Infectious Diseases of Our Native Herps and Disinfection Protocols

Ranavirus (RV)

Massive die-offs of amphibians are often caused by ranaviruses. USGS scientists have isolated ranaviruses associated with die-offs in over 25 states involving more than 20 species of turtles and amphibians in mortality events ranging from one to thousands of individuals affected. Some events may involve a single species, others may involve multiple species. Frogs and salamanders in the same pond, for example, may die from ranaviral infections at the same time.

Map data derived from published and unpublished literature, and lab results from NWHC, MSU, UTK and UVA.

Ranavirus Infected Wood Frog larvae

Ranavirus-caused die-offs in amphibians have occurred on private, State, and Federal lands, including several National Parks and Wildlife Refuges. Many of the amphibian species involved in die-offs are fairly common and widespread in the United States, but some are either declining in number or are already threatened or endangered.

Host species: The USGS National Wildlife Health Center has isolated amphibian ranaviruses from 16 species of frogs, one species of toad and six species of salamanders. Mortality events due to ranaviruses occur most commonly in larval amphibians such as mole salamanders (Ambystoma spp.), true frogs (Lithobates spp. and Rana spp.) and chorus frogs (Pseudacris spp.). Infrequent isolates have been obtained from adult newts (Notophthalmus viridescens), adult tree frogs (Hyla spp.) and post-metamorphic Columbia spotted frogs (Lithobates luteiventris). In states east of the Mississippi River, especially Atlantic coastal states, mortality events tend to involve all species within the wetland (frogs, toads and salamanders) while those in western states, with less amphibian species diversity, tend to involve only one species.

Ranavirus infections in turtles occur mostly in captive colonies of eastern box turtles (Terrapene carolina carolina) and true tortoises, but die-offs of free-ranging box turtles also have been observed. Because box turtles in the wild usually are solitary animals, it has been difficult to document die-offs of multiple box turtles from an area.

Distribution: Amphibian ranaviruses probably are present in every state with the possible exception of Hawai'i. Globally, ranavirus diseases in amphibians have been diagnosed in North and South America, Europe, Asia, and Australia.

All confirmed cases of ranaviral infection in wild eastern box turtles on file at the USGS NWHC are from Maryland and Virginia. Additional ranaviral disease outbreaks in box turtles have been reported by others in New York, Pennsylvania, Georgia, and Florida.

Seasonality: Because mortality events due to ranaviruses mostly affect larval amphibians, there is a strong correlation between the presence of amphibian larvae in the spring and summer with ranaviral die-offs. Mortality events often are first detected in April when large populations of wood frogs (Lithobates sylvaticus, formerly Rana sylvatica) are present in eastern and northern wetlands. Early and mid-summer die-offs due to ranaviruses tend to involve a variety of amphibian species nationwide. Late summer and autumn mortality events involve mostly larval bullfrogs (Lithobates catesbeianus) and tiger salamanders (Ambystoma tigrinum).

Cause/Etiology: Ranaviruses are DNA-based viruses of the genus Ranavirus, in the family Iridoviridae. Occasionally, amphibian ranaviruses are called iridoviruses; however, this can be confusing because there is a genus of insect viruses called Iridovirus. Some isolates of amphibian ranaviruses have been named; most noteworthy are Frog Virus-3 (FV-3), first isolated in the 1960s, and Ambystoma tigrinum (tiger salamander) Ranavirus. Other strains or isolates of ranaviruses have informal names (e.g., Bohle virus in Australia, Redwood Creek virus in northern California, Southern High Plains virus, etc.), but the status of most isolates as species or strains of Ranavirus has yet to be clarified.

Signs and Lesions: Field signs of a ranaviral epizootic include sudden or explosive onset of illness in amphibians in a wetland, often with hundreds or thousands of sick and dead amphibians found in a 1–5 day period. Overall mortality rates in juvenile frogs and salamanders in a wetland can exceed 90%. Affected individuals usually present with subtle to severe hemorrhages in the ventral skin, especially at the base of the hind limbs and around the vent opening. Hemorrhages may be present from tip of chin to tip of tail ventrally and may be pinpoint or irregular patches.

Other clinical signs include lethargy, swimming erratically, weakly, or on their sides, and mild to severe fluid accumulation under the skin (in lymphatic sacs) of the abdomen and proximal hind limbs. Internally, there may be fluid accumulation (clear or red-tinged) in the body cavity (called hydrocoelom), and hemorrhages on the serosal surfaces of viscera, especially heart, stomach and liver. Occasionally, white minute foci of necrosis are evident in the liver or spleen. Ulcers of the skin and palate tend to be randomly scattered, but are detected in a low percentage of casualties.

Turtles with ranavirus infection show weakness, swollen eyelids, discharge from the nose and mouth, and the tongue and palate may show dull white or thick yellow plaques. At dissection, these plaques also may be found in the pharynx and esophagus. Occasionally, turtles may show ulcers on the bottom of their feet. Like ranaviral infections in tadpoles and salamanders, infection in box turtles spreads throughout the body affecting many organs including blood vessels. Additional research is needed to determine whether ranaviruses from box turtles and amphibians are identical and may be transmitted between the different genera and species.

