Introduction
It has been well established that intramammary infections (IMI) in dairy cows are caused by bacterial pathogens that gain access to the interior of the udder by way of the teat canal. However, other than via bacteria-laden impacts against the teat end during the milking process due to liner slips, improper vacuum, and faulty pulsation, we have yet to discover just how bacteria enter the teat end orifice, traverse the teat canal, and enter the teat cistern. We as scientists have speculated that between milkings, bacteria pass through the teat canal by multiplying within the keratin lining, through physical movement resulting from pressure placed on the teat end as the cow moves about, or inadvertently when antibiotics are infused into the teat end by insertion of the syringe cannula. However, the exact mechanisms have yet to be scientifically demonstrated.
Whatever these mechanisms may be, it has been well established that new IMI are a function of bacterial numbers present at the teat end, and that the practices of pre- and postmilking teat antisepsis reduce these bacterial populations and significantly reduce the chances of them entering through the teat canal and establishing IMI. Predipping both reduces the chances of environmental bacteria on the teat skin, such as Streptococcus uberis and Escherichia coli, from entering the bulk tank, and minimizes the exposure of teat ends to these pathogens during milking.
Postdipping effectively destroys bacteria prior to teat skin colonization or penetration of the teat canal, and reduces the incidence of new IMI caused by contagious bacteria, such as Staphylococcus aureus and Streptococcus agalactiae, which are transferred among cows during the milking process. Although postmilking teat dipping has been shown to markedly reduce teat end bacterial populations of staphylococci and streptococci during the intermilking period, especially on pastured cows compared with those confined to housing, the practice, in general, does not influence the incidence of new IMI caused by environmental pathogens.
The germicidal components of teat dips effectively and rapidly destroy microorganisms by chemical or biological action. Germicides include iodophors, chlorhexidines, linear dodecyl benzene sulfonic acid (LDBSA), sodium hypochlorite, sodium chlorite/lactic or mandelic acid, hypochlorous acid, quaternary ammonium, and antimicrobial proteins and fatty acids. Some of these germicides may have deleterious effects on teat skin and cause chapping (12). Irritation may be due to the low pH or high titratable acidity or alkalinity of a formulation. In addition, the incorrect use of concentrated udder washes or pipeline cleaners as teat dips can result in severe teat lesions, as can improper mixing, freezing, and production accidents in the formulation of teat dips (3). Because of the potential for causing irritation, skin conditioning agents are often added to teat dip formulations to serve as humectants, like glycerine, to draw water onto the teat skin surface, or as emollients, like lanolin, which serve to coat the teat skin and prevent evaporative water loss. However, the germicidal activity may be reduced if concentrations of conditioners are incorporated at levels above 10 to 12%.
Influence of Weather on Teat Chapping, Bacterial Colonization, and Germicidal Activity
The teat skin surface is coated with bacteriostatic acids that are derived from the dermal layer, which retard the growth of bacterial pathogens. When exposed to cold, wet, and windy conditions, the teat skin may become chapped and irritated, and the protective surface coating may be removed, allowing colonization of bacteria such as S. aureus. The germicidal component of a teat dip can also be irritating to the teat end, and the interaction of the germicide effect plus the effects of inclement weather promote chapping (7).
Iodophor and chlorhexidine germicides containing glycerine help to reduce colonization of the teat skin with S. aureus (6). It would seem that such conditioners would help to reduce chapping during cold and windy weather, but not dipping teats may be preferable to dipping them and letting the germicide remain on teats under such weather conditions. However, if teats ends are blotted dry after 15 to 20 seconds of exposure to a teat dip, good skin condition is maintained and bacterial colonization is reduced.
The use of salves (i.e., containing 1% chlorhexidine) instead of dips to prevent chapping is not advantageous and actually increases S. aureus colonization. It was suggested that the germicide component of the salve could not come in contact with the entire teat skin surface because of its hydrophobic properties (5). For example, when water-based teat dips are used, the germicidal component comes in contact with the entire skin surface and penetrates all cracks and crevices. The water eventually evaporates and leaves behind the germicide, which may be rehydrated and activated by moisture from the skin. However, the salve probably does not contact the cracks and crevices as well as water-based products do because of its semi-solid nature. In addition, the salve will not completely dissolve or evaporate due to its consistency, and will not leave concentrated germicide behind on teat skin; some of the germicidal component remains inactive while incorporated in the salve.
Chemical Interactions May Lead to Teat End Irritation
Some germicides can have irritating effects on teat skin, resulting in increased colonization of pathogens normally associated with teat skin such as the staphylococci, and the higher the concentration, the greater the potential for irritation. In one study, use of a 1% iodophor postdip product was associated with poorer teat end condition than was a 0.1% iodophor postdip (2).
