Section 4

Udder Health Management for Quality Milk Production

 

The target of udder health management programme is to control udder infections to a reasonable level so as to minimise economic losses. Mastitis by definition is inflammation of udder parenchyma resulting in physical/chemical changes in milk and physical changes in mammary gland. The changes in milk could range from presence of clot and flakes to changes in physical consistency or discoloration. The organ changes could range from no change to severe inflammatory swelling or gangrene.

Causes

Conventionally, with mention of mastitis association of bacteria and other microbes override the thought process. Dairy farmers and veterinarians should realise that although the primary cause may be microbial infection but for its control strategies other than use of antibiotics are often found to be more successful.

A number of pathogenic organisms are associated with mastitis in cows and buffaloes. There are various ways to classify mastitis but for dairy farmers or veterinarians classification is based on the source of organisms should suffice as it helps in taking decisions on treatment and prevention. Contagious mastitis means a type wherein mastitis-causing pathogens are transmitted from one infected animal to other. In environmental mastitis, the source of infection is generally the cow environment, such as, floor, bedding, etc. In addition there are minor pathogens whose association with mastitis in incidental and these usually are involved along with other pathogens.

Epidemiology

Mastitis is widely prevalent in cows and buffalos. Crossbred cows, especially high milk yielders, are more susceptible than buffalos and indigenous cows. Pathogens associated with mastitis keep on altering depending upon a number of factors, such as housing, milking practices, stage of mastitis control programme, etc. Strp. agalactia and Staph. aureus are present in infected animals which are transmitted to the uninfected quarter through milking process.

Transmission can occur during or between milking, dry period or at heifer stage. The disease is more commonly prevalent in relatively older cows and buffalos. In heifers, infection is usually contracted much earlier in pregnancy but expressed only few days before parturition and after calving there are signs of per acute/acute mastitis with severe udder swelling and systemic signs leading to fibrosis and complete loss of milk. New infection usually occurs frequently during early part of the dry period and first few months of lactation.

The type of housing has major influence on the type of pathogen and infection pressure. When the barn floor is made of concrete/bricks and animals are tied on it without bedding, the daily cleaning with water leads to accumulation of dung and urine on the denuded hard floor. As a result the direct contact of teat while lying offers sure chance of transmission of environmental bacteria to enter and colonise in teat canal. In such farms mastitis incidence is high.

Mastitis is more common in organised farms compared to small herds, probably due to stocking density and floor hygiene. Mastitis is also more commonly prevalent in Holstein Friesian and its crosses than in Jersey. Teat conditions such as over size teat and pendulant udder compromise the integrity of teat orifice leading to increased incidence of mastitis. Vitamin A, E and calcium deficiency increases risk of mastitis in herds. For these reasons mastitis is also considered as disease related to farm management rather than problem associated with microbes alone.

 Zoonotic and economic importance

Mastitis causing pathogens may be excreted in milk and if such raw milk is consumed it may lead to transmission of infection to human. Bacterial contamination of milk renders it unsuitable for consumption or processing. Bacteria, such as Salmonella, E.coli, Listeria, compylobacter, M. bovis may be present in milk, but most of these are destroyed by correct pasteurisation, otherwise with consumption of contaminated milk, human health may be endangered. Clinical mastitis causes economic losses due to decrease in milk yield, cost of treatment and increased culling leading to high replacement cost.

The clinical form of the disease is easy to diagnose but when present in sub-clinical form the problem is not evident unless the farmer is very observant. Sub-clinical mastitis causes major economic losses due to lower milk production to the extent of around 7-10 per cent of the lactation yield.

Milk from animals suffering from mastitis may contain large quantities of inflammation chemicals (chemical mediators), such as α1-antitrypsin, that may cause dyspepsia in humans and interference in milk processing. In addition to direct losses udder infection might also be source of embolic infections to other organs such as liver, uterus, spleen and may be cause of diverse symptoms. It is therefore in the interest of farmers and the milk processors to implement mastitis control programme for their farmers.

