KSUCVM • CS 712 • Mammary Images

MAMMARY GLAND DISEASES
(fig 100)

BOVINE MASTITIS
Mastitis is the single most common disease syndrome in adult dairy cows, accounting for 38% of all morbidity. Mastitis may result following the introduction of microorganisms through the teat sphincter. The clinical course varies with the ability of bacteria to colonize and thrive in the udder, virulence, and host response. (fig 71)

General Sequence of Events and Pathology of Bovine Mastitis

  1. the organisms enter the teat duct.
  2. the organisms multiply in the teat duct, streak canal, and mammary gland.
  3. the organisms progress upward into the lactiferous sinus, collecting ducts and alveoli.
  4. organisms localize, resulting in leukocytic attraction, edema, and in some cases, abscess formation.
  5. healing often results in fibrous connective tissue formation with some resolution.

Contagious mastitis

  • transfer of organisms from infected mammary glands to healthy mammary glands.
  • Streptococcus agalactiae, S. aureus, and Mycoplasma spp.
  • Streptococcus dysgalactiae, Staphylococci-coagulase negative

Environmental mastitis

  • contaminated bedding, water, fecal material, or other fomites
  • coliform bacteria
  • E. coli, Klebsiella pneumoniae, Enterobacter aerogenes, Streptococcus fecalis, and foecum.

TYPES OF MASTITIS
Subclinical

  • the milk appears grossly normal, there is no visible sign of inflammation of the udder.
  • detected by routine tests such as California Mastitis Test (CMT) SCCs reported on Dairy Herd Improvement Association (DHIA) records, or routine culturing of all quarters.
  • results in decreased milk production

Acute mastitis

  • swollen, painful gland, fever, anorexia.
  • frequently associated with flare-ups of S. agalactiae or S. aureus
  • toxic mastitis due to coliforms may result in low serum calcium and paraplegia.

Chronic mastitis

  • no clinical signs for prolonged intervals
  • SCCs are generally elevated.
  • mammary gland secretions periodically contain flakes, clots or shreds of fibrin
  • mammary gland is replaced with scar tissue

Gangrenous mastitis

  • caused mostly by Staphylococcus
  • parts of the mammary gland become cold and secretions are watery and sanguinous.
  • areas of the mammary gland may slough within 10 to 14 days.

Non-Lactating Dairy Heifer Mastitis

  • researchers are finding that heifers that haven't calved are an important reservoir for many of the contagious mastitis organisms which are found in most dairy herds.
  • heifer mastitis is defined as an intramammary infection at first freshening, either subclinical or clinical.
  • Nickerson (1992) found 34% coagulase negative staphylococci, 12% Staphylococcus aureus, and 20% environmental pathogens in infected heifers.

Beef Cattle Mastitis

  • as reported in the literature, the prevalence of intramammary infections in beef cattle ranges from 5%–27.5% for quarters and 10.7% –54.4% for cows.
  • subclinical mastitis in the beef cow is common. The differences in average adjusted weaning weights of calves nursing cows with subclinical mastitis is not statistically different from those calves nursing cows without subclinical mastitis

MICROBIOLOGIC TECHNIQUES

  • wash and dry the mammary gland before sampling.
  • each teat end and orifice should be scrubbed thoroughly with a separate cotton ball or gauze section moistened with 70% alcohol
  • tube should be gripped in a horizontal plane during filling, with the cap held with its inside facing downward
  • sample each quarter into sterile tube after stripping each teat two or three times, collect 5 to 10 ml from each quarter.
  • samples should be cooled to 39.2 to 41E F until culture procedures are performed.
  • the task of sample collection on a herd basis is substantially reduced by collection of composite samples, i.e., samples from all quarters in one collection tube.
  • microbiologic testing can be done on the basis of elevated SCCs.
  • milk samples from each lactating cow should be cultured once every six weeks. Many variations of sampling schedules can be arranged, but any schedule should include culturing of all cows with clinical mastitis, all purchased cows, and all fresh cows and heifers.

BULK-TANK MILK CULTURES

  • monitoring the herd health status by routine, monthly culturing of bulk-tank milk. Allows the monitoring of milk quality and mastitis status in the herd.

STAPHYLOCOCCUS AUREUS MASTITIS

  1. Bovine mastitis caused by Staphylococcus aureus represents a significant problem to the dairy industry. The disease is usually seen in a subclinical state during most of the lactation period, but can become acute shortly following parturition. Losses from this disease result from treatment costs, decreased milk production, and the need to cull some affected cows. The disease does not respond to treatment well and satisfactory methods to eradicate staphylococcal mastitis from infected herds have yet to be devised.
  2. Infection during early lactation often results in the appearance of the peracute form, with gangrene of the udder due to the acute necrotizing action of the alpha toxin. During the later stages of lactation or during the dry period, new infections are not usually accompanied by a systemic reaction, but result in an acute or chronic form.
  3. Classified as a coagulase positive bacteria

Pathogenic Factors Attributed to S. aureus

  1. Alpha Toxin - this is product of the organism, and when injected as a cell-free fraction can produce clinical disease. It has been shown to be responsible for the gangrenous form of mastitis. Immunological titers to this toxin can be demonstrated to be at a higher levels in older cattle than in younger cattle, and this may account for clinical signs of disease being more common in younger cows at parturition. Purified alpha toxin when injected into the skin of cattle, will cause vasoconstriction and results in ischemia and coagulative necrosis. The toxin is also leukocidal, and will lyse red blood cells.
  2. Protein A - Protein A produced by S. aureus positively influences the immune system, but negatively it has antiphagocytic properties, which can be attributed to the inactivation of compliment and inhibition of heat labile opsonization. Protein A can also cause delayed hypersensitivity with repeated exposure.
  3. Teichoic acid - This acid is a component of the S. aureus cell wall and animals are capable of developing antibodies to this factor. The organism may have the capability to alter its metabolic pathways to protect teichoic acid.
  4. Leukocidin - Leukocidin is elaborated by S. aureus and is known to attack bovine granulocytes.
  5. Pigments - The amount of pigment produced by the organism is correlated to the incidence of persistent infections.
  6. Extracellular Proteins - Extracellular proteins such as coagulase, hyaluronidase, phosphatase, nuclease, lipase, catalase, staphylokinase (fibrinolysin), and proteases all aid the growth and spread of S. aureus.

Pathogenesis

  1. The organism must enter the mammary gland through the teat sphincter. (fig 102) (fig mam 004)
  2. Coagulase-positive S. aureus can normally inhabit the skin of the teats and the population of the organism can be high if the quarter is also shedding the organism. In addition, the organism may be deposited on the teat end by contaminated wash cloths or sponges used in the normal premilking cleaning procedure. Contaminated inflations from previously milked infected quarters may easily transmit the organism. (fig mam 006)
  3. Another factor that can potentiate the organism is damage to the epithelium of the teat end, caused by viral infection, chemical irritation from teat dips, or physical damage from excessive milking or high vacuum which will allow the organism to colonize on the teat end.
  4. Following entry into the mammary gland of the organism, the subsequent course is determined by the ability of the neutrophils to control the growth and multiplication of the bacteria. When growth and multiplication is not prevented, the gangrenous form of staphylococcal mastitis will frequently occur. The cow can die of toxemia or the quarter may slough with this form.
  5. If neutrophils are able to adequately control S. aureus multiplication, mild clinical signs, which are usually confined to the mammary gland, will be observed.
  6. Repeated cycles of clinical and subclinical infection throughout the lactation period is typical of S. aureus mastitis.
  7. The initial pathological finding is degeneration and denuding of duct epithelium with stromal swelling which decreases the size of the lumen. The alveolar secretory cells nearest the ducts decrease in numbers. Microabscesses will form in the secretory areas and the majority of viable staphylococcal organisms are found within somatic cells. These are some of the factors that make this infection difficult to treat.