The interaction of different chemicals incorporated into predips and postdips may cause teat irritation, especially if much of the predip residue remains on teats after machine removal prior to postdipping. A survey performed in the Pacific Northwest suggested that combinations with different germicides in the pre- and postdips were more likely to be associated with chapping compared with using the same germicide in the pre- and postdip (1). Also, the predip and postdip combinations that contained no teat skin conditioner were more likely to be associated with teat chapping than combinations that did contain conditioning agents in the pre- and postdips. A follow-up study based on a systematic scoring of teat skin and teat end condition showed no effects of various pre- and postdip combinations on skin condition. However, the type of postdip used had a marked effect on visual teat scores and on measurements of transepidermal water loss. One barrier type product exhibited a greater barrier to water loss, which was associated with poorer skin condition, and greater teat end irritation compared with the other conventional and barrier products tested.
The stronger and more persistent adherence of barrier dips to the teat skin compared with conventional products may influence the degree of irritation. In one study, barrier products were generally associated with poorer teat end condition scores compared with nonbarrier postmilking teat dip products (2). It was theorized that such irritation could be due to the mechanical damage resulting from removing the residual barrier film prior to milking, and to the occlusion of the skin surface, which increases the permeability of the stratum corneum, thereby promoting penetration and amplifying the effects of any irritant.
Potential Influence of Barrier Components on Teat End Colonization
The interaction of certain barrier products with the teat skin surface has the potential to promote bacterial growth. During the testing of an acrylic latex dip without germicide, concern was expressed that bacteria remaining on the teat end after milking and trapped under the latex product may proliferate under the barrier film (4). However, an investigation to determine the degree of bacterial growth under the film showed that fewer S. aureus were recovered from dipped teats vs. control teats; thus, the barrier product did not promote multiplication of these microorganisms. Likewise, following challenge with E. coli after application of an acrylic latex product without germicide, slightly fewer organisms were recovered from quarters of dipped vs. undipped control teats (9). This acrylic latex product was shown to be effective in reducing new coliform IMI (4), but in a subsequent study (14), the product was no more effective than a nonbarrier iodophor dip, and concern was expressed about possible skin irritation due to use of this barrier product.
Experimental challenge and natural exposure studies have shown that some experimental and commercial barrier teat dip formulations are either ineffective in reducing new IMI or actually increase the development of new IMI (10). Two experimental challenge studies showed that new S. aureus and new S. agalactiae IMI were increased in quarters dipped in experimental formulations of antimicrobial-based and chlorhexidine products compared with undipped controls; the percentage increase was greater for S. aureus than for S. agalactiae.
It is possible that germicide concentrations are insufficient in some barrier products to provide the level of microbicidal activity at the teat end to reduce mastitis-causing bacterial populations and decrease the chances for the development of new IMI. In one 6-mo natural exposure trial, a 0.3% iodine barrier was less effective in reducing new IMI by all bacterial species compared with a conventional 1% iodophor product; the numbers of new S. aureus IMI in this trial were 9 and 5, respectively. In another study, after dipping with a 0.3% iodine barrier product in a natural exposure trial for 6 mo, number of new IMI across all pathogens in dipped quarters was not different from undipped controls. This product was reformulated to increase the iodine concentration from 0.3% to 0.5%, and after dipping in the reformulated product, new IMI were significantly reduced 43.2%; coagulase-negative staphylococci were reduced 39.7%, Streptococcus sp. were reduced 61.3%, and coliforms were reduced 30.4%. The interaction of the 0.3% iodine barrier product and the teat end evidently did not provide a sufficient level of germicide to effectively eliminate bacteria that were exposed to teats after milking. Thus, increasing the germicide concentration in this barrier product increased its efficacy, possibly by providing sufficient microbicidal activity.
Oil-based products are no longer used, but were shown to enhance new IMI, possibly by providing a barrier or protective film at the teat end. In two natural exposure studies, use of a 0.5% iodine-based postdip increased the rate of new S. aureus IMI over undipped controls as well as a 0.5% water-based iodophor. In an experimental challenge study, the same 0.5% oil-based dip also increased new S. aureus IMI compared with undipped controls (12). It was suggested that the oil film remaining on the teat skin surface afforded physical protection for bacteria, thereby increasing the bacterial load on the teat end and increasing the chances for new IMI. Similarly, Schultz et al. (13) found that use of a similar iodine-in-oil product increased the number of new S. aureus IMI, and suggested that the oil carrier created a favorable environment for bacterial multiplication. The testing of a 1% oil-based iodine dip under natural and experimental challenge conditions showed no difference in rate of new S. aureus IMI between dipped and undipped controls (12). The higher concentration of germicide in the latter study may have overcome the deleterious effect of the oil.
