Veterinary Microbiology 134 (2009) 143–149

Periparturient use of parenteral micronised procaine penicillin to reducethe risk of clinical mastitis in heifers after calving

Mark Bryan *, Kath Taylor

VetSouth Ltd, PO Box 12, Winton, Southland, New Zealand

A R T I C L E I N F O

Keywords:

Mastitis

Heifers

Periparturient

Penicillin

A B S T R A C T

Mastitis in primiparous heifers immediately postpartum can be both a significant welfare

concern and a heavy economic loss. Interventions successfully researched include

intramammary therapies. This study considered the clinical and practical effects of a

parenteral approach to controlling clinical mastitis in heifers immediately postpartum.

The objective of this field trial was to determine whether preventative treatment of heifers

with a single parenteral treatment of 15 million iu micronised procaine penicillin within

12 h after calving would reduce the incidence of clinical mastitis in early lactation as

detected by farmers. All heifers (n = 609) calving on three commercial dairy farms in New

Zealand during the spring of 2006 were randomly allocated to either treatment or no

treatment. Treatment (15 million iu micronised procaine penicillin) was given at the first

milking following calving. All clinical mastitis was recorded. Treatment reduced the odds

of having clinical mastitis within the first 7 days in milk by over half (Mantel-Haenszel

adjusted OR = 0.456; p = 0.044); and reduced the odds of having mastitis within the first

100 days in milk by just under half (Mantel-Haenszel adjusted OR = 0.518; p = 0.027).

Treatment had a significant effect on increasing the median days to clinical mastitis

(p = 0.019; b = 1.961, LCI 1.117, UCI 3.445). Preventative treatment of heifers immediately

following calving with 15 million iu micronised procaine penicillin parenterally could be

of benefit as part of a control programme aimed at reducing the incidence of clinical

mastitis in heifers in their first lactation.

� 2008 Elsevier B.V. All rights reserved.

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1. Introduction

Peripartum mastitis in heifers can be a significantproblem on seasonally calving dairy farms in New Zealand,with reported incidences ranging from 13% (Williamson,2002), to 22% (Parker et al., 2005), to 35% (Pankey et al.,1996), and is recognised and being of higher incidencegenerally in heifers than in older herd cohorts (Barkemaet al., 1998). In large herds of approximately 1000 cowsand heifers, with a seasonal calving pattern, on any one dayin the spring there may be up to 50 cows and heiferscalving. Calving is predominantly outside on pasture, and

* Corresponding author. Tel.: +64 3236 6090; fax: +64 3236 8518.

E-mail address: markb@thevets.co.nz (M. Bryan).

0378-1135/$ – see front matter � 2008 Elsevier B.V. All rights reserved.

doi:10.1016/j.vetmic.2008.09.021

often heifers are grouped together as a single group and arecalved separately from the main herd. In contrast to othercountries, where Staphylococcus aureus is the predominantheifer pathogen (Owens et al., 2001), the predominantbacterial isolate from clinically infected heifers in NewZealand is Streptococcus uberis (Pankey et al., 1996; Parkeret al., 2005; Compton et al., 2007).

There is a growing awareness of the welfare aspects ofthis disease: authors have reported that 11% of heifers withclinical mastitis immediately pre- or postpartum are culledwithin 28 days in milk (DIM) (Waage et al., 2000); and anincreased risk of culling was associated with an increasedincidence of clinical mastitis (De Vliegher et al., 2005a;Compton et al., 2007). Furthermore, clinical mastitis inheifers in early lactation leads to greater economic loss byhaving an increased risk of mastitis in the subsequent

M. Bryan, K. Taylor / Veterinary Microbiology 134 (2009) 143–149144

lactation (Rupp et al., 2000). Some authors have reportedthat heifers experiencing clinical mastitis have lower longterm production (Oliver et al., 2003; De Vliegher et al.,2005b), but this effect has not been found in New Zealand(Compton et al., 2007), where heifers experiencing clinicalmastitis were not found to have reduced milk solids oryield.

In recent years, several novel approaches have beenresearched in an attempt to minimise the risk of mastitis inprimiparous heifers. Infusion of intramammary injectorsprepartum is effective in reducing clinical mastitis inheifers post calving (Trinidad et al., 1990; Owens et al.,1991, 1993, 2001; Oliver et al., 2003; Sampimon and Sol,2004). Both lactational and extended (dry period) anti-biotic intramammary preparations have been used.

