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MAMMARY RESISTANCE MECHANISMS | Anatomical
MAMMARY RESISTANCE MECHANISMS Contents Anatomical Endogenous
Anatomical S C Nickerson, University of Georgia, Athens, GA, USA ª 2011 Elsevier Ltd. All rights reserved.
Introduction Tissues associated with the teat duct or teat canal form the first barrier against mastitis-causing bacteria and include the exterior skin, sphincter muscle, stratified squamous epithelium of the teat canal lining, and keratin (Figure 1). These structures provide both a physical barrier and a chemical deterrent to bacterial colonization. Physical properties of the teat, such as length, width, and shape, also influence the incidence of mastitis as do teat end shape, milk flow rate, and presence of teat end lesions. Similarly, udder conformation and position are associated with mammary health. Fortunately, some of these traits are heritable, and to a certain degree, selection for resistance to mastitis is possible.
Teat Skin The healthy exterior teat skin composed of stratified squamous epithelium serves as a defense mechanism by providing a hostile environment for microbial survival, including an impenetrable keratinized layer as well as bacteriostatic fatty acids. However, abnormalities such as cuts, abrasions, lesions, and chapping provide an environment for bacterial growth, especially the staphylococci, for example, Staphylococcus aureus and Staphylococcus spp. Proper milking machine function and use of appropriate teat dips containing teat skin conditioning agents, such as emollients and humectants, are important in maintaining a healthy, smooth, and intact teat skin.
Teat Canal Keratin The teat canal is approximately 8.5 mm (5–13 mm) in length and between 0.4 and 1.63 mm in diameter, averaging 0.46 mm
at its midportion. Keratin is a gummy substance produced by the stratified squamous epithelium that lines the teat canal. This epithelial layer is actually continuous with the external skin and results from an invagination of the epidermis during fetal development. This lining terminates abruptly at Furstenberg’s rosette at which the stratified squamous epithelium becomes a double-layered epithelium. The stratum corneum of the teat canal epithelium is synonymous with keratin. Below this layer lie the stratum granulosum, stratum spinosum, and stratum germinativum. The epithelium is arranged in a series of longitudinal folds that interlock to form a seal as the sphincter muscle contracts after milking. In cross-section, the teat canal lumen has a mesh-like appearance where it is occluded with keratin, and is surrounded by layers of epithelium. The keratinized cells are derived from the stratum granulosum, and this dedifferentiation is associated with loss of nuclei and cellular organelles. One function of keratin is to provide bacteriostatic and bactericidal lipids and proteins to repress growth of microorganisms in the teat canal. The other function of keratin is to help block the teat orifice, serving as a physical barrier to bacterial penetration between milkings. During lactation, keratin exists in a dynamic state of generation and degradation as it sloughs from the stratified squamous epithelial lining. Portions of keratin are removed during each milking, probably as a result of the shearing forces of milk through the teat canal, but the substance is regenerated during the intermilking period within 24–60 h. Thus, immediately after milking, some degree of teat canal patency exists because of keratin removal, and this is the period during which the teat canal is most susceptible to penetration by mastitis-causing miroorganisms. However, keratin sloughing and removal are important because these processes help to remove colonized bacteria as does the flow of milk through the teat canal during machine milking. In fact, the mere flushing action of milk as it jets through the
381
382 Mammary Resistance Mechanisms | Anatomical
Figure 1 Longitudinal section through the distal teat end with lateral teat walls stretched and pinned to expose the teat canal and teat cistern. Furstenberg’s rosette is found at the junction of the canal and cistern where numerous longitudinal tissue folds of the cistern converge. Keratin is observed as a white gummy substance lining the teat canal lumen.