Clinical presentation

Clinical signs depend on the type of organisms associated but it is difficult to accurately diagnose causal pathogens before conducting the laboratory tests. Initial signs are related to milk abnormality, udder size, consistency, udder temperature and systemic reaction. For milk examination strip cup is the best method to detect blood clots, discoloration, flakes and pus, which indicates udder inflammation. In acute mastitis, mammary gland may be swollen, hot and painful to touch. The systemic signs are due to toxic substances produced by bacteria in udder tissues and absorbed in blood. The systemic signs are fever, increased heart rate, rumen stasis, recumbence and anorexia. Death may occur if the inflammation becomes gangrenous.

More number of cases clustered around up to 2 months of calving is suggestive of new infections acquired during dry period. High proportion of cases during 2-4 months of lactation is suggestive of contagious pathogens. In heifers, prevalence of infection is common in third trimester of pregnancy to several days before parturition. It is mostly caused by minor pathogens or coagulase-positive staphylococcus. Table 6 summarises the diagnosis and treatment strategy based on clinical symptoms.

Diagnostic tests

In clinical cases diagnosis of udder inflammation is evident but the challenge is to find out causal organism. In number of cases the results of laboratory culture test may mislead choice of antibiotics. Since the technicians conducting culture and sensitivity tests require skill to identify and pick up the correct pathogen colony for culture which takes at least 48-72 hours, the antibiotic sensitivity done in the laboratory may not be a true reflection of sensitivity in the clinical case hence too much reliance on sensitivity tests is unwarranted. The correct strategy is to isolate bacteria from clinical cases before any treatment is administered and do antibiotic sensitivity to find out common mastitis pathogens and sensitivity patterns, which can be used to decide on routine treatment strategy for the farm. The key to manage mastitis in a farm set-up is to implement proactive and preventive udder health management programme.

 Detection of sub-clinical mastitis

Since in this form clinical signs are not present, it is necessary to employ laboratory tests on milk to detect underlying inflammation or infection. The current udder health management programmes rightly focus on detecting sub-clinically affected animals, and to identify the organisms involved and understand the route of transmission. With this data mastitis control strategy can be planned scientifically. It is important to maintain animal records for analysis. For example, it is helpful to know if mastitis incidence is associated with lactation length or lactation phases. It is important to note that useful interpretation can be drawn if the laboratory diagnosis data is read with other data as described in following flow chart:

 

 

(a) Laboratory investigations: The investigation can be done at individual or herd level. For individual animal, pooled milk sample can be obtained after milking whereas for herd level investigations bulk tank milk can be sampled for examination. The correct sequence is to first find out, based on the data, if animals are having problem of contagious mastitis or the source is environmental pathogens. Then find out what pathogens are involved, especially at herd level. Unlike in clinical cases, bacterial culture in sub-clinical mastitis cases must be done at the herd level. In order to keep costs low, it is advisable to first detect if the sample is positive for subclinical form and then culture tests can be performed. It is advisable to send few milk samples from negative tested animals also for bacterial culture to prove the hypothesis that the pathogens are present only in affected and absent from healthy animals.

(b) Bacterial count: From the point of view of public health safety, it is important to know bacterial count in bulk tank milk samples. These bacteria in bulk milk may originate from udder, teat, udder surface or other environmental sources. The bulk tank milk culture gives an idea of major pathogens involved in mastitis. Total bacterial count is also undertaken which is regarded as measure of quality of udder health and fitness to consumption. In sub-clinically affected quarters, bacterial count could be 10,000 to 100,000 per ml but in normal milk counts are less than 1,000 bacteria/ ml.

(c) Somatic Cell Count (SCC): Somatic cell count is an indirect method to detect udder inflammation. The SCC in bulk tank milk is a superior indirect measure of mastitis detection within a dairy herd. SCC can be done by preparing milk smear and the somatic cells can be counted under microscope. This method has higher technician-to-technician variation and needs lot of time. Nowadays electronic cell counters are available but they are prohibitive due to high cost. Amongst contagious pathogens, infection due to Streptococci leads to significant increase in SCC but with Staphylococcus sp., it is less significantly correlated.

