The effect on inflammation of the bovine mammary gland of vaccination with a cell wall extract of Staphylococcus aureus

Alan Frost, Tiina Mattila

Research output: Contribution to journalArticleScientific

Abstract

Two pregnant cows were immunized with a cell wall factor of Staphylococcus aureus and were challenged during subsequent lactation with both endotoxin and later with homologous S. aureus. Compared with control animals, the response to both endotoxin and S. aureus was delayed and the severity of the clinical response was markedly reduced. Inflammation was monitored by changes in antitrypsin and NAG‐ase. The mechanism of this protective effect remains obscure.
Original languageEnglish
Pages (from-to)688-694
JournalZentralblatt für Veterinärmedizin, Reihe B: Infektions- und Invasionskrankheiten, Bakteriologie, Virologie, Parasitologie, Hygiene, Lebensmittelhygiene, Pathologie
Volume35
Issue number1-10
DOIs
Publication statusPublished - 1988
MoE publication typeB1 Article in a scientific magazine

Fingerprint

Human Mammary Glands
Cell Extracts
mammary glands
Cell Wall
Staphylococcus aureus
Vaccination
inflammation
vaccination
cell walls
endotoxins
Inflammation
Endotoxins
cattle
extracts
beta-N-acetylhexosaminidase
Acetylglucosaminidase
Lactation
animal behavior
protective effect
lactation

Cite this

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abstract = "Two pregnant cows were immunized with a cell wall factor of Staphylococcus aureus and were challenged during subsequent lactation with both endotoxin and later with homologous S. aureus. Compared with control animals, the response to both endotoxin and S. aureus was delayed and the severity of the clinical response was markedly reduced. Inflammation was monitored by changes in antitrypsin and NAG‐ase. The mechanism of this protective effect remains obscure.",
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AB - Two pregnant cows were immunized with a cell wall factor of Staphylococcus aureus and were challenged during subsequent lactation with both endotoxin and later with homologous S. aureus. Compared with control animals, the response to both endotoxin and S. aureus was delayed and the severity of the clinical response was markedly reduced. Inflammation was monitored by changes in antitrypsin and NAG‐ase. The mechanism of this protective effect remains obscure.

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