Egg production systems have become subject to heightened levels of scrutiny. Multiple factors such as disease, skeletal and foot health, pest and parasite load, behavior, stress, affective states, nutrition, and genetics influence the level of welfare hens experience. Although the need to evaluate the influence of these factors on welfare is recognized, research is still in the early stages. We compared conventional cages, furnished cages, noncage systems, and outdoor systems. Specific attributes of each system are shown to affect welfare, and systems that have similar attributes are affected similarly. For instance, environments in which hens are exposed to litter and soil, such as noncage and outdoor systems, provide a greater opportunity for disease and parasites. The more complex the environment, the more difficult it is to clean, and the larger the group size, the more easily disease and parasites are able to spread. Environments such as conventional cages, which limit movement, can lead to osteoporosis, but environments that have increased complexity, such as noncage systems, expose hens to an increased incidence of bone fractures. More space allows for hens to perform a greater repertoire of behaviors, although some deleterious behaviors such as cannibalism and piling, which results in smothering, can occur in large groups. Less is understood about the stress that each system imposes on the hen, but it appears that each system has its unique challenges. Selective breeding for desired traits such as improved bone strength and decreased feather pecking and cannibalism may help to improve welfare. It appears that no single housing system is ideal from a hen welfare perspective. Although environmental complexity increases behavioral opportunities, it also introduces difficulties in terms of disease and pest control. In addition, environmental complexity can create opportunities for the hens to express behaviors that may be detrimental to their welfare. As a result, any attempt to evaluate the sustainability of a switch to an alternative housing system requires careful consideration of the merits and shortcomings of each housing system.

Human illness due to Camplyobacter jejuni infection is closely associated with consumption of poultry products. We previously demonstrated a 50 % shift in allele frequency (phase variation) in contingency gene Cj1139 (wlaN) during passage of C. jejuni NCTC11168 populations through Ross 308 broiler chickens. We hypothesized that phase variation in contingency genes during chicken passage could promote subsequent colonization and disease in humans. To test this hypothesis, we passaged C. jejuni strains NCTC11168, 33292, 81-176, KanR4 and CamR2 through broiler chickens and analysed the ability of passaged and non-passaged populations to colonize C57BL6 IL-10-deficient mice, our model for human colonization and disease. We utilized fragment analysis and nucleotide sequence analysis to measure phase variation in contingency genes. Passage through the chicken reservoir promoted phase variation in five specific contingency genes, and these 'successful' populations colonized mice. When phase variation did not occur in these same five contingency genes during chicken passage, these 'unsuccessful' populations failed to colonize mice. Phase variation during chicken passage generated small insertions or deletions (indels) in the homopolymeric tract (HT) in contingency genes. Singlecolony isolates of C. jejuni strain KanR4 carrying an allele of contingency gene Cj0170 with a 3These authors contributed equally to this work. Two supplementary tables, listing PCR primer sequences for fragment and sequence analysis used in this study, and results of sequence and fragment analysis to confirm large shifts in allele frequency, with a supplementary reference, are available with the online version of this paper. 10G HT colonized mice at high frequency and caused disease symptoms, whereas single-colony isolates carrying the 9G allele failed to colonize mice. Supporting results were observed for the successful 9G allele of Cj0045 in strain 33292. These data suggest that phase variation in Cj0170 and Cj0045 is strongly associated with mouse colonization and disease, and that the chicken reservoir can play an active role in natural selection, phase variation and disease.

Since the initial report of West Nile virus in the northeastern United States in 1999, the virus has spread rapidly westward and southward across the country. In the summer of 2002, several midwestern states reported increased cases of neurologic disease and mortality associated with West Nile virus infection in various native North American owl species. This report summarizes the clinical and pathologic findings for 13 captive and free-ranging owls. Affected species were all in the family Strigidae and included seven snowy owls (Nyctea scandiaca), four great-horned owls (Bubo virginianus), a barred owl (Strix varia), and a short-eared owl (Asio flammeus). Neurologic signs identified included head tilt, uncoordinated flight, paralysis, tremors, and seizures. Owls that died were screened for flaviviral proteins by immunohistochemical staining of formalin-fixed tissues, followed by specific polymerase chain reaction assay to confirm West Nile virus with fresh tissues when available. Microscopic lesions were widespread, involving brain, heart, liver, kidney, and spleen, and were typically nonsuppurative with infiltration by predominantly lymphocytes and plasma cells. Lesions in owls were much more severe than those previously reported in corvids such as crows, which are considered highly susceptible to infection and are routinely used as sentinel species for monitoring for the presence and spread of West Nile virus. This report is the first detailed description of the pathology of West Nile virus infection in Strigiformes and indicates that this bird family is susceptible to natural infection with West Nile virus.