teat canal is a defense mechanism because it removes colonized bacteria. Cows milked 3 or 4 times a day are generally less susceptible to mastitis than are cows milked twice a day. In addition, when the frequency of milking increases, the pressure within the udder is reduced, especially just before the next milking. This reduction in pressure is important because an excess of pressure within the teat cistern shortens the teat canal and increases the susceptibility to intramammary infection by mastitis-causing bacteria. The loss of the keratin lining may be accentuated during conventional pulsation milking through the cyclic opening and closing of the teat canal, which tends to loosen the surface keratinized cells and promotes desquamation. In fact, it has been shown that more keratin is retained in the teat canal after pulsationless milking as compared with conventional pulsation milking. In one study, 50% more keratin was removed by pulsation milking as compared with milking without pulsation. However, by using pulsationless milking, the patency of the teat canal increases, making the quarter markedly more susceptible to intramammary infection. A decrease in the removal of keratin, as well as the bacteria entrapped in this substance, caused by milking without pulsation may also contribute to increased susceptibility to mastitis (Figure 2). Physical properties of the teat end are influenced by the milking machine, which affect susceptibility to infection. Teat congestion or edema, as measured by teat end thickness, usually decreases after conventional milking, but where there exists a milking-induced increase in teat end thickness that exceeds 5%, colonization with mastitis-causing bacteria increases significantly. Likewise, teat end thickness increases after pulsationless milking, thereby increasing susceptibility to infection. In addition, the reduced blood flow to the teat end that accompanies edema may alter the redox potential of the teat end tissues and compromise defense mechanisms such as the activity of xanthine oxidase. Within 2–3 weeks after drying off, a keratin plug completely occludes the teat duct and inhibits bacterial
Figure 2 Longitudinal histological section of the teat illustrating the teat duct (TD) and teat cistern (TC). The junction of these two structures at Furstenberg’s rosette is observed at the arrow. Note that the exterior teat skin (epidermis-E) is continuous with the teat duct.
Figure 3 Cross section through the midportion of the teat canal illustrating the lumen (L) occluded with mesh-like keratin and the stratified squamous epithelium (E).
penetration (Figure 3). Research has shown that the udder is highly resistant to mastitis at this time. Keratin also contains certain proteins and fatty acids harmful to microorganisms; however, bacteria have been shown to survive in teat duct keratin for months. Thus, the value of these antimicrobial substances is questionable, and keratin serving as a barrier probably plays a greater part in host resistance to mastitis than the antimicrobial proteins and fatty acids.
Sphincter Muscle The teat canal is surrounded by bundles of smooth muscle fibers. The fibers are arranged longitudinally immediately adjacent to the epithelial lining, and in a circular manner around the canal deeper in the connective tissue. The circular smooth muscles in their contracted state function to maintain tight closure of the teat canal between milkings to prevent leakage, and to keep keratin occluding the canal lumen compressed as an aid in preventing bacteria
Mammary Resistance Mechanisms | Anatomical
from progressing upward into the teat cistern. The elastic fibers in the dermis associated with the teat end also aid in closing the teat canal. During milking, the barrel of the teat elongates and the teat canal becomes dilated and shortened. However, after milking, contraction of the teat sphincter leads to a shortening of the teat barrel and lengthening of the teat canal. Shortened teats are less prone to injury, and the lengthened and closed teat canal is less prone to bacterial penetration. For a diagram of the teat sphincter (see Mammary Gland: Anatomy). Teats with weak, relaxed, or incompetent sphincters are termed ‘patent’ or ‘leaky’. Cows having such teats milk out fast in 2–3 min, but the incidence of mastitis is greater in quarters with patent teat canals. This is likely inherited, and such cows will be more susceptible to mastitis. Cows having teats with tight sphincters are called ‘hard or slow milkers’ because milk is expressed as a fine spray and rate of milk flow is reduced, thus they take longer to milk. The teat duct may remain dilated for 0.5–2 h after milking, and feeding the cows during this period keeps them on their feet, keeps the teats clean, and provides time for the sphincter muscle to tighten and close around the duct, thereby preventing bacterial entry. Because the teat canal remains dilated for a period of time after machine removal, the dipping of teats into a germicide is recommended to reduce bacterial populations at the teat end and to prevent subsequent colonization and infection. If the milking machine malfunctions due to excessive vacuum or faulty pulsation, then teat end congestion or edema may develop as mentioned above. Such edema decreases tissue elasticity as well as muscle contractions at the teat end, which may enhance bacterial penetration.
