Teat canal keratin (n = 461) and mammary gland secretions (n = 370) were collected from 31 unbred and 85 primigravid Jersey heifers from one research and three commercial dairy herds. Of 97 heifers from which secretion samples were obtained, 96.9% had intramammary infections and 29% showed clinical symptoms. Seventy-five percent of quarters were infected. Staphylococcus aureus were isolated from 36 (37.1%) heifers and 55 (14.9%) quarters. One hundred and eight (93.1%) heifers and 326 (70.7%) quarters had teat canals colonized with mastitis pathogens. Staphylococcus aureus were isolated from teat canal keratin samples from 36 (31%) heifers and 57 (12.3%) quarters. The three most common species isolated from secretion and teat canal keratin samples were Staphylococcus chromogenes, Staphylococcus hyicus, and S. aureus. Secretions from infected (n = 240) and uninfected (n = 85) quarters had SCC of 13.6 X 10(6)/ml and 5.7 X 10(6)/ml. Macrophages were the most numerous cell type in secretions of infected and uninfected quarters. Quarters with teat canal colonization, but with no intramammary infections, exhibited higher SCC in secretion (9.3 X 10(6)/ml) than quarters without both teat canal colonizations and intramammary infections (4.9 X 10(6)/ml). Data indicated that intramammary infections and teat canal colonizations were more prevalent and SCC higher than previously realized in dairy heifers.
Initial studies to determine the prevalence of mastitis in heifers of breeding age and in pregnant dairy heifers demonstrated that IMI were present in 97% of heifers and 75% of quarters. The most common isolates were Staphylococcus aureus, Staphylococcus hyicus, and Staphylococcus chromogenes; SCC ranged from 12.4 to 17.3 x 10(6)/ml. Approximately 29% of heifers and 15% of quarters exhibited clinical mastitis at breeding age, as evidenced by clots or flakes in mammary secretions. Histologic examination of mammary tissues demonstrated significant reductions in alveolar epithelial and luminal areas and increases in connective tissue stroma and leukocytosis, illustrating limited development and marked inflammation of infected tissues. A one-time infusion of antibiotic for nonlactating cows into infected quarters > or = 45 d prepartum reduced incidence of IMI by 59% at calving compared with the pretreatment level; the cure rate for Staph. aureus IMI was > 90%. Prophylactic treatment of uninfected quarters > or = 45 d prepartum reduced new Streptococcus sp. IMI by 93%. The mean SCC was 50% lower at calving for treated heifers, and milk yield over the first 2 mo of lactation was 10% greater than that of untreated controls. Heifers from herds using fly control had a lower prevalence of IMI than herds without fly control. Prevalences of IMI and SCC in dairy heifers were higher than previously realized, but mastitis at calving was controlled by use of therapeutic products for nonlactating cows during pregnancy.
Frequency of new intramammary infection is greatest during early involution, decreases during middle stages, and then increases prepartum. Penetrability of the teat canal, antibacterial properties of keratin, bacterial adherence, and epithelial sensitivity to toxins play a role in resistance. Leukocytes phagocytose bacteria and regulate expression of immune mechanisms, although their function is compromised during certain stages of involution. These cells increase to millions per milliliter as involution progresses and then decrease prepartum. Macrophages predominate in lacteal secretions, followed by lymphocytes and neutrophils. Lactoferrin, a major whey protein and iron chelator, is also associated with resistance to infection during the nonlactating period and may have immunomodulatory properties. Lacteal immunoglobulins increase throughout involution peaking prepartum and function by opsonizing bacteria, neutralizing toxins, and preventing bacterial adherence. Immunoglobulins are derived from blood or are produced locally by plasma cells present in the subepithelial mammary stroma. Plasma cells, lymphoid cells, and other protective leukocytes present in teat end tissues accumulate during infection and concentrations increase in response to local antigenic stimulation. Various aspects of the mammary immune system are compromised during periods of functional transition. Thus, vaccination, immunostimulation, accelerated involution, and intramammary devices are some methods now being tested to amplify local immunity and protect the gland from bacterial infection.
It is a given in biology that structure and function go hand-in-hand. At the level of the mammary alveoli, copious milk production depends on the proliferation of mammary epithelial cells and the biochemical and structural differentiation of these cells after parturition. For example, data from quantitative structural studies demonstrate that differences in milk production between beef and dairy cows correspond with a relative failure of alveolar cell differentiation in cattle not specifically selected for milk yield. It is likely, but not proven, that production differences within or between dairy breeds are also determined by differences in the capacity of alveolar cells to differentiate or to maintain an adequate state of differentiation. These observations strongly support the belief that insults from mastitis that lead to losses in mammary function are directly related to disruption of alveolar cell integrity, sloughing of cells, induced apoptosis, and increased appearance of poorly-differentiated cells. Ironically, reduced milk production in cases of subclinical mastitis, is also associated with increases in milk somatic cell count. Thus the elevated neutrophil migration evoked to fight inflammation can inadvertently rendered alveolar epithelial cells non-secretory. A challenge to future researchers will be to devise mastitis treatments and therapies that prevent and/or repair damage to alveolar structure and maximize subsequent secretory cell differentiation.
A survey was conducted to determine and contrast prevalence of IMI in nulligravid and primigravid dairy heifers pre- and postpartum. Contrasts were made to evaluate the risk factors of location of dairy, trimester of gestation, and season of sampling on IMI. Twenty-eight dairies in California, Louisiana, Vermont, and Washington were studied. Lacteal secretions were collected aseptically from heifers at breeding age (8 to 19 mo) from one side of the gland and again at 4 d postpartum from all quarters. Of the quarters sampled, 65.6% prepartum and 64.0% postpartum were free of IMI. The percentages of quarters with IMI from coagulase-negative staphylococci or Staphylococcus aureus IMI were 27.1 and 9% prepartum and 21.8 and 2.9% postpartum. Staphylococcus aureus IMI were most prevalent in Louisiana during the months other than summer. Location, herd, and season significantly influenced prevalence of IMI. The prevalence of IMI was greatest during the last trimester of pregnancy, ranging from 49.2% in the winter to 36.8% in the summer. The significant effects of herd location and season suggest that management variables influence prevalence of heifer IMI. Because prevalence of IMI was greatest during the last trimester of pregnancy compared with prevalence during earlier stages of pregnancy, the heifer may be most susceptible to this disease during this period of first gestation.
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