Clinical Findings

  1. The peracute form occurs usually in the first few days after calving and is highly fatal. There is a severe systemic reaction with elevation of rectal temperature of 106-107E F., rapid heart rate (100-120), complete anorexia, profound depression, absence of ruminal movements, and muscular weakness, often to the point of recumbency. The quarter is grossly swollen, hard, and sore to touch. A bluish discoloration may develop and this may spread to involve the floor of the udder. Within 24 hours, (fig 103) the gangrenous areas become black and ooze serum. The secretion is reduced to a small amount of blood-stained serous fluid without odor, clots, or flakes. Even with early treatment, the quarter is usually lost and gangrenous areas will slough.
    (fig 104)
  2. Acute staphylococcal mastitis occurs most commonly in early lactation. There is severe swelling of the gland and the milk is purulent or contains thick clots. Extensive fibrosis and severe loss of function result.
    (fig 105)
  3. The most important herd losses are caused by the chronic form where up to 50% of the herd can be affected. Only a few cows may show sufficient signs to be recognized by the dairyman. Many cases are characterized by a slowly developing induration and atrophy with occasional appearance of clots in the milk or wateriness of the first streams.
    (fig 78)

Identifying Staphylococcus Aureus as a Herd Problem
Monitoring the herd health status of the dairy herd by routine, monthly culturing of the bulk-tank milk can be an important management tool for the dairy producer. The absence of S. aureus from routine bulk-tank milk samples can be found because of the low and intermittent shedding of organisms in the milk from infected cows.

Bulk-tank somatic cell counts (SCC) can be used to determine the severity of a staphylococcus mastitis herd problem. The prevalence of staphylococcal species isolated from bovine mammary glands was determined in four dairy herds. Staphylococcus aureus and S. hyicus were the predominant organisms isolated from cows in a herd with a bulk milk somatic cell count (SCC) of 900,000 or greater. Another herd with a bulk-tank SCC of 565,000 had a high incidence of S. aureus and coagulase-negative species S. epidermidis and S. hyicus. When S. hyicus was prevalent in two herds, S. aureus was low, and the bulk-tank SCC count was >200,000. A dairyman with a severe S. aureus mastitis problem may not receive a warning from the milk processor until his SCC begins to approach 1,000,000.

The standard plate count (SPC) taken from bulk tank milk measures the number of bacterial colonies per milliliter of raw milk. It does not identify the responsible organisms and is not a reliable indicator of mastitis incidence in the herd. A good tank sample should have less than 5,000 colonies per milliliter of milk. Herds with chronic staphylococcus mastitis problems can have low to moderately elevated SPC's, even when half the cows are infected with the organism. Standard plate counts for S. aureus from bulk-tank milk rarely exceeds 20,000 per ml. The absence of a pathogen on the SPC blood agar plate should not be interpreted that a pathogen is absent in the herd, but it may mean that there is less than 100 organisms per ml of milk.

Attainable goals for bulk-tank milk samples are SPC >1,000 and SCC of >150,000. Coagulase positive S. aureus should be absent from the samples. A staphylococcus infection should be suspected when the SPC is at least 12,500, SCC at least 750,000, and the bulk-tank is culture positive for S. aureus.

On an individual cow basis, the California Mastitis Test (CMT) grade is correlated with the infection status of a quarter. When approaching a S. aureus herd problem, an initial CMT is done on all four quarters of every cow in the herd. All cows that score two or three on the CMT test are then cultured. Trace and one grade are usually not cultured because they are often self-limiting environmental or coagulase-negative staphylococcus infections. The second most widely used screening test for subclinical mastitis is the direct somatic cell count (SCC) of milk reported on Dairy Herd Improvement Association (DHIA) records. If the cow is infected, the SCC code usually increases. An infected S. aureus quarter may not be detected because the SCC is diluted by milk from the other three quarters.

Detection of S. aureus on the farm has some limitation, but a new method for detecting S. aureus infected cows has become available through the DHIA. The test (ProStaph, ProScience Corp., Sterling, VA) is an enzyme-linked immunosorbent assay (ELISA) which will bind S. aureus antibodies in milk from infected lactating cows with a purified antigen preparation. The accuracy of the test compared to culture techniques was 96%, with a sensitivity of 90% (the ability to identify culture positive) and a specificity of 97% (identification of culture negatives). Recommendations for using the test procedure are as follows: herds with a high somatic cell count (SCC) average should be tested. If S. aureus is found, the Pro-Staph test should be conducted on all cows in the herd. S. aureus positive cows should be segregated from the herd or culled. In addition, first-lactation cows, and newly purchased cows should be tested and isolated when necessary.

A definitive diagnosis of S. aureus infection can be made by microbiological examination of aseptically collected milk. Composite culturing of all cows in the herd is suggested when a contagious pathogen such as S. aureus is found. The objective is to identify infected cows for segregation, treatment, or culling.

Treatment

  1. Decreased duct lumen size probably will allow only minimal success with local treatment, indicating the need for systemic treatment. The intracellular location, inability of an antibiotic to penetrate the cell wall will provide the organism with resistance to many antibiotics.
  2. In regard to systemic treatment, the degree of ionization and lipid solubility of antibiotics are major factors in establishing a milk-to-serum ratio.
  3. Most staphylococcus isolated are not sensitive to penicillin in vitro
  4. Development of penicillin-resistant staphylococci has brought about the increased use of the following antibacterial drugs:
    Cloxacillin Erythromycin
    Novobiocin Hetacillin
    Cephapirin Pirlimycin
  5. Greater treatment success is found when dry cow therapy is used as opposed to lactating cow therapy and it also reduces the number of new infections at parturition.

Prevention
Vaccines are available, but S. aureus is classified as a facultative intracellular parasite and the establishment of mammary infection is controlled by antibody levels only in the early course of the disease. Immunization against staphylococcal antigens is effective only against challenge by a homologous strain. Also, another problem with vaccination is the rapid decline of the antibody levels within 1-4 months.

Commercially Available Staphylococcus Aureus Vaccines
Commercial Name Company Type Recommendations
Lysigin Bio-Ceutic Bacterin 5 mL IM, repeat in 14 days, and booster every 6 months
Somato-Staph Ancher Bacterin 5 mL IM, repeat in 14 days, and booster every 6 months
Somato-Staph/Lepto-5 Ancher Bacterin 2 mL IM, repeat in 14 days and booster every 6 months
Staphoid A-B Coopers Bacterin toxoid 5 mL, repeat in 14 days, and booster every 6 months

Other effective preventative procedures can be broadly categorized as either sanitation or segregation. Use paper towels for washing udder only once, clean milkers' hands and milking units with germicidal solution between cows. Automatic backflushing equipment is an integral component of many newer milking facilities. Properly functioning milking equipment will minimize the reverse flow of potentially contaminated milk and reduce trauma to the teat end. A thorough analysis of milking machine performance, including vacuum levels, vacuum reserve, pulsation rates, and pulsation ratios, must be an integral part of any mastitis control program.

Most teat dips marketed in the United States effectively prevent many new intramammary infections when used properly and concurrently with a complete mastitis control program. Good milking techniques with correctly functioning equipment is also necessary for the best results from postmilking teat antisepsis. Backflushing of milking units between cows has been suggested as S. aureus control. Backflushing was effective in reducing new coagulase-positive staphylococci infections in one study, but was not confirmed by a second study.

Physically separating infected and noninfected cattle eliminates the spread of infection between the two groups, thus decreasing the rate of new infections. Such isolation procedures can be accomplished either by culling infected cattle or by segregating the herd into culture-positive and culture-negative groups or some combination thereof. The most effective method of reducing the prevalence of S. aureus infection within a herd is by culling of infected cows. Culling should be done judiciously with respect to production, breeding performance, genetic potential, and other health problems and may be limited by the need to maintain ample milk production for cash flow. Segregation of S. aureus infected cows and milking them last to help avoid exposure to noninfected cows has been suggested as a method of prevention.

Other Staphylococcus Recognized as Pathogens

  • Staphylococcus hyicus–coagulase positive
  • Staphylococcus epidermidis and micrococcus.–coagulase negative
  • these are all minor mastitis pathogens and are readily found on teat skin. They are commonly found in bulk tank milk and elevated somatic cell counts may be associated with infected quarters or teat sanitation problems

STREPTOCOCCUS AGALACTIAE MASTITIS  (fig mam 013)

  1. Any large dairy herd which has no mastitis control program can commonly be infected with Streptococcus agalactiae. The average morbidity rate will be about 25%, while the herd loss in milk production may be in the order of 10-15%. When mastitis control programs are used, the morbidity will be low.
  2. Deaths rarely occur due to Str. agalactia and complete loss of productivity of a quarter is uncommon.
  3. The main source of infection is the udder of infected cows although, when hygiene is poor, contamination of the environment may provide a ready source of infection. The teats and skin of cattle, milkers' hands, floors, utensils, and clothes are often heavily contaminated. Sores on teats are the most common site outside the udder for persistence of the organism.
  4. The teat canal is an important portal of entry, suction into the teat during milking or immediately afterwards does occur, but growth of bacteria between milkings also appears to be an important method of entry.

