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Title: Variation in the underlying mechanisms of innate defense and outcome of bovine mammary E. coli infections

item Burvenich, C
item Bannerman, Douglas
item Lefever, S
item Peelman, L
item Paape, Max

Submitted to: International Conference on Production Diseases in Farm Animals
Publication Type: Proceedings
Publication Acceptance Date: 7/23/2007
Publication Date: 7/29/2007
Citation: Burvenich, C., Bannerman, D.D., Lefever, S., Peelman, L., Paape, M.J. 2007. Variation in the underlying mechanisms of innate defense and outcome of bovine mammary E. coli infections. International Conference on Production Diseases in Farm Animals. pp. 437-456. July 29-August 4, 2007. Leipzig. Germany

Interpretive Summary:

Technical Abstract: Mastitis is the most costly production disease in dairy herds worldwide. During the last years the proportion of Gram-positive mastitis has declined, while Gram-negative mastitis has risen. Progress was made in reducing subclinical contagious mastitis but these measures didn’t have any impact on Gram-negative mastitis. Gram-negative pathogens commonly implicated are E. coli and Klebsiella pneumoniae. Neutrophils migrate from blood to the mammary gland in response to infection and constitute a major host defense mechanism. Many factors related to stage of lactation and parity may influence normal neutrophil function. The innate defense mechanisms become temporarily impaired during the periparturient period and the greatest effect of E. coli on the mammary gland is at that period. Of those cows with severe Gram-negative infections, nearly 25% will either die or culled. Endotoxin or lipopolysaccharide (LPS), the major constituent of the Gram-negative cell wall is released during bacterial growth and destruction, and is implicated in the pathogenesis. LPS provokes host cells to produce large amounts of pro-inflammatory mediators by activating transcription factors. One target is NF-kappa B, a key regulator of the inflammatory response. Cellular recognition of LPS is mediated by the transmembrane Toll receptor-4 (Tlr-4). LPS also binds to CD14 and this is greatly enhanced by LBP. There is strong evidence for a protective role for CD14 and LBP in mediating the host response to Gram-negative infections. Although the detection of LPS is a critical event in the activation of the innate response to Gram-negative bacteria, excess of LPS signaling can lead to exaggerated host responses culminating in the development of septic shock. Although antimicrobial agents are continuously being developed, intramammary infection with E. coli in a compromised host remains a serious problem. No antibiotic can clear infections without a good functional immune system. Therefore, the development of novel interventions that modulate the inflammatory response elicited by LPS and/or contribute to the elimination of the pathogen, remains an important animal health priority.