Factors Affecting Anatomical Resistance Mechanisms To maintain healthy teat end tissues, it is necessary to maintain recommended milking machine function and operation, namely, proper teat end vacuum level, optimum pulsation ratio, appropriate milking time, and proper teat cup removal. Awareness of these protective tissues of the teat end also becomes important when administering therapy by infusing antibiotics into the mammary gland. Bacteria living in or colonizing teat duct keratin require mechanical assistance to penetrate into the teat and the gland cisternal areas and cause an intramammary infection. Full insertion of the antibiotic treatment syringe cannula may push portions of keratin colonized by bacteria into the teat cistern and induce intramammary infection. In addition, keratin could be forced against the interior teat duct wall by the syringe cannula,
383
creating a larger than normal opening, thereby enhancing bacterial penetration. The conventional syringe cannula averages 3.1 mm in diameter, and teat duct diameters range from 0.40 to 1.63 mm for distal through proximal portions of the duct. Full insertion of a commercial cannula can result in temporary dilation of the duct lumen beyond the normal diameter (up to 8 times the normal diameter of the teat duct if the lower diameter range is considered). Tissue trauma caused by full insertion of the cannula may cause gaps or spaces in keratin, providing areas in which bacteria can adhere and colonize. A comparison of the histological cross sections of teat ducts that were inserted with a syringe cannula by partial or by full insertion revealed that the teat ducts inserted partially had a thicker keratin layer as compared with the teat ducts infused by full insertion. The latter exhibited partial loss of keratin, and it has been shown that removal of keratin decreases resistance to intramammary infection. Similarly, glands susceptible to infection have been shown to have canal keratin that was thinner, less dense, and detached from the epithelium in many areas. Sanitation of teat ends prior to antibiotic infusion destroys many bacteria, but organisms lodged in microscopic cracks and crevices near the teat orifice and in the teat duct may be protected and may survive. In these sites, they could be carried upward as full insertion of the cannula is applied. If bacteria gaining access to the teat cistern by these various aforementioned routes are resistant or inaccessible to the infused drug, a new intramammary infection may result. Studies designed to compare methods of cannula insertion for administration of intramammary drug therapy at dry off showed that the depth of cannula insertion had an effect on number of new intramammary infections at freshening. A 58.8% reduction in the number of new intramammary infections with Streptococcus uberis, S. aureus, Streptococcus agalactiae, and the coliforms at calving was found in quarters treated by partial insertion (2–3 mm) of the cannula as compared with those treated with full insertion. Commercial syringes are now available that facilitate partial insertion by providing a twist-off tip, which when removed, allows the protrusion of 3.0 mm of the syringe cannula, and at the same time forms a seal with the teat orifice to provide support during infusion and to ensure upward movement of the antibiotic (Figure 4). Use of such cannulas has reduced the incidence of new intramammary infections caused by S. aureus and Str. uberis by 40–50%. Teat orifice lesions also affect resistance to mastitis, and include abnormalities such as eversions, hyperkeratosis, and hemorrhagic blisters. Such lesions are a result of leaving the milking machine on the cow for long periods of time (overmilking), excessive vacuum levels,
384 Mammary Resistance Mechanisms | Anatomical
claw, ultimately impacting the opposite teat end. These impacting droplets are carried with such a high velocity that they penetrate the teat canal and enter the teat cistern. If such droplets are contaminated with bacteria from other quarters of the cow being milked or with bacteria that contaminate the milk tubes and cluster from previously milked mastitic cows, they can cause a new infection in the quarter into which they are propelled. Cluster removal under vacuum also may lead to droplet impacts.
Figure 4 Syringe with removable tip, allowing partial insertion into teat canal.
inadequate pulsation, or a combination of these factors. Lesions are readily colonized by pathogenic bacteria such as S. aureus, and an increase in teat end lesions is associated with an outbreak of mastitis. The tissues lining the teat cistern can likewise be irritated by hard-liner mouthpieces under conditions of excessive vacuum, which leads to teat cup crawl or its upward movement on the teat barrel. This leads to a pinching-off of the teat cistern at the point where the teat attaches to the ventral surface of the udder, leading to constriction and tissue irritation as the opposite walls of the teat cistern lining rub against one another resulting in lesions. As stated above, such lesions are readily colonized by pathogenic bacteria and lead to intramammary infection. Use of functionally adequate milking machines is also important to udder health. Research has confirmed that the milking machine can be a vector for transferring mastitis organisms from teat to teat and from cow to cow, and can serve as a means of transferring those organisms through the teat canal and into the udder. Every effort should be made to ensure that milking machines meet functional standards as well as operator use such as meeting internationally accepted design and installation standards, providing a relatively stable milking vacuum level of 275–300 mm of mercury or 37–41 kPa at the claw during peak milk flow, avoiding slipping or squawking teat cup liners during milking, and shutting off the vacuum to the claw before removing the teat cups. Milking machine vacuum fluctuations and inadequate vacuum reserve may lead to teat cup liner slippage. When this occurs, the teat cup liner drops or slips down on the teat barrel as milk volume and pressure in the teat cistern decreases, often resulting in a squawking sound as air enters the space between the liner and outer teat wall. This air travels down the liner, through the short milk tube, and across the cluster. Here, the air agitates milk in the cluster and forms tiny droplets of milk that are carried by the air to the opposite short milk tube and teat cup liner of the
