Mature female red-tailed boa constrictor (Boa constrictor).This snake became listless, inappetant, and died approximately one month after birthing. It had
regurgitated recently. One other snake (also a red-tailed boa) also died recently.
This boa was in good nutritional condition and had ample internal body fat stores.Â No gross
lesions were seen.
Inclusion body disease of boids, with widespread intracytoplasmic
inclusion bodies in epithelial cells of liver hepatocytes and biliary epithelial cells and hepatocellular degeneration
Boid Inclusion Disease
Inclusion body disease of boid snakes has been recognized for the past 30 years, and is
named for the characteristic intracytoplasmic inclusion bodies seen in a variety of epithelial cells.Â These include
epithelial cells of the pancreas, renal tubules, gastrointestinal tract, respiratory tract, hepatocytes, biliary epithelium,
thyroid follicular cells, and neurons of brain and spinal cord.(4) All tissues involved are reported to have varying
degrees of degenerative changes, including vacuolation, cellular collapse and necrosis.Â Meningoencephalitis has
been reported in both boas and pythons; however, the severity of both the neural histopathologic changes and
clinical signs is much higher in Burmese pythons than in boa constrictors.(4)
Workers at the University of Florida found this disease to be caused by a retrovirus through the use of transmission electron microscopy.Â Further characterization efforts conducted demonstrated reverse transcriptase activity. Western blot analysis of viruses from different snakes was also done; these different isolates from different snakes were found to be similar.(1)
Clinical signs are quite variable.Â Regurgitation and signs of central nervous system (CNS) disease are commonly seen in boa constrictors.Â Stomatitis, pneumonia, undifferentiated cutaneous sarcomas, and lymphoproliferative disorders have all been seen.Â Burmese pythons generally show signs of CNS disease without manifesting any other clinical signs; regurgitation is not seen in Burmese pythons.(4)
This snake was one of several in this household that died with similar clinical presentations and pathologic findings. There is no treatment, and the disease is highly contagious and always fatal.Â As the disease seems to be occurring with increasing incidence, it is imperative that all new boids brought into a collection be quarantined from acquisition for at least 3-6 months, and that appropriate precautions be taken when visiting other collections, pet stores, expositions, and swap events.
Although slides submitted from this snake for the conference were all from the liver, similar inclusion bodies were also seen in most of the tissues cited above.
1.Â Liver: Hepatocellular degeneration, diffuse, moderate, with scattered single hepatocellular necrosis, and many hepatocellular and biliary epithelial intracytoplasmic eosinophilic inclusion bodies.
2.Â Liver: Hepatitis, necrotizing, random, acute, multifocal, moderate, with colonies of coccobacilli.
Conference participants noted the characteristic eosinophilic intracytoplasmic inclusion
bodies both in hepatocytes and biliary epithelial cells.Â Additionally, scattered randomly throughout the liver are foci
of lytic necrosis with colonies of coccobacilli, which participants ascribed to embolic showering resulting from
terminal sepsis, thus accounting for the lack of associated inflammation.
Despite an abundance of research on this important entity, fulfillment of Kochs postulates remains elusive, and the cause of inclusion body disease (IBD) is still enigmatic.Â As noted by the contributor, a retroviral etiology has been strongly suspected, and clinicopathologic evidence (e.g.Â stomatitis, lymphoproliferative disorders, etc.) supports this conclusion.Â Moreover, retroviruses have been isolated from various species of snakes with IBD; however, a causal role has not been established, and it remains possible that retroviruses play only an incidental role in IBD.Â Similarly, reoviruses and adenoviruses have also been isolated from snakes with IBD, and may play causal and/or incidental roles in the disease.Â Notably, electron microscopy demonstrates that IBD inclusions are nonviral, and consist of radio-dense round particles that accumulate at the periphery of the inclusion; particles are composed of a 68-KDa protein deposited by polyribosomes.(2)
As noted by the contributor, epidemiologic evidence suggests that IBD is indeed contagious, and quarantine measures are therefore warranted.Â Antemortem diagnosis is achieved by biopsy examination of the liver or kidney, or the esophageal tonsil, in which inclusions are generally present in the overlying epithelial cells.(2) In a recent study, investigators readily identified inclusions in the leukocytes of boas with IBD using concentrated buffy coat examinations, and hence recommended the screening technique as a less invasive alternative to biopsy; however, the technique may not be applicable in pythons, in which the distribution of inclusions is often limited to the central nervous system.(3)
1.Â Jacobson ER, OrÂ³s J, Tucker SJ, Pollock DP, Kelley KL, Munn RJ, Lock BA, Mergia A, Yamamoto JK: Partial
characterization of retroviruses from boid snakes with inclusion body disease.Â Am J Vet Res 62:217-224, 2001
2.Â Jacobson ER: Viruses and viral diseases of reptiles.Â In: Infectious Diseases and Pathology of Reptiles, ed. Jacobson ER, pp.Â 410-412.Â CRC Press, Boca Raton, FL, 2007
3.Â Pees M, Schmidt V, Marschang RE, Heckers KO, Krautwald-Junghanns M-E: Prevalence of viral infections in captive collections of boid snakes in Germany.Â Vet Rec 166:422-425, 2010
4.Â Schumacher J, Jacobson ER, Homer BL, Gaskin JM: Inclusion body disease in boid snakes.Â J Zoo Wildl Med 25:511-524, 1994