Barrier products were developed to reduce exposure of teat ends to environmental bacteria between milkings. Thus, the use of the experimental exposure procedure to evaluate the efficacies of certain barrier products may have limitations when using contagious pathogens as challenge organisms. During exposure to S. aureus and S. agalactiae, teats are immersed immediately after milking with solution containing approximately 50 million colony-forming units (cfu)/ml of each microorganism followed immediately by dipping of half of the teats in the barrier product (8). Due to the interaction of the teat dip germicide, barrier components, milk, teat skin, and the massive bacterial load, it is possible that the antimicrobial activities of the products were compromised and unable to kill enough bacteria left on the teat end after challenge to prevent new IMI. Likewise, the products may have formed a protective film that promoted the growth of challenge organisms at the teat end, thereby increasing the opportunity for invasion into the teat canal and inducing new IMI when certain products are used. Protocols are now being developed to evaluate barrier products under natural exposure conditions.
Bacterial populations on teat skin increase markedly shortly after drying off and remain elevated through calving. This increase is thought to be due to the cessation of udder hygiene practices, such as washing or predipping, drying with paper towels, and postdipping, all of which would allow bacterial populations to grow unchecked during this time. Bacterial numbers are also found to increase markedly on the day of calving, which is attributed to greater exposure of teat ends in cows confined to maternity areas as well as to leakage of mammary secretion that may favor bacterial growth.
Several experimental barrier teat dip products and one commercially available product have been applied at drying off and again prepartum to protect against the development of new IMI that occur during the early dry and prepartum periods. One such product was found to persist on teat ends for greater than 3 days and exhibited an overall 37% reduction in new IMI at calving for cows and heifers, but had no effect on Gram-negative infections. In addition, this dip had no observable deleterious effect on teat skin or teat end tissue (15); however, a systematic evaluation of teat skin and teat end parameters was not performed in this evaluation. The long-term influence of persistent barrier films on teat end condition remains to be resolved. i
Teat Germicide Type, Viscosity, and Influence on Teat Canal Infections
The type of teat germicide may alter the distribution of mastitis-causing bacteria on cows' teats, especially the staphylococci. As cited in (16), three herd studies showed an increase in staphylococcal IMI when teats were postdipped in LDBSA compared with an iodophor product. In one investigation, the incidences of S. aureus and Staphylococcus epidermidis IMI were higher in herds using LDBSA than in those using iodine. Similarly, changing from the use of an iodophor as a postdip for 15 years to LDBSA led to an increase in overall IMI, with increases in S. aureus, Staphylococcus hyicus, and S. epidermidis. In a third study, the prevalence of S. aureus was found to be highest in a herd using LDBSA for 4 years compared with herds using iodophor dips.
In an effort to determine how the LDBSA and iodophor dips may affect bacterial populations at the teat end and subsequent development of IMI, Watts et al. (16) designed a study to measure the influence of the two dips used above on incidence of teat canal infections and IMI over a 1-year period. Across bacterial species, total teat canal infections increased 28.9% in the LDBSA group and 14.3% in the iodophor group; new IMI rates were +30% and -17.4%, respectively. No differences in S. aureus IMI were observed across dips. However, teat canal infections caused by the human-associated staphylococci (S. epidermidis and Staphylococcus xylosus) persisted with greater frequency in the LDBSA-dipped quarters, and persistence of animal-associated staphylococcal (S. hyicus for example) teat canal infections was higher in the iodophor-dipped quarters. Thus, the use of the LDBSA product was not as effective as the iodophor product in preventing teat canal infections or in preventing the progression of teat canal infections to IMI. Whether this was due to germicide activity differences or a consequence of other formulation differences, such as viscosity or type of conditioner, remains unresolved.
An effective teat dip should eliminate existing teat canal infections and prevent new ones from developing. But such infections may persist despite regular teat dipping, and this suggests that germicide is not reaching the bacteria growing in the teat canal. The viscosity of barrier product may prevent the germicide from contacting bacteria colonizing the crevasses on the teat skin as well as the teat canal. Less viscous products may have a better chance of capillary movement into these areas. This contention is supported by a trial in which two products were evaluated for their ability to prevent new teat canal infections (11). A less viscous iodophor product was provided as a concentrate, which upon dilution (1:42) with distilled water, contained 0.18% iodine. A more viscous fatty acid/lactic acid product was also provided as a concentrate, which upon dilution (1:3) with distilled water, contained 0.25% Lauricidin7, 1.25% caprylic and capric acids, and 1.5% lactic acid. The less viscous product was 90% effective in preventing new S. aureus teat canal infections, but the more viscous dip had no effect. Thus, the less viscous product performed in a superior manner, possibly by more easily penetrating the teat canal and contacting colonized bacteria. However, two different germicides were used in this comparison, and valid conclusions cannot be drawn.