Hereditary Factors Heritability of udder and teat shape is moderate to high, and selection for cows with desirable traits may reduce the incidence of mastitis. For example, studies have demonstrated that deep or pendulous udders are more susceptible to intramammary infections and have higher somatic cell counts (SCCs) than shallow, tight, nonpendulous udders. The correlation between udder height and incidence of clinical mastitis is 0.13, while that between udder height and SCCs is 0.11. The heritability of udder depth is 0.25. Teats, according to their shape, are generally classified as funnel-shaped, cylindrical, or bottle-shaped. Research suggests that cows with funnel-shaped teats have lower incidence of intramammary infection than those with cylindrically shaped teats. The former may offer greater resistance to teat cup crawl, pinching-off of the teat cistern during milking, and subsequent tissue damage to the delicate tissues of teat end. In fact, teat end erosion is more common in cylindrically shaped than in funnel-shaped teats. Udders with funnel-shaped teats also have been shown to produce more milk, milk out more completely, and exhibit lower SCC. Teat length and diameter are also associated with mastitis, and these traits are heritable. Teats with smaller diameters milk out more completely and are probably less prone to mastitis, whereas teats of larger diameter have larger orifices and are more susceptible to infection. One study indicated that the heritability of teat diameter may be as high as 0.67. The heritability of teat length ranges from 0.25 to 0.60; shorter teats are less prone to teat-treading injuries, milk out faster and more completely, and are associated with greater milk yield. Teat end shape also affects resistance and appears to be highly heritable as well. Teat end shape is generally classified as pointed, round, flat (disk or plate-shaped), or inverted. Pointed teats tend to be longer and are predisposed to damage of the orifice. Inverted or disk-shaped teat ends are associated with larger-diameter teat ducts, which are less resistant to bacterial invasion. One study showed that as teat end shape varied from pointed to
Mammary Resistance Mechanisms | Anatomical
inverted, milk flow rate increased, which suggests largerdiameter teat canals. It has been suggested that after milking, milk may have a greater tendency to adhere to the bottom of the cone of inverted teat ends and serve as a source of nutrients for bacterial growth and subsequent penetration. In general, cows with round teat ends have lower incidence of infection and lower SCC than those with pointed, inverted, or flat teat ends. As stated above, wider-diameter teat canals with increased milk flow rates are more susceptible to infection, whereas narrow canals are more resistant. The speed of milking is positively correlated with yield, that is, greater yields mean greater flow rates; thus, increasing the selection for yield will increase milk flow rates. However, the keratin that occludes the teat canal between milkings serves as the primary defense by forming a physical barrier, and research has shown that bacteriostatic lipids and proteins associated with this substance are also heritable.
See also: Mammary Gland: Anatomy. Mastitis Therapy and Control: Management Control Options; Role of Milking Machines in Control of Mastitis. Milking Machines: Principles and Design.
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Further Reading Blowey R and Edmondson P (eds.) (1995) Teat and udder defences against mastitis. In: Mastitis Control in Dairy Herds, pp. 17–26. Ipswich: Farming Press. Chandler RL, Lepper AWD, and Wilcox J (1969) Ultrastuctural observations on the bovine teat duct. Journal of Comparative Pathology 79: 315–319. Craven N and Williams MR (1985) Defences of the bovine mammary gland against infection and prospects for their enhancement. Veterinary Immunology and Immunopathology 10: 71–127. National Mastitis Council (eds.) (1996) Cow factors in mastitis. In: Current Concepts of Bovine Mastitis, pp. 21–24. Madison, WI: National Mastitis Council. Nickerson SC (1985) Immune mechanisms of the bovine udder: An overview. Journal of the American Veterinary Medical Association 187: 41–45. Nickerson SC (1995) Milk production: Factors affecting milk composition. In: Harding F (ed.) Milk Quality, pp. 3–24. London: Blackie Academic & Professional. Paape MJ, Schultze WD, Guidry AJ, and Pearson RE (1979) Leukocytes: Second line of defense against invading mastitis pathogens. Journal of Dairy Science 62: 135–153. Philpot WN and Nickerson SC (eds.) (2000) Defense mechanisms against mastitis. In: Winning the Fight against Mastitis, pp. 18–21. Naperville, IL: Westfalia-Surge. Sandholm M and Korhonen H (eds.) (1995) Antibacterial defence mechanisms of the udder. In: The Bovine Udder and Mastitis, pp. 37–48. Helsinki: University of Helsinki. Schalm OW, Carroll EJ, and Jain NC (eds.) (1971) Gross and microscopic structure of the bovine mammary glands. In: Bovine Mastitis, pp. 36–47. Philadelphia, PA: Lea & Febiger. Seykora AJ and McDanial BT (1985) Udder and teat morphology related to mastitis resistance: A review. Journal of Dairy Science 68: 2087–2093.