Pathogenesis

  1. There is variation in resistance to infection, but invasion takes 1-4 days, and the appearance of inflammation 3-5 days.
  2. The initial stages of infection are characterized by rapid multiplication of the organism in the lactiferous ducts, followed by passage of the bacteria through the duct walls into lymphatic vessels and to the supramammary lymph nodes, and an outpouring of neutrophils into milk ducts. At this stage, a short-lived systemic reaction occurs, milk yield drops due to acinar and ductal epithelium damage. Some fibrosis develops even when the organism is cleared rapidly. Subsequently, similar crises develop and more lobules are affected in the same way resulting in a step-wise loss of secretory function with increasing fibrosis of the quarter and eventual atrophy.

Clinical Signs

  1. In natural cases, fever, lasting for a day or two, is occasionally observed with the initial attack, but the inflammation of the gland persists and subsequent crises are usually of a mild nature.
  2. The degrees of severity may be classified as peracute when the animal is febrile and off its feed, acute when the inflammation of the gland is severe, but there is no marked systemic reaction, and chronic when the inflammation is mild, the gland is not greatly swollen, pain and heat are absent, and the presence of clots in watery foremilk may be the only apparent abnormality.
  3. The milk yield of affected glands is reduced during each crisis but with proper treatment administered early, the milk yield may return to almost normal. Even without treatment, the appearance of the milk will soon appear normal, but the yield will be significantly reduced.

Treatment

  1. Procaine penicillin G is universally used as a mammary infusion at a dose rate of 100,000 units. To provide a broader spectrum of antibiotic efficiency, penicillin is often combined with other drugs such as novobiocin.
  2. As a general rule, clinical cases should be treated with three infusions and subclinical cases, particularly those detected by routine examination in a control program, with one infusion.
  3. Recovery, both clinically and bacteriologically, should be achieved in at least 90% of quarters if treatment has been efficient. In dry cows, one infusion is usually sufficient.
  4. On rare occasions, a penicillin-resistant strain of streptococci is encountered, a mixed infection with bacteria which produce penicillinase, may inactive the penicillin.
  5. Penicillin can be administered parenterally and is effective, but more expensive than intramammary infusion. Three doses of at least 6 million units of procaine penicillin G injected intramuscularly every 12 hours is an efficient treatment regimen.
  6. Lincomycin is also effective.

Control
Eradication on a herd basis of mastitis caused by Str. agalactiae can be accomplished. In general, it can be anticipated that about 80% of the herds can be rid of infection within a year of commencing a preventative program. The control program will be outlined later in this section.

MASTITIS CAUSED BY MISCELLANEOUS STREPTOCOCCI
Streptococcus uberis - can survive outside the mammary gland, is very contagious infection, most common after teat canal injury or abnormal milk machine function. This organism is one of the most common Streptococcus infections during the dry period.

Streptococcus dysgalactiae - can survive outside the mammary gland, is very contagious. The main source of this organism is infected udders, tonsils, and skin lesion.

Streptococcus bovis - found frequently in feces and discharge of the reproductive tract.

Streptococcus zooepidemicus - usually a subacute or chronic mastitis.

In general, there appears to be a causal relationship between Streptococcus infection and teat injuries caused by milking technique and improper housing.

Clinical Signs

  1. Infection is usually acute, with severe swelling of the quarter and abnormality of the milk, with occasional cases showing a moderate systemic reaction.

Treatment
In general, Str. dysgalactiae and Str. uberis respond well to penicillin, erythromycin, and tetracyclines, while Str. zooepidemicus does not respond well to penicillin.

Control
Control programs for these organisms typically involve lactating cow therapy of clinical cases, routine dry cow therapy, and rigorous application of milking sanitation procedures.

COLIFORM MASTITIS

  1. Cause
    1. in most herds, E. coli, Klebsiella species, are most commonly isolated, while Enterobacter and Citrobacter are isolated less frequently. In some herds, coliform bacteria can account for 20% to 80% of all organisms isolated from acute mastitis.
    2. the source of the coliforms is environmental compared to Staphylococcus aureus which is infectious. Environmental sanitation and milking hygiene are important in controlling coliform mastitis.
    3. coliform bacteria enter the mammary gland via the streak canal. They grow rapidly to high concentrations, and products of bacterial growth and tissue damage stimulate a marked influx of polymorphonuclear leukocytes into the gland.
    4. endotoxin is believed to be a major initiating factor in the clinical signs observed in coliform mastitis. Endotoxin is considered to be a factor in the severe systemic derangements observed in patients with peracute coliform mastitis. When endotoxins are absorbed, a complex cascade of pathophysiologic events are triggered. Endothelial damage and activation of the coagulation system may occur as a consequence of direct endotoxin membrane injury. It is however activation of the body's own inflammatory mechanisms by endotoxin that lead to most of the damage. In this regard, activation of neutrophils, platelets, vascular endolthelium, mast cells, and most importantly macrophages leads to the release of critical mediators such as tumor necrosis factor(TNF), interleukins(especially IL-1), platelet activating factor, phospholipase, prostaglandins, thromboxane, and leukotrienes. Numerous other mediators and toxins have also been implicated and include histamine, serotonin, beta endorphins, and toxic oxygen metabolites. Cytotoxicity occurs due to direct actions, mediator effects, oxygen radical formation and lysosomal enzyme release. (fig 83)

      The cellular damage leads to an escalating cascade of microvascular injury, increased capillary permeability, and decreased tissue perfusion.
  2. Environmental and Management Factors in Coliform Mastitis
    1. It has been shown that numbers of Klebsiella and total coliform organisms increase markedly when sawdust is in use under cows. It was found that sawdust had higher numbers of Klebsiella and total coliforms than did wood shavings or straw.
    2. Several other environmental or management factors may influence the incidence of coliform mastitis. One such factor is the effect of milking time hygiene on coliform infections. One hypothesis is that coliform bacteria may reach the teat end at any time between milkings, but that implantation of bacteria into the teat canal may occur during the milking process due to the action of the milking machine. If this hypothesis is correct, then premilking procedures which substantially reduce coliform numbers on the teat end might be expected to reduce the number of coliform infections. Careful washing of udders, avoidance of excessive amounts of water, and drying of teat and udder surfaces before applying the milking machine are common sense measures which may prove useful.
    3. Automated udder washing - large volumes of water are leaving the udder of the cow prior to the application of the milking units.
    4. Faulty, unsanitary infusion techniques.
  3. Route of Infection
    1. It is generally agreed that the route of entry of coliform bacteria into the mammary glands is through the streak canal. Coliform bacteria are not active tissue invaders, there is production and elaboration of endotoxin.
    2. Increasing the numbers of bacteria on the teat end will increase the incidence of intramammary infection.
    3. Numbers of coliforms recoverable from teat ends are usually low compared with numbers of staphylococci and streptococci recovered; this is true despite the fact that under most conditions teat ends are exposed to large numbers of coliform organisms. When large numbers of coliforms are found on teat ends, the condition is usually transitory and probably results from chance contamination from the environment.
  4. Stage of Lactation and Coliform Infection
    1. Coliform mastitis frequently occurs shortly after parturition. In 2 studies, more than one-third of all coliform infections were first detected in colostrum or in samples collected between 5 and 11 days postpartum. Most coliform infections probably occur in the few days immediately before calving.
    2. Approach to the prevention of coliform mastitis at calving, some investigators reported that thorough cleaning of corrals and dipping of teats twice daily for 3 days before expected calving appeared to halt a serious occurrence of E. coli mastitis in parturient cows.
    3. During the early hours after inoculation, bacterial numbers increased rapidly, followed by leukocyte diapedesis into the mammary gland. Bacterial concentrations then decreased rapidly, presumably due to phagocytosis by polymorphonuclear leukocytes. Phagocytosis resulted in endotoxin release, with maximal swelling of the udder, and systemic signs, including fever, depression, and inappetence. Endotoxin is believed to be the primary stimulus to the inflammatory response, and the appearance of systemic signs is believed due to endotoxin absorption from the mammary gland. A subnormal temperature then develops rapidly.
    4. Clinicopathologic changes in acute coliform or endotoxin mastitis include early leukopenia, with reduced numbers of neutrophils, lymphocytes, monocytes, and eosinophils. It has been suggested that leukopenia is due in part to migration of leukocytes into the infected gland.
    5. Marked alterations of the complement system may occur and this sets into action blood coagulation and eventually results in a disseminating intravascular coagulopathy.
    6. Other features of acute coliform mastitis include hyperglycemia, hypercortisolemia, and hypocalcemia.
    7. In a more recent California report of a herd in which about 20 cases were treated per month, most were mild and responded readily to treatment; only about 10% were characterized as peracute. However, among cows with the peracute form, it was estimated that 20% returned to milk if lactating, 10% died of the disease, and 70% were culled for agalactia.