A barrier approach to treatment by infusing a teatsealant into udders prior to calving was effective inreducing the incidence of mastitis by any organism within2 weeks of calving by 64–68%; and to reduce the risk ofmastitis caused by S. uberis by 41–84% (Parker et al., 2007).In this study and others (Owens et al., 2001; Oliver et al.,2003) heifers were treated from approx. 4 weeks pre-calving. Under many management systems in NewZealand, primiparous heifers are grazed outside on Brassica

spp. through the winter away from the milking platformprior to calving, and often facilities are poor andcontamination high. Under these systems, administrationof either intramammary teat sealant or antibiotics is bothimpractical and likely to pose contamination risks.

For this reason, some New Zealand researchers haveinvestigated treatment options closer to calving, and inparticular using parenteral therapy. Parenteral treatmentof mastitis in New Zealand with penicillin is both commonand effective in treating clinical mastitis in both cows andheifers during lactation (McDougall, 1998; McDougallet al., 2007a). In a small study using 21 sets of identicaltwin heifers, parenteral treatment of heifers at approxi-mately 7 days before calving with 15 million iu ofmicronised procaine penicillin was found to lower newintramammary infections (IMI) following calving,although this difference was not statistically significant(Williamson, 2002). Parenteral treatment at approxi-mately 7 days prepartum using penethamate penicillinin heifers has also been shown to reduce the risk of mastitiswithin 7 days following calving (Bryan and Friton, 2004;Bryan, 2005), but the data from all of these parenteral NewZealand studies in heifers have not been replicated inlarger scale studies.

There are two potential problems with parenteraltreatment prior to calving: the first is the risk of antibioticresidues in the resulting calf, should that calf be sent forslaughter shortly after birth, a practice that is notuncommon in New Zealand; the second is that groupingand yarding heifers close to calving is itself a potential riskfactor in the development of mastitis by increasing uddercontamination (Compton et al., 2007), and may be bestavoided. To address these concerns, this study investigatedthe effects of treating primiparous heifers within 12 h postcalving with a single parenteral dose of 15 million iu ofmicronised procaine penicillin on subsequent mastitisincidence.

2. Materials and methods

2.1. Herds and animals

This study was performed under the auspices of theInvermay Animal Ethics Committee, New Zealand, AECnumber 10652. From a database of 250 farms, threecommercial dairy farms with a history of a high incidence(>15% within the first 2 weeks of calving) of heifermastitis in the previous season were chosen. Herd sizeswere 950, 1110 and 550 respectively (mean herd sizeVetSouth database = 630, median 600, S.D. 412; August2006). All heifers (n = 609) calving on these threecommercial dairy farms were examined at the firstmilking after calving and included for allocation to oneof three groups.

An initial power analysis was performed using PASS(NCSS.com), based on previous data obtained by the authorin earlier pilot studies (Bryan and Friton, 2004; Bryan,2005). In these studies, heifers treated with Penethamatepenicillin immediately prior to calving had approximatelyhalf the subsequent incidence of mastitis during the first 7DIM compared to heifers who were left untreated. Theincidence of mastitis in New Zealand is 14 cases/100 cows/lactation (McDougall et al., 2007b). The majority of thesecases occur in the first 4 weeks following calving, and thepredominant bacterial isolate is S. uberis (Pankey et al.,1996; Parker et al., 2005). Based on this data, using analpha of 0.05, a Beta of 0.8, a two-tailed outcome and anassumption of a mean mastitis level in untreated heifers ofbetween 15 and 20% (Pankey et al., 1996), requiredbetween 220 and 291 heifers per group.

Heifers were managed as a single group on each farmand calved on pasture, with supplementary feeding inthe form of baleage and hay. Standard New Zealandfarming practices were followed with regard to calvingand pericalving management. Heifers were allowed tocalve on pasture and were brought to the dairy shedtwice daily, such that the maximum time betweencalving and first milking would be 12 h. Calves wereremoved at this time.

2.2. Data collection

For each of the three herds, a designated farmtechnician was assigned the task of identifying heifers atfirst milking and allocating them to one of either treatmentor control groups. Assignation was by preformed, ran-domly allocated listing based on order of entry to the dairyshed at the time of first milking. The randomisation of theorder was performed a priori using a skewed ZRANDfunction in Excel. Specifically, a ZBernoulli function takingthe probability of treatment as 0.4 was used, such thatcontrols outnumbered treatments at a ratio of approxi-mately 60:40. This was designed to minimise the numberof treatment cases required within the initial poweranalysis.

