A review of prevention and control of heifer mastitis via non-antibiotic strategies.

Clinical and subclinical mastitis is a significant problem in primiparous dairy cattle (heifers) with a higher prevalence and incidence in heifers than cows, especially early in lactation. Differences in management (e.g. nutrition, pasturing, no use of dry cow therapy) as well as differences in physiological status (e.g. continuing growth in heifers) are likely contribute to the observed differences between heifers and cows. These differences may result in the requirement for different approaches for mastitis management in heifers than for cows. Mastitis is a multifactorial disease, hence control requires an understanding of the risk factors before effective interventions can be defined. Control strategies are aimed at reducing the incidence of new intramammary infections and eliminating existing infections. Potential strategies can include improved environmental and animal hygiene, application of internal and external teat sealants, prepartum application of teat antiseptics, prepartum milking and control of horn fly in environments where it acts as vector. Other less well-proven strategies to control heifer mastitis include management of heifers as a physically separate group from older cows and not feeding mastitic milk to calves. It is concluded that several well-proven strategies are available to manage heifer mastitis. However, further research is likely to improve understanding of heifer mastitis and lead to novel managerial approaches to mastitis control in this age group.

Effect of application of an external teat sealant and/or oral treatment with a monensin capsule pre-calving on the prevalence and incidence of subclinical and clinical mastitis in dairy heifers.

AIM: To assess the effect of applying an external teat sealant or a slow-release intraruminal monensin capsule pre-calving on the prevalence and incidence of subclinical or clinical mastitis in dairy heifers post-calving. METHODS: The studies were undertaken in 13 herds. In two herds application of an external teat sealant was compared with a negative control; in nine herds treatment with monensin was compared with controls, and in two herds treatments were applied in a 2 x 2 factorial design. Heifers were randomly assigned within herd to be treated with a slow-release intraruminal device containing 32 g monensin (n=383), or left as untreated controls (n=389), approximately 30 days before the start of the spring calving period; or to be treated with a latex external teat sealant (n=206) when calving was impending, or be left as untreated controls (n=205). Milk samples were collected from each gland between 0 and 5 days after calving and from any gland diagnosed with clinical mastitis. The effect of the treatments on the prevalence of intramammary infection (IMI), i.e. subclinical mastitis, and clinical mastitis were initially analysed at the univariate level, with associated variables (p<0.2) being used in construction of multivariable models. RESULTS: The prevalence of IMI was 18.4% at the gland level, and coagulase-negative staphylococci followed by Streptococcus uberis were the most common isolates. Treatment with an external teat sealant reduced the prevalence, compared with controls, of any IMI (12.1 (SE 1.7)% vs 16.5 (SE 2.1)%, respectively; p=0.05) or IMI caused by a major pathogen (3.8 (SE 0.8)% vs 6.0 (SE 1.1)%, respectively; p=0.05). Monensin treatment did not affect the prevalence of any IMI (p=0.68) or IMI due to a major pathogen (p=0.11). The cumulative incidence of clinical mastitis was 14.2%. Neither monensin treatment (p=0.47) nor application of an external teat sealant (p=0.71) altered the risk of clinical mastitis. There was no interaction between the monensin and external teat sealant in the two herds where the treatments were applied in a 2 x 2 factorial design. CONCLUSIONS: Application of an external teat sealant resulted in a lower prevalence of any IMI and of an IMI caused by a major pathogen. Despite monensin reducing the mobilisation of body tissue and the risk of subclinical ketosis, it had no effect on the prevalence or incidence of IMI or clinical mastitis. CLINICAL RELEVANCE: Application of an external teat sealant is an option for reducing the prevalence of IMI in pasture fed dairy heifers.

Quarter-level analysis of subclinical and clinical mastitis in primiparous heifers following the use of a teat sealant or an injectable antibiotic, or both, precalving.