The SCC at the farm or the milk processing unit level is now accepted as the indicator of udder health and milk quality on which even acceptance and pricing of milk is proposed to be regulated. With bulk tank SCC the number of quarter-affected can be fairly predicted, but this needs generation of internal data for benchmarking. The cut-off level of SCC varies from country to country and species of animal. In cows the alarm level for farm-level SCC is 3-4 x105 per ml. SCC in buffalo milk is appreciably lower than in cows (100,000 per ml). SCC is high in first two weeks after parturition and in late lactation. Older cows have more SCC than young ones. If the level remains elevated for three-month period, the herd should be investigated for mastitis.

(d) Indirect tests:

  • California Mastitis Test (CMT): This is a cheap, quicker and accurate method of diagnosis but requires special milk collection. The result is read as negative, 1, 2, 3 reaction score, depending on amount of gel formed. The test reflects somatic cell count in milk indirectly.
  • High Mast test The test can be used to differentiate infection due to gram positive, gram negative pathogens and no growth. The test is a good aid to decide on the choice of antibiotic.
  • N-acetylglucosoaminidate (NAGAse) test: This test is considered as the gold standard indirect test for mastitis. Its sensitivity, specificity and predictive values are as good as SCC. It requires availability of expensive reagents and instruments.
  • Other tests: Determination of a a1 anti-trypsin in milk is also a useful test. A spot test has been developed to detect threshold a1 antitrypsin in milk.

Other indirect tests have low sensitivity and specificity hence devising control strategies based on results of low quality tests should be avoided.

Treatment

Up to early 1990s, while treating clinical mastitis, emphasis was on antimicrobial therapy. But now it is recognised that the cure rate with intra-mammary antimicrobial is not uniform specially in treating environmental (coliforms and streptococcal) infections. Due to increased public awareness and government regulations on antibiotic residue in milk the criteria for treating lactating cow and buffalo have changed radically. In subclinical mastitis the accepted strategy is not to treat animals during lactation but at the end of lactation when animals are being dried off by administering a slow release antibiotic and sealing formulation. The key question is to decide if antimicrobial therapy is necessary in a particular case. Such decisions can be made on clinical examination with or without bacterial culture report. In case of acute mastitis the onset is fast and the systemic signs are usually due to endotoxins, such cases should be treated without loss of time to save udder and animal.

In order to decide whether an anti-microbial is to be administered or not through intra-mammary infusion or parenteral route simple thumb rules can be followed. Intra-mammary microbial therapy with udder infusion is convenient and efficient but strict hygiene is necessary at the time of infusion otherwise bacteria, fungi and yeast may be introduced which would result in further complications. Before intra-mammary infusion complete emptying of udder is critical and if possible oxytocin 10–20 IU may be injected to facilitate complete emptying.

Selection of an anti-microbial to treat clinical mastitis cases is rather difficult in most cases due to lack of diagnostic support. It is advisable to develop a micro-level strategy for mastitis control based on routine culture and sensitivity data collected for the area. This becomes easy if dairy cooperatives and organised herds set up data recording for milk yield, disease incidence and routine SCC. The first and second choice antibiotic recommendation for mastitis then can be developed on a rational basis. For clinical mastitis the antibiotic should maintain minimum inhibitory concentration (MIC) in udder tissues up to 72 hours whereas for dry cow therapy the antibiotic must persist for 8 weeks.

Since merely on clinical signs it is difficult to diagnose mastitis pathogens, broad-spectrum antibiotic effective against gram positive and gram-negative organisms can be considered. Neomycin, framycetin, ampicillin, cloxicillin, and third generation cephalosporins are drug of choice in the treatment of mastitis. Ampicillin, cloxicillin erythromycin, tylosin, etc also have good mammary diffusion, whereas, penicillin G, cloxicillin, and tetracycline have medium efficacy. Aminoglycosides like gentamycin should not be used in treating mastitis as these have strong tissue binding and the residue period is long.

