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.

Peritonitis is the major disease problem of laying hens in commercial table egg and parent stock operations. Despite its importance, the etiology and pathogenesis of this disease have not been completely clarified. Although avian pathogenic Escherichia coli (APEC) isolates have been incriminated as the causative agent of laying hen peritonitis, Gallibacterium anatis are frequently isolated from peritonitis lesions. Despite recent studies suggesting a role for G. anatis in the pathogenesis of peritonitis, little is known about the organism’s virulence mechanisms, genomic composition and population dynamics. Here, we compared the genome sequences of three G. anatis isolates in an effort to understand its virulence mechanisms and identify novel antigenic traits. A multilocus sequence typing method was also established for G. anatis and used to characterize the genotypic relatedness of 71 isolates from commercial laying hens in Iowa and 18 international reference isolates. Genomic comparisons suggest that G. anatis is a highly diverse bacterial species, with some strains possessing previously described and potential virulence factors, but with a core genome containing several antigenic candidates. Multilocus sequence typing effectively distinguished 82 sequence types and several clonal complexes of G. anatis, and some clones seemed to predominate among G. anatis populations from commercial layers in Iowa. Biofilm formation and resistance to antimicrobial agents was also observed in several clades. Overall, the genomic diversity of G. anatis suggests that multiple lineages exist with differing pathogenic potential towards birds.

An Iowa grain processor attempted to alter the typical 12-h preharvest fasting period by giving broilers cornstarch derivative pellets and water for 6 h followed by 6 h of no feed or water. After slaughter, plant food inspectors determined that livers from the treatment group were lighter in color than normal, and consequently a significant number of chicken carcasses were condemned for human consumption. The study reported herein was conducted to determine the effects of fasting or 3 feeding programs applied before processing on liver color, liver lipids, and liver glycogen of broilers. Dietary treatment groups consisted of 1) full-fed control broilers, 2) fasted broilers, 3) maltodextrin-fed broilers, and 4) and chickens given maltodextrin and methionine. Full-fed chickens had lighter liver coloration than chickens without access to feed for 6 or 12 h immediately prior to slaughter (P < 0.05). Lightness values for livers from full-fed control chickens (L* = 54.41) were 38% higher than those for livers from fasted broilers (L* = 39.30). Lighter liver colors in full-fed broilers were associated with higher hepatic lipid concentrations (6.38%) and more total liver lipid (4.96 g/liver) than was found in broilers without feed for 12 h. In contrast, darker livers from fasted broilers had lower levels of lipid (4.42%) and less total lipid (2.68 g/liver) than the full-fed broilers. Feeding maltodextrin pellets resulted in liver colors that were lighter (P < 0.05) than those found in fasted chickens but darker (P < 0.05) than livers from full-fed broilers. If carbohydrate supplements are fed prior to slaughter, producers should notify processing plant officials so that inspectors do not interpret light livers as an abnormal physiological state.

Recent research has demonstrated that swine and poultry professionals, especially those who work in large confinement facilities, are at markedly increased risk of zoonotic influenza virus infections.

Cecal spirochetosis in chickens has been associated with enteric disease and reduced egg production in the United States and Europe. This report describes spirochete overgrowth of cecal mucosa in chickens from a flock of 100,000 commercial layers experiencing diarrhea and a 5% drop in egg production. Spirochetes were demonstrated in the ceca by darkfield and light microscopy. Apical surfaces of cecal enterocytes were covered by a dense layer of spirochetes aligned parallel to each other and perpendicular to the mucosal surface. Weakly beta-hemolytic, indole-negative spirochetes were isolated from the ceca on BJ media under anaerobic conditions at 42 C. Chicken cecal spirochetosis may represent an economically significant enteric disease of laying hens which has heretofore been infrequently recognized.