This study investigated the effect of infusion of a bismuth subnitrate teat canal sealant or an injectable antibiotic, or both, in heifers on the cure of existing intramammary infection (IMI), incidence of new IMI, prevalence of postcalving IMI, and incidence of clinical mastitis in the first 2 wk postcalving at the quarter level. Heifers (n = 1,067) in 30 seasonally calving, pasture-fed dairy herds were randomly assigned at the heifer level to 1 of 4 treatments (no treatment; 3 intramuscular injections of 5 g of tylosin antibiotic at 24-h intervals; infusion of a teat sealant into all 4 quarters; 3 intramuscular injections of 5 g of tylosin antibiotic and infusion of teat sealant into all 4 quarters). Mammary gland secretion samples were collected from each quarter of every heifer before treatment. Heifers within a herd were enrolled on one calendar day, 27 d (on average) before the planned start of the seasonal calving period. Duplicate milk samples were collected from each gland within 5 d after calving for bacterial culture and from glands the herdowners diagnosed as having clinical mastitis. The relative risk of effect of treatment on the incidence of cure, incidence of new IMI, prevalence of postcalving IMI, and incidence of clinical mastitis were calculated at the gland level using multivariate logistic regression analyses. Neither infusion of a teat sealant nor treatment with the injectable antibiotic increased the cure of precalving IMI. Infusion of the teat sealant reduced the risk of new IMI with any pathogen by 74%, reduced the prevalence of postcalving IMI by 65%, reduced the risk of new infection with Streptococcus uberis by 70% in quarters with an IMI precalving, and reduced the incidence of clinical mastitis from which a pathogen was isolated by 70% in quarters with an IMI precalving. Parenteral antibiotic treatment had no effect on any of these outcomes. In conclusion, use of an internal teat-canal sealant in heifers reduced the postcalving IMI prevalence and the incidence of pathogen-associated clinical mastitis postcalving by decreasing the incidence of new infections over this high-risk peripartum period, and may be a useful tool for reducing the risk of mastitis in heifers.

Management of dairy heifers and its relationships with the incidence of clinical mastitis.

AIM: To describe aspects of management of dairy heifers before calving and determine risk factors for clinical mastitis postpartum in heifers, at the herd level, under pasture-based management systems in the Waikato and Taranaki regions of New Zealand. METHODS: Dairy herdowners (n=578) provided information via a prospective survey about their practices for rearing heifers and management of mastitis. A proportion of herdowners (n=250) subsequently provided data on the cases of clinical mastitis in their herds, including the date, cow identification, age and quarter affected from cases occurring in the 4 months after the planned start of calving (PSC) in the subsequent lactation. The relationship between management factors and the proportion of heifers diagnosed with clinical mastitis within a herd was examined using bivariate and multivariate analyses. RESULTS: The herd average percentage of heifers with clinical mastitis was 13.6 (95% confidence interval (CI)=12.3-14.9)%, and multiparous cows with clinical mastitis was 9.0 (95% CI=8.2-9.8)% in the first 4 months of lactation. There were positive relationships between the proportion of heifers with clinical mastitis and average milk production per cow (kg milksolids/ lactation; p<0.001), number of cows milked per labour unit (p=0.003), stocking rate (<> 3.30 cows/ha; p=0.002), and incidence of clinical mastitis in multiparous cows (%/120 days; p<0.04), in the final multivariate model. The proportion of heifers with clinical mastitis per herd was lower in herds that milked their lactating cows in multiple groups (p=0.02). CONCLUSIONS: The risk of clinical mastitis in heifers was significantly associated with management practices. It may be possible to reduce the incidence of clinical mastitis in heifers by modification of management practices at the herd level, and further studies are required to investigate this.

Subclinical and clinical mastitis in heifers following the use of a teat sealant precalving.

This study investigated the effect in heifers of infusion of a bismuth subnitrate teat-canal sealant and bacterial intramammary infection (IMI) precalving on prevalence of postcalving IMI and incidence of clinical mastitis in the first 2 wk postcalving. Glands (n = 1,020) from heifers (n = 255) in 5 seasonally calving, pasture-fed dairy herds were randomly assigned within heifer to 1 of 4 treatment groups (no treatment; mammary gland secretion collection; infusion of a teat sealant; or sample collection with infusion of teat sealant). Heifers within a herd were enrolled on one calendar day, 31 d on average before the planned start of the seasonal calving period. Duplicate milk samples were collected from each gland within 4 d after calving for bacterial culture. Herd owners collected duplicate milk samples, before treatment, for bacterial culture from glands they defined as having clinical mastitis. The gland prevalence of IMI precalving was 15.5% and did not differ between herds. Bacteria isolated precalving included coagulase-negative staphylococci (76.9% of all bacteriologically positive samples), Streptococcus uberis (14.1%), Staphylococcus aureus (5.1%), Corynebacterium spp. (3.8%), and others (0.1%). The presence of an IMI precalving increased the risk of an IMI postcalving 3.6-fold and the risk of clinical mastitis 4-fold, relative to no IMI precalving. Infusion of the teat sealant reduced the risk of postcalving IMI due to Strep. uberis by 84%, and of clinical mastitis by 68%. Sampling the glands precalving had no effect on postcalving IMI or on clinical mastitis incidence. Use of an internal teat canal sealant in heifers precalving may be a useful tool for reducing the risk of subclinical and clinical mastitis in heifers.

