A simulation model for studying the role of pre-slaughter factors on the exposure of beef carcasses to human microbial hazards.

A Monte Carlo simulation model was constructed for assessing the quantity of microbial hazards deposited on cattle carcasses under different pre-slaughter management regimens. The model permits comparison of industry-wide and abattoir-based mitigation strategies and is suitable for studying pathogens such as Escherichia coli O157:H7 and Salmonella spp. Simulations are based on a hierarchical model structure that mimics important aspects of the cattle population prior to slaughter. Stochastic inputs were included so that uncertainty about important input assumptions (such as prevalence of a human pathogen in the live cattle-population) would be reflected in model output. Control options were built into the model to assess the benefit of having prior knowledge of animal or herd-of-origin pathogen status (obtained from the use of a diagnostic test). Similarly, a facility was included for assessing the benefit of re-ordering the slaughter sequence based on the extent of external faecal contamination. Model outputs were designed to evaluate the performance of an abattoir in a 1-day period and included outcomes such as the proportion of carcasses contaminated with a pathogen, the daily mean and selected percentiles of pathogen counts per carcass, and the position of the first infected animal in the slaughter run. A measure of the time rate of introduction of pathogen into the abattoir was provided by assessing the median, 5th percentile, and 95th percentile cumulative pathogen counts at 10 equidistant points within the slaughter run. Outputs can be graphically displayed as frequency distributions, probability densities, cumulative distributions or x-y plots. The model shows promise as an inexpensive method for evaluating pathogen control strategies such as those forming part of a Hazard Analysis and Critical Control Point (HACCP) system.     

Sudden death of two horses associated with pulmonary aspergillosis.

The sudden death of two horses was attributed to the rapid and acute development of pulmonary aspergillosis. One horse was making excellent postoperative progress after a jejunal resection and anastomosis for intestinal adhesions. The other horse was being treated routinely for equine protozoal myeloencephalitis (EPM). Signs of fever and an increased respiratory rate were detected shortly before death in the first horse, but no premonitory clinical signs characteristic of pulmonary infection were detected in the horse being treated for EPM. Both horses developed rapidly debilitating, acute pulmonary mycosis and died unexpectedly.     

Canine X-linked severe combined immunodeficiency.

Canine X-linked severe combined immunodeficiency (XSCID) is due to mutations in the common gamma (gamma c) subunit of the IL-2, IL-4, IL-7, IL-9 and IL-15 receptors. The most striking clinical feature is a failure to thrive or 'stunted' growth. Recurrent or chronic infections begin at the time of decline of maternal antibody, usually between six and eight weeks of age. Affected dogs rarely survive past three to four months of age. The major pathologic feature of canine XSCID is a small, dysplastic thymus. Grossly identifiable lymph nodes, tonsils, and Peyer's patches are absent in XSCID dogs. During the neonatal period, XSCID dogs have few, if any, peripheral T cells and increased number of peripheral B cells. Some XSCID dogs do develop phenotypically mature, nonfunctional T cells with age, however, the absolute number of peripheral T cells remain significantly decreased compared to age-matched normal dogs. An interesting finding is that as soon as T cells begin to appear in XSCID dogs they rapidly switch from a CD45RA+ (naive) phenotype to a CD45RA- (activated or memory phenotype). One of the characteristic findings in XSCID dogs is an absent or markedly depressed blastogenic response of T cells in response to stimulation through the T cell receptor and when the necessary second messengers for cellular proliferation are directly provided that by-pass signals delivered through ligand-receptor interaction. The proliferative defect is due to the inability of T cells to express a functional IL-2 receptor. Canine XSCID B cells do not proliferate following stimulation with T cell-dependent B cell mitogens, however, they proliferate normally in response to T cell-independent B cell mitogens. Canine XSCID B cells are capable of producing IgM but are incapable of class-switching to IgG antibody production following immunization with the T cell-dependent neoantigen, bacteriophage phiX174. The number of thymocytes in the XSCID thymus is approximately 0.3% of the thymocytes present in the thymus of age-matched normal dogs. The proportion of CD4-CD8- thymocytes in XSCID dogs is increased 3.5-fold and the CD4+CD8+ population is decreased 2.3-fold. These findings demonstrate that (1) a functional gamma c is required for normal B and T cell function, (2) early T cell development is highly dependent upon a functional gamma c, and (3) B cell development can occur through a gamma c-independent pathway.     