Anatomical S C Nickerson, University of Georgia, Athens, GA, USA ª 2011 Elsevier Ltd. All rights reserved.
Introduction Tissues associated with the teat duct or teat canal form the first barrier against mastitis-causing bacteria and include the exterior skin, sphincter muscle, stratified squamous epithelium of the teat canal lining, and keratin (Figure 1). These structures provide both a physical barrier and a chemical deterrent to bacterial colonization. Physical properties of the teat, such as length, width, and shape, also influence the incidence of mastitis as do teat end shape, milk flow rate, and presence of teat end lesions. Similarly, udder conformation and position are associated with mammary health. Fortunately, some of these traits are heritable, and to a certain degree, selection for resistance to mastitis is possible.
Teat Skin The healthy exterior teat skin composed of stratified squamous epithelium serves as a defense mechanism by providing a hostile environment for microbial survival, including an impenetrable keratinized layer as well as bacteriostatic fatty acids. However, abnormalities such as cuts, abrasions, lesions, and chapping provide an environment for bacterial growth, especially the staphylococci, for example, Staphylococcus aureus and Staphylococcus spp. Proper milking machine function and use of appropriate teat dips containing teat skin conditioning agents, such as emollients and humectants, are important in maintaining a healthy, smooth, and intact teat skin.
Teat Canal Keratin The teat canal is approximately 8.5 mm (5–13 mm) in length and between 0.4 and 1.63 mm in diameter, averaging 0.46 mm
at its midportion. Keratin is a gummy substance produced by the stratified squamous epithelium that lines the teat canal. This epithelial layer is actually continuous with the external skin and results from an invagination of the epidermis during fetal development. This lining terminates abruptly at Furstenberg’s rosette at which the stratified squamous epithelium becomes a double-layered epithelium. The stratum corneum of the teat canal epithelium is synonymous with keratin. Below this layer lie the stratum granulosum, stratum spinosum, and stratum germinativum. The epithelium is arranged in a series of longitudinal folds that interlock to form a seal as the sphincter muscle contracts after milking. In cross-section, the teat canal lumen has a mesh-like appearance where it is occluded with keratin, and is surrounded by layers of epithelium. The keratinized cells are derived from the stratum granulosum, and this dedifferentiation is associated with loss of nuclei and cellular organelles. One function of keratin is to provide bacteriostatic and bactericidal lipids and proteins to repress growth of microorganisms in the teat canal. The other function of keratin is to help block the teat orifice, serving as a physical barrier to bacterial penetration between milkings. During lactation, keratin exists in a dynamic state of generation and degradation as it sloughs from the stratified squamous epithelial lining. Portions of keratin are removed during each milking, probably as a result of the shearing forces of milk through the teat canal, but the substance is regenerated during the intermilking period within 24–60 h. Thus, immediately after milking, some degree of teat canal patency exists because of keratin removal, and this is the period during which the teat canal is most susceptible to penetration by mastitis-causing miroorganisms. However, keratin sloughing and removal are important because these processes help to remove colonized bacteria as does the flow of milk through the teat canal during machine milking. In fact, the mere flushing action of milk as it jets through the
381
382 Mammary Resistance Mechanisms | Anatomical
Figure 1 Longitudinal section through the distal teat end with lateral teat walls stretched and pinned to expose the teat canal and teat cistern. Furstenberg’s rosette is found at the junction of the canal and cistern where numerous longitudinal tissue folds of the cistern converge. Keratin is observed as a white gummy substance lining the teat canal lumen.
teat canal is a defense mechanism because it removes colonized bacteria. Cows milked 3 or 4 times a day are generally less susceptible to mastitis than are cows milked twice a day. In addition, when the frequency of milking increases, the pressure within the udder is reduced, especially just before the next milking. This reduction in pressure is important because an excess of pressure within the teat cistern shortens the teat canal and increases the susceptibility to intramammary infection by mastitis-causing bacteria. The loss of the keratin lining may be accentuated during conventional pulsation milking through the cyclic opening and closing of the teat canal, which tends to loosen the surface keratinized cells and promotes desquamation. In fact, it has been shown that more keratin is retained in the teat canal after pulsationless milking as compared with conventional pulsation milking. In one study, 50% more keratin was removed by pulsation milking as compared with milking without pulsation. However, by using pulsationless milking, the patency of the teat canal increases, making the quarter markedly more susceptible to intramammary infection. A decrease in the removal of keratin, as well as the bacteria entrapped in this substance, caused by milking without pulsation may also contribute to increased susceptibility to mastitis (Figure 2). Physical properties of the teat end are influenced by the milking machine, which affect susceptibility to infection. Teat congestion or edema, as measured by teat end thickness, usually decreases after conventional milking, but where there exists a milking-induced increase in teat end thickness that exceeds 5%, colonization with mastitis-causing bacteria increases significantly. Likewise, teat end thickness increases after pulsationless milking, thereby increasing susceptibility to infection. In addition, the reduced blood flow to the teat end that accompanies edema may alter the redox potential of the teat end tissues and compromise defense mechanisms such as the activity of xanthine oxidase. Within 2–3 weeks after drying off, a keratin plug completely occludes the teat duct and inhibits bacterial
Figure 2 Longitudinal histological section of the teat illustrating the teat duct (TD) and teat cistern (TC). The junction of these two structures at Furstenberg’s rosette is observed at the arrow. Note that the exterior teat skin (epidermis-E) is continuous with the teat duct.