Clinical Signs

  1. sudden onset
  2. okay or normal at previous milking and then found at next milking depressed, completely anorexic, may be shivering, and has a watery diarrhea (fig 84)
  3. quarter may not be noticeable, swollen quarter may be smaller than normal because of hypogalactia
  4. first 6-8 hours of peracute disease the temperature is usually 106-108 F
  5. increased heart and respiratory rate
  6. sunken eyes - loss of elasticity of skin - progresses very rapidly
  7. cow may become recumbent within hours, becomes sore, depressed, and there is a decline in temperature, 98-102 F
  8. later the gland may swell and be painful to touch
  9. gross change in milk is characteristic - in a few hours, small particles are visible in the milk which becomes watery and then serous and straw-colored
  10. in severe cases, the secretion may become serosanguineous
  11. the affected quarter may not return to normal during that lactation but should feel normal to palpation in about 10 days
  12. 10-15% of coliform mastitis cows show severe systemic signs including significant dehydration, weakness, hypothermia, injected mucous membranes, and scleral vasculature, severe gastrointestinal stasis, and rumen atony, and diarrhea.

Therapy

  • Four therapeutic principles have been identified for the management of acute coliform mastitis: eliminating bacteria from the mammary gland, neutralizing endotoxin, neutralizing the effects of endotoxin, and providing supportive therapy.
  • Antimicrobial agents are commonly administered by systemic and intramammary routes to treat coliform mastitis. More recent research evidence would suggest that intramammary treatment is not justified
  • Recent research would suggest that some cows not only have endotoxemia, but also have a bacteremia. On this basis, the use of systemically administered antimicrobials should be strongly considered, particularly if the economic value of the cow warrants aggressive treatment. If antibiotics are used, the most effective agents will include the aminoglycosides, cephalosporins, or potentiated sulfonamides. Because the use of aminoglycosides results in extremely prolonged tissue drug resides, their use is strongly discouraged.
  • Frequent stripping out of affected quarters is an important aspect of therapy. The rationale is that evacuation of bacteria and toxins minimizes the local effects on the gland. Affected quarters should be stripped out as often as is practical.
  • Intravenous or intramuscular oxytocin (20 to 40 IU) can facilitate the removal of contaminated milk.
  • Fluid therapy in peracute and toxic cases, as much as 20 L of a balanced electrolyte solution IV during the first one to two hours. The rest of the total dose (60 to 110 ml/kg) can be given during the next 10-12 hours.
    (fig 1036)
  • Hypertonic saline therapy is advocated in cases where large volumes of fluids are not possible. Hypertonic saline, equivalent to 7.2% sodium chloride, at 5 ml/kg IV given over 3-5 minutes via a catheter or large gauge needle placed in the jugular vein. The plasma volume expansion and increased cardiac output, although rapid following administration of hypertonic saline, is short-lived, generally lasting less than 2 hours. Hypertonic saline solution administration is, therefore, a rapid mode of resuscitation which must be followed by IV isotonic fluids. In circumstances where economic issues preclude the administration of IV isotonic crystalloid fluids, hypertonic saline can be followed by intraruminal administration of water. This can be accomplished by pumping 5 gallons of water into the rumen through an esophageal tube. Treated ruminants should also be provided with free access to water, as most will be thirsty.
  • Total doses of 150 to 250 g of sodium bicarbonate, at a maximum concentration of 5%, can be useful in treating the metabolic acidosis.
  • Many cases can benefit from intravenous glucose to help in maintaining hepatic detoxification of endotoxins. The recommended dose is 250 g of glucose.
  • Hypocalcemia has been documented in many cases of coliform mastitis. Caution should be given to giving calcium preparations, because it can be fatal. It is probably best to give SQ rather than IV, or else give very slowly or diluted.
  • Anti-inflammatory agents - in experimental studies using an E. coli intramammary endotoxin model, parenteral flunixin meglumine at 1.1 mg/kg IV every 8-12 hours prevented pyrexia, reduced clinical depression, and reduced local signs of quarter inflammation. Aspirin 100 mg/kg orally and repeated every 12 hours is another possibility. Ibuprofen at 2.2 mg/kg, IM, q 24h significantly improved the clinical course of endotoxin-induced mastitis of cattle and is probably the NSAID of choice when treating coliform mastitis. Recognize that the half life of ketoprofen is short( 30 minutes) suggesting that it should be administered more frequently than at 24h intervals. Phenylbutazone at a loading dose of 10 to 20 mg/kg and daily maintance dose of 2.5 to 5 mg/kg IV is also recommended.

    Dexamethasone at 1-3 mg/kg is beneficial for approximately 48 hours. but can also cause abortion. The drug is beneficial in acute endotoxemia because it prevents the activation of phospholipase.

Prevention

  • The primary source of coliform mastitis infections is the environment. Infections may occur either at milking, between milkings, or during the dry period. The focus of control efforts centers not on the infected cow, but on sanitizing the general environment and preventing the contamination of the teat end during the variable interval in which the streak canal remains open after milking. Therefore, management programs that incorporate ways in which the lactating cow can remain standing for at least 30 minutes after milking will allow the sphincter muscles of the teat end to contract, making it difficult for bacteria to enter the streak canal.
  • Improper application of premilking sanitation procedures, particularly milking cows with wet udders, will dramatically increase the incidence of coliform mastitis. Contaminated wash water dripping off either the cow's back or mammary gland will carry bacteria to the teat end. If mammary glands are handwashed, individual paper towels should be used, both to wash and dry each quarter. If automatic wash pens are used, careful attention must be paid to their design and function. The angle of sprinkler heads should be sufficiently low. In addition to postmilking dipping, premilking teat dipping, has been reported to reduce the incidence of infections with environmental pathogens.
  • Control measures effective against the contagious pathogens are of little value in the control of coliform mastitis. An effective coliform mastitis control program reduces teat end exposure and maximizes the resistance of the mammary gland.
  • Exposure of teat ends to the coliform bacteria involves the following factors: housing, bedding materials, access to muddy or manure-covered lots, milking time hygiene, and machine function. The use of inorganic bedding materials can significantly reduce teat end exposure to the coliform bacteria. Predipping can reduce exposure to the coliform bacteria during the milking process. Cows resistance to infection can be optimized by reducing stress and feeding well-balanced diets containing adequate amounts of vitamin E and selenium.
  • Antibiotics are of little or no value for the control of coliform mastitis in dairy herds.
  • A coliform vaccine based on a mutant strain of E. coli called J5 has been shown to reduce the incidence of clinical coliform mastitis during lactation but not the prevalence of infected quarters at calving. An 80% reduction in coliform mastitis in cows vaccinated with a vaccine (J5 TC) made of the mutant has been demonstrated. Three doses of the vaccine are recommended. Examples of vaccines are J5 Bacterin (Upjohn) and J-VacJ5 (Sanofi).
  • Cross-protective vaccines have also been manufactured using genetically engineered mutants such as the patented R/17 strain of Salmonella typhimurium. A vaccine called ENDOVAC-Bovi (IMMVAC Inc., Columbia, MO) is available.

BOVINE MASTITIS CAUSED BY PSEUDOMONAS AERUGINOSA
In most dairy herds, occurrence of Pseudomonas mastitis is only sporadic, but occasionally it may be a serious herd problem. In surveys, overall incidence is not over 3%, with most reports showing less than 1% of udder infections caused by P. aeruginosa.

Pseudomonas aeruginosa is usually regarded as an opportunist, being relatively non-invasive and producing disease more often after injury of debilitating conditions, or it is secondary to other infectious agents. Use of common or nonsterile teat cannulas for intramammary administration of antibiotics has been involved in the introduction and spread of Pseudomonas mastitis. Home-mixed antibiotic preparations have also contributed to herd epizootics. Access to ponds of stagnant water has been associated with some herd problems.

  1. Description of Disease
    Pseudomonas mastitis of the dairy cow is usually an acute local process. Some cases become chronic or subacute. Occasional cases are acute with systemic signs and a fatal outcome. The infected gland is swollen, and the secretion is altered in gross appearance (watery and clotted). A few days after the acute attack, swelling may subside, and milk gradually becomes grossly normal. Spontaneous recovery may occur; but in some cases, the disease becomes chronic with flare-ups occurring over weeks or months.
  2. Therapy
    1. In general, specific treatment is unsatisfactory. While most isolates of P. aeruginosa are inhibited by gentamicin, administration of this drug may not succeed in elimination of the organism.