At the first presentation following calving, heiferswere examined by the trained farm technician for signsof systemic illness (rectal temperature) and, followingstripping of the foremilk, the milk examined for signs of

M. Bryan, K. Taylor / Veterinary Microbiology 134 (2009) 143–149 145

clinical mastitis. Clinical mastitis was defined as thepresence of either 1 or more of: clots in the milk; or heator swelling within the udder. In addition, the presence ofblood in the milk without any of the previous threesignals did not constitute a clinical mastitis case.Following this initial presentation, heifers were allo-cated to either compulsory treatment and removal fromthe trial (presence of clinical mastitis), or to one of eithertreatment or control as per the pre-determined listorder.

Control heifers received no further intervention. Treat-ment heifers received a single treatment (split into twoequal simultaneous doses of 15 mls) of 15 million iu ofmicronised procaine penicillin (Masticillin, StockguardLaboratories Ltd., Hamilton, New Zealand) by intramus-cular injections. Both treatment and control heifers weremanaged together as a group within the main milkingherd. On all farms they were not housed at any time andwere fed a predominantly pasture based diet. All weremilked twice daily. The milk from both treatment andcontrol heifers was not included in the bulk milk for 12milkings (144 h) following calving.

At each milking, all heifers were examined by the farmtechnician for signs of clinical mastitis by examining themilk (following foremilk stripping) for clots; and the udderfor signs of heat, swelling and/or oedema (Nestor et al.,1988). Clinical mastitis was defined as the presence of clotsonly; or the presence of 1 of the other signals and thepresence of clots. These heifers were recorded as havingclinical mastitis and treated appropriately. No bacteriology

Fig. 1. Distribution of calving dates of

was performed on cases deemed clinical to determinebacteriological presence.

Primary outcomes of interest were: incidence of clinicalmastitis within 7 DIM; incidence of clinical mastitis from 8to 100 DIM; and overall incidence of clinical mastitis.Secondary outcomes of interest were DIM to first mastitiscase. Somatic cell count, milk volume and culling incidencewere also measured and will be used as part of a longerterm assessment of survivability and reported accordingly.Quarterly herd tests were performed (by LIC, Riverlea,Hamilton, New Zealand) to determine milk production(milk solids, fat, protein) and SCC.

2.3. Statistical analysis

Data were recorded on preprinted forms and tran-scribed to electronic media. All farms were visited at leastweekly by a veterinarian during the initial spring period,and in addition to uplifting and verification of data, regularassessment of farm technicians was made. Data was storedin Excel (Microsoft.com) and transferred for statisticalanalysis to SPSS (SPSS.com). Initial analysis was performedusing Chi-square and relative risks on the incidence ofclinical mastitis for each identified period. The farm effectlead to the use of Mantel-Haenszel adjusted odds ratios toallow for the effect of farm. For days to event data, Kaplan-Meier survival analyses were performed on postulated riskfactors. All those where log rank test was significant atp < 0.2 were used in a final Cox Proportional Hazardsanalysis of significant variables.

all heifers included in the study.

Fig. 2. Days relative to calving for first clinical mastitis case by treatment

group.

M. Bryan, K. Taylor / Veterinary Microbiology 134 (2009) 143–149146

3. Results

Heifers with evidence of mastitis at the time of initialexamination (n = 3) were allocated to a separate, immedi-ate treatment group and removed from the analysis.Twelve heifers calved before the start of the study period.The remainder were randomly allocated as described oneach farm on the day of calving to one of either the controlgroup (n = 376) or the treatment group (n = 218). Heiferscalved from 13/7/06 to 19/10/06, with a median calvingdate of 12/08/2006 (Fig. 1).

The overall incidence of clinical mastitis in heifers for all3 farms for the first 100 DIM was 11.6% (Table 1). For eachfarm, the incidence of clinical mastitis during the first 100DIM was lower within the treatment group compared tothe control group, and overall, the incidence of clinicalmastitis was significantly lower in the treatment groupcompared to the control group (Table 1). After adjusting forfarm, treatment had a significant effect on the incidence ofclinical mastitis within 100 DIM (p = 0.03). It reduced theodds of having clinical mastitis by under half (Mantel-Haenszel adjusted OR = 0.52; 95% CI: 0.29–0.94.

In the first 7 DIM, all farms had a lower incidence ofclinical mastitis in the treatment group compared with thecontrol group (Table 1). After adjusting for any farm effect,the incidence of clinical mastitis within the first week aftercalving was significantly lower in the treatment groupthan in the control group (p = 0.04). Treatment reduced theodds of having clinical mastitis by over half (Mantel-Haenszel adjusted OR = 0.46; 95% CI: 0.21–0.98.

The overall incidence of clinical mastitis from 8 to 100DIM was 4.38% (Table 1). There was no treatment effect(Mantel-Haenszel adjusted OR = 0.77, p = 0.55), but therewas a farm effect (p = 0.023).

