The onset of virus shedding and clinical signs in chickens infected with high-pathogenicity and low-pathogenicity avian influenza viruses

Abstract

Some avian influenza viruses may be transmissible to mammals by ingestion. Cats and dogs have been infected by H5N1 avian influenza viruses when they ate raw poultry, and two human H5N1 infections were linked to the ingestion of uncooked duck blood. The possibility of zoonotic influenza from exposure to raw poultry products raises concerns about flocks with unrecognized infections. The present review examines the onset of virus shedding and the development of clinical signs for a variety of avian influenza viruses in chickens. In experimentally infected birds, some high-pathogenicity avian influenza (HPAI) and low-pathogenicity avian influenza (LPAI) viruses can occur in faeces and respiratory secretions as early as 1 to 2 days after inoculation. Some HPAI viruses have also been found in meat 1 day after inoculation and in eggs after 3 days. There is no evidence that LPAI viruses can be found in meat, and the risk of their occurrence in eggs is poorly understood. Studies in experimentally infected birds suggest that clinical signs usually develop within a few days of virus shedding; however, some models and outbreak descriptions suggest that clinical signs may not become evident for a week or more in some H5 or H7 HPAI-infected flocks. During this time, avian influenza viruses might be found in poultry products. LPAI viruses can be shed in asymptomatically infected or minimally affected flocks, but these viruses are unlikely to cause significant human disease.

Pathobiology of Clade 2.3.4.4 H5Nx High-Pathogenicity Avian Influenza Virus Infections in Minor Gallinaceous Poultry Supports Early Backyard Flock Introductions in the Western United States in 2014-2015

“…Birds were considered infected if they had detectable virus shedding and clinical disease or if they seroconverted by 14 days postchallenge (dpc). Susceptibility (i.e., infectious dose and transmission to contact-exposed birds) varied among species (Tables 1 and 2); the least susceptible birds were Japanese quail, which required 3.7 and 3.2 log 10 mean bird infectious doses (BID 50 ) for the H5N2 virus and the H5N8 virus, respectively, and for which transmission to contact birds occurred only at the high H5N2 dose. The most susceptible birds were bobwhite quail, with infection at Ͻ2 log 10 BID 50 for both viruses and transmission to 100% of contact birds at all doses (Tables 1 and 2).…”

“…Susceptibility (i.e., infectious dose and transmission to contact-exposed birds) varied among species (Tables 1 and 2); the least susceptible birds were Japanese quail, which required 3.7 and 3.2 log 10 mean bird infectious doses (BID 50 ) for the H5N2 virus and the H5N8 virus, respectively, and for which transmission to contact birds occurred only at the high H5N2 dose. The most susceptible birds were bobwhite quail, with infection at Ͻ2 log 10 BID 50 for both viruses and transmission to 100% of contact birds at all doses (Tables 1 and 2). The surviving birds did not show evidence of clinical disease and were all serologically negative based on hemagglutination inhibition (HI) data; therefore, all were considered uninfected.…”

“…The surviving birds did not show evidence of clinical disease and were all serologically negative based on hemagglutination inhibition (HI) data; therefore, all were considered uninfected. In this study, the BID 50 and the mean bird lethal dose (BLD 50 ) for both viruses were the same for each species. Time of death varied according to both bird species and challenge dose.…”

Persistence of highly pathogenic avian influenza virus (H7N1) in infected chickens: feather as a suitable sample for diagnosis

“…Fragmented information on HPAIV detection and isolation from the tissues of infected chickens already exists (Serena Beato et al, 2006, 2009Spickler et al, 2008;Starick & Werner, 2003;Swayne, 2007, Swayne & Beck, 2005; however, complete studies on HPAIV detection in several samples during active infection as well as at different times post-mortem (p.m.) have not been carried out. In addition, most recent studies have focused on the H5N1 strain (Swayne, 2006) and little information is currently available on the detection and persistence of other HPAIV subtypes in animal tissues.…”

“…Both these subtypes are compulsorily notifiable (OIE, 2009) as they could potentially mutate from low-pathogenic AIV to HPAIV (Stech et al, 2009;Webster et al, 1992). HPAIV causes multisystemic disease with high viraemia levels in poultry, where virus is detected not only in respiratory and enteric organs but also in internal organs (Spickler et al, 2008;Starick & Werner, 2003;Swayne & Beck, 2005). In susceptible poultry species, HPAIV infection leads to severe depression and high morbidity and mortality rates (Spickler et al, 2008;Swayne, 2007), causing important economic losses Tiensin et al, 2005).…”