Plasma concentrations of inhibin a and follicle-stimulating hormone differ between cows with two or three waves of ovarian follicular development in a single estrous cycle.

Patterns of ovarian follicle development were monitored daily in Holstein-Friesian cows that had two (n = 4) or three (n = 4) waves of ovarian follicle development during a single estrous cycle. The plasma from daily blood samples was used in assays for inhibin A, FSH, progesterone, and estradiol-17beta. Mean cycle lengths for cows with two and three waves were 21.8 and 25.3 days, respectively (P < 0.02). Although the average number of follicles >3-mm diameter on each pair of ovaries was similar for two- and three-wave cows on Days 2, 3, and 4 (Day 0 = day of ovulation; 8.6 vs. 9.6 follicles), there were more follicles >6-mm diameter on the ovaries of cows with two waves on Days 3 and 4. This difference was associated with a shorter interval from wave emergence to peak concentrations of inhibin A during the first wave in two-wave cows (2.0 vs. 3.8 days; P = 0.03) and with higher peak concentrations (474 vs. 332 pg/ml; P = 0.03). Differences in peak FSH concentrations were not significant (1.7 vs. 1.3 ng/ml; P = 0.10) and were inversely related to inhibin A concentrations. The peak concentrations of inhibin A and FSH in the second nonovulatory wave in the three-wave cows were similar to the low concentrations measured in the first wave (292 vs. 332 pg/ml of inhibin A, 1.3 vs. 1.3 ng/ml of FSH; P > 0.20). Average peak concentrations of inhibin A and FSH were similar during the ovulatory wave for cows with either two or three waves in a cycle (432 vs. 464 pg/ml of inhibin A, 2.3 vs. 2.1 ng/ml of FSH; P > 0.3). The lower concentrations of FSH during the emergence of the first follicular wave in cows with three-wave cycles may have reduced the rate of development of some of the follicles and reduced the concentrations of inhibin A. This pattern of lower concentrations of FSH and inhibin A was repeated in the second nonovulatory wave but not in the ovulatory wave. Subtle differences in the concentrations of these two hormones may underlie the mechanism that influences the number of waves of ovarian follicle development that occur during the bovine estrous cycle.

Effect of treatment with progesterone and oestradiol when starting treatment with an intravaginal progesterone releasing insert on ovarian follicular development and hormonal concentrations in Holstein cows.

Ovarian follicular development and concentrations of gonadotrophin and steroid hormones were studied in non-lactating Holstein cows following administration of progesterone (P(4)) or oestradiol benzoate (ODB) at the start of treatment with an intravaginal progesterone releasing insert (IVP(4)) in a 2 by 2 factorial experiment. Cows were treated at random stages of the oestrous cycle with an IVP(4) device (Day 0) and either no other treatment (n=8), 200 mg of P(4) IM (n=9), 2.0 mg of ODB IM (n=8) or both P(4) and ODB (n=9). Seven days later devices were removed and PGF(2alpha) was administered. Twenty-four hours later 1.0mg of ODB was administered IM. Oestrus was detected in 97.1% and ovulation in 64.7% (effect of treatment, P=0.41) of cows within 96 h of removing inserts. In the cows that ovulated, day of emergence of the ovulatory follicle was delayed (P<0.01) and more precise (P<0.05) in cows treated with ODB compared to the cows treated with P(4). Interval from wave emergence to ovulation and the diameter of the ovulatory follicle was less (P<0.05) in cows treated with ODB compared to cows treated with P(4). Combined treatment with P(4) and ODB at the time of starting treatment with an IVP(4) device did not significantly change the pattern of ovarian follicular development compared to treatment with ODB alone. Concentrations of LH and FSH in plasma were less in cows treated with ODB between Days 0 and 4 (P<0.05) while treatment with P(4) increased concentrations of FSH in plasma between Days 0 and 4 (P<0.05). When anovulatory cows were compared to ovulatory cows, diameters of follicles (P<0.001) and growth rate of follicles (P<0.01) were less in anovulatory cows between Days 7 and 9, while concentrations of FSH in plasma were greater (P<0.01), concentrations of LH similar (P>0.90) and concentrations of oestradiol were less (P=0.01) in the anovulatory cows between Days 4 and 10. Our findings support a hypothesis that ovarian follicular development following administration of P(4) or ODB at the start of treatment with an IVP(4) device differs. Anovulatory oestrus may have been associated with reduced maturity and/or later emergence of ovarian follicles.