Ohio State University Research/Extension Bulletin

Animal Sciences Research and Reviews

Special Circular 156


Efficacy of a Barrier Teat Dip Containing 0.55% Chlorhexidine for Prevention of Bovine Mastitis

J.S. Hogan, K.L. Smith, D.A. Todhunter, and P.S. Schoenberger
Department of Animal Sciences

Summary

A natural exposure trial was conducted for 12 months in a commercial herd of 125 lactating cows to compare the efficacy of an experimental barrier teat dip containing 0.55% chlorhexidine gluconate with the efficacy of a 1% iodophor for preventing new intramammary infections (IMI) and clinical mastitis. Teats of half of the cows were dipped in the experimental barrier product, and teats of the remaining half of the herd were dipped in the 1% iodophor product. Quarters dipped with the experimental barrier product had fewer new IMI caused by Escherichia coli, coagulase-negative staphylococci, and Gram-positive bacilli than did quarters dipped in the 1% iodophor. A greater incidence of new IMI caused by Serratia spp. and Pseudomonas spp. occurred in quarters dipped in the experimental barrier product compared with quarters dipped in the 1% iodophor. Efficacy of the two teat dips against new IMI caused by Staphylococcus aureus, environmental streptococci, and Klebsiella spp. did not differ. Incidence of bacteriologically negative clinical cases was greater in quarters dipped in the 1% iodophor than in quarters dipped in the experimental barrier product. Incidence of clinical mastitis cases caused by Staph. aureus, environmental streptococci, E. coli, Klebsiella spp., Serratia spp., and Pseudomonas spp. did not differ between treatment groups.

Introduction

Postmilking application of germicidal teat dip is an effective and widely practiced means to reduce the incidence of new IMI. The use of germicidal teat dips postmilking effectively reduces the incidence of new IMI caused by the contagious mastitis pathogens Staphylococcus aureus, Streptococcus agalactiae, and Corynebacterium bovis (Pankey et al., 1984). These bacteria are primarily transferred among cows at milking. In contrast, the use of a germicidal teat dip postmilking has a limited effect on the incidence of new IMI caused by environmental streptococci and coliform bacteria (Eberhart et al., 1983). The primary sources of environmental streptococci and coliforms include bedding, manure, soil, and feedstuffs. Therefore, exposure to environmental pathogens is continuous throughout both the milking and intermilking periods. Although most germicidal products kill coliforms and environmental streptococci on teat skin (Godinho and Bramley, 1980), exposure to these pathogens occurs primarily between milkings, long after the bactericidal activity of the dips has diminished.

A latex barrier teat dip that formed a physical seal between the teat and the environment was reported to reduce the incidence of new coliform IMI during lactation (Farnsworth et al., 1980). The efficacy of this barrier product was reported to be due to the persistency of the dip on teats between milkings. However, others have reported that barrier teat dips did not cause a significant reduction in coliform IMI and were ineffective in preventing IMI caused by contagious pathogens (McArthur et al., 1984; Seryies et al., 1983). Subsequently, barrier teat dips containing germicidal agents were reported to be ineffective in preventing IMI during the dry period (Matthews et al., 1988) and in lactating cows challenged by immersing teats in cultures of contagious pathogens (Nickerson and Boddie, 1995). The purpose of the present study was to compare the efficacy of an experimental barrier teat dip containing 0.55% chlorhexidine gluconate with the efficacy of a 1% iodophor teat dip in a commercial herd under natural exposure conditions.

Materials and Methods

Experimental Cows. Experimental cows were in a commercial herd of approximately 125 lactating Holsteins. The DHIA rolling herd averages for the month the trial began were 19,200 pounds of milk, 660 pounds of fat, and 598 X 103 SCC/ml. Cows were milked at 12-hour intervals in a double-nine herringbone parlor equipped with automatic takeoffs. The milking system was serviced prior to the trial and bimonthly during the experiment. Management procedures were consistent between experimental groups and included housing, nutrition, and milking management. Premilking sanitation included predipping all teats in a 0.25% iodophor solution (Quarter-Bac®, IBA, Inc., Millbury, MA) and drying all teats with single-service paper towels.