Feather pecking in groups of growing bantams in relation to floor litter substrate and plumage colour

1. As part of a programme investigating the causation of pecking damage in fowls, this experiment tested a proposal that birds may receive more feather pecks when their plumage colour contrasts with floor litter colour, because litter particles on plumage (as a consequence of dustbathing) may then have greater stimulus value. 2. Groups consisting of 7 light- and 7 dark-coloured bantams were reared from 1 to 11 weeks of age in pens with either wood shavings (light coloured, n=6) or peat (dark coloured, n=6) floor litter. 3. Feather loss from pecking commenced in the 3rd week of life and increased thereafter, but observed pecking damage scores were not consistent with the hypothesis being tested. 4. Despite many more pecks at birds being seen (over 10 weeks) in the wood shavings groups' (661 at particles on plumage, 1795 not at particles) than in peat groups (205, 787), there was no effect of litter substrate on pecking damage. The only evidence supporting the proposal was the finding that, in groups on wood shavings, significantly more pecks at particles on plumage were directed from light coloured birds towards dark ones, than from light to light, dark to light, or dark to dark. 5. Feather eating was confirmed from the presence of feather material in 2% to 15% of faecal droppings collected from each group at 11 weeks, but these proportions were not correlated with pecking damage scores. 6. The results imply that only some feather pecks/pulls were damaging and only some eaten feathers were pulled from other birds.     

Analgesic effects of butorphanol and buprenorphine in conscious African grey parrots (Psittacus erithacus erithacus and Psittacus erithacus timneh)

OBJECTIVE: To evaluate effects of butorphanol tartrate and buprenorphine hydrochloride on withdrawal threshold to a noxious stimulus in conscious African grey parrots. ANIMALS: 29 African grey parrots (Psittacus erithacus erithacus and Psittacus erithacus timneh). PROCEDURE: Birds were fitted with an electrode on the medial metatarsal region of the right leg, placed into a test box, and allowed to acclimate. An electrical stimulus (range, 0.0 to 1.46 mA) was delivered to each bird's foot through an aluminum perch. A withdrawal response was recorded when the bird lifted its foot from the perch or vigorously flinched its wings. Baseline threshold to a noxious electrical stimulus was determined. Birds then were randomly assigned to receive an i.m. injection of saline (0.9% NaCl) solution, butorphanol (1.0 mg/kg of body weight), or buprenorphine (0.1 mg/kg), and threshold values were determined again. RESULTS: Butorphanol significantly increased threshold value, but saline solution or buprenorphine did not significantly change threshold values. CONCLUSIONS AND CLINICAL RELEVANCE: Butorphanol had an analgesic effect, significantly increasing the threshold to electrical stimuli in African grey parrots. Buprenorphine at the dosage used did not change the threshold to electrical stimulus. Butorphanol provided an analgesic response in half of the birds tested. Butorphanol would be expected to provide analgesia to African grey parrots in a clinical setting.     

Development of a polyclonal-antibody-based immunohistochemical method for the detection of type 2 porcine circovirus in formalin-fixed, paraffin-embedded tissue.

An immunohistochemical method for the detection of type 2 porcine circovirus (PCV2) in paraffin-embedded tissue was developed. Rabbits were inoculated with purified PCV2 to obtain a polyclonal antiserum. Antiserum was applied to sections of porcine tissue that contained lesions consistent with postweaning multisystemic wasting syndrome and in which PCV2 genome had been demonstrated by in situ hybridization. In all cases (18/18), the density and distribution of positive cells detected by in situ hybridization or immunohistochemistry were identical. The immunohistochemical method is more rapid and less expensive than in situ hybridization and is thus more suitable for routine diagnostic use.