MAMMARY GLAND DISEASES
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.
General Sequence of Events and Pathology
of Bovine Mastitis
- the organisms enter the teat duct.
- the organisms multiply in the teat duct, streak canal, and mammary
- the organisms progress upward into the lactiferous sinus, collecting
ducts and alveoli.
- organisms localize, resulting in leukocytic attraction, edema, and in
some cases, abscess formation.
- healing often results in fibrous connective tissue formation with
- transfer of organisms from infected mammary glands to healthy mammary
- Streptococcus agalactiae, S. aureus, and Mycoplasma
- Streptococcus dysgalactiae, Staphylococci-coagulase negative
- contaminated bedding, water, fecal material, or other fomites
- coliform bacteria
- E. coli, Klebsiella pneumoniae, Enterobacter
aerogenes, Streptococcus fecalis, and foecum.
TYPES OF MASTITIS
- 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
- results in decreased milk production
- 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
- no clinical signs for prolonged intervals
- SCCs are generally elevated.
- mammary gland secretions periodically contain flakes, clots or shreds
- mammary gland is replaced with scar tissue
- caused mostly by Staphylococcus
- parts of the mammary gland become cold and secretions are watery and
- 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
- 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
- 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
- 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
- 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
- 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
- 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.
- 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
- Classified as a coagulase positive bacteria
Pathogenic Factors Attributed to S.
- 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.
- 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.
- 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
- Leukocidin - Leukocidin is elaborated by S. aureus
and is known to attack bovine granulocytes.
- Pigments - The amount of pigment produced by the organism is
correlated to the incidence of persistent infections.
- 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.
- The organism must enter the mammary gland through the teat sphincter.
102) (fig mam 004)
- 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)
- 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.
- 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.
- If neutrophils are able to adequately control S. aureus
multiplication, mild clinical signs, which are usually confined to the mammary gland, will
- Repeated cycles of clinical and subclinical infection throughout the
lactation period is typical of S. aureus mastitis.
- 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.
- 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.
- 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.
- 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
Identifying Staphylococcus Aureus as a
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
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
- 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.
- In regard to systemic treatment, the degree of ionization and lipid
solubility of antibiotics are major factors in establishing a milk-to-serum ratio.
- Most staphylococcus isolated are not sensitive to penicillin in vitro
- Development of penicillin-resistant staphylococci has brought about
the increased use of the following antibacterial drugs:
- 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
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
|Commercially Available Staphylococcus Aureus
||5 mL IM, repeat in 14 days, and booster every 6 months
||5 mL IM, repeat in 14 days, and booster every 6 months
||2 mL IM, repeat in 14 days and booster every 6 months
||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 hyicuscoagulase 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
- 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.
- Deaths rarely occur due to Str. agalactia and complete
loss of productivity of a quarter is uncommon.
- 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.
- 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.
- There is variation in resistance to infection, but invasion takes 1-4
days, and the appearance of inflammation 3-5 days.
- 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.
- 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.
- 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.
- 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.
- 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.
- 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.
- 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
- On rare occasions, a penicillin-resistant strain of streptococci is
encountered, a mixed infection with bacteria which produce penicillinase, may inactive the
- 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
- Lincomycin is also effective.
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
In general, there appears to be a causal relationship between Streptococcus
infection and teat injuries caused by milking technique and improper housing.
- Infection is usually acute, with severe swelling of the quarter and
abnormality of the milk, with occasional cases showing a moderate systemic reaction.
In general, Str. dysgalactiae and Str. uberis respond well
to penicillin, erythromycin, and tetracyclines, while Str. zooepidemicus
does not respond well to penicillin.
Control programs for these organisms typically involve lactating cow therapy of
clinical cases, routine dry cow therapy, and rigorous application of milking sanitation
- 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.
- 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.
- 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.
- 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.
- Environmental and Management Factors in Coliform Mastitis
- 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.
- 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.
- Automated udder washing - large volumes of water are leaving the
udder of the cow prior to the application of the milking units.
- Faulty, unsanitary infusion techniques.
- Route of Infection
- 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.
- Increasing the numbers of bacteria on the teat end will increase the
incidence of intramammary infection.
- 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.
- Stage of Lactation and Coliform Infection
- 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.
- 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.
- 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
- 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.
- Marked alterations of the complement system may occur and this sets
into action blood coagulation and eventually results in a disseminating intravascular
- Other features of acute coliform mastitis include hyperglycemia,
hypercortisolemia, and hypocalcemia.
- 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.
- sudden onset
- 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)
- quarter may not be noticeable, swollen quarter may be smaller than
normal because of hypogalactia
- first 6-8 hours of peracute disease the temperature is usually
- increased heart and respiratory rate
- sunken eyes - loss of elasticity of skin - progresses very rapidly
- cow may become recumbent within hours, becomes sore, depressed, and
there is a decline in temperature, 98-102 F
- later the gland may swell and be painful to touch
- 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
- in severe cases, the secretion may become serosanguineous
- the affected quarter may not return to normal during that lactation
but should feel normal to palpation in about 10 days
- 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.
- 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.
- 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
- 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
- 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
- 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.
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.
- 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.
- 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
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
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.
- 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.
- 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.
A reasonably accurate diagnosis of C pyogenes mastitis can be made based on the gross
appearance of the exudate and by a gram stain.
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.
Credit to: John Kirk
- 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.
- 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.