Experimental Design. Teats of half of the cows were dipped postmilking in the experimental barrier product containing 0.55% chlorhexidine gluconate (Ultra-Shield®, IBA, Inc.), and teats of the remaining half of the herd were dipped in a 1% iodophor (FS-103®, IBA, Inc.). Cows were balanced between treatment groups by parity, stage of lactation, and bacteriological status at the beginning of the trial. Cows were assigned alternately to treatment and control groups following calving. Cows within treatment groups were identified by colored leg bands. The trial was conducted from February 1994 through January 1995.

Sample Schedule. Duplicate samples of quarter foremilk were collected from all cows prior to the trial. When bacteriological results of duplicate samples did not agree, a third sample was obtained 14 days later. All quarters were eligible for the trial except those with teats that were obviously deformed from previous injury. Quarters with teats that were injured during the trial were excluded for the remainder of that lactation; such quarters re-entered the trial after a dry period if healing was complete.

Single quarter milk samples were collected monthly during the trial. A second quarter milk sample was collected within 7 days from all quarters in which the bacteriological status of the gland had changed. Duplicate milk samples were collected from all lactating quarters of cows within 7 days after calving, from quarters with clinical mastitis prior to treatment, and within 7 days prior to drying off or leaving the herd. Samples taken from quarters with clinical mastitis were collected by the herd owners and were stored frozen for no longer than 7 days. All other milk samples were collected by laboratory personnel and stored on ice until primary bacteriological culturing was initiated within 14 hours.

Diagnosing IMI and Clinical Mastitis. Methods for confirmatory identification of bacterial isolates were as outlined by Todhunter et al. (1991). A quarter was determined to be free of infection when it entered the trial if the quarter was bacteriologically negative for two of the three initial samples. An IMI was diagnosed when the same bacterial species was isolated from two consecutive samples taken during the trial. Clinical mastitis and IMI diagnosed during the first 7 days of lactation were not included in data analyses of teat dip efficacy. An episode of clinical mastitis was defined as described by Hogan et al. (1989). The status of a clinical quarter was recorded as a bacteriologically negative when bacteriological results were negative for both samples or when the results of duplicate samples from a clinical quarter did not match.

Statistical Analyses. Differences between the efficacy of the teat dips were tested within pathogen groups as described by Hogan et al. (1990).

Results and Discussion

Incidence of total IMI did not differ between cows dipped with the experimental barrier product and cows dipped with the 1% iodophor (Table 1). The predominant bacterial group isolated from IMI was Gram-negative bacilli.

Table 1. New IMI in quarters dipped with an experimental barrier containing 0.55% chlorhexidine or a 1% iodophor dip.
Bacteriological

status

Iodophor
(n1=2888)
Barrier
(n=2772)
P <
Staphylococcus aureus 7 3 NS2
CNS3 32 13 0.01
Streptococci 15 9 NS
Total Gram-negatives 55 63 NS
Escherichia coli 19 9 0.08
Klebsiella spp. 12 11 NS
Serratia spp. 12 23 0.05
Pseudomonas spp. 8 16 0.07
Unidentified 4 4 NS
Gram-positive bacilli 9 2 0.05
Yeast 2 0 NS
Total 120 90 NS
1 Total number of quarters tested at monthly samplings.

