Exotis ISSN 2398-2985

Reptiles

Inclusion body disease

Synonym(s): IBD

Contributor(s): Mark Naguib, Nadene Stapleton

Introduction

  • Cause: disease of mainly boids and pythons present since 1970s and previously attributed to retroviral infection, but recently novel arenaviruses have been discovered as the main cause. The disease is thought to be spread by snake mites but feces, urine and shed skin may be involved.
  • Signs: neurological signs especially opisthotonos, torticollis and tremors, regurgitation, pneumonia, anorexia, wasting and lethargy.
  • Diagnosis: demonstration of characteristic inclusions on histopathology from biopsies or post mortem samples alongside detection of arenavirus via PCR.
  • Treatment: no successful treatment recorded.
  • Prognosis: some carriers may live for a long period without signs, but once clinical signs develop prognosis is grave. Animals eventually die of secondary infection.

Pathogenesis

Etiology

  • Infection with novel arenaviruses from a new genus reptarenavirus.
  • Concurrent infection with more than one reptarenavirus is likely to be common.
  • Snake mites (Ophionyssus natricis) likely spread infection between animals via contaminated blood.
  • The precise method of horizontal transmission has not yet been proved but large amounts of reptarenaviruses have been found in feces, urine and shed skin of infected animals.
  • Inclusions develop within glia and a variety of other cells.
  • In animals that develop clinical signs, an inflammatory response occurs leading to meningitis and neurological signs.
  • Secondary bacterial, protozoal and fungal infections and occasionally lymphoma lead to death.

Predisposing factors

General

  • Generally seen in boids and pythons but other species can be affected and may act as carriers.
  • Some selectively bred color variations such as the Spider morph of the royal python (Python regius) demonstrate very similar neurological signs due to inbreeding. These snakes can on occasion also have IBD that is overlooked and will act as a source of infection in a collection.
  • Presence of snake mites (Ophionyssus natricis) in collection.
  • History of snakes being brought into collections without suitable quarantine Quarantine or testing.

Pathophysiology

  • Inclusions develop within glia and a variety of other cells.
  • In animals that develop clinical signs, an inflammatory response occurs leading to meningitis and neurological signs.
  • Secondary bacterial, protozoal and fungal infections and occasionally lymphoma lead to death.

Timecourse

  • Extremely variable timecourse.
  • Some snakes may remain asymptomatic for many years.
  • Some may act as carriers and never develop inclusions or clinical disease.
  • Some may act as carriers and develop inclusions without clinical disease.
  • Once neurological signs are evident, secondary disease and eventually death will follow.
  • Pythons and jevenile boids often have a more acute course and die within weeks after the onset of clinical signs.
  • Adult boids may survive for months to years after the onset of clinical signs and many may still be feeding and aside from neurological signs, appear normal.

Epidemiology

  • Usually spreads rapidly within collections and breeding groups, particularly where there is high stocking density.
  • Often brought in on purchased animals that have not been quarantined.
  • Suspected to be spread between enclosures and individuals by snake mites (Ophionyssus natricis).
  • The precise method of horizontal transmission has not yet been proved but large amounts of reptarenaviruses have been found in feces, urine and shed skin of infected animals.

Diagnosis

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Treatment

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Prevention

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Outcomes

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Further Reading

Publications

Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Stenglein M D et al (2017) Differential disease susceptibilities in experimentally reptarenavirus-infected boa constrictors and ball pythons. J Virol 91 (15), e00451-17 PubMed.
  • Hepojoki J et al (2015) Arenavirus coinfections are common in snakes with Boid inclusion body disease. J Virol 89 (16), 8657-8660 PubMed.
  • Schilliger L et al (2014) Antemortem diagnosis of multicentric lymphoblastic lymphoma, lymphoid leukemia, and inclusion body disease in a boa constrictor (Boa constrictor imperator). J Herpetol Med Surg 24 (1-2), 11-19 VetMedResource.
  • Stenglein M D et al (2012) 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 3 (4): e00180-12 PubMed
  • Schilliger L, Selleri P & Frye F L (2011) Lymphoblastic lymphoma and leukemic blood profile in a Red-Tail Boa (Boa constrictor constrictor) with concurrent inclusion body disease. J Vet Diag Invest 23 (1), 159-162 PubMed.
  • Chang L-W & Jacobson E R (2010) Inclusion body disease, a worldwide infectious disease of boid snakes: A review. J Exotic Pet Med 19 (3), 216-225 SciDirect

Other sources of information

  • Schumacher M (2006) Inclusion Body Disease Virus. In: Reptile Medicine and Surgery. Ed: Mader D. Saunders Elsevier, USA. pp 836-840.


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