Risk Factors for Clinical Mastitis In Herds with a Low Bulk Milk Somatic cell Count. 1. Data and Risk Factors for All Cases Y. H. SCHUKKEN, F. J. GROMMERS, D. VAN DE GEER, H. N. ERB,1 and A. BRAND Department of Herd Health and Reproduction. Yalelaan 7 3584 CL Utrecht, The Netherlands ABSTRACT
The incidence rate of clinical mastitis in 125 herds with a low annual bulk milk sec «150,000 cells/mI) 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. (Key words: mastitis, epidemiology, somatic cell count) INTRODUCTION
Clinical mastitis remains a problem in daily herds throughout the world Efforts to reduce mastitis in herds with high bulk milk sec
involved improvement of the milking procedures, postmilking teat disinfection, and dry cow therapy. 1bese programs successfully reduced the prevalence of subclinical mastitis with major pathogens as evidenced by decreasing sec; however, the rate of clinical mastitis is less affected (5, 8, 20). As a consequence of mastitis control programs, the distribution of pathogens in clinical mastitis cases altered. In high bulk milk sec herds, Streptococcus agalactiae and Staphylococcus aureus are the predominant pathogens, whereas in low bulk milk sec herds the predominant pathogens are Escherichia coli and environmental streptococci (Streptococcus dysgalactiae, Streptococcus uberis) (5, 8, 14, 20). Controlling the rate of clinical mastitis due to these pathogens has not been successful. Ample variation exists in the rate of clinical mastitis in low bulk milk sec herds (5, 8, 20). In a survey in herds in Ohio with a bulk milk sec less than 300,000 cells/mI, the rate varied between 8.9 and 24.5 cases per 10,000 cow-days at risk (8). Variations of this size may be explained in part by host defense mechanisms, but certainly a considerable part of this variation can be explained by herd factors such as housing, nutrition, and hygiene. Epidemiological techniques offer important tools to study herd risk indicators (17). The identification of risk indicators in the herd will contribute to the formulation of the pathogenesis of clinical mastitis on low bulk milk sec herds and thereby enhance the prospects of implementing a successful control program. The purpose of this study was to identify risk indicators for the rate of clinical mastitis in daily herds with a low bulk milk sec. MATERIALS AND METHODS The Herds
Received 11U1W1JY 2, 1990.
tccepted 1u1y 9, 1990. Section of Epidemiology, Depal1Inent of Clinical Sciences, Cornell UniveJSity, Itbaca, NY. 1990 1 Dairy Sci 73:346l-3471
Clinical mastitis was observed during 12 mo on 125 farms with a low mean bulk milk sec.
3463
SCHUKKEN BT AL.
3464
The annual mean in the 12 mo preceding the study in each herd was
The incidence rate of clinical mastitis in 125 herds with a low annual bulk milk sec «150,000 cells/mI) 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. (Key words: mastitis, epidemiology, somatic cell count) INTRODUCTION
Clinical mastitis remains a problem in daily herds throughout the world Efforts to reduce mastitis in herds with high bulk milk sec
involved improvement of the milking procedures, postmilking teat disinfection, and dry cow therapy. 1bese programs successfully reduced the prevalence of subclinical mastitis with major pathogens as evidenced by decreasing sec; however, the rate of clinical mastitis is less affected (5, 8, 20). As a consequence of mastitis control programs, the distribution of pathogens in clinical mastitis cases altered. In high bulk milk sec herds, Streptococcus agalactiae and Staphylococcus aureus are the predominant pathogens, whereas in low bulk milk sec herds the predominant pathogens are Escherichia coli and environmental streptococci (Streptococcus dysgalactiae, Streptococcus uberis) (5, 8, 14, 20). Controlling the rate of clinical mastitis due to these pathogens has not been successful. Ample variation exists in the rate of clinical mastitis in low bulk milk sec herds (5, 8, 20). In a survey in herds in Ohio with a bulk milk sec less than 300,000 cells/mI, the rate varied between 8.9 and 24.5 cases per 10,000 cow-days at risk (8). Variations of this size may be explained in part by host defense mechanisms, but certainly a considerable part of this variation can be explained by herd factors such as housing, nutrition, and hygiene. Epidemiological techniques offer important tools to study herd risk indicators (17). The identification of risk indicators in the herd will contribute to the formulation of the pathogenesis of clinical mastitis on low bulk milk sec herds and thereby enhance the prospects of implementing a successful control program. The purpose of this study was to identify risk indicators for the rate of clinical mastitis in daily herds with a low bulk milk sec. MATERIALS AND METHODS The Herds
Received 11U1W1JY 2, 1990.
tccepted 1u1y 9, 1990. Section of Epidemiology, Depal1Inent of Clinical Sciences, Cornell UniveJSity, Itbaca, NY. 1990 1 Dairy Sci 73:346l-3471
Clinical mastitis was observed during 12 mo on 125 farms with a low mean bulk milk sec.
3463
SCHUKKEN BT AL.
3464
The annual mean in the 12 mo preceding the study in each herd was