2 Not significant (P > 0.1).

3 Coagulase-negative staphylococci.

Efficacy of the two products differed within genera of Gram-negative bacilli. The use of the barrier teat dip reduced (P < 0.08) incidence of Escherichia coli IMI by 50.6% compared with the use of the 1% iodophor. These data support the findings of Farnsworth et al. (1980) that a barrier teat dip was efficacious against coliform IMI. In contrast, cows dipped with the barrier in the current trial had a 52.1% increase (P < 0.07) in Pseudomonas spp. IMI and a 49.9% increase (P < 0.05) in Serratia spp. IMI compared with incidence for cows dipped with the 1% iodophor. Both Serratia spp. and Pseudomonas spp. have been reported to contaminate chlorhexidine gluconate solutions (Russell et al., 1986). However, both teat dip products tested in the current study were bacteriologically negative when samples were taken from the shipping containers and from the reservoirs of teat dip cups during milking (data not shown). In addition, rates of IMI by these bacteria within both treatment groups were elevated relative to results from previous surveys (Nickerson and Boddie, 1995) and were influenced by season of the year. Between 70 and 75% of Serratia spp. IMI in iodophor-dipped and barrier-dipped cows occurred during March, April, May, June, and July. A total of 87.5% of Pseudomonas spp. IMI were first diagnosed during July, August, September, and October in both treatment groups. These data suggest that exposure to these pathogens may have been similar between treatment groups relative to housing and climatic changes. Housing conditions, such as ventilation, manure management, and free-stall maintenance, were generally poor throughout the trial and may have contributed to the high incidence of IMI in both treatment groups. The reasons for increased rates of Serratia spp. and Pseudomonas spp. IMI in barrier-dipped quarters compared with 1% iodophor-dipped quarters are unknown but appeared to be independent of contaminated product.

The pathogen group isolated second most frequently from new IMI was coagulase-negative staphylococci. The use of the experimental barrier product reduced (P < 0.01) incidence of IMI caused by coagulase-negative staphylococci by 57.7%. These results agreed with a previous report (Nickerson et al., 1995) that cows with teats dipped with a barrier teat dip containing germicide had a lower incidence of coagulase-negative staphylococcal IMI during lactation than cows with teats dipped with a 1% iodophor solution (Nickerson et al., 1995). In addition, IMI caused by Gram-positive bacilli were reduced (P < 0.05) by 76.8% for teats dipped with the experimental barrier compared with cows with teats treated with the 1% iodophor.

Rate of environmental streptococcal IMI did not differ between cows with teats dipped with the experimental barrier product and cows with teats dipped with the 1% iodophor. Environmental streptococci primarily contaminate teats between milkings. Nevertheless, in a previous trial (Oliver et al., 1990), the use of chlorhexidine solutions as postmilking teat dips reduced the incidence of new IMI caused by environmental streptococci during lactation. Godinho and Bramley (1980) reported that dipping of teats with a chlorhexidine product reduced IMI during the early dry period in an experimental challenge trial. Those scientists (Godinho and Bramley, 1980; Oliver et al., 1990) hypothesized that the bacteriocidal activity of chlorhexidine on teat skin may be greater than that of other common germicides. However, in the current trial, the efficacy of the barrier product containing 0.55% chlorhexidine was comparable with that of the 1% iodophor.

Nickerson and Boddie (1995) reported from experimental challenge trials that the rate of Staph. aureus IMI in quarters dipped in barrier products was greater than in undipped quarters. Nickerson and Boddie (1995) suggested that the elevated rate of Staph. aureus IMI may have been caused by improper experimental design, excessive challenge, or improper timing of teat end exposure. Therefore, a primary concern in the current study was to determine the efficacy of the barrier product against Staph. aureus IMI compared with a 1% iodophor under natural exposure conditions in a herd with a high prevalence of Staph. aureus IMI. At the beginning of the trial, prevalence of Staph. aureus IMI occurred in > 20% of cows in both treatment groups, and rates of IMI caused by Staph. aureus did not differ between treatments. The results of the current natural exposure field trial did not support those of experimental challenge trials in which incidence of IMI caused by Staph. aureus increased in quarters dipped with barrier products (Nickerson and Boddie et al., 1995).

Rate of total clinical cases did not differ between treatment groups (Table 2). Incidence of bacteriologically negative clinical cases was greater in quarters dipped in the 1% iodophor than in quarters dipped in the experimental product. Incidence of clinical mastitis cases caused by Staph. aureus, environmental streptococci, E. coli, Klebsiella spp., Serratia spp., and Pseudomonas spp. did not differ between treatment groups.

Conclusions

The primary purpose of using a barrier plus germicide teat dip is to reduce IMI caused by both environmental and contagious pathogens. Results of the current study indicated that selective protection against environmental pathogens was afforded by the experimental barrier dip. Escherichia coli IMI were reduced, Serratia spp. and Pseudomonas spp. IMI were increased, and environmental streptococcal IMI were unchanged by using the experimental barrier compared with results using the 1% iodophor dip. Rates of IMI caused by Staph. aureus did not differ between treatments. The total efficacy of the barrier containing 0.55% chlorhexidine was comparable with that of the 1% iodophor.

