Proventriculitis in broiler chickens: effects of immunosuppression

Proventriculitis in broilers causes carcass condemnation when swollen proventriculi tear during evisceration. The cause of this proventriculitis is unknown, but several infectious agents have been associated with it. One such agent, infectious bursal disease virus (IBDV), has been implicated as a cause of proventriculitis, but a direct effect of this virus on the proventriculus has not been proven. The role of IBDV in proventriculitis may be indirect as a result of its ability to cause immunosuppression. The objective of this study was to understand how immunosuppression affects the incidence of proventriculitis in broiler chickens. Immunosuppression was induced in commercial and specific-pathogen-free broiler chickens using chemicals (cyclophosphamide and cyclosporin) or virus (IBDV). All groups were then exposed to a proventricular homogenate produced from diseased birds. At 7 and 14 days postinoculation, the incidence of proventriculitis in these groups was compared to that produced by homogenate exposure in immunocompetent broilers. All birds exposed to the proventricular homogenate from diseased birds developed proventriculitis. Cyclophosphamide and IBDV, both B cell suppressors, did not significantly affect the incidence or characteristics of the proventriculitis observed, although they did have an effect on the size of the proventriculus at 7 days postinoculation. Chickens immunosuppressed with cyclosporin, a T cell suppressor, developed more severe lesions and had a higher incidence of proventriculitis. These findings indicate that both B and T cells are involved in the immune response against proventriculitis, but cell-mediated immunity appears to have a more important role in controlling the disease. IBDV affects both humoral and cellular immunity in the chicken, so although under experimental conditions it didn't have a major effect on proventriculitis, it may explain why control of IBDV in the field seems to reduce the incidence of proventriculitis.     

Mycotoxin interactions in poultry and swine

Mycotoxins are toxic compounds produced by fungi. When one mycotoxin is detected, one should suspect that others also are present in a contaminated feed ingredient or finished feeds. The toxicity and clinical signs of observed in animals when more than one mycotoxin is present in feed are complex and diverse. Some mycotoxins, such as the combination of aflatoxin with either ochratoxin A or T-2 toxin, interact to produce synergistic toxicity in broiler chicks. The effects observed during multiple mycotoxin exposure can differ greatly from the effects observed in animals exposed to a single mycotoxin. For example, fatty livers in poultry are used for presumptive diagnostic identification of aflatoxicosis. However, simultaneous presence of ochratoxin A prevents fatty livers. Of the mycotoxin combinations that have been investigated in poultry and swine, the aflatoxin + ochratoxin A and aflatoxin + T-2 toxin interactions appear to be the most toxic.     

Spatial variability in ocean‐mediated growth potential is linked to Chinook salmon survival

Early ocean survival of Chinook salmon, Oncorhynchus tshawytscha, varies greatly inter‐annually and may be the period during which later spawning abundance and fishery recruitment are set. Therefore, identifying environmental drivers related to early survival may inform better models for management and sustainability of salmon in a variable environment. With this in mind, our main objectives were to (a) identify regions of high temporal variability in growth potential over a 23‐year time series, (b) determine whether the spatial distribution of growth potential was correlated with observed oceanographic conditions, and (c) determine whether these spatial patterns in growth potential could be used to estimate juvenile salmon survival. We applied this method to the fall run of the Central Valley Chinook salmon population, focusing on the spring and summer period after emigration into central California coastal waters. For the period from 1988 to 2010, juvenile salmon growth potential on the central California continental shelf was described by three spatial patterns. These three patterns were most correlated with upwelling, detrended sea level anomalies, and the strength of onshore/offshore currents, respectively. Using the annual strength of these three patterns, as well as the overall growth potential throughout central California coastal waters, in a generalized linear model we explained 82% of the variation in juvenile salmon survival estimates. We attributed the relationship between growth potential and survival to variability in environmental conditions experienced by juvenile salmon during their first year at sea, as well as potential shifts in predation pressure following out‐migration into coastal waters.     

