Epidemiologic Studies of the 1975 Avian Influenza Outbreak in Chickens in Alabama

Abstract

The epidemiology of the first reported non-fowl-plague avian influenza (AI) virus, A/Chicken/Alabama/75 (Hav4Neq2), isolated from chickens in the United States is discussed. The signs and pathologic changes have been described. The environment, nutrition, and stress factors are discussed as possible contributors to the disease syndrome observed in 3 commercial egg-laying flocks. Avian influenza antibody was demonstrated by agargel precipitation in convalescent chickens through 83 days postinfection. A serological survey of 321 additional poultry flocks was negative for antibodies against avian influenza. A survey was made by serology and virus isolation techniques on 387 wild free-flying birds that fed and roosted in the area. Wild waterfowl are discussed as a possible source of the AI virus.

Type a influenza viruses in birds in southern Spain: Serological survey by enzyme‐linked immunosorbent assay and haemagglutination inhibition tests

“…Alexander (1985) noted that cases of influenza virus infection in turkeys have been reported in fewer countries than hen influenza virus infection, though this may be due to the limited number of countries breeding turkeys. Other authors report lower (Samadieh et al 1975) or similar infection rates (Johnson et al, 1976) to those found in this study, although the latter study was performed after a clinical outbreak.…”

“…The distribution of infection by areas was 44% at the marshes (232 samples), 33% by the inland lakes (48 samples) and 26% in the sierra (51 samples). (Beard, 1970;Anraku et al, 1971 ;Belusova et ai, 1979), and always in order to detect and assess the involvement of carriers within an avian population following the appearance of clinical outbreaks in the area (Smithies et al, 1969a,b;Homme et al, 1970;Johnson et al, 1976).…”

“…Antibody titres to type A influenza virus antigens in poultry were highly variable (SD 452), with a mode of 456. Given that antibodies to type-specific antigens of influenza virus are possible evidence of recent infection (Beard, 1970), that titres may fall rapidly after infection (Johnson et al, 1976) and that samples in this study were collected over a period of 27 months, it can be assumed that influenza viruses circulate actively and continuously among poultry.…”

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

“…Although marked clinical signs are possible (Johnson & Maxfield, 1976;Johnson et al, 1977;Brugh et al, 1996;Swayne et al, 1997;Bano et al, 2003;Nili & Asasi, 2003), most LPAI viruses tend to cause disease when chickens are co-infected with other pathogens or are subject to environmental stresses (Hooper & Selleck, 1998;Bano et al, 2003;Nili & Asasi, 2003). Clinical signs reported in infected chickens include depression/lethargy, decreased feed and water consumption, decreased egg production, decreased fertility and hatchability of eggs, misshapen eggs, and increased mortality (Johnson & Maxfield, 1976;Alexander & Stuart, 1982;Bean et al, 1985;Hooper & Selleck, 1998;Ziegler et al, 1999;Kinde et al, 2003;Mutinelli et al, 2003;Nili & Asasi et al, 2003;Bowes et al, 2004;Swayne & Pantin-Jackwood, 2006).…”

“…Although reproductive lesions including salpingitis and oophoritis have been reported in some LPAIinfected flocks (Johnson & Maxfield, 1976;Johnson et al, 1977;Hooper & Selleck, 1998;Ziegler et al, 1999;Kinde et al, 2003;Mutinelli et al, 2003;Swayne & Pantin-Jackwood, 2006), as well as in intravenously inoculated hens (Shalaby et al, 1994), there is no definitive evidence that LPAI viruses are shed in eggs. The most direct evidence for shedding is the recovery of a non-pathogenic H5N2 virus (intravenous patho genicity index00) from the internal contents of two of 120 eggs laid by an asymptomatically infected, commercial layer flock in Virginia during the H5N2 (HPAI) Pennsylvania outbreak (Cappucci et al, 1985).…”