Mastitis in Dairy Cattle in India
ABSTRACT Mastitis is multi factorial and a costly problem affecting all milk producing ruminants in India Unfortunately, there is no simple solution to it. As per 2006 estimates referred in ICAR’s National Agricultural Innovation Project, the estimated annual loss due to mastitis alone is nearly Rs16,702 millions. Mastitis reduces milk yield and alters its composition. The magnitude of these changes in individual animal varies with the severity and duration of the infection and the causative microorganisms. Mastitis is almost always caused by bacteria. These microorganisms produce toxins which directly damage milk-producing tissue of the mammary gland, and the presence of bacteria initiates inflammation within the mammary tissue in an attempt to eliminate the invading microorganisms. The inflammation contributes to decreased milk production and is primarily responsible for the compositional changes observed in milk from infected quarters and cows. In general, compositional changes involve an increase in blood components present in milk and a decrease in normal milk constituents.
Electronic copy available at: http://ssrn.com/abstract=1798382
Mastitis in Dairy Cattle in India
By: Dr Kishore T Motwani
Mastitis is multi factorial and a costly problem affecting all milk producing ruminants in
India Unfortunately, there is no simple solution to it. As per 2006 estimates referred in
ICAR’s National Agricultural Innovation Project, the estimated annual loss due to mastitis
alone is nearly Rs16,702 millions.
Mastitis reduces milk yield and alters its composition. The magnitude of these changes
in individual animal varies with the severity and duration of the infection and the
causative microorganisms. Mastitis is almost always caused by bacteria. These
microorganisms produce toxins which directly damage milk-producing tissue of the
mammary gland, and the presence of bacteria initiates inflammation within the mammary
tissue in an attempt to eliminate the invading microorganisms. The inflammation
contributes to decreased milk production and is primarily responsible for the
compositional changes observed in milk from infected quarters and cows. In general,
compositional changes involve an increase in blood components present in milk and a
decrease in normal milk constituents.
Three major factors involved in mastitis are namely: (1) the microorganisms as the
causative agent, (ii) the cow or a buffalo as host, and (iii) the environment, which can
influence the cow / buffalo and the microorganisms.
(1) The Causative Agent:
Over 100 different microorganisms can cause mastitis, which vary greatly in its route by
which they reach the mammary gland and in the nature of the disease they cause. Of
these pathogenic organisms, one can divide it into 2 groups: contagious pathogens and
environmental pathogens The major contagious pathogens are Streptococcus
agalactiae, Staphylococcus aureus, and Mycoplasma spp. which gain entry into
mammary gland through teat canal-with exception of some mycoplasmal infections
whereas, other important bacteria are environmental coliforms like Escherichia coli and
(2) The Host Animal
Cows get udder infection at different ages and stages of the lactation cycle-usually
animals in 4-5th month of lactation being more susceptible(59%) whereas, hind quarters
being more affected(57%) than fore quarters(43%). The immunological status of the
animal also affects the risk for mastitis. During certain stressful periods, e.g. around
calving, the immune functions of the dairy animal are suppressed. This peri-partum and
early lactation period, is also associated with a high susceptibility to udder infections and
mastitis. Other diseases, like different viral infections, which cause immune suppression,
stress of high milk yield or injuries also increase the risk of mastitis .Cows also vary in
their ability to overcome an infection once it has been established and so plays an active
role in the development of mastitis.
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(3) The environment:
The cows' environment influences both the numbers and types of bacteria they are
exposed to and their ability to resist these microorganisms. However, through
appropriate management practices, the environment can be controlled to reduce this
exposure and enhance resistance to udder disease. Most literature deals with heat
stress and its detrimental effect on milk production. Exposure of cattle to high
temperature in tropics like India can increase the stress of the animal. The total cell
counts in both blood and milk are higher in heat stressed cows. The heat stress
depresses leukocyte responses in vitro and so probably, the migration of leukocytes into
the mammary gland
Practical measures are now available to maintain common forms of mastitis at relatively
low and acceptable levels in the majority of herds. While continued research is needed
to control the less common forms of intra mammary infection, herd problems are often
the result of failure to apply the proven mastitis control practices consistently and to
consider all aspects of the disease problem. It is not too a distant future when milk from
organic dairy farming would start fetching a premium price in India and other Asian
Types of Mastitis:-
Clinical Mastitis -- visible signs of mastitis include:
Mild signs: Flakes or clots in the milk, may have slight swelling of infected
Severe signs: Secretion, abnormal, hot, swollen quarter or udder; cow
may have a fever, rapid pulse, loss of appetite, dehydration and
depression; even death may occur.
Sub clinical Mastitis -- no visible signs of the disease:
Somatic cell count (SCC) of the milk is elevated.
Bacteriological culturing of milk will detect bacteria in the milk.
Causes the greatest financial loss to dairy farmers through lowered milk
For every clinical case of mastitis, it is estimated that there will be 10 to
20 sub-clinical cases.
In cows and buffaloes, sub clinical mastitis is of high economic importance than the
clinical mastitis in developing countries.
What is Somatic Cell Count (SCC) – It is the number of leukocytes or white blood cells
per milliliter of milk.
Normal milk will have less than 200,000 cells per milliliter.
An elevated SCC is an indication of inflammation in the udder.
Bulk milk tank SCC gives an indication of the level of sub-clinical mastitis
and the loss of milk production in a herd due to mastitis.
Contagious Versus Environmental Mastitis: The Difference
Streptococcus agalactiae (S. agalactiae)
Staphylococcus aureus (S. aureus)
Streptococcus dysgalactiae (S. dysgalactiae)
Contaminated udder & udder of infected cows.