Figure 3 Cross section through the midportion of the teat canal illustrating the lumen (L) occluded with mesh-like keratin and the stratified squamous epithelium (E).
penetration (Figure 3). Research has shown that the udder is highly resistant to mastitis at this time. Keratin also contains certain proteins and fatty acids harmful to microorganisms; however, bacteria have been shown to survive in teat duct keratin for months. Thus, the value of these antimicrobial substances is questionable, and keratin serving as a barrier probably plays a greater part in host resistance to mastitis than the antimicrobial proteins and fatty acids.
Sphincter Muscle The teat canal is surrounded by bundles of smooth muscle fibers. The fibers are arranged longitudinally immediately adjacent to the epithelial lining, and in a circular manner around the canal deeper in the connective tissue. The circular smooth muscles in their contracted state function to maintain tight closure of the teat canal between milkings to prevent leakage, and to keep keratin occluding the canal lumen compressed as an aid in preventing bacteria
Mammary Resistance Mechanisms | Anatomical
from progressing upward into the teat cistern. The elastic fibers in the dermis associated with the teat end also aid in closing the teat canal. During milking, the barrel of the teat elongates and the teat canal becomes dilated and shortened. However, after milking, contraction of the teat sphincter leads to a shortening of the teat barrel and lengthening of the teat canal. Shortened teats are less prone to injury, and the lengthened and closed teat canal is less prone to bacterial penetration. For a diagram of the teat sphincter (see Mammary Gland: Anatomy). Teats with weak, relaxed, or incompetent sphincters are termed ‘patent’ or ‘leaky’. Cows having such teats milk out fast in 2–3 min, but the incidence of mastitis is greater in quarters with patent teat canals. This is likely inherited, and such cows will be more susceptible to mastitis. Cows having teats with tight sphincters are called ‘hard or slow milkers’ because milk is expressed as a fine spray and rate of milk flow is reduced, thus they take longer to milk. The teat duct may remain dilated for 0.5–2 h after milking, and feeding the cows during this period keeps them on their feet, keeps the teats clean, and provides time for the sphincter muscle to tighten and close around the duct, thereby preventing bacterial entry. Because the teat canal remains dilated for a period of time after machine removal, the dipping of teats into a germicide is recommended to reduce bacterial populations at the teat end and to prevent subsequent colonization and infection. If the milking machine malfunctions due to excessive vacuum or faulty pulsation, then teat end congestion or edema may develop as mentioned above. Such edema decreases tissue elasticity as well as muscle contractions at the teat end, which may enhance bacterial penetration.
