Avian rotavirus (AvRV) is a major cause of viral GI disease in mammals and birds. The severity of disease is dependent upon AvRV strains, concomitant infections, maternal antibodies (with protection of up to 4 weeks) and environmental factors. Infection occurs at <6 weeks of age, with 1- to 2-week-old birds most susceptible, resulting in high mortality. Turkey poults succumb to infection at 1 week, whereas peak mortality of broiler chickens is at 4 weeks of age.
The global prevalence of avian rotavirus ranges from 19%–70% in turkeys and 10%–47% of chicken flocks. The AvRVs are classified in genogroups/serologic groups RVA and RVD and genogroups F (RVF) and G (RVG). RVD, RVF, and RVG are exclusive to avian species. RVA and RVD are the most prevalent, and interspecies transmission is known to occur within group A. Broiler and turkey flocks often have simultaneous and sequential disease with different AvRV groups. Transmission occurs by horizontal infection via the fecal-oral route. AvRV co-infects with other pathogens, most commonly avian astroviruses, but also secondary bacterial pathogens.
The primary signs of avian rotavirus infection are:
Other signs can include dehydration, anorexia, and weight loss with increased mortality. AvRV is associated with growth retardation or runting-stunting syndrome Malabsorption Syndrome in Poultry Malabsorption syndrome is characterized by stunted growth and lack of pigmentation in growing chickens. A viral cause is suspected but has not been confirmed. There are no confirmatory tests... read more in poultry. Carcases are often dehydrated and stunted, and yellow, watery, scour fluid with gas is seen in the intestine and cecum. Prolific viral replication in the small intestinal villus epithelium disrupts the villus structure, causing enteritis and diarrhea by epithelial detachment, villus atrophy, and malabsorption. Other gross lesions include whitish-transparent intestinal walls, enlarged gall bladder, and atrophy of the pancreas and bursa. Histopathologic lesions include vacuolation of enterocytes with separation from the lamina propria and infiltration of inflammatory cells into the lamina propria. The main cells affected are the mature villous absorptive epithelium of the distal third of the small intestine.
Laboratory diagnosis of avian rotavirus from intestinal and fecal content by electron microscopy will show a virion 70 nm in diameter with a wheel-like appearance. Polyacrylamide gel electrophoresis can detect extracted viral RNA and differentiate each AvRV group; however, it is considered to have low sensitivity. Virus isolation is limited to group RVA. A multiplex real-time reverse transcriptase PCR assay is available to detect and quantify RVA and RVD.
Strict biosecurity measures are advised to prevent the spread and persistence of avian rotavirus infection. There is no commercially available vaccine against AvRV. AvRV is extremely stable and resistant to some disinfectants yet sensitive to phenol and formaldehyde. Beneficial treatments during the acute phase include: avoiding dehydration through use of an oral electrolyte solution, increasing temperature of housing, improving ventilation, and adding fresh litter. Antibiotics may be used to treat secondary bacterial infections.
Avian rotavirus infections range from subclinical to acute with enteritis and diarrhea.
Infection occurs at <6 weeks of age, with 1- to 2-week-old birds most susceptible, resulting in high mortality.
Transmission occurs by horizontal infection via the fecal-oral route.
No commercial vaccine is available.
Good biosecurity is important to prevent the spread of infection.