Poult enteritis syndrome (PES) is characterized by enteritis and decreased body weight gain in growing turkey poults between one d and 7 wk of age. Another syndrome called light turkey syndrome (LTS) causes a decrease in body weight of adult tom turkeys in Minnesota leading to huge economic losses. Reovirus, rotavirus, and astrovirus have been found in LTS and PES flocks in Minnesota. We tested 80 fecal pools collected from four LTS flocks and 35 fecal pools from non-LTS flocks for the presence of parvovirus. In addition, 116 fecal and meconium samples from turkeys submitted to the Minnesota Veterinary Diagnostic Laboratory (MVDL) also were tested. The samples were tested by PCR using primers for the non-structural 1 (NS1) gene of parvovirus. Of the 80 samples from LTS flocks, 41 were positive for parvovirus while 20 of 35 samples from non-LTS flocks were positive. The prevalence of parvovirus in fecal samples submitted to MVDL was relatively low; only five of the 116 pools were positive. The partial NS1 gene sequences from LTS and non-LTS samples showed 98 to 100% nt identity except for one divergent turkey parvovirus (TuPV) strain that revealed 90% identity and clustered with chicken-like parvoviruses. The presence of this divergent strain suggests circulation of a recombinant strain of TuPV in Minnesota turkeys. Our results indicate that TuPVs are circulating in both LTS and non-LTS flocks of turkeys in Minnesota, and further experimental studies are indicated to study the role of TuPV in LTS.

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.

2011 Poultry Science doi:10.3382/ps.2010-00794

Upon photostimulation, restricted ovulator (RO) female chickens exhibit endogenous hyperlipidemia, develop atherosclerotic lesions, and generally fail to lay eggs. This phenotype results from a point mutation in the gene specifying the very low density lipoprotein receptor (VLDLR), whose protein product normally mediates the massive oocytic uptake of egg yolk precursors from the circulation. Taking advantage of the single base change in the mutant VLDLR allele, a PCR-based method for the rapid identification of RO chickens was developed at the Biocenter and University of Vienna, Austria. However, this procedure was incompletely validated because phenotypic data were not obtained and conventional progeny testing of sons and grandsons was not performed. Here, the assay validation was completed by providing plasma lipid concentrations, plasma very low density lipoprotein particle sizes, or egg production records of PCR-genotyped females and their brothers and sires to demonstrate that each bird's phenotypic traits substantiated their genotypic classification. Moreover, several methodological modifications resulted in improved chemical safety, speed, and cost of preparing and analyzing genomic DNA from chicken erythrocytes. Because the ovaries of mutant RO females generally contain numerous vitellogenic follicles in the absence of a functional oocyte plasma membrane VLDLR, the existence of an alternate system for the oocytic uptake of plasma very low density lipoprotein and vitellogenin is suggested, whereas a physiological explanation as to why some, but not all, mutant RO hens are able to ovulate and lay eggs is lacking.

The purpose of this study was to determine the virulence of raptorial Pasteurella multocida for ducks and the effect of various routes of inoculation on virulence. Four-week-old Pekin ducks (Anas platyrhynchos) were challenged with one of three raptorial isolates (RTHA-2, RTHA-4, or WESO-1) by one of five inoculation routes (intranasal, intraocular, intravenous, oral, and subcutaneous). Ducks were monitored daily for mortality until 2 wk postchallenge. Results indicated that the intravenous route caused the most mortality for all isolates and that significant variation existed in the virulence among the sources of P. multocida, with WESO-1 causing the least mortality of the isolates tested.

