus is able to persist in keratinized mouthparts of larvae (tadpoles) and they may act as a reservoir; persistence further enhanced by saprophytic development in the environment; development outside of host may greatly increase impact and accelerate population declines; species with declining populations are regionally endemic rain forest specialists with low fecundity that reproduce in streams and live at high altitudes.
Leg Deformities of Amphibians
Background: 1992-1993 high frequencies of hindlimb deformities in anurans occupying ponds or ditches exposed to agricultural pesticides was observed; several degrees of ectromelia (absence of all or part of limb) and ectrodactyly (absence of digits) seen; Green frogs, leopard frogs, American toads and bullfrogs affected.
Prevalence: ranged from 12-69%; characterized by segmental hypoplasia or agenesis; interfered with swimming and hopping.
Etiology: Authors proposed a teratogenic action of exogenous factors as most likely etiology; agricultural contaminants were suspected as the primary cause; amphibians may be subject to more environmental stressors and toxins due to biphasic life cycle and skin permeability.
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