Survival analysis showed that both Farm and Treatmentfactors were significant using a Log Rank test at theunivariate level (Log Rank [Mantel-Cox] treatment effect:0.013; farm effect: 0.026) (Figs. 2 and 3), and so both were

Table 1

Incidence of mastitis in the three farms in the two intervals after calving.

Farm No. of heifers Clinical mastitis

0–7 DIM 8–100 DIM

# % # %

1

Control 131 16 12.21 5 3.82

Treatment 50 2 4.00 3 6.00

Total 181 18 9.94 8 4.42

2

Control 158 13 8.23 12 7.59

Treatment 106 6 5.66 5 4.72

Total 264 19 7.20 17 6.44

3

Control 87 5 5.75 1 1.15

Treatment 62 1 1.61 0 0.00

Total 149 6 4.03 1 0.67

All

Control 376 34 9.04* 18 4.79

Treatment 218 9 4.13* 8 3.67

Total 594 43 7.24 26 4.38

* p = 0.044.

included in a final Cox model. In the final model, Treatmenthad a significant effect (p = 0.02; b = 1.961, LCI 1.117, UCI3.445) on the median time to clinical mastitis afteradjusting for farm (Fig. 4).

4. Discussion

There is a growing awareness of both the economic andwelfare aspects of heifer mastitis. In New Zealand, wherethe vast majority of heifers are calved outside on pastureover a short period in the spring, S. uberis is the mostcommon isolate (Pankey et al., 1996; Parker et al., 2005), incontrast with Northern Hemisphere data where coagulase-negative staphylococci predominate (Owens et al., 2001;Oliver et al., 2004). The incidence of clinical mastitis inheifers within 7 DIM in New Zealand obviously variessignificantly from farm to farm and season to season.However, for farmers affected by high incidence rates,control and/or prevention becomes critical. It has beensuggested that in many heifers that develop mastitiswithin 7 DIM, infection may have originated as long as 9months prior to calving (Meaney, 1981; Trinidad et al.,

Fig. 3. Days after calving for first clinical mastitis case by farm.

Fig. 4. Final Cox proportional hazards model for day after calving to first

clinical mastitis case.

M. Bryan, K. Taylor / Veterinary Microbiology 134 (2009) 143–149 147

1990; Parker et al., 2007). Consequently, treatment beforecalving or immediately after calving may be expected toremove some subclinical infection before it becomesclinical.

The use of antibiotic therapy prior to calving has beenshown to be effective (Trinidad et al., 1990; Owens et al.,1991, 1993, 2001; Oliver et al., 2003; Sampimon and Sol,2004). There are also some data showing a beneficial effectwith the use of parenteral antibiotic therapy prior tocalving on reducing clinical mastitis immediately aftercalving (Williamson, 2002; Bryan and Friton, 2004; Bryan,2005; McDougall et al., 2005), However, these data onparenteral studies are limited and have not been validatedin larger scale, peer reviewed studies, and all carry the riskof antibiotic residues in both the milk and the calf. Thereare considerable risks associated with widespread par-enteral metaphylaxis prepartum, including residue risks inboth milk and calf meat, and the risk of developingantibiotic resistance. In New Zealand, many calves arecollected at 4 days of age and slaughtered for humanconsumption. Thus, antibiotic therapy of any sort prior tocalving carries a high risk.

Treatment of heifers at 4 weeks pre-calving with anintramammary barrier formulation reduced the incidenceof clinical mastitis by 68% (Parker et al., 2007), and thiswould seem to be the control option of choice for herdswith a high incidence of heifer mastitis. More recently, pre-calving IMI, Friesian breed, low teat height above ground,udder oedema and low post calving serum non-esterifiedfatty acid concentration increased the incidence ofperipartum mastitis in heifers in New Zealand (Comptonet al., 2007). These findings give hope that a non-antibioticapproach to controlling peripartum mastitis may be anoption.

New Zealand dairy farmers have been reluctant toadopt intramammary teat sealant as a control measure,and this may be due to practical considerations. Heifers arefrequently grazed off-farm through the winter outside,with no access to housing, on Brassica spp. They arebrought home immediately prior to calving, and so

opportunities to infuse intramammary teat sealants arepoor. In New Zealand, parenteral treatment of mastitisusing either a tylosin-based or penicillin-based therapy is awidespread and effective practice (McDougall et al.,2007a), and based on previous reports of success farmerswho are experiencing high levels of heifer mastitis duringan intense spring period are turning to parenteral therapyprepartum. This study was an attempt to provide somedata on the efficacy of parenteral therapy immediatelypostpartum, to avoid the high risk of antibiotic residues inthe calf caused by prepartum parenteral therapy. Post-partum therapy also poses potentially less risk with regardto antibiotic contamination of milk supply, because there isless likely to be error in recording of treated heifers if theyhave already calved and are on the milking platform.

