|
|
|
|
MASTITIS DEFINITION Inflammation of the mammary gland which may manifest as clinical mastitis when the milk is grossly abnormal or subclinical mastitis when the milk appears normal. ECONOMIC IMPORTANCE AND INCIDENCE Mastitis, along with lameness and infertility, ranks as one of the major sources of economic loss to the U.K. dairy industry, both in the effects of the disease itself and the number of cows culled because of repeated incidents of mastitis. The incidence of mastitis is affected by various factors including (I) Age of the animal The incidence of mastitis increases with age. This is particularly the case with regard to the incidence of Streptococcal infection. (ii) Stage of lactation The incidence of clinical mastitis is highest in early lactation with a marked peak during the first few days post-partum. On the other hand, the incidence of subclinical mastitis increases steadily as lactation proceeds and is particularly obvious with Streptococcus agalactiae infections. (iii) Management of husbandry Many different management and husbandry practices can affect the incidence of mastitis, but by far the most important is hygiene particularly with reference to the milking regime. AETIOLOGY Mastitis can be caused by a number of micro-organisms especially bacteria such as Streptococcus agalactiae, Streptococcus dysgalactiae, Streptococcus uberis, Staphylococcus aureus and Actinomyces pyogenes. Other bacteria occasionally involved include Proteus vulgaris, Pseudomonas aeruginosa, Klebsiella spp, M.bouzgenitalium and M.bovimastidis. Tuberculous mastitis caused by Mycobacterium bovis is extremely rare. Leptospiral and fungal mastitis may occur. CLINICAL MASTITIS Four degrees of clinical mastitis are recognised.
Usually occurs very shortly after calving. Sudden onset with the cow changing from being apparently normal to severely ill within a period of 12 hours. Both local and systemic reactions are evident. The local reaction is very severe with one or more quarters (more frequently hind quarters) becoming hard, hot, swollen and painful. The secretion is small in amount, thin, serous, may be bloodstained, and is often foul-smelling. The systemic reaction is characterised by marked fever and may proceed to a fatal toxaemia. Other clinical features include marked depression, anorexia and a markedly abnormal gait due to the pain associated with the local reaction. Foetal membranes are often retained. Recumbency is common.If the animal survives affected quarter(s) may become gangrenous (particularly associated with Staphylococcal infections). The quarter becomes cold to the touch, discoloured blue-black and, if death does not occur, sloughs off within 1-2 weeks. Very severe (peracute) clinical mastitis is often associated with Staphylococci or E.coli.Clinically severe E.coli mastitis presents as follows: Initially anorexia, pyrexia and in some cases diarrhoea are seen. The udder and milk may appear normal. However within twelve hours the udder becomes hot, swollen and painful and the secretion is abnormal being yellow in colour and containing small clots. The fever is usually transient and by the time clinical signs develop in the udder and milk the temperature may be normal. Gangrene rarely develops.
More common than the very severe form and may occur at any stage of lactation. However it also most frequently occurs shortly after calving. There is a marked local reaction. The onset is rapid with one or more quarters becoming hot, swollen and painful. The secretion is thin and serous, but contains large yellow clots which often clog the teat orifice. Pus may also be present. The systemic reaction is characterised by moderate fever. This frequently subsides within one or two days, but persists if the lesion spreads or septicaemia develops. A wide variety of micro-organisms may be responsible for this form of mastitis. Amongst the most common are staphylococci, streptococci and coliforms.
Can occur at any stage of lactation. Usually there is only a local reaction. Any systemic reaction is mild and transient. The local reaction is mainly evident as changes in the milk. The secretion is thinner than normal, containing small clots and in many cases pus. Repeated episodes of mild clinical mastitis in the same lactation are common and this is referred to as "chronic" mastitis. Again a wide variety of bacteria may be responsible, although staphylococci and streptococci are most frequently isolated.