Factors Affecting Anatomical Resistance Mechanisms To maintain healthy teat end tissues, it is necessary to maintain recommended milking machine function and operation, namely, proper teat end vacuum level, optimum pulsation ratio, appropriate milking time, and proper teat cup removal. Awareness of these protective tissues of the teat end also becomes important when administering therapy by infusing antibiotics into the mammary gland. Bacteria living in or colonizing teat duct keratin require mechanical assistance to penetrate into the teat and the gland cisternal areas and cause an intramammary infection. Full insertion of the antibiotic treatment syringe cannula may push portions of keratin colonized by bacteria into the teat cistern and induce intramammary infection. In addition, keratin could be forced against the interior teat duct wall by the syringe cannula,
383
creating a larger than normal opening, thereby enhancing bacterial penetration. The conventional syringe cannula averages 3.1 mm in diameter, and teat duct diameters range from 0.40 to 1.63 mm for distal through proximal portions of the duct. Full insertion of a commercial cannula can result in temporary dilation of the duct lumen beyond the normal diameter (up to 8 times the normal diameter of the teat duct if the lower diameter range is considered). Tissue trauma caused by full insertion of the cannula may cause gaps or spaces in keratin, providing areas in which bacteria can adhere and colonize. A comparison of the histological cross sections of teat ducts that were inserted with a syringe cannula by partial or by full insertion revealed that the teat ducts inserted partially had a thicker keratin layer as compared with the teat ducts infused by full insertion. The latter exhibited partial loss of keratin, and it has been shown that removal of keratin decreases resistance to intramammary infection. Similarly, glands susceptible to infection have been shown to have canal keratin that was thinner, less dense, and detached from the epithelium in many areas. Sanitation of teat ends prior to antibiotic infusion destroys many bacteria, but organisms lodged in microscopic cracks and crevices near the teat orifice and in the teat duct may be protected and may survive. In these sites, they could be carried upward as full insertion of the cannula is applied. If bacteria gaining access to the teat cistern by these various aforementioned routes are resistant or inaccessible to the infused drug, a new intramammary infection may result. Studies designed to compare methods of cannula insertion for administration of intramammary drug therapy at dry off showed that the depth of cannula insertion had an effect on number of new intramammary infections at freshening. A 58.8% reduction in the number of new intramammary infections with Streptococcus uberis, S. aureus, Streptococcus agalactiae, and the coliforms at calving was found in quarters treated by partial insertion (2–3 mm) of the cannula as compared with those treated with full insertion. Commercial syringes are now available that facilitate partial insertion by providing a twist-off tip, which when removed, allows the protrusion of 3.0 mm of the syringe cannula, and at the same time forms a seal with the teat orifice to provide support during infusion and to ensure upward movement of the antibiotic (Figure 4). Use of such cannulas has reduced the incidence of new intramammary infections caused by S. aureus and Str. uberis by 40–50%. Teat orifice lesions also affect resistance to mastitis, and include abnormalities such as eversions, hyperkeratosis, and hemorrhagic blisters. Such lesions are a result of leaving the milking machine on the cow for long periods of time (overmilking), excessive vacuum levels,
384 Mammary Resistance Mechanisms | Anatomical
claw, ultimately impacting the opposite teat end. These impacting droplets are carried with such a high velocity that they penetrate the teat canal and enter the teat cistern. If such droplets are contaminated with bacteria from other quarters of the cow being milked or with bacteria that contaminate the milk tubes and cluster from previously milked mastitic cows, they can cause a new infection in the quarter into which they are propelled. Cluster removal under vacuum also may lead to droplet impacts.
Figure 4 Syringe with removable tip, allowing partial insertion into teat canal.
inadequate pulsation, or a combination of these factors. Lesions are readily colonized by pathogenic bacteria such as S. aureus, and an increase in teat end lesions is associated with an outbreak of mastitis. The tissues lining the teat cistern can likewise be irritated by hard-liner mouthpieces under conditions of excessive vacuum, which leads to teat cup crawl or its upward movement on the teat barrel. This leads to a pinching-off of the teat cistern at the point where the teat attaches to the ventral surface of the udder, leading to constriction and tissue irritation as the opposite walls of the teat cistern lining rub against one another resulting in lesions. As stated above, such lesions are readily colonized by pathogenic bacteria and lead to intramammary infection. Use of functionally adequate milking machines is also important to udder health. Research has confirmed that the milking machine can be a vector for transferring mastitis organisms from teat to teat and from cow to cow, and can serve as a means of transferring those organisms through the teat canal and into the udder. Every effort should be made to ensure that milking machines meet functional standards as well as operator use such as meeting internationally accepted design and installation standards, providing a relatively stable milking vacuum level of 275–300 mm of mercury or 37–41 kPa at the claw during peak milk flow, avoiding slipping or squawking teat cup liners during milking, and shutting off the vacuum to the claw before removing the teat cups. Milking machine vacuum fluctuations and inadequate vacuum reserve may lead to teat cup liner slippage. When this occurs, the teat cup liner drops or slips down on the teat barrel as milk volume and pressure in the teat cistern decreases, often resulting in a squawking sound as air enters the space between the liner and outer teat wall. This air travels down the liner, through the short milk tube, and across the cluster. Here, the air agitates milk in the cluster and forms tiny droplets of milk that are carried by the air to the opposite short milk tube and teat cup liner of the
