Avian Metapneumovirus, Turkey Hemorrhagic Enteritis Virus and Escherichia coli interaction in finishing turkey flocks suffering from colibacillosis-associated mortality.

This paper investigates the spectrum of mortality-associated pathogens by longitudinal studies carried out in two Italian finishing tom turkey flocks. The surveys focus on the interaction between Avian Metapneumovirus (AMPV), Turkey Hemorrhagic Enteritis Virus (THEV) and Avian Pathogenic Escherichia Coli (APEC). Cloacal swabs, rhino-pharyngeal swabs and blood samples were collected weekly from 10 birds until turkeys were 14 weeks old for virus isolation and/or PCR detection. Mortality was recorded and 10 % of deceased birds were examined post mortem. Where colibacillosis was suspected, microbiological examinations were performed from selected organs. All E. coli strains detected were assessed for the presence of virulence-associated genes and were serotyped. Random amplified polymorphic DNA (RAPD) was used to analyse the relationship between E.coli clones. AMPV was detected from rhino-pharyngeal swabs by RT-PCR and virus isolation. Cloacal swabs and spleen samples collected from the examined carcasses were tested for THEV by PCR. Serum samples were examined for antibodies against AMPV, THEV, and other avian respiratory pathogens. Colisepticaemia associated mortality, due to O78 APEC strains, was observed in both flocks. In the first flock the highest mortality rate was recorded in young birds, at week four of age, in association with subtype B AMPV. In the second flock the highest E.coli associated mortality was observed late in the production cycle, in turkeys of 11-12 weeks. In this instance colisepticaemia was triggered by both previous and/or attendant THEV and subtype B AMPV infections. While other different APEC strains were detected during the studies, they were not responsible for significant clinical outbreaks. It is widely believed and experimentally reported that co-infection with AMPV and E. coli can lead to an increased morbidity and a higher incidence of gross E.coli lesions. The results reported in the current study supports this notion, and suggests that THEV, having an immunosuppressive effect, plays a further predisposing role.