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• Mastitis in the late dry period decreases colostral volume and total IgG₁ in colostrum. However, the IgG₁ concentration of the colostrum is not affected by mastitis.
• Because Holstein cows generally produce more colostrum than is fed to their calves, the reduction in colostral volume and total IgG₁ due to mastitis is unlikely to be an important contributor to the high rate of failure of passive transfer of colostral immunoglobulins. Factors that reduce colostral IgG₁ concentration would be more important.

INTRODUCTION

The importance of adequate passive transfer of colostral immunoglobulins (antibodies) for calf health is well recognized. Calves depend entirely upon absorption of immunoglobulins (particularly IgG₁) across the intestine during the first day of life to establish protective immunoglobulin concentrations in their blood. Failure of adequate passive transfer of colostral immunoglobulins is associated with increased disease occurrence and mortality, and occurs in > 40 percent of dairy heifer calves in the United States. It has been estimated that at least 22 percent of dairy heifer calf deaths could be avoided by preventing failure of passive transfer.

Adequate passive transfer requires 1) ingestion of a sufficient mass (> 100 grams) of IgG₁, which is dependent upon the volume of colostrum ingested and its IgG₁ concentration; and 2) absorption of IgG₁ from the intestine into the blood, which is dependent upon the timing of colostrum ingestion (absorption decreases with time after birth). Breed and lactation number of the cow influence the volume and IgG₁ concentration of colostrum produced. Also, prepartum milking, delay in time to first milking, leakage of colostrum, selenium deficiency, and heat stress have all been associated with low colostral immunoglobulin concentrations. However, much of the variation in colostral volume and IgG₁ concentration among cows remains unexplained.

Dairy cows are most susceptible to mastitis during the early and late stages of the dry period. Mastitis acquired during the dry period typically remains subclinical (inapparent) until after calving. Because subclinical mastitis during lactation results in reduced milk production and altered milk composition, we hypothesized that colostral volume, and possibly IgG₁ concentration, would be reduced when mastitis was present during the last two weeks of the dry period when colostrum is being formed. The objectives of this study were to investigate these effects, using matched (infected and uninfected) quarters of the same cow.

MATERIALS AND METHODS

One hundred and six Holstein cows from the University of Illinois Dairy Research Farm that were calving for at least the second time were studied. Mammary glands and secretions were examined at approximately 14 and 7 days before calving and within 3 hours after calving. The color, size, temperature, and consistency of each quarter were recorded, along with the presence or absence of edema, pain, or teat lesions. The color, viscosity, opacity, consistency, and pH of the secretions were recorded, along with results of the California Mastitis Test. Secretions from each quarter were cultured and tested for somatic cell count, protein percent, and fat percent Cows were milked with a quarter milker within 3 hours after calving, and the volume and IgG₁ concentration of colostrum from each quarter determined. Cows were eligible for inclusion in the analysis only if they had a pair (front or rear) of quarters in which one quarter was infected (at > 1 sampling time) and one quarter was uninfected (at all 3 sampling times).

RESULTS AND DISCUSSION

Thirty-one cows had 33 paired of quarters that met the criteria for inclusion in the analysis when only persistent infections (> 2 sampling times) were considered, and another 33 cows had 36 paired quarters that met the inclusion criteria when transient (1 sampling time only) infections were considered. Staphylococci other than Staphylococcus aureus were the bacteria isolated most frequently from infected quarters, followed by coliform bacteria. Colostrum from infected quarters had higher somatic cell counts, California Mastitis Test scores and pH than colostrum from uninfected quarters, and the presence of flakes or clots in the colostrum was associated with infection.

Colostral volume was lower (median = 17%) from persistently infected glands than matched uninfected glands. Colostral IgG₁ concentration, fat percent and protein percent did not differ for persistently infected and uninfected glands, but because of the reduced volume, the total mass of IgG₁ and protein in colostrum were decreased. The effects of mastitis on colostral volume and IgG₁ and protein mass were not significant when quarters with transient infections were included in the analysis, indicating that persistent infection was required to alter colostral volume and composition. Because the volume of first-milking colostrum produced by Holstein cows is so high (mean = > 2.5 qt/uninfected quarter and 2.3 L/infected quarter in this study), and because Holstein calves are typically fed < 4 qt of first-milking colostrum, the mastitis-associated reduction in colostral volume would not be expected to limit calf colostrum intake, even if all four quarters were persistently infected. Also, because mastitis did not alter colostral IgG₁ concentration, it is not expected to be an important contributor to the high rate of failure of passive transfer in calves in this country. However, until it is determined that the IgG₁ in mastitic colostrum is absorbed as efficiently as from uninfected colostrum, and that calves fed mastitic colostrum are not at increased risk for gastrointestinal or generalized bacterial infections (septicemia), we recommend that feeding of visibly abnormal colostrum or colostrum from cows with inflamed (swollen, hot, red) quarters be avoided, when other sources of colostrum are available.