Ultrastructure of hepatic and renal lesions in chickens fed aflatoxin

Male broiler chicks were given feed and water ad libitum from hatching through 3 weeks of age. The feed contained 0, 1.25, 2.5, and 5.0 micrograms of aflatoxin/g of feed. The chicks were killed by cervical dislocation and specimens of liver and kidney were obtained for electron microscopy on days 3, 6, 9, 17, and 21. In chicks fed 5.0 micrograms of aflatoxin, the primary lesions in liver were hepatocellular lipidosis, enlargement of bile canaliculi, reduction in mitochondrial size, mild lymphocytic infiltration, and hepatocellular degeneration and necrosis. Similar lesions were noticed in some chicks fed 2.5 micrograms of aflatoxin, but none was observed in chicks fed at 1.25 micrograms of aflatoxin. At 5 micrograms of aflatoxin, the most consistent lesion in the kidney was thickening of the glomerular basement membrane. Similar glomerular lesions were observed at 2.5 micrograms of aflatoxin, but not at 1.25 micrograms of aflatoxin. Some foot processes of the glomerular epithelial cells were poorly developed. Fusion of foot processes was not observed and fibrous material was not evident in the basement membrane. The pseudopodia of endothelial cells lining the thickened basement membrane were depleted in number or were absent. Degenerative changes also were observed in the cells of the proximal convoluted tubules, but these were less consistent than those of the glomerulus.     

Pathogenicity of Listeria monocytogenes Scott A after oral and oculonasal challenges of day-old turkey poults

Listeria monocytogenes is a ubiquitous, environmental pathogen that has contaminated poultry ready-to-eat products resulting in large-scale recalls. Research is needed to determine the source of product and processing plant contamination with L. monocytogenes. The purpose of this study was to compare the oral and oculonasal routes of infection on the pathogenicity of L. monocytogenes in turkey poults under different housing conditions. One-day-old turkey poults were challenged by either route with the Scott A strain of L. monocytogenes and placed either in paper-lined battery-brooder cages for 1 wk or in floor pens on fresh pine-shaving litter. On day 7, birds challenged in battery cages were transferred to floor pens. Challenge by the oculonasal route resulted in higher mortality (P = 0.05) and lower body weights (P < 0.0001) compared with both nonchallenged controls and those challenged by the oral route. Birds contained in battery cages for 1 wk had higher mortality (P = 0.002) and higher body weights (P < 0.0001) compared with floor-pen-reared birds. Using direct plating, the challenge strain was isolated from the gall bladder, brain, and knee joint of only one dead poult challenged by the oculonasal route. These results suggest that day-old turkey poults may be more susceptible to an oculonasal challenge with L. monocytogenes than to an oral challenge and that containment in battery cages for the first week increased contact exposure to the challenge.     

Effects of treatment of growing swine with aflatoxin and T-2 toxin

Effects of dietary aflatoxin (AF) and T-2 toxin, singly and in combination, were evaluated in growing crossbred (Yorkshire x Landrace x Hampshire) pigs. The experimental design consisted of 4 treatment groups of 6 barrows each fed diets containing 0 mg of AF and T-2/kg of feed (controls; group 1), 2.5 mg of AF/kg of feed (group 2), 10 mg of T-2/kg of feed (group 3), or 2.5 mg of AF plus 10 mg of T-2/kg of feed (AF + T-2; group 4) ad libitum for 28 days (7 to 11 weeks of age). Production performance, and serum biochemical, and hematologic evaluations were made weekly. Body weight and body weight gain were depressed by all toxin treatments, but the effect of AF and T-2 toxin in combination was less than additive. Liver and kidney weights, as a percentage of body weight, were increased by AF treatment, and heart weight, as a percentage of body weight, was increased by T-2 treatment. Treatment with T-2 toxin induced necrotizing contact dermatitis on the snout, buccal commissures, and prepuce. Consumption of AF resulted in increased serum activities of alkaline phosphatase, aspartate transaminase, cholinesterase, and gamma-glutamyltransferase, and decreased serum concentrations of urea nitrogen, cholesterol, albumin, total protein, calcium, potassium, magnesium, and phosphorus. Consumption of T-2 toxin resulted in increased serum triglyceride concentration and decreased serum iron concentration. Treatment with AF induced lower serum unsaturated iron-binding capacity and high RBC count, PCV, hemoglobin concentration, WBC count, and prothrombin time.(ABSTRACT TRUNCATED AT 250 WORDS)