The Welfare Quality(®) Assessment protocol for poultry ( WQA: ) provides animal-based measures allowing welfare comparisons across farms and housing systems. It was used to compare Lohmann LSL Classic White hens housed in an enriched colony ( EC: ), aviary ( AV: ), and conventional cage system ( CC: ) on a commercial farm over 2 flock cycles. Hens (n = 100/system) were scored on a variety of measures. A baseline measurement was made at placement at 19 wk of age for 1 flock, since AV hens had been reared in an aviary pullet facility ( AVP: while EC and CC hens were reared in a conventional pullet facility ( CCP: ). Hens in all systems were then assessed at 52 and 72 wk of age. Necropsies were performed on all mortalities 1 wk before and after the WQA sampling. WQAs were analyzed using Mann-Whitney U and Kruskal-Wallis tests for prevalence and Fisher's exact tests for severity. There was an effect of rearing, with AVP having shorter claws (P = 0.01), dirtier feathers (P = 0.03), and more keel abnormalities (P< 0.0001) than CCP at placement. For the hens, there were several significant housing system effects across flocks and age periods (all P ≤ 0.05). AV and EC hens had more keel abnormalities than CC hens. They also had fewer foot abnormalities than CC hens, although those in AV hens were more severe. AV hens had consistently dirtier feathers than EC and CC hens. While AV hens had the best overall feather cover, feather loss patterns suggested that loss was due to head pecking for AV, whereas in EC and CC it was due to cage abrasion. The necropsy findings and the WQA results were similar, except that the WQA failed to find enteritis at 19 wk, although it was detected in the necropsies during this sampling period. These results show that the WQA is a useful tool for detecting hen condition differences across housing systems.

Commercial egg-laying chickens were vaccinated for infectious laryngotracheitis (ILT) with one of five commercially available vaccines (designated A, B, C, D, and E) on five separate farms by either eyedrop (e), spray (s), or double dose in the water (w) method. Groups were identified by the vaccine designation and the method of vaccination. Birds from the test groups were transferred to an isolation facility and challenged intratracheally 3 wk after vaccination. The remaining birds were given a second vaccination with the original chicken embryo origin vaccine by spray or a chicken embryo origin vaccine if the first vaccine was of tissue culture origin. After challenge, birds were monitored for clinical signs. Those surviving were euthanatized on day 6 postchallenge, and tissues and blood were collected for histopathology, virus isolation, and serology. On the basis of histopathology and enzyme-linked immunosorbent assay (ELISA) results, after one vaccination, all chickens given vaccines by eyedrop were provided better protection than nonvaccinated controls (CTLs). Birds in groups Bs and Ds had lower microscopic lesion scores whereas only birds given Bs had higher ELISA titers than CTLs. Birds in groups As and Cs and groups Bw birds taken from the rear of the barn (r) had microscopic lesion scores that were no different from those of CTLs. These same birds in addition to vaccine Ds had ELISA titers no different from those of CTLs. Of all vaccines, only A given by eyedrop or spray produced higher virus isolation titers than those of CTLs. The remainder of the vaccines produced virus isolation titers that were no different from those of CTLs. After two vaccinations, all groups had lower microscopic lesion scores than CTLs. Only Bw birds from the middle of the barn Bs, EeDs, and AsAs had virus isolation results that were higher than those of CTLs. Only groups BwrBs, CsCs, and DsDs had ELISA titers no different from those of controls. These results suggest that a priming vaccination followed by a booster dose offers better protection against ILT than a single vaccination alone. Vaccine application by eyedrop provides more uniform protection if only one vaccination is given, whereas spray vaccination may serve as an alternative method of vaccination for birds receiving two doses of vaccine.