Hereditary Factors Heritability of udder and teat shape is moderate to high, and selection for cows with desirable traits may reduce the incidence of mastitis. For example, studies have demonstrated that deep or pendulous udders are more susceptible to intramammary infections and have higher somatic cell counts (SCCs) than shallow, tight, nonpendulous udders. The correlation between udder height and incidence of clinical mastitis is 0.13, while that between udder height and SCCs is 0.11. The heritability of udder depth is 0.25. Teats, according to their shape, are generally classified as funnel-shaped, cylindrical, or bottle-shaped. Research suggests that cows with funnel-shaped teats have lower incidence of intramammary infection than those with cylindrically shaped teats. The former may offer greater resistance to teat cup crawl, pinching-off of the teat cistern during milking, and subsequent tissue damage to the delicate tissues of teat end. In fact, teat end erosion is more common in cylindrically shaped than in funnel-shaped teats. Udders with funnel-shaped teats also have been shown to produce more milk, milk out more completely, and exhibit lower SCC. Teat length and diameter are also associated with mastitis, and these traits are heritable. Teats with smaller diameters milk out more completely and are probably less prone to mastitis, whereas teats of larger diameter have larger orifices and are more susceptible to infection. One study indicated that the heritability of teat diameter may be as high as 0.67. The heritability of teat length ranges from 0.25 to 0.60; shorter teats are less prone to teat-treading injuries, milk out faster and more completely, and are associated with greater milk yield. Teat end shape also affects resistance and appears to be highly heritable as well. Teat end shape is generally classified as pointed, round, flat (disk or plate-shaped), or inverted. Pointed teats tend to be longer and are predisposed to damage of the orifice. Inverted or disk-shaped teat ends are associated with larger-diameter teat ducts, which are less resistant to bacterial invasion. One study showed that as teat end shape varied from pointed to
Mammary Resistance Mechanisms | Anatomical
inverted, milk flow rate increased, which suggests largerdiameter teat canals. It has been suggested that after milking, milk may have a greater tendency to adhere to the bottom of the cone of inverted teat ends and serve as a source of nutrients for bacterial growth and subsequent penetration. In general, cows with round teat ends have lower incidence of infection and lower SCC than those with pointed, inverted, or flat teat ends. As stated above, wider-diameter teat canals with increased milk flow rates are more susceptible to infection, whereas narrow canals are more resistant. The speed of milking is positively correlated with yield, that is, greater yields mean greater flow rates; thus, increasing the selection for yield will increase milk flow rates. However, the keratin that occludes the teat canal between milkings serves as the primary defense by forming a physical barrier, and research has shown that bacteriostatic lipids and proteins associated with this substance are also heritable.
See also: Mammary Gland: Anatomy. Mastitis Therapy and Control: Management Control Options; Role of Milking Machines in Control of Mastitis. Milking Machines: Principles and Design.
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Further Reading Blowey R and Edmondson P (eds.) (1995) Teat and udder defences against mastitis. In: Mastitis Control in Dairy Herds, pp. 17–26. Ipswich: Farming Press. Chandler RL, Lepper AWD, and Wilcox J (1969) Ultrastuctural observations on the bovine teat duct. Journal of Comparative Pathology 79: 315–319. Craven N and Williams MR (1985) Defences of the bovine mammary gland against infection and prospects for their enhancement. Veterinary Immunology and Immunopathology 10: 71–127. National Mastitis Council (eds.) (1996) Cow factors in mastitis. In: Current Concepts of Bovine Mastitis, pp. 21–24. Madison, WI: National Mastitis Council. Nickerson SC (1985) Immune mechanisms of the bovine udder: An overview. Journal of the American Veterinary Medical Association 187: 41–45. Nickerson SC (1995) Milk production: Factors affecting milk composition. In: Harding F (ed.) Milk Quality, pp. 3–24. London: Blackie Academic & Professional. Paape MJ, Schultze WD, Guidry AJ, and Pearson RE (1979) Leukocytes: Second line of defense against invading mastitis pathogens. Journal of Dairy Science 62: 135–153. Philpot WN and Nickerson SC (eds.) (2000) Defense mechanisms against mastitis. In: Winning the Fight against Mastitis, pp. 18–21. Naperville, IL: Westfalia-Surge. Sandholm M and Korhonen H (eds.) (1995) Antibacterial defence mechanisms of the udder. In: The Bovine Udder and Mastitis, pp. 37–48. Helsinki: University of Helsinki. Schalm OW, Carroll EJ, and Jain NC (eds.) (1971) Gross and microscopic structure of the bovine mammary glands. In: Bovine Mastitis, pp. 36–47. Philadelphia, PA: Lea & Febiger. Seykora AJ and McDanial BT (1985) Udder and teat morphology related to mastitis resistance: A review. Journal of Dairy Science 68: 2087–2093.