Hill Farm Research Station,
Louisiana Agricultural Experiment Station,
Louisiana State University Agricultural Center,
Rt. 1, Box 10,
Homer, LA, U.S.A. 71040.
Management practices and disease control for heifers include proper housing, adequate nutrition, artificial insemination, and vaccination against calfhood diseases, with little or no concern about mastitis. However, these animals do become infected, and in some herds, the overall mastitis level is greater than 95%, with Staphylococcus aureus causing 35% of these infections. Heifer mastitis is not to be confused with "summer mastitis", which is caused by Actinomyces pyogenes, Peptococcus indolicus, and/or Streptococcus dysgalactiae, and spread by the fly, Hydrotae irritans.
The mammary glands of heifers have traditionally been regarded as uninfected, and they are not examined until the first milking or during the first episode of clinical mastitis following calving. The greatest development of milk-producing tissue in heifers occurs during the first pregnancy, so it seems logical to protect these young animals from the harmful effects of mastitis-causing bacteria to ensure maximum future milk production.
Milk somatic cell counts (SCC) are considered an important parameter for assessing mammary health status in lactating cows, and it is well recognized that milk production decreases as SCC and level of mastitis increase. Thus, SCC in heifer mammary gland secretions were analyzed to measure degree of inflammation and potential reductions in future milk yield. Somatic cell counts were elevated in all infected quarters, averaging 8.1 million/mL for CNS-infected quarters and 9.2 million/mL for S. aureus-infected quarters. Histological examination of chronically infected quarters of the developing udders from two heifers revealed inflammation of the mammary parenchymal tissues characterized by an intense lymphocyte infiltration. Samples taken from the teat skin and teat canal keratin contained many species of staphylococci, suggesting these sites as potential sources of bacteria for infecting the developing mammary glands.
Results demonstrated that teat canal infections were found in 93% of heifers or 71% of teats (8). Similarly, intramammary infections were found in 97% of heifers or 75% of quarters, and 29% of heifers showed clinical symptoms of mastitis as evidenced by clots, flakes, or blood in mammary secretions. Staphylococcus aureus was isolated from 20% of all quarters and from 25% of quarters with clinical symptoms. These bacteria cause severe damage to mammary tissue, and it is known that infections are very difficult to eliminate in lactating cows. Such infections in heifers are of great concern because of the possible deleterious effect on future milk production. Examination of mammary gland tissues from seven heifers demonstrated marked inflammation in S. aureus-infected quarters, and limited development of milk secretory tissues (7).
Reasons why young dairy animals become infected with mastitis-causing bacteria are largely unknown. Nevertheless, management practices such as fly control, use of individual calf hutches to avoid suckling among calves (particularly those fed mastitic milk), and segregation of pregnant heifers from dry cows may help to prevent the development of mastitis in heifers. In addition, replacement heifers should be cultured for presence of contagious mastitis-causing bacteria prior to purchase or before entering the milking herd. Protecting the developing milk-producing tissues of heifers from bacterial invasion is important to ensure optimum future milk yield.
Results showed that in treated heifers, 97.1% of animals were infected at time of treatment, but at calving, numbers of infected heifers in the treatment group were reduced to 40% (Figure 2; 9). Only 2.9% of quarters had antibiotic residues at time of calving. Residues were limited to two heifers treated within three weeks of calving because estimated due dates were miscalculated, but all quarters were negative after five days. In the untreated control group, 100% of heifers were infected at initial sampling (Figure 2), and at calving, mastitis in control heifers was reduced only slightly to 97.4%.
Staphylococcus aureus was isolated from 11 quarters of six treated heifers before antibiotic infusion (45.8%), but at calving, this organism was isolated from only one quarter of one heifer (4.2%). In the control group, 18 quarters of 10 heifers were infected with S. aureus at time of treatment (45%). At calving, six of the control heifers still had S. aureus mastitis in 11 quarters (55%). Thus, the overall level of infection was reduced 60% and that caused by S. aureus was reduced more than 90%.
In lactating cows, approximately 30% of animals or 25% of quarters with S. aureus mastitis are typically cured after antibiotic therapy. In this heifer study, 83.3% of animals or 90.9% of quarters were cured, thus antibiotic therapy in heifers was highly effective in eliminating mastitis compared with therapeutic success in lactating cows. Reasons are unclear, but the relatively small udders of heifers may have limited the microorganisms to areas of mammary tissue in which the antibiotic would be present in adequate concentrations to eliminate infection. In addition, scar tissue, common in S. aureus infections, may not have formed, which may have permitted the antibiotic to reach all infecting bacteria.
Antibiotic therapy in heifers is advantageous over treatment of lactating cows because treatment can be performed before calving, and the risk of antibiotic residues at freshening is minimal. In one commercial herd, heifers that received dry cow therapy during pregnancy produced an average of 5.5 lbs more milk per day over the first two months of lactation compared with herdmates that did not receive therapy. This amounted to a $42.12 increase per cow for the first two months of lactation, which would have paid for the cost of four mastitis tubes approximately eight-fold.