A trial was conducted to determine whether the delayed footpad reaction (DFR) induced by killed Staphylococcus aureus in chickens is a delayed-type hypersensitivity (DTH) reaction. Five criteria were used to assess DTH: 1) DFR with a peak response at 24 to 48 h postchallenge, 2) inhibition of monocyte/macrophage migration, 3) lymphocyte blastogenic response, 4) mononuclear cell infiltration at the challenge site, and 5) passive transfer of DFR by splenic lymphocytes. Broilers were sensitized twice with a s.c. injection in the neck of S. aureus antigen (150 microg/bird) diluted in polyethylene glycol at 3 and 4 wk of age. Controls were s.c. injected with polyethylene glycol. At 6 wk of age, a migration inhibition test was conducted before the birds were challenged intradermally with S. aureus antigen (75 microg/bird) in PBS in the right footpad. The left footpad was injected with PBS. The thickness of the footpad was measured at 0, 4, 24, and 48 h postchallenge to evaluate the DFR. After challenge, blood was collected for the lymphocyte blastogenesis assay. Birds were euthanatized, and both footpads were removed for histology. The spleens were collected aseptically; splenic lymphocytes were injected i.v. into recipient birds. Sensitized birds showed an increase in the DFR (P < 0.02) and blastogenic response (P < 0.01) compared with nonsensitized birds. Delayed footpad reaction reached a maximum response at 24 h postchallenge. The in vitro migration of monocytes/macrophages from sensitized birds was significantly inhibited (P < 0.01). The histological appearance of S. aureus-injected footpads was characterized by dermal edema and perivascular infiltrates of small lymphocytes and macrophages. Birds that received sensitized splenic lymphocytes had a significantly pronounced DFR following challenge with S. aureus when compared with birds that received nonsensitized lymphocytes (P < 0.0001). These results indicated that the DFR can be used as a standard in vivo test for cell-mediated DTH reaction induced by killed S. aureus antigen in chickens.

Enteric bacterial infections in poultry pose a threat to intestinal health and can contribute to poor feed efficiency and livability of a flock. A variety of enteric bacterial diseases are recognized in poultry. Three of these bacterial diseases, necrotic enteritis, ulcerative enteritis, and spirochetosis, primarily infect the intestine, whereas other bacterial diseases, such as salmonellosis, colibacillosis, mycobacteriosis, erysipelas, and fowl cholera, affect a variety of organ systems in addition to the intestine. Diagnosis of bacterial enteritis requires monitoring of clinical signs in the flock and proper use of diagnostic methods such as necropsy, histopathology, bacteriology, and serology.

A simple polymerase chain reaction (PCR)-based procedure was developed for the detection of avian infectious laryngotracheitis virus (ILTV) in chicken trachea, chorio-allantoic membrane (CAM), infected hepatoma cells and infectious cell culture supernatant. Samples were prepared by dilution in distilled water. After boiling and low speed centrifugation, samples were used for PCR analysis with two primers without special labeling. The PCR analysis for ILT virus could be completed in less than 8 h. Standard agarose gel electrophoretic analysis of the PCR products revealed a prominent band of 300 base-pairs in samples from ILTV-infected specimens, but not from specimens containing Newcastle disease virus, infectious bronchitis virus, avian adenovirus, fowlpox virus, Pachecoz or Marek's disease virus. One single ILTV infected cell or 10 plaque forming units of ILTV could be detected with this procedure. The procedure can be used for the identification of ILTV and the differentiation of ILTV from other avian respiratory tract infectants.

Previous work in the authors' laboratory had shown that inducing molt using a 2-wk feed removal protocol in 58- to 84-wk-old White Leghorn hens increased the severity of intestinal infection by Salmonella enteritidis (SE). As susceptibility to infection can be influenced by age, a study was conducted to compare the effect of the feed removal on infection by SE in 20-, 40-, and 74-wk-old hens. Birds were orally infected with 5 to 10 x 10(6) SE on Day 4 of fast and were sampled for SE shedding 3, 10, 17, and 24 days later. Significantly higher numbers of SE were shed in fasted birds on Day 3 (20 and 40 wk of age), Day 10 (40 and 74 wk of age), and Day 17 (74 wk of age). Transmission of SE to uninfected, contact-exposed birds was observed in all three trials for both the fed and fasted groups. However, significantly more fasted contact-exposed birds became positive for SE on Day 3 (20-wk-old), Day 10 (74-wk-old), and Day 17 (74-wk-old). Significantly more SE was also shed in these fasted contact-exposed birds on Day 3 (20-wk-old), Day 10 (all age groups), and Day 17 (74-wk-old). The current results indicate that the fasting conditions used to induce a molt in hens increase the shedding of SE in direct-infected and contact-exposed hens and this effect does not appear to be affected by age.