There are numerous diseases of snakes both infectious and noninfectious. This lecture is not meant as a review of all common snake diseases but an overview of some of the most common infectious diseases encountered in captive snakes.
Cryptosporidiosis in snakes is most commonly caused by the organism Cryptosporidium serpentis, although other species, such as Cryptosporidium saurophilum, have also been implicated in clinical disease.4,8 Cryptosporidium is an apicomplexan parasite with a simple life cycle that infects the gastric mucosa of many snake species. Once ingested, the organism infects the gastric mucosal cells where it replicates. As the gastric mucosal cells are sloughed, the oocysts are shed in the feces. Transmission is fecal-oral or by fomite transmission and oocysts are infective immediately after they are shed.4 There are many species of Cryptosporidium; however, only a few species are pathogenic to reptiles. Many rodents carry Cryptosporidium species, including Cryptosporidium muris, and the oocysts may be seen in the feces of a snake after eating an infected mouse or rat.8 These organisms do not infect the gastric mucosal cells and do not cause clinical disease in snakes. Infected snakes may not exhibit clinical signs of disease, but continue to intermittently shed oocysts in the feces. Snakes that develop clinical disease typically present with weight loss, mid-body swelling, and/or regurgitation.4 Diagnosis of the disease is based on clinical signs in conjunction with diagnostic testing. Asymptomatic carriers of the disease can be very challenging to diagnose. Cryptosporidium organisms stain positively using acid-fast stains and immunofluorescent antibody (IFA) stains (Merifluor). Cytology with acid-fast staining can be performed on feces and regurgitated food material. Acid-fast and IFA staining techniques may also be used on gastric lavage samples; however, false positive results will occur if the snake is shedding noninfective rodent Cryptosporidium species. Polymerase chain reaction (PCR) is a much more specific diagnostic test and can be performed on gastric lavage, fecal or gastric biopsy specimens. On histopathology infected snakes will typically have severe gastric mucosal hyperplasia with intralesional organisms.4 Several treatments have been reported for reptile cryptosporidiosis including trimethoprim-sulfa, hyperimmune bovine colostrum and paramomycin.4 Many of these treatments did reduce shedding and clinical signs but failed to eliminate the organism completely. Cryptosporidium is very stable in the environment; therefore, strict hygiene and quarantine is essential to prevent the spread of disease. The organism is resistant to many common disinfectants and only ammonia and formal saline were proven to be effective at killing the oocysts.4
Inclusion Body Disease
Inclusion body disease (IBD) is a suspected viral disease of boid snakes with an unknown etiology. The cause of the disease has long been suspected to be a retrovirus-like organism, but more recently an arenavirus has been detected in association with clinical disease.9,10 The disease is characterized by large eosinophilic inclusions in the cytoplasm of cells in infected animals. Clinical presentation of disease varies between the Boidae and Pythonidae families. Boas typically have inclusions noted in all visceral tissues and present with regurgitation and progressive weight loss. In later stages of the disease, secondary infections such as stomatitis and pneumonia, and severe neurologic disease may be evident.9 Pythons typically have inclusions noted in the central nervous system and present with acute severe neurologic disease. The disease in pythons typically progresses more rapidly than in boas.9 Although boas may live with IBD for extended periods of time, the disease is ultimately fatal. Antemortem diagnosis of IBD is difficult and clinical signs are nonspecific. A thorough history may indicate possible exposure. Routine CBC and chemistry may show a leukocytosis with lymphocytosis in infected animals and inclusion bodies can sometimes be detected in the cytoplasm of white blood cells on a buffy coat smear.9 The most useful diagnostic tool is reported to be organ biopsy, including skin, esophagus, liver and stomach, for histopathology to identify inclusion bodies.9 Treatment for the disease consists of supportive care. Infected animals should be strictly isolated from all other collection animals to prevent transmission or euthanized and strict hygiene is necessary to help prevent spread of the disease. The snake mite Ophionyssus natricis may be a mechanical vector of the disease and infestations should be promptly treated.