SERRATIA LIQUEFACIENS MASTITIS
Serratia spp. are gram-negative motile bacilli of the family Enterobacteriaceae. Commonly found in soil and water, they were considered nonpathogenic saprophytic bacteria.

Serratia marcescens and Serratia liquefaciens have been incriminated as causes of mastitis in dairy cows. Australian investigators found S. liquefaciens in the milk of 5 cows with clinical mastitis in a 120-cow herd.

Abnormal physical findings included rectal temperature of 39.7E C and moderate edema of one udder quarter. Milk from the affected quarter was of normal color, but was slightly watery, with occasional clots. The cow responded favorably to intramammary infusion of gentamicin sulfate and IV administration of chloramphenicol.

S. liquefaciens isolants were shown to be susceptible to chloramphenicol, gentamicin, kanamycin, and trimethoprim-sulfadiazine, but were resistant to ampicillin, cephalothin, streptomycin, and tetracycline.

Either gentamicin sulfate, kanamycin sulfate, or amikacin sulfate was used in intramammary treatments in addition to and in conjunction with several commercially prepared udder infusion products containing cephapirin sodium, hetacillin potassium, or procaine penicillin-novobiocin oil suspension.

CORYNEBACTERIUM (Actinomyces) PYOGENES MASTITIS
Not more than 1 to 2% of all acute cases of bovine mastitis in a herd are caused by this organism. In Great Britain, incidence is higher in summer months and it is commonly referred to as "summer mastitis." In the United States, definite seasonal trends have not been reported. Trauma or lesions initiated by other agents greatly favor establishment of infection by C pyogenes.

  1. Transmission and Predisposing Factors
    It has been reported that increased incidence of C pyogenes mastitis has occurred during rainy periods when cows are forced to walk through or stand in deep muddy lots. Flies have been thought to play an important part in the transmission of "summer mastitis." A number of isolations of C pyogenes have been made from flies.
  2. Description of Disease
    Onset is usually sudden, with acute swelling of the gland and grossly altered secretion. Exudate may be seropurulent at first, changing to a thick purulent character in a few days.
    (fig 88) Blood also may be a component of the exudate. The infected animal may have a substantial increase in body temperature and exhibit signs of a toxemia. Acute and systemic manifestations subside, but condition of the udder does not improve after a few days as in most other forms of mastitis. Exudate remains purulent, and secretion of milk ceases. Necrosis of the gland parenchyma extending through the skin covering the udder is not uncommon. (fig 89) Resulting fistulous tracts are characteristic of C pyogenes mastitis and are not observed with other etiologic agents. Metastasis of the organism from the udder is to internal organs often results in the formation of abscesses in liver, lungs, spleen, or kidney. The disease may continue for several weeks or months as an acute local condition, often causing the death of the animal.
  3. Diagnosis
    A reasonably accurate diagnosis of C pyogenes mastitis can be made based on the gross appearance of the exudate and by a gram stain.
  4. Treatment
    Prolonged intensive treatment of early cases with penicillin has occasionally given results. Surgical drainage by teat removal is often beneficial to the extent that the process heals sufficiently for market salvage of the cow. Bacterins, toxoids, or combinations of these have been given a fairly extensive trial, but benefits from these products have been limited.

MYCOPLASMA MASTITIS                                 Credit to: John Kirk

  1. Mycoplasma species are important causes of mastitis, arthritis, urogenital disease, and respiratory infections in dairy cattle. With respect to mastitis in dairy cows, Mycoplasma species are highly contagious and economically important causes of milk loss and increased culling in infected cows.
  2. Distribution
    1. The disease has been reported in regions worldwide, including Europe, Japan, Australia, Israel, Canada, New Zealand, and many areas of the United States, such as New York, Massachusetts, Pennsylvania, Florida, Arkansas, California, Idaho, Oregon, Hawaii, Washington, Alaska, and Arizona.
  3. Prevalence
    1. The prevalence of Mycoplasma in bulk tanks (where routine microbiological screening is performed) varies between 1% to 4% in the dairies tested.
    2. In very large herds with low prevalence, Mycoplasma may remain undetected because of a dilution effect.
  4. Species
    1. At least 11 species of Mycoplasma have been isolated from milk. These species are: Acholeplasma laidlawii, M. alkalenscens, M. arginini, M. bovigenitalium, M. bovirhinis, M. bovis, M, californicum, M. canadense, M. capricolum, Group 7 bovine, and F-38.
    2. M. bovis is the most frequently isolated and most pathogenic species in the United States.
  5. Route of Infection
    1. Herd outbreaks are often traced back to the introduction of infected cows to a herd.
    2. Heifers that have never been milked may be noted as infected during their first milking and, therefore, may be the source of Mycoplasma entry into a herd.
    3. Cows in all stages of lactation, including dry cows, are susceptible to infection, but most infections occur during the milking process. The usual route of infection for cows is through the teat canal.
    4. Mycoplasma mastitis developed in the noninoculated quarters of four cows that were all inoculated in a single quarter.
    5. Authors have observed spread of the disease to the mammary gland via the blood stream.
  6. Reservoir
    1. Cows infected with Mycoplasma mastitis may become chronic carriers.
    2. Infections may spread from other sites on animals, such as the respiratory tract (especially from calves with subclinical pneumonia) and the reproductive tract of cows as well as from arthritic cows or calves.
    3. Mycoplasma has also been isolated from the dairy environment. Mycoplasma bovis survives for long periods in manure (236 days); milk (2 months) at 4E C; and urine, water, straw, and air.
  7. Clinical Syndromes
    1. increased incidence of clinical mastitis that is resistant to therapy.
    2. clinical mastitis in multiple quarters without systemic signs of illness in animals; systemic signs, such as fever or anorexia, are usually transitory and may go undetected; often, two quarters on the same side become infected.
    3. marked loss of milk production to the extent that some cows cease lactating; this usually occurs three to six days after onset of infection.
    4. obviously abnormal milk, which is often brown to tan with flaky sediment in a watery or serous fluid; the milk may later become purulent.
    5. The somatic cell count is elevated in individual cows infected with subclinical mastitis.
  8. Herd Effects
    1. In dairies where monitoring is not in place, losses can be great. Prevalences of up to 70% have been reported. High levels of infection have resulted after intramammary infusion drugs and nonhygienic infusion techniques were contaminated.
    2. Clinical mastitis results in production loss; destroyed quarters; prolonged milking time; and increased treatment costs as a result of discarded milk, culling, and possibility of milk antibiotic residue.
    3. In addition to the effects of mastitis, the number of calf replacements may be reduced because of arthritis and pneumonia.
  9. Detection Methods
    1. The primary method of detection has been microbiological culture of milk samples taken from suspect cows or bulk tanks. Four to seven days is needed for isolation of Mycoplasma.
    2. Other laboratory methods have been developed to detect species of Mycoplasma.
  10. Treatment
    1. Treatment regimens reported in studies from the United States have been overwhelmingly unsatisfactory.
    2. Drugs that have been reported to be sensitive in vitro include erythromycin, lincomycin, demeclocycline, kanamycin, spiramycin, doxycycline, tetracycline, and tylosin.
    3. Drugs reported with positive effects are tylosin and oxytetracycline.
    4. It should be noted that most of the drugs showing sensitivity are not approved by the Food and Drug Administration for lactating dairy cows.
  11. Prevention
    1. Cows or calves should not be purchased from herds with a history of Mycoplasma mastitis or elevated somatic cell counts. Likewise, animals of unknown origin should not be purchased.
  12. Control
    1. Some investigators recommend that discarded milk infected with mastitis should not be fed to young calves. Some have suggested that the milk fed to calves should be pasteurized to prevent spread of infection.
    2. Physical separation of young replacement stock from older animals has been advised.
    3. The backbone of any control program should be routine bulk tank milk monitoring for somatic cell count level and culture with media designed specifically for the detection of Mycoplasma and other pathogenic bacteria.
    4. Another early warning control measure is to culture all cows that have clinical cases of mastitis.
    5. At the first discovery of disease, individual cows infected with Mycoplasma should be quickly identified and then culled or permanently segregated.