Table 2. Clinical mastitis in quarters dipped with an experimental barrier containing 0.55% chlorhexidine or a 1% iodophor dip.
Bacteriological status Iodophor
(n1=2888)
Barrier
(n=2772)
P <
Staphylococcus aureus 6 6 NS2
CNS3 3 6 NS
Streptococci 1 7 NS
Total Gram-negatives 32 28 NS
Escherichia coli 18 14 NS
Klebsiella spp. 8 2 NS
Serratia spp. 4 6 NS
Pseudomonas spp. 2 6 NS
Other microbes 0 1 NS
Bacteriologically

negative

36 16 0.001
Total 79 64 NS
1 Total number of quarters tested at monthly samplings.

2 Not significant (P > 0.1).

3 Coagulase-negative staphylococci.

References

Eberhart, R.J., P.L. LeVan, L.C. Griel, and E.M. Kesler. 1983. Germicidal teat dip in a herd with low prevalence of Streptococcus agalactiae and Staphylococcus aureus mastitis. J. Dairy Sci. 66:1390.

Farnsworth, R.J., L. Wyman, and R. Hawkinson. 1980. Use of a teat sealer for prevention of intramammary infections in lactating cows. J. Am. Vet. Med. Assoc. 177:441.

Godinho, K.S., and A.J. Bramley. 1980. The efficacy of teat dips of differing persistence on teat skin in preventing intramammary infection by Streptococcus uberis and Escherichia coli in dry cows. Br. Vet. J. 136:574.

Hogan, J.S., D.M. Galton, R.J. Harmon, S.C. Nickerson, S.P. Oliver, and J.W. Pankey. 1990. Protocols for evaluating efficacy of post-milking teat dips. J. Dairy Sci. 73:2580.

Hogan, J.S., K.L. Smith, K.H. Hoblet, P.S. Schoenberger, D.A. Todhunter, W.D. Hueston, D.E. Pritchard, G.L. Bowman, L.E. Heider, B.L. Brockett, and H.R. Conrad. 1989. Field survey of mastitis in low somatic cell count herds. J. Dairy Sci. 72:1547.

Matthews, K.R., R.J. Harmon, B.E. Langlois, W.L. Crist, and R.W. Hemken. 1988. Use of a latex teat dip with germicide during the periparturient period. J. Dairy Sci. 71:1940.

McArthur, B.J., T.P. Fairchlid, and J.J. Moore. 1984. Efficacy of a latex teat sealer. J. Dairy Sci. 67:1331.

Nickerson, S.C., and R.L. Boddie. 1995. Efficacy studies on barrier teat dips. Page 38 in Proc. 34th Annu. Mtg. Natl. Mastitis Counc., Natl. Mastitis Counc., Inc., Arlington, VA.

Oliver, S.P., S.H. King, M.J. Lewis, P.M. Torre, K.R. Matthews, and H.H. Dowlen. 1990. Efficacy of chlorhexidine as a postmilking teat disinfectant for prevention of bovine mastitis during lactation. J. Dairy Sci. 72:2230.

Pankey, J.W., R.J. Eberhart, A.L. Cumming, R.D. Daggett, R.J. Farnsworth, and C.K. McDuff. 1984. Update on postmilking teat antisepsis. J. Dairy Sci. 67:1336.

Russell, A.D., S.A. Hammond, and J.R. Morgan. 1986. Bacterial resistance to antiseptics and disinfectants. J. Hosp. Infect. 7:213.

Seryies, F., C. Lerondelle, and B. Poutrel. 1983. Utilisation du Teat Shield 3M pour la prevention par trempage de nouvelles infections mammaires pendant la lactation. Bull. Soc. Vet. Prat. Fr. 67:225.

Todhunter, D.A., K.L. Smith, and J.S. Hogan. 1991. Serratia species isolated from bovine intramammary infections. J. Dairy Sci. 74:1860.


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