Ophidian paramyxoviruses are enveloped RNA viruses categorized into two distinct subgroups containing several isolates.3,6 Recently, a new isolate was identified and may represent a third distinct group.1 Ophidian paramyxovirus affects all major families of snakes but is most prevalent in the crotalids.3 Clinical signs of the disease are nonspecific, but include anorexia, regurgitation, dyspnea, star gazing, head tremors and flaccid paralysis.3 Due to immunosuppression, secondary bacterial infections are common. Some individuals die acutely, but some remain asymptomatic for extended periods of time (up to 10 months) before exhibiting clinical signs of disease.3 Diagnosis of the disease is based on history, clinical signs and serology. Titers to the virus can be detected using hemagglutination inhibition (HI). The University of Florida, University of Tennessee and Texas State Diagnostic Laboratories all perform HI serologic testing. A positive titer indicates exposure only and a rising titer is required to diagnose active disease. Each of these labs utilizes different test antigens from different paramyxovirus isolates; therefore, results are not necessarily comparable between labs and because of potential variable cross-reactivity between strains false positive and false negative results can occur.2 Further research is needed to determine the sensitivity and specificity of each of the serologic assays. Reverse transcriptase polymerase chain reaction (RT-PCR) has also been described and may be used to detect viral antigen and identify specific isolates.7 Virus transmission is mainly airborne although transmission can occur via contaminated utensils.3 Strict quarantine and isolation of infected individuals is required to prevent an outbreak. Treatment consists mainly of supportive care and treatment of secondary bacterial or parasitic infections. A necropsy should be performed on any snake that dies with suspected ophidian paramyxovirus. Histologically, lesions are located mainly in the lung, central nervous system and liver and are characterized by inflammation and necrosis. Eosinophilic intracytoplasmic inclusion bodies can be seen in the tissues but are rare. Definitive diagnosis is by virus isolation or electron microscopy.
Ectoparasites are commonly found on captive snakes with ticks and mites (Acarids) most commonly seen. A wide variety of species can parasitize snakes but one of the most important ectoparasites for the private practitioner is the snake mite, Ophionyssus natricis. The adult and protonymph stages of the snake mite are parasitic and feed on the blood of the snake.5 The life cycle of the snake mite is short (7–16 days), which can rapidly lead to severe infestations.5 Ophionyssus is considered a typical nest parasite and snake habitats are ideal for proliferation. The mites are often found between skin folds of the snake, under the chin and under scutes. The most common clinical signs noted with infection are behavioral change, dysecdysis, blood-loss anemia, anorexia and dehydration.5 Snake mites have also been implicated in the transmission of some viral diseases, notably inclusion body disease.5 Treatment of snake mites is difficult due to the complex life cycle and must include treatment of the animal as well as the environment. A variety of insecticide products are available but not all are safe for use on snakes. Commonly used treatments include dichlorvos strips, ivermectin and fipronil although safety and efficacy data have not been determined. Recurrence is common and vigilant treatment and hygiene is critical to cure the infestation.
1. Abbas MD, Marchang RE, Schmidt V, et al. A unique novel reptilian paramyxovirus, four atadenovirus types and a reovirus identified in a concurrent infection of a corn snake (Pantherophis guttata) collection in Germany. Vet Microbiol. 2011:150:70–79.
2. Allender MC, Mitchell MA, Dreslik MJ, et al. Measuring agreement and discord among hemagglutination inhibition assays against different ophidian paramyxovirus strains in the Eastern massasaugua (Sistrurus catenatus catenatus). J Zoo Wildlife Med. 2008;39:358–361.
3. Bronson E, Cranfield MR. Paramyxovirus. In: Mader DR, ed. Reptile Medicine and Surgery. 2nd ed. St. Louis, MS: Saunders Elsevier; 2006;858–861.
4. Cranfield MR, Graczyk TK.Cryptosporidiosis. In: Mader DR, ed. Reptile Medicine and Surgery. 2nd ed. St. Louis, MS: Saunders Elsevier; 2006:756–762.
5. Fitzgerald KT, Vera R. Acariasis. In: Mader DR, ed. Reptile Medicine and Surgery. 2nd ed. St. Louis, MS: Saunders Elsevier; 2006:720–741.
6. Marching R, Papp T, Frost JW. Comparison of paramyxovirus isolates from snakes, lizards, and a tortoise. Virus Res. 2009;144:272–279.
7. Papp T, Pees M, Schmidt V, Marchang RE. RT-PCR diagnosis followed by sequence characterization of paramyxoviruses in clinical samples from snakes reveals concurrent infections within populations and/or individuals. Vet Microbiol. 2010;144:466–472.
8. Pedraza-Diaz S, Ortega-Mora LM, Carrion BA, et al. Molecular characterization of Cryptosporidium isolates from pet reptiles. Vet Parasitol. 2009;160:204–210.
9. Schumacher J. Inclusion body disease virus. In: Mader DR, ed. Reptile Medicine and Surgery. 2nd ed. St. Louis, MS: Saunders Elsevier; 2006:836–840.
10. Stenglein MD, Sanders C, Kistler AL, et al. Identification, characterization, and in vitro culture of highly divergent arenaviruses from boa constrictors and annulated tree boas: candidate etiological agents for snake inclusion body disease. MBio. 2012;3(4):e00180-12.