BOVINE MYCOTIC MASTITIS
Mycotic infections of the mammary gland can occur as natural sporadic infections affecting a small percentage of cows in a herd or from treatment-related outbreaks affecting the majority of animals within a herd.

  1. Causative Organisms
    The most common mycotic organisms causing mastitis belong to the genera Candida, Cryptococcus, and Trichosporon. Candida is the most frequently isolated yeast from milk or the mammary gland. It has been reported to have been isolated from 56% to 86% of the yeast-positive milk samples tested.
  2. Epidemiology - Spread of Infection
    Mycotic organisms are common in the environment in which dairy cows are confined. For example, Cryptococcus neoformans is a soil-borne organism that is often isolated in pigeon droppings and bird manure. Candida spp. are part of the normal flora of the skin and digestive tract and have also been isolated from brewer's grain fed to dairy cows. Nocardia organisms are found naturally in the soil, water, air, and herbage and on the skin of udders of healthy cows. Trichosporon spp. are common in air, soil, body surfaces, and stagnant water.

    In a seven-year study in Minnesota, nearly all yeast infections of the mammary gland were associated with homemade veterinary udder infusion products or multiple-dose commercial products given with reused syringes or teat cannulas. In still another case study, the source of mycotic organisms was found to be an intramammary infusion product produced by the attending veterinarian. In at least one case study, the source was found to be contaminated udder wash and teat cups.
  3. Prevalence of Mycotic Mastitis
    In a variety of reported studies, between 2% and 7% of the milk samples that were taken from dairy cows on a routine basis were positive for mycotic organisms. Levels in problem herds ranged from 8-70%.

    During a period of 4 years, 950 cows became infected with yeast mastitis within a herd of about 3300. In all of these herds, streptococcal mastitis and treatment with antibiotics (usually penicillin) were common precursors to mycotic mastitis.
  4. Economic Losses
    Cows that suffer from acute clinical Candida or Trichosporon yeast infection recover to near normal production one week to one month following onset of the infection. Other animals infected with Cryptococcus, Aspergillus or Nocardia spp. usually developed chronic, progressive mammary lesions resulting in marked decreases in production and eventual sale to slaughter. Deaths may occur from yeast infections.
  5. Pathogenesis
    Yeasts are known to be ubiquitous in the natural surroundings of dairy cattle, and therefore challenges to the mammary gland may occur frequently. The severity of infection, however, relates to the species of yeast involved, the number of organisms introduced into the gland, and the ability of the organism to grow at 40E C.
  6. Clinical Findings
    Clinical findings vary from nonclinical to severe life-threatening systemic infections. The nonclinical infections may spontaneously resolve or become chronic and long-term. Peak in clinical signs by about 10 days post infection. Initial signs of infection include fever, reduced milk flow, abnormal milk, swelling, and inflammation of the mammary gland, inappetence, ataxia, and depression. The appearance of the abnormal milk is usually watery to mucoid with clots varying from gray-white to yellowish. (fig 92)
  7. Laboratory Findings and Diagnosis
    Diagnosis is made by culture of mycotic organisms from milk of infected glands. A direct smear of milk should be stained for microscopic examination. The presence of large oval bodies with or without budding projections resembling baseball bats is indicative of mycotic infection.

    Media that restrict the growth of bacteria are often used for attempts at mycotic isolation. Sabouraud's agar medium is often used in this way to increase the opportunities to isolate yeast organisms from milk samples.

    Organisms are usually visible after growth of 24 to 48 hours on Sabouraud's agar glucose medium.

    In animals with chronic infections, nodular lesions develop within the mammary gland. Nodules are often granulomatous with caseous centers and fibrous capsules. Cryptococcus and Nocardia may also cause generalized fibrosis of the gland.
  8. Treatment
    No FDA-approved agents are now available. Most experimental cases spontaneously regress with only supportive treatment, as do most naturally occurring cases caused by Candida or Trichosporon. Beneficial supportive therapy during the acute phase includes hydrotherapy, massage, frequent striping (1-2 hour intervals during the day), and the use of oxytocin (40-100 USP units intramuscularly or subcutaneously) to cause milk letdown and removal of the organisms.

    In vitro, most yeasts are reported to be sensitive to nystatin, amphotericin B, and 5-fluorocystosine. These agents, however, may often cause damage to the mammary gland during treatment. Less toxic antifungal agents include undecylenic acid, primaricin, and miconazole. In vitro studies using isolates from 91 cases indicated that 96% were sensitive to clotrimazole; over 65% were sensitive to ketoconazole and nystatin; while less than 50% were sensitive to miconazole, amphotericin B, and 5-fluorocystosine.

    In a field trial without controls, treatment with nystatin (1,500,000 IU/treatment) or miconazole (50-100 mg/treatment) has been described as useful used as an intramammary injection in 60 mo of sterile water.

    Other treatments that have been reported include systemic use of thiabendazole at recommended deworming doses repeated for several days or oral thiabendazole for three days at 45 g/treatment. Other clinicians have used iodine with apparent clinical cures. Iodine can be used as 2 grams of iodide crystals dissolved in 30 ml of ether to which 150 mo of mineral oil is added and 40 ml of the mixture infused intramammarily per treatment. Some drugs used for this purpose are 3% silver nitrate (30-60 ml), 5% copper sulfate (20 ml), and 1:500 acriflavine (100-300 ml) as udder infusions.
  9. Prevention
    Most herd outbreaks can be avoided by using properly prepared commercial products in single-dose syringes (i.e., no reusable teat cannulas) and by following proper sanitary measures during intramammary infusion of therapeutic products.

General Detection of Infected Quarters

  1. Strip cup
  2. Submission of all quarters from all cows to California Mastitis Test (CMT)
    (fig 1200)
  3. Bacteriological examination of CMT positive quarters
  4. Antibiotic sensitivity of pathogens isolated
  5. ProStaph test
California Mastitis Test
CMT Reaction Leukocyte Count/ML Percent of Milk Yield Lost
trace 150,000–500,000 6
1 400,000-1,500,000 10
2 800,000-5,000,000 16
3 >5,000,000 24

Function of the test is to determine the quantity DNA and therefore approximately the number of leukocytes.

MILK + PREPARED REAGENT = REACTION (gel formation)

SOMATIC CELLS IN MILK (fig 1205)

  • The displaced alveolar epithelial cells, phagocytes, and white blood cells comprise the somatic cells of the milk. The phagocytes or white blood cells represent from 65 to 70% of the cells in milk from uninfected quarters. In response to irritation within the gland, the percentage of white blood cells may reach 95% of the total somatic cells in the milk. Recent changes in the Pasteurized Milk Ordinance have decreased the legal limit for milk SCC from 1,000,000 to 750,000 cells/ml in bulk tank samples. Most herds with bulk tank SCC exceeding the new legal limit have ongoing contagious mastitis problems.
  • A recent study of Virginia herds reported 45%, 66%, and 76% of the cows with counts <100,000, <200,000, and <300,000 cells/ml, respectively.
  • A level of >400,000 cells/ml has been suggested as indicative of serious infection with a major pathogen. Levels between 100,000 and 400,000 cells/ml suggested a developing infection, while cows with <100,000 cells/ml were usually not infected (62.2%).
  • Efforts have also been made to relate the bulk tank somatic cell count or herd somatic cell count to infection status.

Other Factors Affecting the Somatic Cell Count
Season
. Data from Wisconsin shows a peak somatic cell count from July through August and a low count in March. Data from Quebec, Canada, indicates a low count in May, with a steady increase beginning in June and registering the highest count in December. The increase which began when the cows went to pasture and peaked when they returned to housing. In most cases, the somatic cell count for a herd measures the lowest in the spring.

Age. In general, researchers believe that a minimal or no increase in the count occurs with age if a cow is free of infection. Heifers following parturition usually have counts between 20,000 and 100,000 cells/ml. Older cows usually have high cellular readings, possibly because older cows have more resolved infections or tend to respond more frequently to infections caused by minor pathogens.

Stage of Lactation. Most cows (especially older cows) have higher counts at the beginning and end of lactation periods, with the lowest count occurring at the peak level of production during the lactation. Caution is advised when interpreting the count during the initial or final 14 days of lactation.

Production Level. A sudden decline in milk production generally causes an increase in the count because of a concentration of somatic cells. This event is most pronounced when milk production drops lower than 20 lb/cow/day. Reduced production can be caused by numerous factors, such as illness or lack of water, and can in turn cause an increased somatic cell count.

