JPC SYSTEMIC PATHOLOGY

DIGESTIVE SYSTEM

November 2024

D-V30

 

Signalment (JPC #2548995): Red-tailed boa constrictor (Boa constrictor constrictor).

 

HISTORY: This 3-year-old animal was in a collection of over 40 exotic snakes of various species. It had a 5-month history of lethargy, intermittent anorexia, weight loss, and fetid loose feces. It was dehydrated and had petechiation of its oral mucosa and ventral scutes. 

 

HISTOPATHOLOGIC DESCRIPTION: Intestine: Multifocally 75% of the mucosal epithelial cells, lymphocytes within gut-associated lymphoid tissue (GALT), and rarely ganglion cells of the myenteric plexus contain one to multiple, 3-10 µm, intracytoplasmic, brightly eosinophilic viral inclusion bodies. Extending from the superficial mucosal epithelium into the submucosa are multifocal, large (up to 3mm) ulcers characterized by loss of mucosal architecture and replacement by eosinophilic cellular and karyorrhectic debris, fibrin, edema, scattered bacterial colonies with 1-2µm cocci and 1x3µm rods, and many macrophages, fewer multinucleated giant cells, and heterophils, often centered on fungal hyphae. Fungal hyphae are 5-20 µm wide, non-septate, with 2µm thick, non-parallel walls and irregular, non-dichotomous branching. Hyphae often infiltrate the submucosal vessel walls, where they are admixed with necrotic debris, edema, and few inflammatory cells which expand the tunica media and efface the tunica intima (necrotizing vasculitis). Multifocally scattered vessels contain fibrin thrombi with enmeshed fungal hyphae. 

 

MORPHOLOGIC DIAGNOSIS: 1. Intestine, enterocytes; lymphocytes; and ganglion cells: Eosinophilic intracytoplasmic inclusion bodies, numerous, Red-tailed boa constrictor (Boa constrictor constrictor), reptile.

2. Intestine: Enteritis, ulcerative and granulomatous, subacute, multifocal, severe, with necrotizing vasculitis, fibrin thrombi, and fungal hyphae, etiology consistent with Mucorales (order) fungi (formerly Zygomyces sp.).

 

CONDITIONS: Inclusion body disease (IBD) of boid snakes and mucormycosis (formerly zygomycosis) 

 

ETIOLOGY: Arenavirus; secondary infection with a mucormycete

 

ETIOLOGIC DIAGNOSES: Arenaviral and zygomycotic enteritis

 

SYNONYMS: Boid inclusion body disease

 

GENERAL DISCUSSION:

• Disease caused by Reptarenavirus (or reptile-associated Arenavirus) that naturally infects boa constrictors (Boa constrictor) and Corrallus annulatus (ringed tree boa, annulated tree boa, norther annulated tree boa) with worldwide distribution in captive populations
  • Virions: pleomorphic, two segments of single-stranded RNA denoted as large (L) and small (S)
• Transmissible, progressively fatal disease almost exclusively in captive boids (boas and pythons)
• Disease characterized by formation of intracytoplasmic inclusions in peripheral blood (lymphocytes, and rarely thrombocytes, basophils, and granulocytes), in lymphocytes within lymphoid aggregates in the esophagus (esophageal tonsils), myeloid precursors in bone marrow, and virtually all tissues, especially within neurons in central nervous system, liver, stomach, esophageal tonsils, and pancreas
• Snakes may have a concurrent lymphoid neoplasm
• Other non-Boidae species have been diagnosed with similar histologic findings to this disease
• Mortality often associated with secondary infections (bacterial, fungal)

 

PATHOGENESIS: 

• Numerous routes of transmission proposed:

• Possible vector: Snake mite Ophionyssus natricis (common in epizootics) 
• Direct contact, intrauterine, or venereal transmission

• Incubation period unknown

 

TYPICAL CLINICAL FINDINGS:

• No treatment; invariably fatal; euthanasia recommended if diagnosed
• Clinical signs and progression of disease differ between boas and pythons
• In boas:

• Chronic regurgitation and CNS abnormalities are the most common 
• Progressive debilitation, anorexia, weight loss 
• Head tremors, disorientation, incoordination, paresis, stargazing, torticollis; can progress to flaccid paralysis
• Secondary bacterial infections (ulcerative stomatitis, pneumonia)

• In pythons:

• No regurgitation, but anorexic
• Earlier, more severe, rapidly progressing CNS signs with death in weeks

 

TYPICAL GROSS FINDINGS:

• Atrophy and fibrosis of spleen and pancreas
• May see pneumonia, ulcerative stomatitis, nodular lesions in stomach & esophagus

 

TYPICAL LIGHT MICROSCOPIC FINDINGS:

• Hepatocytes and renal tubular epithelial cells most commonly affected

• Inclusions are often limited to the central nervous system in those snakes (particularly pythons) with a rapid progression of neurological disease 
• Inclusions can be seen in more systems (enteric, respiratory, and renal epithelial cells, hepatocytes, pancreatic acinar cells, and mononuclear cells) in chronic disease which is reported in boa constrictors

• Intraneuronal inclusions in brain (neurons and glial cells) and spinal cord with nonsuppurative meningoencephalitis, neuronal degeneration, gliosis, and demyelination
• Intralymphocytic inclusions

• Pancreatic exocrine atrophy
• Renal granulomas
• Hepatocyte vacuolation and hydropic degeneration
• Lymphoid depletion
• Rare concurrent sarcomas, lymphoid neoplasia reported
• Secondary bacterial, fungal, and protozoal infections are common

 

ULTRASTRUCTURE:

 

ADDITIONAL DIAGNOSTIC TESTS:

 

DIFFERENTIAL DIAGNOSIS: 

• Ophidian paramyxovirus: Proliferative pneumonia with syncytia & eosinophilic intracytoplasmic inclusion bodies resembling those of morbillivirus in size & shape

• Commonly reported in captive viperids and crotalids, but susceptibility spans colubrids, elapids, boids

• Sunshine virus (reclassified from paramyxovirus into its own viral family): Snakes exhibit neurologic signs and inappetence; lesions include white matter spongiosis and gliosis
• Secondary bacterial and fungal diseases are frequently blamed for IBD lesions

 

COMPARATIVE PATHOLOGY:

Other selected Arenaviridae; all in genus Mammarenavirus:

• Lymphocytic choriomeningitis

• Mice (N-V18): Lymphocytic choriomeningitis; clinical signs are rare; causes vasculitis, glomerulonephritis, lymphocytic inflammation in the brain, liver, adrenal gland, kidney, lung
• Marmosets and tamarins (D-V27): transmitted through ingestion or contact with infected mice; causes enlarged liver and spleen, jaundice, possible coagulopathy, hemorrhage within muscle, pericardial and pleural effusion; microscopically, multifocal hepatic necrosis with neutrophilic and lymphocytic inflammation
• Other primates (including humans): transmitted through ingestion or contact with infected mice; causes transient typically nonfatal meningoencephalitis

• Lassa virus  
• Machupo virus

 

REFERENCES:

1. Ossibof RJ. Serpentes. In: Terio KA, McAloose D, St. Leger J, eds. Pathology of Wildlife and Zoo Animals. San Diego, CA: Elsevier; 2018: 908-909, 911.
2. Vancraeynest D, Pasmans F, Martel A, et al. Inclusion body disease in snakes: a review and description of three cases in boa constrictors in Belgium. Vet Rec. 2006;158:757-761.

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