Chicken Parvovirus and Turkey Parvovirus Infections
Chicken parvoviruses (ChPV) and turkey parvoviruses (TuPV) are members of the aveparvovirus genus and are distinct from the dependoparvoviruses affecting waterfowl. These viruses were first discovered in the early 1980s and have been shown to have a worldwide range. Aveparvoviruses have been linked to a number of enteric “production disease” syndromes affecting growth rates, such as malabsorption syndrome, poult enteritis complex, and the more damaging poult enteritis/mortality syndrome. Recent studies have corroborated the role of ChPV in malabsorption syndrome. Chicken and turkey parvoviruses require actively dividing host cells to replicate, eg, intestinal or lymphoid tissues.
Although vertical transmission from hen to egg has been observed, the major route of transmission appears to be horizontal through environmental and fecal-oral routes. ChPV and TuPV appear to be confined to their homologous host (chicken or turkey). In broiler chickens, molecular detections of ChPV tend to be observed within the first week after hatch and tend to peak in the second or third week. These infections can then persist at high levels throughout the lifetime of the flock.
Aveparvoviruses have been shown to be stable within the environment.
The main findings with production diseases, such as those listed above, are poor or uneven weight gain, poor feed conversion, and failure to thrive. Diarrhea, feather abnormalities, and increased mortality have also been reported in more severe cases.
Acute catarrhal enteritis of the small intestine has been observed histologically, as well as moderate to severe distension of intestinal crypts with associated eosinophilic intranuclear inclusions within epithelial cells. Parvovirus has been detected by molecular means in broilers presenting with enteric diseases, curvature of the duodenal loop, pancreatic atrophy, and mesenteric inflammation. Gross observations have included atrophy of pancreas, bursa of Fabricius, and spleen. Recent reports have associated ChPV with the development of lymphocytic pancreatitis, heterophilic pancreatitis, and pancreatic atrophy. Immunohistochemistry techniques have been used to detect parvovirus in the follicles of the bursa of Fabricius in turkeys.
A diagnosis with one of the production disease syndromes will commonly be based on poor performance metrics of the flock along with other clinical findings as above. A number of molecular methods have been used to detect ChPV and TuPV viral nucleic acid, such as polymerase chain reaction (PCR) and real-time quantitative PCR (qPCR). Aveparvoviruses have been detected using immunohistochemistry on tissue sections as well as ELISA tests for use on sera.
There is currently no commercial aveparvovirus vaccine available, and these viruses are not easily grown in culture, precluding the use of endogenous vaccines. Exposure to the virus can be minimized through robust biosecurity, good husbandry, and effective sanitation measures in both parent and broiler flocks. These measures include the use of disinfection of machinery and housing, “all in, all out” production systems, and adequate downtime between flocks.