Control

(a) Improving sanitation and hygiene by shifting from tie-barn to lose housing with earth floor: A major factor leading to mastitis is animal is the faulty housing wherein cows/buffaloes are tied concrete/brick floor (without bedding). I have very often advocated open housing with earth floor (an old concept but revisited and refined). A large number of farmers have successfully tried this system in districts of Ahmednagar, Sangli, Kolahpur, Satara in Maharashtra and the message is spreading to other districts and states. For various intensity rainfall, different types of floor and housing models have been developed and tried. A major advantage of shifting to open housing with earth floor is dramatic improvement in udder heath including milk quality. A sample of such a house is given in Figure 11.

 

Figure 11: Simple and cost effective open housing in a village in Maharashtra – The barricade is of bamboo. The earlier shed has been included as rest area. The animals are loose. This farm is using tie barn system earlier. After shifting to the open housing farmer experienced significant reduction in udder infections. The cleanliness score and health of animals can be appreciated. A large number of farmers have adopted this system.

 

(b) Animal records: Mastitis control planning requires elaborate animal record keeping and periodic data analysis. This is important for organised herd or at milk cooperative level since mastitis control costs money and therefore it should be well-spent. The planning of preventive programmes should be based on scientific investigation and economic analysis. The target of control should be restricted to keep the problem at manageable level to minimise possible economic losses and should offer substantially high benefits compared to cost. The herd should have carefully laid policy of treatment of clinical mastitis based on previous investigations. In case of chronic mastitis it is better to dry-off the affected teat as otherwise it may become source of infection to others. Only drying-off the affected quarter (follow instructions in the box) would not affect milk production from other quarters, rather other quarters may compensate to some extent. 

(c) Good milking practices: This involves washing of udder, use of disposable paper towel to wipe udder, post milking teat-dip and complete emptying of milk. A number of post-milking dips are available. For Indian conditions a barrier-type teat dip will be most suitable rather than a plain formulation. A novel barrier type teat dip developed jointly by the author would be soon available in India. The laboratory tests and field studies have shown that once dipped the barrier formed at the teat sphincter does not permit entry of bacteria until it is removed by washing in the next milking. Iodophors and several other disinfectants can be employed. Teat dipping is an important management decision and once started it should be continued throughout lactation. Stopping teat dipping in the middle usually increases risk of pathogens. Post-milking teat dip is a good tool to reduce contagious and environmental mastitis. All chronically affected quarters should be dried off.

Ensuring that the animals are milked completely is very critical since it affects animals’ health as well as productivity. If milk is present in udder even after milking there is a feed back because of which production is decreased in next lactation; and residual milk would increase risk of mastitis. At least every three months a test should be done to ascertain if animals are being milked completely. The farm/dairy cooperative should have sub-clinical mastitis testing campaign at least twice in a year. The mastitis affected animals should be milked last so that there is no transmission. Milkers’ hands and use of towels to wipe udder after washing are major sources of spread of mastitis in herd. Milkers should be encouraged to wash hand with some disinfectant and as far as possible disposable paper towels should be used.

The animals should be given fodder to eat after milking so that they don’t sit. After each milking the teat sphincters are relaxed for about 30 minutes; during this time if the animal sits, the floor microbes can enter the teat canal. It is always advisable to get serum of few randomly selected animals examined for calcium level with the help of veterinarian. The average level should not be less than 9 mg/dl whereas 11 mg/dl is a realistic target. In case there is any deficiency, calcium should be supplemented in feed and blood levels should be checked after 2-3 months.

