Snake Fungal Disease
Causitive Agent and Affected Species
The organism responsible is the fungus Ophidiomyces ophiodiicola. It is characterized as an environmental saprobe, meaning that it normally feeds on decaying organic matter in the environment. This is evident due to its highly tolerant nature; it can thrive in a wide pH range (5 – 11), it is drought tolerant, and can utilize a number of complex carbon, nitrogen and sulfur compounds. Evidence that this organism is a saprobe makes it likely that infection of snakes is of opportunistic nature.
O. ophiodiicola is within the family Onygenacea and is closely related to Chrysosporium anamorph Nannizziopsis vriessii (CANV) complex; many early reports of snake fungal disease identify CANV as the causative organism but the fungus has since been reclassified. Snake Fungal Disease was first definitively identified in a population of Timber Rattlesnakes residing in New Hampshire in 2006. Since then, both colubrids and pit vipers in Eastern and Midwestern United States have been identified with SFD. However, recent advances in molecular diagnostics have allowed identification of cases dating back as far as 1986.
Affected species include milk snakes, black rat snakes, garter snakes, timber rattle snake, eastern massasauga, cotton mouth snakes and black racer snakes.
The fungus is believed to be spread from the environment-to-snake. Since O. ophiodiicola is an environmental saprobe, it is likely that the fungus resides in the soil. Spread of the fungus may occur through anthropogenic causes such as people moving contaminated soil imbedded in clothing or shoes. There have been a number of cases of captive snake populations becoming infected as well. This brings to question the origin of the fungus and that it may have come to the United States via the exotic captive snake trade. There is no definitive evidence of snake to snake transmission. However, since it is a lesion that predominates on the skin, it is possible that shedding of fungal particles from the external lesions can result in further dissemination of the disease, especially in species that share dens.
Several studies have indicated that temperature is a signiﬁcant factor affecting the growth of O. ophiodiicola. This suggests that populations hibernating in the lower thermal range of 0 °C - 10 °C should have a reduced infection during the spring and summer than snakes that hibernate in the upper thermal range of 0 °C - 10 °C. In addition, data suggest that with increasing global temperatures, snake populations will be more vulnerable to O.ophiodiicola.
Incubation period is between 30 to 37 days with some showing clinical signs as early as day 12 of inoculation. The characteristic clinical sign of SFD is facial swelling. The disease progresses from the nasal cavity internally via the eyes, throat and lungs causing ocular infections and pneumonia in some cases. The fungus additionally spreads externally along the neck, body and tail forming scattered nodules under the scales. In rare cases where there are wounds secondary to the infection, the fungus can penetrate the body and cause a systemic fungal infection resulting in nodules on the coelomic fat pad, kidneys, liver and air sac. Experimental data shows snakes surviving an average of 90 days with SFD and having a 40% mortality rate.
Diagnosis of SFD involves visual identification of the fungus or lesions consistent with an infection as well as laboratory identification of the fungus. Methods to identify the fungus include histopathological examination via skin biopsy, fungal culture and real-time or quantitative polymerase chain reaction (rtPCR and qPCR).
Due to its close relation to Chrysosporium anamorph Nannizziopsis vriessii (CANV) complex, O. ophiodiicola infections may have been misdiagnosed previously due to a lack of specific testing for the fungus. Treatment with antifungal medications has not been successful in colubrid snakes.
Clark RW, MN Marchand, BJ Clifford, R Stechert, and S Stephen. "Decline of an isolated timber rattlesnake (Crotalus horridus) population: interactions between climate change, disease, and loss of genetic diversity." Biological Conservation, vol. 144, no. 2, 2011, pp. 886-891. Accessed November 10 2016.
Sigler L, S Hambleton, and JA Paré. "Molecular characterization of reptile pathogens currently known as members of the Chrysosporium anamorph of Nannizziopsis vriesii complex and relationship with some human-associated isolates." Journal of Clinical Microbiology, vol. 51, no. 10, 2013, pp. 3338-3357. Accessed November 10 2016.
Guthrie AL, S Knowles, AE Ballmann, and JM Lorch. "Detection of snake fungal disease due to Ophidiomyces ophiodiicola in Virginia, USA." Journal of Wildlife Diseases, vol. 52, no. 1, 2015, pp. 143-149. Accessed November 10 2016.
Robertson J, SK Chinnadurai, DB Woodburn, MJ Adkesson, and JA Landolfi. "Disseminated Ophidiomyces ophiodiicola infection in a captive eastern massauga (Sistrurus catenatus catenatus).” Journal of Zoo and Wildlife Medicine, vol. 47, no. 1, 2016, pp. 337-340. Accessed November 10 2016.
Allender MC, S Baker, D Wylie, D Loper, MJ Dreslik, CA Phillips, C Maddox, and EA Driskell. "Development of Snake Fungal Disease after Experimental Challenge with Ophidiomyces ophiodiicola in Cottonmouths (Agkistrodon piscivorous)." PLOS ONE, vol. 10, no. 10, 2015. Accessed November 10 2016.
Allender MC, DB Raudabaugh, FH Gleason, and AN Miller. "The natural history, ecology, and epidemiology of Ophidiomyces ophiodiicola and its potential impact on free-ranging snake populations." Fungal Ecology, vol. 17, 2015, pp. 187-196. Accessed November 10 2016.