Management Practices. In general, lower counts are reported from herds using milking parlors (compared with higher counts when barn pipelines are used), from herds that routinely use postmilking teat dips (compared with higher counts for nondipping herds), when single-use towels are used for udder preparation, and with selective dry cow therapy (particularly when teat dipping is also practiced). Herds involved in comprehensive programs to improve udder health have lower counts than those not included in udder health programs.

Using Composite Cow Results. The composite (individual) cow count can be used in a general way to predict the probability of infection in cows. The composite cow count can be used to help identify cows for culling. Cows with persistent elevations throughout the lactation are potential culls, particularly if dry cow treatment has failed to lower the counts. Removing these cows decreases the spread of infection by removing the source.

The composite cow count can be used to identify cows for early dry off. The use of somatic cell counts is valuable in determining the effectiveness or response to treatment.

Using Bulk Tank Sample Results.

  • Regulatory agencies and milk cooperatives use the bulk tank count to determine the acceptability of milk for shipment. Herds with counts <250,000 cells/ml are approaching the optimal level of udder health, while herds with bulk tank counts >500,000 cells/ml have definite problems with subclinical mastitis.
  • The somatic cell count (either the bulk tank count of weighted averages) of a herd can be used as an early warning to detect problems in udder health. One accepted warning signal is when 15% of cows in a herd have counts >800,000 cells/ml. In this case, a complete review of the udder health plan is indicated, including the milking equipment, milking procedure, environmental condition of housing, evaluation of the detection and treatment system, and reevaluation of the dry cow treatment program.
  • The bulk tank count can also give an estimate of the influence of herd udder health on production. For herds with counts measuring between 500,000 and 1,000,000 cells/ml, an estimated 12% reduction in production has been made. Herds with counts >1,000,000 cells/ml may be losing up to 20% of their production.

MASTITIS THERAPY  (fig mam 028)
There are a variety of approaches to mastitis control. They can relate to the locale, the specific herd, the value of an individual cow or the entire herd, the size of the herd, farm management, and the knowledge or feeling of the veterinarian involved. However, a veterinarian's first concern has to be the patient's life, productivity, and the economics involved. His second concern has to be the probable cause of the mastitis and the predisposing factors. A veterinarian becomes involved in mastitis therapy for these reasons: (1) a herd health mastitis program is planned for a dairy; (2) he is called to treat a cow with peracute or acute clinical mastitis; (3) he is called to treat a cow with chronic or nonresponsive clinical mastitis; or (4) he is called because milk quality has deteriorated to a point of nonacceptance by the processor.

The therapeutic and preventive effectiveness of antimicrobial drugs for bovine mastitis is dependent upon the following factors: the etiologic organism, proper use of the drug under consideration, dairy husbandry and sanitation procedures, and phase of the disease.

Several antibiotic residue detection kits are currently marketed in the U.S. Although test kits are useful adjuncts in residue avoidance programs, these tests do not guarantee a residue free milk supply. Equally of concern to the dairy industry, some commercially available tests are plagued by false-positive test results. When extra-label use of antibiotics is necessary, a veterinarian should be prepared to provide instruction to the client as to appropriate withdrawal times. Guidelines for antibiotic withdrawals can be obtained from the Food Animal Residue Avoidance Databank.

Some dairymen and veterinarians have already decided that the risks of antibiotic use in most clinical mastitis cases exceed the benefits and have stopped treating clinical mastitis cows with antibiotics in herds with a low prevalence of the contagious organisms. They emphasize protocols of frequent milkout aided by oxytocin injections and anti-inflammatory drugs, along with heightened attention to management of housing, bedding, and premilking hygiene to prevent infection with environmental pathogens.

FARAD Recommended withdrawl intervals for Nonsteroidal Anti-inflammatory Drugs
Drug Species Dosage Milk withdrawl(h) Meat withdrawl(d)
Aspirin All food 100 mg/kg q12hrs 24 1
Ketoprofen Cattle 3.3mg/kg IV or IM
q 24 h
24 7
Flunixin Cattle 1.1-2.2 mg/kg IV
or IM, q 24 h
72 10
Phenylbutazone Cattle 4-6 g/animal IV or
IM, followed by up
to 2 g/animal daily
120 21

Sources of Drug Residue Information

  • FARAD                            Food Animal Residue Avoidance Databank
  • AMDUCA                         Animal Medicinal Drug Use Clarification Act
  • Food Animal Residue
    Avoidance Databank        (1-888-US-FARAD) or (1-888-873-2723)
                                          http://ace.orst.edu/info/farad
                                          http://cptc.ncsu.edu/farad
                                          E-mail addresses farad@ucdavis.edu (California)
                                                                    farad@ncsu.edu (North Caroline)
                                          Fax numbers–916-752-0903 California
                                                               919-829-4358 North Carolina
  • FARAD Compendium       A comprehensive compendium of FDA-CVM approved food animal drugs
  • VetGram                          Windows-based computer program which contains complete label information for all approved food animal veterinary drugs
  • ProGram                          Windows-based "Producer’s Guide to Residue Avoidance Management"–contains label information for over-the-counter drugs only.
  • Journal of the American
    Veterinary Medical Ass     "Farad Digest" a regular feature to help veterinarians implement AMDUCA
  • ISI/NOAH World
    Veterinary Index                Subscription to NOAH available at www.avma.org
  • Toxicologic monographs
    from the Joint FAO/WHO
    Expert Committee on Food
    Additives                           www.fao.org and www.who.org
  • U.S. Pharmacopoeia
    drug monographs              (301)881-0666

Drugs and Classes of Drugs For Which Extra-Label Use in Food Animals is Prohibited By FDA-CVM

  • Chloramphenicol
  • Clenbuterol
  • Diethylstilbestrol
  • Dipyrone
  • Fluoroquinolones(any products labeled for either humans or companion animals may not be used in food animals. Any deviation from a food animal label( such as use with a different species, dosage, route of administration, or disease indication) is similarly illegal. In the case of the approved beef cattle formulation of enrofloxacin (Baytril 100), this prohibition extends to all nonbeef-production animals, including lactating and nonlactating dairy cows, heifer replacements, and veal calves. Enrofloxacin may not be stored in dairy farm drug cabinets.)
  • Furazolidone
  • Nitrofurazone
  • Nitroimidazoes (eg, dimetridazole, ipronidazole
  • Sulfonamides in lactating dairy cattle ( with the exception of approved uses of
    Sulfadimethoxine in dairy cattle older than 20 months) Additionally, extralabel use of Sulfadimethoxine in lactating dairy cattle is prohibited( for example, use of a higher dose or slow-release Sulfadimethoxine boluses in dairy cattle is not permitted)
  • Glycopeptides antibiotics( vancomycin)
  • Extralabel use of medicated feed. Also ionophore compounds(ie, monensin, lasalocid) in lactating dairy cattle rations is prohibited

–aminoglycosides– a number of veterinary organizations such as the American Association of Bovine Practitioners support policies that discourage the extralabel use of aminoglycosides. These are nonbinding and should not be confused with legal prohibitions described above

TEAT DIPPING  (fig mam 032)
Teat dipping or spraying with a germicidal solution immediately following milking reduces at least 50% of new intramammary infection for the majority of dairy herds. The procedure is regarded as the single most effective practice for prevention of intramammary infections of lactating dairy cows. Organisms that cause intramammary infections absorb strongly to lipids in the stratum corneum of the teat canal lining, and can exist for months and serve as reservoirs for subsequent intramammary infections. Most S. aureus intramammary infections originate from teat canal infections and most of intramammary infections arising during lactation are preceded by teat canal infections. Six classes of postmilking teat sanitizers include the following: iodophors, quaternary ammonium compounds, chlorhexidines, sodium hypochlorites, dodecyl benzene sulfonic acid, and acrylic latex (physical barriers).

CHRONIC AND NONRESPONSIVE MASTITIS
In chronic cases, economics again enters into consideration when a veterinarian chooses a course of therapy. Value of the cow, stage of lactation, number of cows involved, and number and severity of involved quarters on an individual must be considered. One should consider marketing the cow as one alternative.

Herd health programs are employed frequently in the dairy herds in this country. The mechanics of these programs involve mainly a program of prevention which assures proper sanitation, milking machine operation, milking procedure, housing, maintenance of equipment, diagnosis, and therapy in cases of clinical mastitis as well as therapy of nonlactating cows.