Conclusions
It is noteworthy that S. aureus is a common denominator in many of the teat end interactions with the germicides described above. For example, inclement weather is conducive to chapping, which may be exacerbated by some germicidal components, promoting colonization with S. aureus. Likewise, the use of oil-based teat dip products led to increased S. aureus IMI, possibly by creating a favorable environment for bacterial multiplication. Also, S. aureus IMI were found to increase in some experimental challenge and natural exposure studies using barrier products, which may have trapped these bacteria under a protective film, allowing multiplication. A less viscous dip was more effective in preventing S. aureus teat canal infections than a more viscous product. In addition, use of a LDBSA teat dip was associated with increased rates of S. aureus IMI. Thus, this mastitis-causing microorganism maintains a delicate position on the teat skin, at the teat end meatus, and in the teat canal, and its ability to colonize these areas and progress to true IMI may be promoted or repressed by different germicide formulations as well as the conditions under which they are used.
References
1. Burmeister, J. E., L. K. Fox, D. D. Hancock, C. C. Gay J. M. Gay S. M. Parish, and J. W. Tyler. 1995. Survey of dairy managers in the Pacific Northwest identifying factors associated with teat chapping. J Dairy Sci. 78:2073.
2. Burmeister, J. E. , L. K. Fox, J. K. Hillers, and D. D. Hancock. 1998. Effects of before milking and after milking teat disinfectants (pre/post dips) on teat skin condition. J. Dairy Sci. 81:In press.
3. Farnsworth, R. J. 1996. Observations on teat lesions. Page 93 in Proc. 35th Annu. Meet. Natl. Mastitis Counc., Natl. Mastitis Council, Inc. Madison, WI.
4. Farnsworth, R. J., D. K. Sorenson, and D. W. Johnson. 1981. Page 28 in The effect of a teat sealer on coliform mastitis. The Bovine Pract. November, No. 16.
5. Fox, L. K. 1994. Dip and blot dry during cold, windy weather. Page 56 in Hoard's Dairyman. Vol. 139.
6. Fox, L. K. 1995. Colonization of Staphylococcus aureus on chapped teat skin. Page 51 in Proc. II, 3rd International Mastitis Seminar. Tel Aviv, Israel.
7. Fox, L. K., and R. J. Norell. 1994. Staphylococcus aureus colonization of teat skin as affected by postmilking teat treatment when exposed to cold and windy conditions. J. Dairy Sci. 77:2281.
8. 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 postmilking teat dips. J. Dairy Sci. 73: 2580
9. McArthur, B. J., T. P. Fairchild, and J. M. Moore. 1984. Efficacy of a latex teat sealer. J. Dairy Sci. 67:1331.
10. Nickerson, S. C., and R. L. Boddie. 1995. Efficacy of barrier-type postmilking teat germicides against intramammary infection. J. Dairy Sci. 78:2496.
11. Nickerson, S. C., J. L. Watts, R. L. Boddie, and C. H. Ray. 1990. Effect of postmilking teat dipping on teat canal infections in lactating dairy cows. J. Dairy Sci. 73:373.
12. Pankey, J. W., R. J. Eberhart, A. L. Cuming, R. D. Dagget, R. J. Farnsworth,and C. K. McDuff. 1984. Update on postmilking teat antisepsis. J. Dairy Sci. 67:1336.
13. Schultz, W. D., H. H. Dowlen, E. D. Moore, E. Casman, and J. R. Owens. 1975. Efficacy of a commercial iodine-in-oil teat dip. J. Milk Food Technol. 38:132.
14. Serieys, F., C. Lerondelle, and B. Poutrel. 1983. Utilization du Teat Shield 3M pour la prevention par trempage de nouvelles infections mammaires pendant la lactation. Bull. Soc. Vet. Prat. Fr. 67:225.
15. Timms, L. L., A. Steffens, S. Piggott, and L. Allen, 1997. Evaluation of a novel persistent barrier teat dip for prevention mastitis during the dry period. Page 206 in Proc. 36th Annu. Meet. Natl. Mastitis Counc., Natl. Mastitis Counc., Inc., Madison, WI.
16. Watts, J. L., S. C. Nickerson, R. L. Boddie, and C. H. Ray. 1991. Effects of a 1.94% sulfonic acid teat dip and a 1% iodophor teat dip on teat canal infections in lactating cows. J. Dairy Sci. 74:1115.