Author
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RAINARD, P - INST NAT DE LA RECHERCHE |
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Paape, Max |
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Submitted to: Veterinary Research Communications
Publication Type: Peer Reviewed Journal Publication Acceptance Date: 3/22/1997 Publication Date: N/A Citation: N/A Interpretive Summary: Researchers at the Immunology and Disease Resistance Laboratory, USDA, Beltsville, MD have discovered a way to prevent clinical mastitis caused by coliform organisms. The udders of dairy cows are constantly exposed and challenged by millions of coliform organisms. These organisms are especially prevalent in the bedding where cows sleep and account for 50% of all the clinical cases in a herd. The disease is especially debilitating if contracted soon after calving, usually resulting in death of the cow. Death is due to the failure of the udder to initiate the inflammation needed to stop the rapidly multiplying coliform organism in the milk. Researchers at the USDA discovered that udders of cows when first exposed to products released by coli- form organisms, did not produce tumor necrosis factor (TNF), an important protein responsible for initiating this infammatory response. A second exposure was required to cause producion of TNF. This important finding indicates that when coliform organism first invade the udder, the cow lacks the ability to mount a sufficient inflammatory reaction to defend itself. This deficiency could account for the high number of clinical cases of mastitis caused by coliform organisms. Administration of these coliform agents to udders of cows will sensitize udders to coliform organisms. Thus, a satisfactory inflammatory response will be initiated that will prevent mastitis to a first time invasion of these organisms. Technical Abstract: The effect of repeated infusions of Escherichia coli endotoxin on the acute phase response in the mammary gland was assessed through the concentrations of tumor necrosis factor-a. Four lactating cows received two intramammary infusions of E. coli endotoxin (33 ug) 24 h apart in the same mammary quarter. Along with the second infusion, the cows received one dose of endotoxin in the contralateral quarter. Following the first infusion at 0 h, mean concentrations of TNF-a augmented from undetectable concentrations to a maximum of 0.4 ng/ml at 6 h and declined to below 0.04 ng/ml at 24 h, the time of the second infusion. In quarters challenged twice, the rise in TNF-a concentrations was abrupt, culminating at 11.7 ng/ml 6 h later. Increases in TNF-a concentrations were similar in the contralateral quarters infused once. After the first infusion, none of the cows developed fever, but following the second infusion, rectal temperature increased markedly. Milk somatic cells increased markedly after the first infusion. These results show that infusion in one quarter of an amount of endotoxin sufficient to induce a pronounced cell recruitment but insufficient to induce a marked TNF-a secretion at first shot sensitized not only that quarter but also the contralateral one to a second infusion with endotoxin. It is thus possible that sensitization of the whole udder follows a first contact with a moderate dose of endotoxin in one quarter. |