Method of spread:
From infected quarters to other quarters and cows/buffaloes primarily at milking
Indicators of problem:
Bulk tank somatic cell count (SCC) above 300,000 cells/ml.
Frequent flare ups of clinical mastitis, often in the same cows and buffaloes.
Bacterial culturing of cows shows S. agalactiae and/or S. aureus infections.
Controlling Contagious Mastitis
Staphylococcus aureus infections remain the largest mastitis problem on dairy farms.
The source of the Staph. aureus to infect these young animals is not known but may be
contaminated bedding, feeding milk from Staph. aureus infected cows, cross suckling, or
exposure to high fly populations. Pregnant heifers should not be housed together with
dry cows, when a significant number of cows in the herd are known to be infected with
Staph. aureus. This pathogen being most common often develops resistance against
general antibiotics and therefore the dairy animal should also be treated systematically
with new generation antibiotics like those containing β-lactamase inhibitor.
Staphylococcus aureus infected cows should be identified and milked last, or milked with
a separate unit from those used on uninfected cows. Clinical mastitis sometimes occurs
following prolonged sub clinical infections. Antibiotic therapy during lactation may
improve the clinical condition but usually does not eliminate infection.
Maintaining a Staph. aureus-free herd is possible but more difficult than maintaining a
Strep. agalactiae-free herd, and Staph. aureus may reappear even in a closed herd. To
achieve a "Staph. aureus-free" status, every infected cow must be identified and treated.
The "uninfected" herd should be closely monitored by individual SCC and milk culturing.
Teat injuries and chapped teat skin should be minimized because they predispose cows
to Staph. aureus intramammary infections.
Streptococcus agalactiae is an obligate parasite of the mammary gland which means
that, in nature, it can only live and reproduce in the gland. Because of this host-parasite
relationship Strep. agalactiae can be controlled and eradicated from a herd by identifying
and treating infected animals. This can be done by obtaining milk samples for
microbiological culture from all cows in the herd, and by treating the Strep. agalactiae
infected udders with an appropriate intramammary infusion product. Streptococcus
agalactiae infection responds well to beta-lactam intra-mammary preparations in both
lactating and dry cows. Using other classes of antibiotics often results in poor cure rates.
And of course some chronic infections also do not recover.
Calves fed discarded milk containing Strep. agalactiae can spread the infection by
suckling themselves or other pen mates. Once Strep. agalactiae is established within the
immature gland, it can persist until first parturition many months later. Therefore, dry
cows and heifers should be cultured at calving before joining the milking herd.
Streptococcus agalactiae responds well to antibiotic therapy and can be eradicated from
dairy herds with good mastitis control practices.
Streptococcus dysgalactiae may live almost anywhere: in the udder, rumen, and feces,
and in the barn. They can be controlled with proper sanitation and are moderately
susceptible to antibiotics.
Mastitis due to mycoplama infection is low, there is no effective treatment for
mycoplasmal mastitis, but the disease can be controlled by identifying infected animals
by sampling and culturing milk samples from all cows in the herd, followed by
segregation and / or culling the infected animals. If Mycoplasma spp. infected cows
remain in the herd, they should be milked last or with a separate unit from those used on
uninfected cows. Rigid sanitary precautions must be followed. Mycoplasmal mastitis
outbreaks have been associated with respiratory problems in calves, heifers, and cows
in poorly ventilated barns.
The environment surrounding the cow.
Indicator of problem:
High rate of clinical mastitis, usually in early lactation or during hot weather.
Somatic cell count may be low (less than 300,000).
Treatment of Clinical Mastitis
Selecting an initial treatment regimen for clinical mastitis cases should be based upon
historical culture and sensitivity results, severity of infection, and documented success of
Antibiotic therapy as well as other treatment methods is useful in reducing the severity of
the clinical condition and perhaps elimination of the infection. Treatment of clinical
mastitis alone will not reduce the prevalence of mastitis in the herd unless it is
accompanied by all other essential parts of a good mastitis control program.
Mild cases of clinical coliform mastitis may respond well to "stripping out" the infected
quarter on a frequent basis. If abnormal clinical signs persist, or in moderate cases with
marked swelling of the gland, commercial intra mammary and intra-muscular
antimicrobial preparations can be used. Careful monitoring and documentation of both
clinical as well as microbiological cure rates are invaluable in maintaining sound clinical
and economical therapeutic decisions.
Reasons for Treatment Failures
Mastitis results after bacteria penetrate teat duct keratin, overcome the defenses in milk,
and multiply within the gland. The interaction of bacteria with milk leukocytes greatly
influences the establishment of infections. These leukocytes function by phagocytosing
bacteria and killing the organisms’ intra cellularly. Thus, antibiotics continue to be relied
upon in attempts to treat clinical quarters during lactation. Reasons for treatment failure
include lack of contact between bacteria and antibiotics due to scar tissue formation,
protection within leukocytes, poor drug diffusion, and inactivation by milk and tissue
proteins; microbial resistance to antibiotics; development of bacterial L-forms;
metabolically inactive organisms; and improper treatment procedures, i.e., stopping
therapy too soon.
For effective intra mammary therapy, it is necessary for antibiotics to reach sites of
infection at concentrations exceeding the minimum inhibitory concentration (MIC) of the
drug and remain at adequate concentrations for sufficient time to kill or inhibit growth of
the infective agent. Unfortunately, therapeutic concentrations may not be achieved in
mammary tissue for a sufficient period of time when presently used doses of antibiotics
are administered intramammarily.