Significance/Zoonotic Risk: At present, ranaviral infections appear to be limited to ectothermic vertebrates (i.e., fish, amphibians and reptiles). The virus generally cannot be cultured at temperatures above 30oC, so it probably is not infectious to domestic mammals and humans. At present, it is unclear how many strains or species of ranavirus are infecting and killing amphibians and turtles. Ranaviral outbreaks involving more than one class of vertebrates (i.e., fish and amphibians, or amphibians and reptiles) at a site are rarely reported in the wild, but such mortality events are of great interest ecologically. Ongoing research by USGS scientists and others will help to determine whether die-offs due to ranavirus are causing or contributing to population declines in turtles and amphibians.


Chytridiomycosis (Chytrid Fungus a.k.a Bd)

Have you heard about the amphibian die-offs occurring around the world? Many of them appear to be caused by a newly discovered fungus, Batrachochytrium dendrobatidis (Bd). Bd is a member of group of fungi called chytrids, which are usually found underwater growing on dead plant or animal matter. Bd is the only chytrid fungus known to feed on living vertebrates. It primarily affects the skin of amphibians, causing the disease known as amphibian chytridiomycosis.

Amphibians breathe and take up water through their skin. Chytridiomycosis interferes with these essential processes. Infected frogs may become lethargic, they are often unable to right themselves if turned upside down, and they may jump or swim in circles. They may rest with their legs outstretched, or sit with their rear end raised up. Sometimes their skin appears bloodshot or sloughs off excessively. They may also sit out in the hot sun, when healthy amphibians would seek shelter in shade or water.

Where did it come from?

Bd is currently found on every continent where amphibians exist, although in Asia it has only been found in Japan. But nobody is sure where it came from, or how long it has been where it is now. One clue lies in museum specimens, which can be examined for tell-tale signs of skin infection. So far, the oldest known instance is from South Africa in the 1930's. One hypothesis is that it was spread around the world in African clawed frogs used for human pregnancy tests.

What can you do to help?

Chytrid fungus can be transported from place to place in water or mud, including on wet or muddy footwear. You can prevent spreading it by making sure to clean your shoes well and let them dry thoroughly between visits to different places. This is also true for anything else that will come into contact with water. To be extra safe, you can brush items clean and then disinfect them with a weak solution of bleach. Also, you can avoid transporting live animals from one place to another.


Snake Fungal Disease (SFD)

Snake Fungal Disease (SFD) is an emerging disease in certain populations of wild snakes in the eastern and midwestern United States. While fungal infections were occasionally reported in wild snakes prior to 2006, recently the number of free-ranging snakes with fungal dermatitis submitted to the USGS National Wildlife Health Center (NWHC) and other diagnostic laboratories has been increasing. Laboratory analyses have demonstrated that the fungus Ophidiomyces (formerly Chrysosporium) ophiodiicola is consistently associated with SFD, but often, additional fungi are isolated from affected snakes. At this time, definitive evidence that O. ophiodiicola causes SFD is inconclusive. As its name implies, SFD is only known to afflict snakes.

To date, the NWHC has confirmed fungal dermatitis (or the suspected fungal pathogen in association with skin lesions) in wild snakes from nine states, including Illinois, Florida, Massachusetts, Minnesota, New Jersey, New York, Ohio, Tennessee, and Wisconsin. However, it is suspected that SFD is more widespread in the United States than is currently documented. Multiple species of snakes have been diagnosed with SFD at the NWHC (see attached figures; view additional photographs at, including northern water snake (Nerodia sipedon), eastern racer (Coluber constrictor), rat snake (Pantherophis obsoletus species complex), timber rattlesnake (Crotalus horridus), massasauga (Sistrurus catenatus), pygmy rattlesnake (Sistrurus miliarius), and milk snake (Lampropeltis triangulum).

The most consistent clinical signs of SFD include scabs or crusty scales, subcutaneous nodules, premature separation of the outermost layer of the skin (stratum corneum) from the underlying skin (or abnormal molting), white opaque cloudiness of the eyes (not associated with molting), or localized thickening or crusting of the skin (hyperkeratosis). Skin ulcers, swelling of the face, and nodules in the deeper tissues of the head have also been documented. Clinical signs of SFD and disease severity may vary by snake species. Aside from the presence of fungi with disease-associated lesions, specific pathological criteria for the disease have not yet been established.

While mortality has been associated with some cases of SFD, population-level impacts of the disease are not yet widely known and are difficult to assess due to the cryptic and solitary nature of snakes, and a general lack of long-term monitoring data. In New Hampshire, clinical signs consistent with SFD were associated with a 50 percent decline of an imperiled population of timber rattlesnakes from 2006 to 2007. In areas where susceptible snake species occur in small, isolated populations, the added threat of SFD may threaten viability of these populations. In other regions, SFD has been observed without suspected or, as yet, documented population declines.

Several agencies, organizations, researchers, and other key stakeholders, including the NWHC, are working together to investigate this potentially emerging disease and to learn more about the impacts

that SFD is having on snake populations in the eastern and midwestern United States. We encourage conservation agencies and natural resource managers to contact the NWHC if snakes with clinical signs consistent with SFD are encountered.


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