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D Van de Geer

Publications and source records attributed to D Van de Geer.

3 recordsLinked to original sources

Risk factors for clinical mastitis in herds with a low bulk milk somatic cell count. 1. Data and risk factors for all cases.

The incidence rate of clinical mastitis in 125 herds with a low annual bulk milk SCC (less than 150,000 cells/ml) was modeled using a Poisson regression model. The rate of clinical mastitis was significantly associated with some variables that increased the exposure to environmental microorganisms: poor cubicle cleanliness increased the mastitis rate; rubber mats in cubicles were associated with a higher incidence; and drinking water from sources other than public water also increased the rate of mastitis. Other variables may be associated with host resistance: an increasing percentage of cows leaking milk increased the rate of mastitis; postmilking teat disinfection was associated with a higher incidence of clinical mastitis; and a high frequency of cubicle disinfection was also associated with more mastitis. Three other variables were associated with the rate of mastitis: breed (Holstein-Friesian had a lower incidence than the Meuse-Rhine-Yssel breed); use of sugar beet pulp in the ration increased the mastitis rate; and in herds with high milk production a higher incidence of mastitis was observed. These items are discussed in respect to their causal relation to clinical mastitis.

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Polymorphonuclear leucocyte function: relationship between induced migration into the bovine mammary gland and in vitro cell activity.

Low doses of 10(-7) mg Escherichia coli endotoxin applied as intramammary infusion into single bovine quarters induced a rise in milk cell count without other inflammatory signs. Significantly fewer quarters responded in early lactation than in mid lactation. Maximum cell count was also somewhat later and less pronounced in early lactation. The rise in milk cell count after infusion of E. coli endotoxin was related to in vitro chemotactic activity of blood polymorphonuclear leucocytes (PMN). PMN isolated from cows which did not respond with a rise in milk cell count upon endotoxin infusion showed a diminished chemotactic activity in vitro as compared to PMN isolated from animals which did respond to an intramammary endotoxin infusion with a rise in milk cell count. No differences in phagocytic and metabolic activity were observed in vitro between the PMN isolated from the two groups of animals.

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Intramammary infections and risk factors for clinical mastitis in herds with low somatic cell counts in bulk milk.

Ten herds with low somatic cell counts in bulk milk had an incidence of clinical mastitis of only 2.2 per 100 cows whereas 10 other herds with similarly low cell counts had an incidence of 53.6 per 100 cows. The major pathogens in the herds with a high incidence were Escherichia coli, Streptococcus uberis, Staphylococcus aureus and the coagulase-negative staphylococci. The percentage of uninfected quarters in the herds with a high incidence of clinical mastitis was 21.4 per cent compared with 12.2 per cent in the herds with a low incidence of clinical mastitis. The prevalence of coagulase-negative staphylococci, Corynebacterium bovis and Micrococcus species was higher in the herds with a low incidence of clinical mastitis. There was a significant linear relationship between the percentage of uninfected quarters and the incidence of clinical mastitis in the herds with a high incidence of clinical mastitis. In herds with a low incidence of clinical mastitis significantly less teat disinfection after milking was practised. The results suggest that infections with minor pathogens tend to protect cows against mastitis, and that teat disinfection after milking may increase the percentage of uninfected quarters and lead to an increased risk of clinical mastitis in herds with low somatic cell counts in bulk milk.

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