Adenoviral Gizzard Erosion in Commercial Broiler Chickens

Abstract

Abstract. Pathologic and immunohistochemical changes caused by group I of the fowl adenovirus (FAV) serotype-1 99ZH strain, isolated from broiler chickens exhibiting gizzard erosion, were investigated in commercial broiler chickens. One hundred twenty-two chickens were inoculated with the strain by both oral and ocular routes at 1, 3, or 5 weeks of age and euthanatized for necropsy within 4-18 days of inoculation. Focal gizzard erosions were observed in the inoculated chickens of each age group. A histologically degenerative koilin layer, necrotic mucosa, intranuclear inclusion bodies in the glandular epithelial cells, inflammatory cell infiltrations in the lamina propria, submucosa, and a muscle layer were seen in the gizzards. Immunohistochemical staining showed evidence of FAV antigens in the intranuclear inclusion bodies. These findings were recognized regardless of their maternal antibody levels for FAV serotype-1. Gizzard lesions appeared later in the lower-dose-inoculated chickens than in the higher-dose-inoculated chickens. Numerous CD3-positive cells and IgY-positive plasma cells were seen in the gizzard lesions. In 5-week-old chickens the heterophil infiltrations in the lesions were milder than in younger chickens. Intranuclear inclusion bodies also were observed in the epithelial cells of the ileum or cecal tonsils of some chickens. Thus, this study shows that FAV-99ZH causes adenoviral gizzard erosion in broiler chickens without hepatic or pancreatic lesions and that cell infiltration is more severe than in dietary gizzard erosions.Key words: Adenovirus; broiler chickens; erosion; gizzard.Fowl adenovirus (FAV) is ubiquitous in chickens, as demonstrated by antibody surveys 11,41 and the high isolation rates of FAV in specimens taken from normal and sick birds. 3,19 FAV is associated with naturally occurring outbreaks of inclusion body hepatitis (IBH), 39 hydropericardium syndrome (HPS), 1 respiratory disease, 5 necrotizing pancreatitis, 32 or gizzard erosion.Gizzard erosions and ulcers in chickens have been associated with diets that are deficient in vitamin B 6 4 or with the ingestion of histamine, 14 gizzerosine, 26 and mycotoxins. 15 Gizzard erosions also have been observed at a high rate in the embryos and chicks of broilers. 36 However, several natural cases of gizzard erosion associated with FAV infection have been reported in layer chickens, broiler chickens, and quails in recent years. 2,10,25,37 Gizzard erosion has been observed in chickens inoculated with group I FAV serotype-8 and affected with hemorrhagic aplastic anemia syndrome. 12 In previous studies, however, the role played by FAV as a pathogen of gizzard erosion was not clearly established, because no viral examinations were conducted and because there were no adenoviral intranuclear inclusion bodies in the gizzard lesions. Some FAVs that had originally been isolated from either the proventriculus or a gastrointestinal pool of the tissues of broiler chickens caused gizzard erosions by experimental infection. 22 In our previous studi...

Association between gizzard lesions and increased caecalClostridium perfringenscounts in broiler chickens

“…GEU has also been found recently in commercial broiler flocks in Norway (unpublished data). Previous studies have linked GEU occurrence with several nutritional and infectious factors (Poupoulis & Jensen, 1976;Okazaki et al 1983;Fossum et al ., 1988;Hedman et al ., 1995;Kaya et al ., 2002;Hetland et al ., 2003;Ono et al ., 2003a;). C. perfringens has been isolated from chickens with gizzard lesions, but the aetiological role of C. perfringens in this condition is uncertain.…”

“…A condition designated ''gizzard erosions'' and/or ''gizzard ulceration'' (GEU) has been reported in commercial broiler chickens in connection with avian adenovirus infection (Ono et al ., 2001(Ono et al ., , 2003a, mycotoxin-contaminated feed (Hedman et al ., 1995;Hoerr, 2003), vitamin B 6 deficiency (Daghir & Haddad, 1981), suboptimal levels of vitamin E (Janssen & Germs, 1973), inadequate levels of sulphur-containing dietary amino acids (Miller et al ., 1975), high levels of dietary copper (Poupoulis & Jensen, 1976), pelleted feed (Ross, 1979), as well as inclusion of certain fish meals in the diets and the consequent presence of histamine and gizzerosine (Harry & Tucker, 1976;Okazaki et al ., 1983;Sugahara et al , 1988;Sharma & Pandey, 1990;Tisljar et al , 2002). The koilin layer of gizzards from affected birds is fissured, thickened, spongy and discoloured (Fossum et al ., 1988).…”

Pathogenicity of Serotype 8 Fowl Adenovirus Isolated from Gizzard Erosions of Slaughtered Broiler Chickens

“…66(12): 1561-1566, 2004 The pathogenicity of serotype 8 fowl adenoviruis (FAV) has been reported in field cases of inclusion body hepatitis (IBH) in chickens [7] as well as in experimental reproduction of IBH in specific-pathogen-free (SPF) chickens [6]. Recently, serotype 8 FAV was isolated from gizzards exhibiting gizzard erosion in slaughterhouses [14]. In pervious reports, however, gizzard erosion was reproduced in SPF white leghorn chickens [9,11] and commercial broiler chickens [12] inoculated with serotype 1 FAV isolated from the gizzards of commercial broiler chickens exhibiting gizzard erosion.…”

“…Recently, serotype 8 FAV was isolated from gizzards exhibiting gizzard erosion in slaughterhouses [14]. In pervious reports, however, gizzard erosion was reproduced in SPF white leghorn chickens [9,11] and commercial broiler chickens [12] inoculated with serotype 1 FAV isolated from the gizzards of commercial broiler chickens exhibiting gizzard erosion.…”

Putative Host Cell Receptor for Fowl Adenovirus Detected in Gizzard

“…FAV serotypes 1 and 8 were isolated from the affected gizzards [2,15,17]. Gizzard erosion was experimentally reproduced in chickens inoculated with isolated FAV serotype 1 [10][11][12][13][14]18]. These results have shown a clear relationship between serotype 1 and virulence in some FAVs.…”