More recent studies with pregnant heifers using a cephalosporin-based nonlactating cow product were also successful (4). Heifers either experimentally or naturally infected with S. aureus were infused 10 weeks prepartum with one dose of a 300 mg cephapirin benzathine product and compared with untreated S. aureus-infected controls. Results demonstrated that 100% of experimentally induced and 87% of naturally occurring S. aureus infections were eliminated in treated animals at the time of calving, and cured quarters remained infection-free for at least two months into lactation (Figure 3). Quarters remaining infected at calving with S. aureus were treated with a lactating cow product containing 200 mg cephapirin benzathine, but cure rate was only 50 to 56%. After antibiotic infusion, SCC in infected quarters that cured decreased from 15 million/mL to 4 million/mL one week later and to 700 x 103/mL at calving. In contrast, none of the untreated S. aureus-infected quarters had spontaneously cured by the time heifers calved. Treated heifers in which S. aureus infections were cured produced over 10% more milk than controls during the first two months of lactation.
Generally, spontaneous cure rates for major mastitis pathogens are low. For example in a subsequent study on heifer mastitis, spontaneous cures for S. aureus and the environmental streptococci were 9% and 6%, respectively (5). Thus, treatment is required to cure such infected quarters in these young dairy animals. New infection rates in uninfected quarters receiving no therapy over the 8- to 10-week prepartum period were very low for most species of bacteria. However, new environmental streptococcal infections were quite common in uninfected, untreated heifers. Prophylactic treatment of such quarters prepartum resulted in a 93% reduction in new environmental streptococcal infections. Thus, use of nonlactating cow therapy not only is very effective in curing existing infections, it is also effective in preventing new infections.
At the initial sampling during pregnancy, frequency of clinical mastitis in infected quarters among heifers in four commercial dairies was 7.5%. At the time of calving, frequency of clinicals increased to 24%, indicating that either the presence of new infections during the prepartum period led to flare-ups of clinical mastitis at freshening, or chronically infected quarters exhibited flare-ups at this time. In either case, it is apparent that clinically infected quarters in heifers should be controlled prepartum rather than at or following freshening.
Somatic cell counts in uninfected quarters decreased from 7.6 million/mL at initial sampling to 1.5 million/mL at time of calving. In infected quarters, SCC decreased from 23.1 million/mL prepartum to 4.1 million at calving. This again indicates the need for infected heifers to be treated so that they enter the milking herd with low SCC. Additionally, the monitoring of mammary secretion characteristics demonstrated that quarters with a honey-like consistency exhibited low frequencies of infection (10%), whereas those with a thin, watery secretion exhibited a high frequency of infection (78%).
The effect of season on prevalence of infected quarters in breeding age heifers in four Louisiana dairies demonstrated that level of infection decreased through winter (55.6%), spring (42.3%), and summer (30.3%), and increased in the fall (49.6%). This trend is just the opposite of what was expected in view of the association of mastitis and the fly season in this region. However, at time of calving, prevalence of infection increased from winter (44.8%), to spring (49.6%) and summer (60.5%), and decreased in the fall (35.9%).
Some dairymen and veterinarians worry that sampling heifers for presence of mastitis may destroy the keratin plug, leading to new infections. However, studies designed to test this theory demonstrated that as long as teat ends were properly sanitized, samples were taken aseptically, and teats were dipped in a barrier type product after sample collection, there was no effect on new infection rate.
The treatment of heifers prepartum with a nonlactating cow product is advantageous because the cure rate is higher than during lactation, especially against S. aureus. There are no milk losses during therapy, the risk of antibiotic residues is minimal, SCC at calving is reduced, and milk production is increased in successfully treated cows. Treatment is indicated only in herds experiencing a high prevalence of heifers calving with clinical mastitis caused by S. aureus or S. uberis. Also, a treatment program should be developed under the supervision of the herd veterinarian. The potential for residues at calving should be considered, especially in animals that calve early. Residue testing should be carried out before mixing milk from treated animals with herd milk.
Overall, approximately 90% of heifers were infected with some type of organism prior to treatment (Figure 4). If left untreated, 78% of heifers freshened with mastitis, but if treatment was administered, only 18% of the heifers were infected. Some quarters did appear to cure spontaneously. For example, in untreated control quarters, 62.2% were infected prior to calving, and postpartum, 44.5% of the quarters remained infected. Among quarters treated with sodium cloxacillin, 50% were infected prepartum versus 8.6% at calving. Among quarters treated with cephapirin sodium, 70.1% were infected prepartum, and 2.1% were infected at calving. Thus, cure rates appeared greatest for the cephapirin sodium product. However, at calving, the percentages of samples with antibiotic residues at calving were 84.7% for cephapirin sodium compared with 17.4% for sodium cloxacillin. Three days after calving, residues were absent from quarters treated with sodium cloxacillin, but residues were still detected in 28.2% of quarters treated with cephapirin sodium. By 10 days, no antibiotic residues were detected in either group.