title: Role of endotoxin and TNF-alpha in the pathogenesis of experimentally induced coliform mastitis in periparturient cows.
abstract: Twelve cows were experimentally infected in two quarters with 1 x 10(4) cfu Escherichia coli per quarter and six cows were infused with 500 microg endotoxin into two quarters. Six cows infected intramammarily with Esch. coli were treated intravenously with a bactericidal antibiotic 10 h after infection and subcutaneously 20 h later. Blood and milk samples were collected from all cows at regular time intervals. Milk production decreased more rapidly, but was less pronounced, after endotoxin infusion than (during Esch. coli mastitis. The milk production losses in the noninflamed quarters were negligible in endotoxin mastitis, but were substantial during Esch. coli mastitis, probably due to more pronounced systemic effects. Reticulorumen motility was inhibited only during Esch. coli mastitis. Changes in plasma haptoglobin were more pronounced during Esch. coli mastitis, although they occurred sooner during endotoxin mastitis. No changes in plasma activities of enzymes such as lactate dehydrogenase, glutamic-oxaloacetic transaminase and gamma-glutamyl transpeptidase were observed. Concentrations of tumour necrosis factor-alpha increased in both types of mastitis. Absorption of these cytokines into the circulation was highest during Esch. coli mastitis, especially in the untreated control group. We found only minor differences between the treated and untreated Esch. coli groups, but there were larger differences between the Esch. coli groups and the endotoxin group. These differences were probably due to differences in kinetics, composition and amounts of different cytokines released in the mammary gland and subsequently absorption into the circulation. Endotoxin is probably not directly responsible for the systemic changes during coliform mastitis.
authors.affiliation: Department of Physiology, Biochemistry and Biometrics, Milk Secretion and Mastitis Research Centre, Faculty of Veterinary Medicine, Ghent University, Merelbeke, Belgium.
authors.forename: D
authors.initials: D
authors.lastname: Hoeben
authors.forename: C
authors.initials: C
authors.lastname: Burvenich
authors.forename: E
authors.initials: E
authors.lastname: Trevisi
authors.forename: G
authors.initials: G
authors.lastname: Bertoni
authors.forename: J
authors.initials: J
authors.lastname: Hamann
authors.forename: R M
authors.initials: RM
authors.lastname: Bruckmaier
authors.forename: J W
authors.initials: JW
authors.lastname: Blum
mesh_terms: D000818:Animals; D002417:Cattle / Q000502:physiology*; D004926:Escherichia coli / Q000254:growth & development; D004927:Escherichia coli Infections / Q000209:etiology / Q000276:immunology / Q000662:veterinary*; D005260:Female; D006242:Haptoglobins / Q000032:analysis; D007774:Lactation; D008070:Lipopolysaccharides / Q000378:metabolism*; D008414:Mastitis, Bovine / Q000209:etiology* / Q000276:immunology / Q000382:microbiology; D008892:Milk / Q000737:chemistry* / Q000378:metabolism; D013997:Time Factors; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis / Q000502:physiology*
chemical_list: D006242:Haptoglobins; D008070:Lipopolysaccharides; D014409:Tumor Necrosis Factor-alpha