Cellular response of chickens to infection with infectious bronchitis virus (IBV) was investigated by lavage of the respiratory tract of five 2-week-old specific-pathogen-free (SPF) chickens at 2, 8, 24, 48, 72, and 96 hours postinfection (PI) with either Massachusetts 41 (IBV-M41) or Australian T (IBV-T) IBV. Tissue response was monitored by microscopic examination of trachea and lung from five non-lavaged infected chickens collected at the same intervals. The total number of cells recovered by lavage from IBV-M41-infected chickens was dramatically higher than the total number recovered from IBV-T-infected chickens and uninfected controls. By contrast, the total number of cells recovered from IBV-T-infected chickens was no higher than that of the uninfected chickens. Heterophils constituted the majority of inflammatory cells recovered from both IBV-M41-infected and IBV-T-infected chickens. Heterophil numbers in IBV-M41-infected chickens paralleled total cell-number recovery, whereas heterophil numbers in IBV-T-infected birds were no higher than those in uninfected chickens. The number of lymphocytes recovered from IBV-M41-infected chickens increased 72 hours PI and continued to increase for the duration of the study. Lymphocyte numbers in IBV-T-infected chickens exceeded those in uninfected chickens only at 96 hours PI. The number of lavage macrophages in IBV-M41-infected chickens increased earlier than the number of lymphocytes but later reached a plateau. IBV-T macrophage numbers did not exceed those of uninfected chickens. Tissue damage occurred most consistently in the trachea and occurred when lavage heterophil numbers were rising or at their peak. Lavage cell recovery and composition reflected tracheal mucosa inflammatory cell infiltrate.

In a large population of animals, it is normal to have some die each day from causes not related to disease, which is often referred to as natural causes. In poultry production, this phenomenon is commonly referred to as daily mortality. In egg-producing chickens, many of the natural causes of death are associated with making an egg. The causes of normal mortality in commercial egg-laying chicken flocks have been described very little to date. A commercial chicken egg farm, housing approximately two million single-comb white leghorn chickens (Gallus gallus domesticus) in 16 egg-producing flocks, was visited on a monthly basis to monitor bird health, body conditioning, skeletal integrity, and causes of daily mortality in an attempt to provide early detection of health abnormalities. A representative sample of daily mortality from each flock was necropsied to determine the cause of death. Reported herein is a summary of visits for a period of 38 mo from June 2011 to July 2014. The top 15 causes of normal mortality, in rank order of prevalence, were determined to be the following: egg yolk peritonitis, hypocalcemia, gout, self-induced molt, salpingitis, caught by spur, intussusception or volvulus (twisted intestine), cannibalism (pick out), tracheal plug, septicemia, fatty liver syndrome, internal layer, layer hepatitis, persecution, and prolapsed vent. Other causes noted were hyperthermia (during summer), trauma, coccidiosis, ovarian neoplasia, being egg bound, urolithiasis, peritonitis (not egg yolk induced), leg fracture, caught in the structure, tumor (other than ovarian origin), wing fracture, exsanguination, and cardiomyopathy.

Ducklings were given egg-derived antibody against Salmonella enteritidis (Ab) in drinking water daily to determine if infection could be prevented. Pekin ducklings in all experimental groups were infected on Day 1 or 5 with 0.7 x 10(6) Salmonella enteritidis (SE). Spleen, liver, and intestine of each bird were collected and cultured on Days 7, 14, 21, and 28. Only livers and spleens were culture positive for SE. Ducklings infected on Day 1 had more SE infections than controls at each observation. Ducklings infected on Day 5 had fewer SE infections than controls on Days 7, 14, and 21. The same experiment was repeated to determine if SE infection could be prevented under production conditions. Only 10 ducks per group were infected with 1.02 x 10(7) SE. In addition to Ab, one group each, infected on Day 1 or 5, received a proprietary probiotic (Pro) daily to determine if Pro was synergistic to Ab. Groups receiving Ab and Pro and infected on Day 1 had fewer birds infected than Ab alone in Day 1-infected birds. Both Day 1-infected groups had more birds infected than controls. Birds infected on Day 5 had fewer ducks infected than controls on Days 7, 14, and 21. Except for Day 14, birds receiving both Ab and Pro and infected on Day 5 had fewer birds infected than Ab alone on Day 21 and 28. Probiotics act synergistically with oral Ab. Oral antibodies may serve as a tool to prevent salmonella infection in poultry.