This study demonstrated that parenteral treatmentwith a single large dose of intramuscular penicillin within12 h after calving was successful in significantly reducingthe incidence of clinical mastitis in heifers. There was astrong farm effect, but after adjusting for farm thetreatment effect was still significant. In this study, clinicalmastitis was diagnosed by trained farm technicians. Thisapproach was chosen to replicate more typical farmconditions, but no bacteriology was undertaken todetermine either the incidence of clinically positive butculture-negative cases; or the pathogenic population ofdefined cases. The outcome measure was clinical mastitisthat would normally be treated by the farmer. The initialallocation was performed using a pre-ordered, randomisedprocess as described, heifers were treated once only andthen all treated and control heifers were managed as asingle mob in exactly the same way. Milk from bothtreatment and control heifers was kept out of the bulk milkfor 12 milkings (144 h) following calving, and neithergroup was identified in any way following the initialtreatment allocation. Nevertheless, there is a risk ofreporting bias and misclassification bias in the recordingby the technician of cases of clinical mastitis. If either wereoccurring however, there is no reason to believe thatmisclassification or false reporting should be more likely tobe associated with one group over another, as thetechnician was essentially blinded to grouping followinginitial allocation and treatment. No data were collected onthe severity of the clinical mastitis, the pathogens involved,or the success or otherwise of lactational treatment.

All current control options carry risks associated withthem. The process of restraining heifers for appropriateintramammary insertion is challenging, with a risk to bothanimal and operator. There is a risk of introducinginfection, especially where large numbers of heifers maybe involved. The act of grouping heifers together in lessthen ideal conditions during winter may in itself be acontributing factor to the development of mastitis.Furthermore, there is a risk of damage to the integrity ofthe teat via sphincter damage or other physical lesions.

Whilst parenteral treatment has the benefit of beingless invasive and of posing less risk to the integrity of theteat canal, to the animal in general, and to the operator, italso carries with it the potential risk of advancing thedevelopment of antimicrobial resistance. The doses ofpenicillin are massive compared with intramammary

M. Bryan, K. Taylor / Veterinary Microbiology 134 (2009) 143–149148

therapy. Furthermore, whilst the risk of calf residue isremoved by treatment postpartum, and the risk ofantibiotic residue in the milk is lessened compared toprepartum parenteral treatment, the risk of antibioticcontamination of the milk is still present, particularlywhen the treatment group makes up a large percentage ofthe herd.

5. Conclusion

Treatment of heifers with a single treatment (split intotwo equal doses) of 15 million iu of micronised procainepenicillin by intramuscular injections at the first milkingafter calving significantly reduced the incidence of mastitiswithin the first 7 DIM. The odds of a treated heiferdeveloping clinical mastitis during the first 7 DIM were lessthan half (adjusted OR 0.456; p = 0.044) of control heifers,after adjusting for Farm. Treatment had no significanteffect beyond 7 DIM. Treatment significantly increased themedian DIM to the development of the first case of mastitis(p = 0.019) after adjusting for the effect of Farm.

Mastitis and udder health are among the leading causesof disease in dairy cows and heifers in both Australasia(Stevenson, 2000), and worldwide (Kaneene and Hurd,1990; Frei et al., 1997), and accordingly, losses from cullingcan be significant. Significantly reducing the incidence ofmastitis and increasing the days to first case of mastitis inheifers could be postulated to have a positive effect on boththe welfare and the long term survivability of heifers, aswell as contributing to improved economic return.Parenteral antibiotic treatment of heifers immediatelypost calving may be an option to help manage highincidences of heifer mastitis. However, other controlmeasures should also be considered such as prepartumintramammary barrier therapy, and attention to recentlyidentified risk factors.

Acknowledgements

This study was performed by VetSouth Ltd. and fundedby Stockguard Animal Health Ltd., New Zealand. Thanks goto the farmers who cooperated in this study, and tocolleagues at VetSouth, Winton.

Conflict of interest

None of the authors (M.A. Bryan, K. Taylor) has afinancial or personal relationship with other people ororganizations that could inappropriately influence or biasthe paper entitled ‘‘Periparturient use of parenteralmicronised procaine penicillin to reduce the risk of clinicalmastitis in heifers after calving’’. However, the study wasfunded by Stockguard Animal Health Ltd., who market anddistribute the micronised procaine penicillin used in thetrial under the trade name Masticillin, manufactured byStockguard Laboratories Ltd.

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