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1 Milk Secretion and Mastitis Research Center, Department of Physiology-Biochemistry-Biometrics, Faculty of Veterinary Medicine, Ghent University, Salisburylaan 133-9820 Merelbeke, Belgium
2 Département de Physiologie, Faculté de Médecine Vétérinaire, Université de Liège Sart-Tilman, 4000 Liège, Belgium
3 Institut National de la Recherche Agronomique, Pathologie Infectieuse et Immunologie Centre de Tours-Nouzilly, 37380 Nouzilly, France
4 Bovine Functional Genomics Laboratory, USDA, ARS, Beltsville, MD 20705
Corresponding author: Christian Burvenich; e-mail: christian.burvenich{at}UGent.be.
Acute Escherichia coli mastitis is one of the major sources of economic loss in the dairy industry due to reduced milk production, treatment costs, discarded milk, and occasional fatal disease. Nonsteroidal anti-inflammatory drugs (NSAIDs) are frequently used as adjunctive therapy to antibiotics. The objective of the current study was to evaluate the effect of carprofen treatment following infusion of Escherichia coli into the mammary glands of primiparous cows during the periparturient period. Severity of mastitis was scored based on the average milk production in the uninfected quarters on d +2 postinoculation and a clinical severity score. Carprofen was administered intravenously at 9 h postchallenge, when clinical signs of mastitis appeared. In previous work, efficacy of NSAIDs was mainly evaluated using clinical symptoms. In the present study, the effect of carprofen on innate immune response was also assessed by quantification of inflammatory mediators. All primiparous cows reacted as moderate responders throughout the experimental period. Primiparous cows were intramammarily inoculated with 1 x 104 cfu of E. coli P4:O32 in 2 left quarters. Analysis of blood and milk parameters, including IL-8, complement component C5a, lipopolysaccharide-binding protein (LBP), soluble CD14, prostaglandin E2, and thromboxane B2 was performed from d 0 to d +6 relative to intramammary inoculation. Rectal temperature in carprofen-treated animals was lower than in control animals at 3 and 6 h posttreatment. Treatment also restored the decreased reticulorumen motility that occurs during E. coli mastitis to preinfection levels faster than in control animals. Carprofen treatment resulted in an earlier normalization of the clinical severity score. Eicosanoid (prostaglandin E2 and thromboxane B2) production in milk tended to be inhibited by carprofen. No significant differences in the kinetic patterns of somatic cell count, IL-8, complement component C5a, LBP, and soluble CD14 were observed. In conclusion, carprofen treatment improved general clinical condition by effective antipyrexia and restoration of reticulorumen motility but did not significantly inhibit eicosanoid production. Carprofen treatment did not result in a significant decrease of chemotactic inflammatory mediators, IL-8 and C5a, and early innate immune molecules, sCD14 and LBP. Therefore, major modulatory effects from NSAID administration were not observed in this mastitis model, although a larger study might confirm some apparent trends obtained in the present results.
Key Words: primiparous cow • carprofen • Escherichia coli mastitis • moderate inflammation
Abbreviation key: C5a = complement component 5a, COX = cyclo-oxygenase, HR = heart rate, LBP = LPS-binding protein, NSAID = nonsteroidal anti-inflammatory drug, PGE2 = prostaglandin E2, PIH = postinfusion hour, RT = rectal temperature, sCD14 = soluble CD14, TMB = tetramethylbenzidine, TXB2 = thromboxane B2.
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  F. Vangroenweghe, W. Van Den Broeck, A. De Ketelaere, H. van Bree, L. Duchateau, and C. Burvenich Endoscopic Examination and Tissue Sampling of the Bovine Teat and Udder Cistern J Dairy Sci, May 1, 2006; 89(5): 1516 - 1524. [Abstract] [Full Text] [PDF]
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