 (d) Dry cow therapy: In order to control new intra-mammary infections dry cow therapy is effective. This therapy can be undertaken in all the animals in the herd or for selective animals, based on results of individual cow indirect test and marked for dry cow therapy at the time of drying off. The dry cow therapy should be infused on the last day of milking and should never be used if the animal is already dry or else it will result in severe mastitis immediately after parturition.

It must be understood that immediate after drying-off for at least 2-3 weeks the teat canal is still open hence there is a chance of contracting new infections. It is always better to shift animals to earthen floor in a loose housing system for at least two weeks after drying-off. In high yielders sometimes drying off is a problem as the animal continues to produce high amount of milk even in last phase presenting a dilemma situation. In my experience, it is a better strategy to dry-off for minimum 30-45 days (ideal 60 days) by forcing the mammary tissues to stop milk synthesis.

In short, focusing on udder health programmes is critical for producing quality milk. It requires implementation of a systemic programme and in turn reward is better yield and safe milk for consumers.

 

Table 6: Key to diagnosis of mastitis based on stage of occurrence and symptoms.

Lactation stage

 Clinical presentation Pathogen involved

 

Treatment recommended

Milk abnormality

 Udder abnormality

Systemic reaction

Two weeks after drying off to two weeks prior to calving

 Watery milk, small flakes Swelling of gland Acute onset, mild systemic response Coliform, E.coli, Klebsiella, Enterobacteria

Trimethoprim plus sulpha 24%, Gentamycin, Cefaquinone, fluids, Oxytocin and frequent stripping

Two weeks after drying off to two weeks prior to calving

 Abnormal milk, thin, watery with small flakes Severe swelling Toxaemia, fever, tachycarida, progressive Coliform, E.coli, Klebsiella, Enterobacteria

Trimethoprim plus sulpha 24%, Gentamycin, Cefaquinone, fluids, Oxytocin and frequent stripping, Ceftiofur intra-mammary

Two weeks after drying off to two weeks prior to calving

 Abnormal milk Swelling of gland No systemic reaction Streptococci uberis, S. dysgalactia, Enterococcus

Oxytocin and stripping 4-5 times, intra-mammary infusion optional

Immediately after calving

 Clotted, discolored milk Acute swelling in later stage function loss Severe systemic reaction Pseudomonas

Antimicrobial, intra-mammary Streptomycin + Neomycin + Polymixin or Cephalosporin

Early lactation

 Thick + clot + pus Indurated, gangrene of teat or udder Fever, tachycardia, depression Staph. aureus

Ampicillin + Cloxicillin; Amoxicillin + Clavulanic acid; Erythromycin or TGC

Early lactation

 Drop or cessation in milk, no physical changes evident All four quarters affected, udder atrophy No systemic reaction Mycoplasma spp.

Tetracycline, Oxytetracycline, Tylosin

Early lactation

 Red tinged, serous consistency Swelling one or more quarter, Fever, toxaemia, recumbency, gangrene B. cereus

Clindamycin, gentamycin, chloromphenicol, erythromycin

Early lactation (post-parturient)

 Bloody milk, clots Swelling, very painful Acute, febrile, systemic reaction B. subtilis

Clindamycin, gentamycin, chloromphenicol, erythromycin

Mid lactation

 Watery, clots Swollen and indurated in later stage Sub-acute or acute in onset, no systemic signs Streptococci spp.

Intra-mammary Penicillin G, Novobiocin or Cloxicillin plus Ampicillin

Mid lactation to any stage

 Viscous, mucoid, gray white Acute swelling, supramammary lymph node No systemic reaction Cryptococci spp.

Iodine in oil intra-mammary

Sodium iodide intravenous

Methioolate 20 ml 0.1% solution, 2-3 days

Mid lactation to any stage

 Fall in milk flow, large yellow clots watery separated fluid Severe inflammatory quarters, supramammary lymph node involved, restricted to milk cistern Severe systemic response Candida spp.

Micanazole 100 mg intra-mammary or 400 mg i.v., Sulphamethoxypyridazine 22 mg per kg