A Fundamental Mastitis Control Program Includes:

  1. Follow precise milking management procedures and use properly functioning milking machines.
  2. Use an approved teat dip on all cows immediately after milking.
  3. Execute approved dry-cow treatment as a standard herd health practice.
  4. Implement appropriate medical management of all clinical cases of mastitis during lactation.
  5. If Streptococcus agalactiae is highly prevalent, initiate therapy during lactation.
  6. Segregate cows with staphylococcal mammary gland infections from the herd.
  7. Cull all cows with chronic mastitis.
  8. Implement routine sanitary procedures to control populations of environmental organisms.
  9. Test replacement animals for detectable mammary gland infections.

HEALTH MANAGEMENT OF DAIRY HERDS TREATED WITH BOVINE SOMATOTROPIN
Bovine somatotropin (BST) is registered by the manufacturers as an alternative name for bovine growth hormone. Drug applications have been submitted to the FDA for 4 forms of recombinant-derived BST. One of these forms is identical to 1 of 4 natural variants of BST, but the other 3 have extra amino acids that served as links between the bovine genome and the bacterial ribosome during manufacture. Certain forms of recombinant BST are more potent metabolically than pituitary BST. Likely efficacy claims for BST are increased milk production and increased efficiency of milk production for 1 or 2 lactations, but probably not for a lifetime.

Milk of BST-treated cows has then been declared equal in composition to that of untreated cows. The effect of long-term BST administration on milk composition is biphasic: saturated long-chain fatty acid content is increased and casein content is decreased early during BST administration, when cows use body tissue stores to make the extra milk; then when tissues are being restored, these changes revert to match the milk composition of control groups.

  1. Milk Production
    1. Milk production responses to BST have been reported as 10 to 25% extra milk in a 305-day lactation by the Animal Health Institute (an association of manufacturers) and as 10 to 15% by the Council for Agricultural Science and Technology.
    2. Dose-response relationship - Milk production increases with BST, up to approximately twice the anticipated approved dose (2D), then flattens or decreases above 2D.
  2. Nutrition and Stress
    1. Catabolic stress - When tissue breakdown to meet the extra metabolic demands of increasing milk production is attended by increased rate of infertility and illness, the condition may be regarded as catabolic stress. In normal lactation, tissue stores of fat and protein are utilized during the first 2 or 3 months, when feed intake is increasing until it matches the extra demand to make milk. This period of tissue utilization is attended by inhibited fertility and a higher frequency of metabolic disorders and infectious diseases. Mastitis incidence is highest in the first 3 months of lactation.
    2. Maximal milk response to exogenous BST is observed in 2 to 5 days, and tissue utilization prevails until feed intake catches up to milk output after 8 weeks or more. Tissue utilization has been detected as loss of body weight and condition as changes in body composition, and as negative energy and protein balances. In effect, BST administration may double the duration of catabolic stress from 2 to 3 months to 4 to 6 months.
    3. Lipid responses - The fat mobilization component of catabolic stress has been manifested by increases of plasma concentrations of free fatty acids (FFA) and acetoacetate (AA) in response to administration of BST.
    4. The catabolic component of BST-stimulated milk production may be detrimental early in lactation but beneficial later, through preventing the fat cow syndrome in the next lactation.
    5. Homeorrhesis - Genetically programmed regulation of nutrient flows to various tissues in proportion to their metabolic rates (nutrient partitioning) during fetal development and growth was called homeorrhesis.
    6. Stimulating milk production with exogenous BST changes the shape of the lactation curve, in contrast to genetic improvement, and thereby extends the period of catabolic stress which is the key to BST-associated infertility and illness.
    7. The combination of sodium bicarbonate and BST had an additive effect on milk production.
    8. The effectiveness of prolonged lactation may be limited by increased culling, mainly for refractory mastitis, infertility, and lameness and for burn-out, a hypermetabolic syndrome that may develop in BST-treated cows. Burn-out is indicated by an abrupt decrease in milk production; by higher body temperature, pulse rate, and respiratory rate; and sometimes, by ketosis.
  3. Heat Intolerance
    1. Thermal balance - Heat production is increased by BST, because it increases with increasing milk production.
    2. Factors other than milk production also are involved in heat intolerance of BST-treated cattle. In nonlactating cattle, higher rectal temperature, breathing rate, and panting frequency were observed when a BST-drug was given.
    3. Control of heat intolerance
      • providing shade to reduce radiant heat load
      • using fans, showers, and ponds to increase heat loss by convection and evaporation
      • including fat in rations to reduce the load of carbon dioxide and to fuel the extra work of heat dissipation
      • providing electrolytes to cover losses
      • incorporating more Bos indicus genes in dairy cows
  4. Infertility
    1. The sterility of cows during the rising phase of lactation has long been known and has been related to cumulative negative energy balance. Stress probably inhibits ovulation when tissue stores are utilized until feed intake matches milk production.
    2. Infertility and high production - A review of reproduction from 27 long-term milk production trials suggested that the percentage of BST-treated cows that failed to become pregnant was about 20% in cows given 1D of BST, compared with about 10% in controls.
    3. Control of infertility
      1. Nutrition
        In general, reproduction is one of the first functions to be impaired when nutrition is less than optimal. The whole ration should be formulated to reach optimal nutrient ranges for specified stages and levels of lactation.
      2. Hormonal drugs
        Gonadotropin releasing hormone and human chorionic gonadotrophin are used to treat follicular cysts, and prostaglandins are used to induce estrus or treat pyometra. Presumably, this treatment reduced adverse effects of BST on reproductive efficiency.
  5. BST-associated Mastitis
    1. Exogenous BST influences the pattern of mastitis in 1 of every 2 or 3 BST-treated herds, by increasing mastitis incidence, duration per case, and days of antibiotic treatment per herd.
    2. Data indicate that BST treatment may introduce a problem into a herd in which mastitis was previously well controlled, or it may mitigate a preexisting problem.
    3. The inconsistency may be attributable partly to conflicting effects of BST on the cow's immune competence. In general, immunity is likely to be suppressed by catabolic stress, contributing to the high mastitis incidence in the first 2 to 3 months of natural lactation.
    4. BST-treated cows needed 4 times the duration of antibiotic treatment in affected herds (0.60% of cow-days) than in unaffected herds (0.15%).
    5. In a summary of mastitis data from 14 milk production trials using 1D of BST, mean mastitis incidence was stated to increase by 8.3% (affected cows) and by 0.07 cases/cow/y.
    6. Exogenous BST increases the incidence of most lesions and diseases common during the rising phase of lactation. So far, the only significant abnormalities other than infertility and mastitis, are lameness and injection site reactions.
  6. Lameness

UDDER EDEMA (fig 99)
Causes

  • inheritance - severity of udder edema is based on an inherent physiological phenomenon, but it has also been concluded that there is little genetic relationship between udder edema and milk production, which there is a genetic relationship.
  • circulatory disturbances - stasis of venous blood or lymph flow. There is increased blood flow to the udder associated with the onset of milk production, but an associated decrease in the amount of blood leaving the udder.
  • diet - prepartum grain feeding has been incriminated. Field studies have suggested a relationship between udder edema and salt intake in the diet.
  • other factors - udder edema becomes more severe as the age of first calving becomes later. The longer the dry period, the greater the chance of udder edema. The disease is more of a problem in heifers, and generally decreases with each calving.

Signs

  • acute - may start forming as early as two to three weeks before calving, peak at parturition, and last for two to three weeks after calving. (fig 109)
  • may involve one or two quarters, but usually involves the whole udder. Swelling may extend ventral to the base of the teats, teats may appear shortened. The skin is tight over the swollen udder and tissue finger pressure will leave a pit.
  • walking and lying down are difficult. Sometimes the edema extends from the udder dorsally, involving the vulva, and extends ventrally and forward on the lower abdomen, as far forward as the sternum.
  • chronic - usually occurs as a sequela to the acute form, frequently present for several months following parturition, disappearing during the middle part of lactation.(fig 101)

Treatment

  • treatment is usually not necessary if condition is not severe. May have permanent damage to the udder and attachments.
  • 20-minute massage, three times daily.
  • hot and cold water applications.
  • udder supports
  • diuretics - hydrochlorothiazide (250 mg once or twice daily) (furosemide IM, IV, or orally, 500 mg once daily or 250 mg twice daily, 1 bolus/cow/day).
  • a combination of corticosteroids and diuretics - caution needs to be exercised, because the product may cause premature calving or abortion.

BLOODY MILK

  • bloody contamination of milk may result from trauma or as a sequela to prepartum udder edema or rupture of small mammary vessels.
  • most of the time, no specific treatment is required
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This section was last updated on: Monday January 31 2005

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