ISSN 2398-2985      

Rotavirus infection


Joanne Sheen

Agata Witkowska


  • Cause: the genus Rotavirus of the family Reoviridae.
  • Signs: diarrhea, can be accompanied by depressed mentation, lethargy and anorexia/dysrexia. Often affecting more than one animal in a colony. Neonates and juveniles usually more severely affected.
  • Diagnosis: tentative diagnosis may be achieved through history, clinical signs and signalment. Confirmation via identification of viral particles in feces using electron microscopy, ELISA or RT-PCR.
  • Treatment: supportive measures only; primarily fluid and nutritional support
  • Prognosis: good in mild cases and in adults, guarded to poor in severely affected cases and juvenile/neonatal animals.



  • The genus Rotavirus of the family Reoviridae comprises icosahedral, nonenveloped viruses with segmented, double-stranded RNA genomes.
  • The rotavirus particle is formed by three concentric layers of proteins. The intermediate layer is formed by viral structure protein 6 (VP6).
  • Epitopes of VP6 are used to classify rotaviruses serologically into ten serogroups (A-J). Each group is genetically distinct, corresponding to a different rotavirus species.
  • Serotypes with each serogroup are further defined by epitopes of the viral structure proteins (VP7 and VP4) in the external layer of the virus particle. These induce neutralizing antibodies in the host animal.
  • Transmission primarily occurs through the fecal-oral route:
    • Other routes of spread include fomites and contaminated food and water.
    • A respiratory route of transmission has also been proposed.

Predisposing factors


  • Poor husbandry and sanitation practices.


  • Direct contact with an infected animal or with a contaminated environment.
  • Naïve immune system or immunosuppression.


  • Rotavirus entry into host cells is a multistep process which varies with different viral strains.
  • Current models suggest endocytosis of the viral particle by the host cell.
  • Intestinal infection:
    • Intestinal luminal virus particles enter enterocytes, followed by viral uncoating, transcription, translation of viral protein, formation of viroplasm and apical release of virus and viral proteins.
    • Adjacent cells can be secondarily infected after virus release from the initial infected cell.
    • Rotavirus infection of enterocytes alters the function of the small intestinal epithelium, resulting in diarrhea.
    • Generally considered to be malabsorptive in nature due to enterocyte destruction:
      • Also, through reduction of digestive enzyme expression on the intestinal epithelial surface.
      • Functional changes in tight junctions between enterocytes leading to paracellular leakage.
      • Transit of undigested mono- and disaccharides, carbohydrates, fats and proteins into the colon results an osmotically active material that affect any resorption of fluids from the colon.
    • Secretory component of diarrhea also suggested:
      • A viral nonstructural protein of rotaviruses (NSP4) can act on intestinal crypt cells to induce secretion of electrolytes and thus water into the lumen.
      • Activation of the enteric nervous system by NSP4 can also have a stimulatory effect on intestinal secretions.
    • NSP4 may also have enterotoxin-like activity.
    • Intestinal transit time is decreased in rotaviral infection, implying increased intestinal motility. This is often identified in diarrheic conditions. The basis of increased intestinal motility in rotavirus infection is not fully determined.
  • Systemic infection:
    • Rotavirus has been documented to spread beyond the intestine after oral infection, resulting in viremia and potential seeding to peripheral tissues.
    • Demonstrated in the mouse model causing viral hepatitis: considered strain dependent.
    • Clinical consequence of systemic infection unclear in natural infections.
  • Diarrhea can potentially result in dehydration, hypovolemia, as well as electrolyte and acid-base derangements. Severe cases can be fatal.


  • Incubation period is generally short, typically between 1-24 h, but can be as long as 3 days.
  • Duration typically ranges between 3-4 days from onset to full resolution of clinical signs.


  • Rotavirus is found in animal populations worldwide.
  • Considered to be highly contagious:
    • Infected animals shed large numbers of viral particles in feces.
    • Limited infectively studies have indicated that 10 or fewer particles are likely required to be infectious.
  • Presence of maternal antibodies can protect neonatal animals from clinical signs:
    • In endemically infected ferret colonies, kits from multiparous jills show decreased morbidity compared to those from primiparous jills.
    • Likely associated with build-up of immunity in jills due to increasing age and virus exposure.
  • Pepsin and gastric acid appear to act as host defense factors against RV infection. Produced at lower levels by the immature gastrointestinal tract of juvenile animals.
  • Both innate and adaptive immunity play a role in viral elimination:
    • Antibodies seem to be the principal mechanism that mediates protection against viral reinfection
    • Animal models demonstrated that total serum rotavirus IgA induced by a primary infection offers the best correlation of protection against subsequent infection.
  • Juvenile animals with insufficient levels of maternal antibodies and naive immune systems therefore most at risk:
    • Infection of juvenile ferrets occurs primarily via contact with infected dams or a contaminated environment.
  • Infected adult animals with an adequate immune response generally show only mild clinical signs or are subclinical.


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Further Reading


Refereed Papers

  • Recent references from PubMed and VetMedResource.
  • Uchiyama R, Chassaing B, Zhang B & Gewirtz A T (2014) Antibiotic treatment suppresses rotavirus infection and enhances specific humoral immunity. J Infect Dis 210 (2), 171-182 PubMed.
  • Greenberg H B & Estes M K (2009) Rotaviruses: from pathogenesis to vaccination. Gastroenterology 136 (6), 1939-1951 PubMed.
  • Wise A G, Smedley R C, Kiupel M & Maes R K (2009) Detection of group C rotavirus in juvenile ferrets (Mustela putorius furo) with diarrhea by reverse transcription polymerase chain reaction: Sequencing and analysis of the complete coding region of the VP6 gene. Vet Pathol 46 (5), 985-991 PubMed.
  • Grimprel E, Rodrigo C & Desselberger U (2008) Rotavirus disease: impact of coinfections. Pediatric Infect Dis J 27 (1), S3-10 Lippincott.
  • Langlois I (2005) Viral diseases of ferrets. Vet Clin North Am Exotic Anim Pract 8 (1), 139-160 PubMed.
  • Cook N, Bridger J, Kentall K et al (2004) The zoonotic potential of rotavirus. J Infect 48 (4), 289-302 PubMed.
  • Ramig R F (2004) Pathogenesis of intestinal and systemic rotavirus infection. J Virol 78 (19), 10213-10220 PubMed.

Other sources of information

  • Palmarini M (2017) Reoviridae. In: Fenner's Veterinary Virology. 5th edn. Eds: Maclachlan N J & Dubovi E J. Academic Press, USA. pp 299-317.
  • Kiupel M & Perpinan D (2014) Viral Diseases of Ferrets. In: Biology and Diseases of the Ferret. 3rd edn. Eds: Fox J G & Mariani R P. John Wiley & Sons, USA. pp 439-517.
  • Angel J, Franco M A & Greenberg H B (2008) Rotaviruses. In: Encyclopedia of Virology. 4th edn. Eds: Mahy B W J & Van Regenmortel M H V. Academic Press, UK. pp 507-513.


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