- The prevalence of Mycoplasma in bulk tanks (where routine microbiological screening is performed) varies
between 1% to 4% in the dairies tested.
- In very large herds with low prevalence, Mycoplasma may remain undetected because of
a dilution effect.
- 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.
- M. bovis is the most frequently
isolated and most pathogenic species in the United States.
- Route of Infection
- Herd outbreaks are often traced back to the introduction of infected
cows to a herd.
- 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.
- 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.
- Mycoplasma mastitis developed in the
noninoculated quarters of four cows that were all inoculated in a single quarter.
- Authors have observed spread of the disease to the mammary gland via
the blood stream.
- Cows infected with Mycoplasma mastitis may become chronic carriers.
- 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.
- 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.
- Clinical Syndromes
- increased incidence of clinical mastitis that is resistant to
- 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.
- marked loss of milk production to the extent that some cows cease
lactating; this usually occurs three to six days after onset of infection.
- obviously abnormal milk, which is often brown to tan with flaky
sediment in a watery or serous fluid; the milk may later become purulent.
- The somatic cell count is elevated in individual cows infected with
- Herd Effects
- 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.
- 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.
- In addition to the effects of mastitis, the number of calf replacements may be reduced
because of arthritis and pneumonia.
- Detection Methods
- 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
- Other laboratory methods have been developed to detect species of Mycoplasma.
- Treatment regimens reported in studies from the United States have been overwhelmingly
- Drugs that have been reported to be sensitive in vitro include erythromycin, lincomycin,
demeclocycline, kanamycin, spiramycin, doxycycline, tetracycline, and tylosin.
- Drugs reported with positive effects are tylosin and oxytetracycline.
- It should be noted that most of the drugs showing sensitivity are not approved by the
Food and Drug Administration for lactating dairy cows.
Mycoplasma mastitis or elevated somatic cell
counts. Likewise, animals of unknown origin should not be purchased.
- Cows or calves should not be purchased from herds with a history of
Mycoplasma and other pathogenic
Another early warning control measure is to culture all cows that have clinical cases of
At the first discovery of disease, individual cows infected with Mycoplasma should be quickly identified and
then culled or permanently segregated.
- 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.
- Physical separation of young replacement stock from older animals has been advised.
- 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
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.
- 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.
- 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.
- 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.
- 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.
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.
- 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)
- 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
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
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.
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.
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
- Strip cup
- Submission of all quarters from all cows to California Mastitis Test
- Bacteriological examination of CMT positive quarters
- Antibiotic sensitivity of pathogens isolated
- ProStaph test
|California Mastitis Test
||Percent of Milk Yield Lost
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
- 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
- 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
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
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
|FARAD Recommended withdrawl intervals
for Nonsteroidal Anti-inflammatory Drugs
||100 mg/kg q12hrs
||3.3mg/kg IV or IM
q 24 h
||1.1-2.2 mg/kg IV
or IM, q 24 h
||4-6 g/animal IV or
IM, followed by up
to 2 g/animal daily
Sources of Drug Residue Information
Food Animal Residue Avoidance Databank
Animal Medicinal Drug Use Clarification Act
- Food Animal Residue
Avoidance Databank (1-888-US-FARAD) or
E-mail addresses email@example.com (California)
firstname.lastname@example.org (North Caroline)
Fax numbers916-752-0903 California
919-829-4358 North Carolina
- FARAD Compendium A comprehensive
compendium of FDA-CVM approved food animal drugs
Windows-based computer program which contains complete label information for all approved
food animal veterinary drugs
Windows-based "Producers 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
Subscription to NOAH available at www.avma.org
- Toxicologic monographs
from the Joint FAO/WHO
Expert Committee on Food
www.fao.org and www.who.org
- U.S. Pharmacopoeia
Drugs and Classes of Drugs For Which Extra-Label Use in Food
Animals is Prohibited By FDA-CVM
- 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.)
- 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:
- Follow precise milking management procedures and use properly
functioning milking machines.
- Use an approved teat dip on all cows immediately after milking.
- Execute approved dry-cow treatment as a standard herd health
- Implement appropriate medical management of all clinical cases of
mastitis during lactation.
- If Streptococcus agalactiae is
highly prevalent, initiate therapy during lactation.
- Segregate cows with staphylococcal mammary gland infections from the
- Cull all cows with chronic mastitis.
- Implement routine sanitary procedures to control populations of
- Test replacement animals for detectable mammary gland infections.
HEALTH MANAGEMENT OF DAIRY HERDS TREATED WITH BOVINE
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.
- Milk Production
- 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.
- Dose-response relationship - Milk
production increases with BST, up to approximately twice the anticipated approved dose
(2D), then flattens or decreases above 2D.
- Nutrition and Stress
- 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.
- 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
- 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.
- 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.
- 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
- 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.
- The combination of sodium bicarbonate and BST had an additive effect
on milk production.
- 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.
- Heat Intolerance
- Thermal balance - Heat production is
increased by BST, because it increases with increasing milk production.
- 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.
- Control of heat intolerance
- providing shade to reduce radiant heat load
- using fans, showers, and ponds to increase heat loss by convection
- 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
- 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
- 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.
- Control of infertility
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.
- 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
- BST-associated Mastitis
- 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.
- 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
- 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.
- 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%).
- 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
- 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.
UDDER EDEMA (fig 99)
- 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
- 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.
- 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
- 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 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