This term is applied to a wide range of chronic lesions within the udder; from a localised area of abscessation to a completely fibrosed quarter. When localised abscesses are present the milk may be normal, but they commonly break down and give rise to episodes of clinical mastitis. Abscesses may also break through the skin of the udder. Affected animals remain a constant source of infection for the rest of the herd. Terminal fibrosis and atrophy are the end-point of most forms of mastitis (proliferative lesions are the exception, the most notable of which is tuberculous mastitis). Once the acute inflammatory signs of an episode of mastitis disappear, they are followed by acinar involution, fibrosis and atrophy. If small, the lesions will be confined to the areas around the base of the teat, but if larger they may involve the greater part or even the whole of the quarter. The teat wall may also be affected. Fibrosis causes induration which can be recognised on palpation. Atrophy results from contraction of the fibrous tissue. The secretion from a quarter undergoing fibrosis and atrophy is usually normal in appearance, although reduced in amount. OTHER SPECIFIC FORMS OF CLINICAL MASTITIS
Although severe clinical mastitis is generally confined to lactating cows, summer mastitis is a severe clinical mastitis which affects dry cows, in-calf heifers and, on occasion, bulling heifers. The cause is Actinomyces pyogenes, probably spread by flies. As the name implies it occurs during the summer months, particularly when warm and wet. Initially the affected quarter becomes swollen, hard and painful. There is either no secretion or just a little watery fluid. This local reaction is usually accompanied by a severe systemic reaction with marked fever. Affected animals may die. Later there is a secretion of thick yellow pus which has a foul smell. The udder then becomes indurated with the formation of multiple abscesses. These frequently burst through the wall of the udder, most commonly at the base of the teat.Gangrene does not develop but the quarter may slough. 2. Mycoplasmal Mastitis The species of Mycoplasma most commonly involved in Britain is M.bovis. There is a sudden onset with all four quarters being involved and milk yield falls to almost zero. The udder is usually swollen, particularly in early lactation. The quarters are smooth and hard but virtually painless. The secretion initially appears normal but on allowing to stand a fine sandy material settles out leaving a turbid whey-like supernatant. Later the secretion resembles colostrum and may contain a little blood. Eventually it becomes purulent but large clots are not seen. Mycoplasmal mastitis may be a persistent problem where the problem is not correctly diagnosed and treatment is inadequate. 3. Leptospiral Mastitis Leptospirae of a number of serotypes (especially L.hardjo) can cause mastitis in cattle. Clinical signs include fever, jaundice and abortion but there is a sudden fall in milk yield for 3-5 days. All quarters can be affected and the milk produced may be stained with blood or be brownish or yellowish in colour. The udder is flabby in this condition SUBCLINICAL MASTITIS By definition, the udder and milk secretion are clinically normal (although, of course, fibrosis and atrophy may be present from a previous clinical attack). However, due to the small, active lesions which exist there is a high cell count in the milk. A high bacterial count may be present. In addition, the milk yield is reduced, butter fat and solids not fat are depressed and the milk has poor keeping qualities. Since the lesions are progressive, subclinical mastitis is often a precursor to clinical mastitis and after an episode of clinical mastitis, the infection may persist at the subclinical level. Even without clinical incidents some degree of fibrosis and atrophy will eventually become clinically apparent. On most farms with a high incidence of clinical mastitis the vast majority of the cows will have subclinical mastitis. The milk from a normal quarter will have a cell count of 100,000 cells/ml, but counts up to 250,000 cells/ml are acceptable. Naturally high counts occur during the first week after calving and at drying off. The usefulness of cell counts is not in the individual animal but as a means of monitoring the herd as a whole. Account should be taken of the trend in cell counts (bulk sample performed once a month) over a six month period, rather than the individual monthly count (for reasons such as a high proportion of the herd being dried of!). As a general guide, continuing counts of <500,000 cells/ml, suggest that a severe mastitis problem is unlikely, whereas counts of 1,000,000 suggest the opposite. Total bacterial counts are carried out by the milk boards on bulk milk samples as a means of assessing hygienic quality on a monthly basis. Micro-organisms which cause mastitis can infect the mammary gland by invasion of the teat canal, e.g. streptococci, staphylococci, coliforms (E.coli, Klebsiella sp., Proteus sp. and Pseudomonas sp.) yeasts, salmonellae, mycoplasmas and Actinomyces pyogenes. The last three organisms may also invade the udder by the haematogenous route, as do Leptospira spp. and Mycobacterium bovis. EPIDEMIOLOGY A few bacteria which cause mastitis are obligate udder pathogens e.g. Streptococcus agalactiae, but the majority can also grow on skin (A.pyogenes, S.dysgalactiae, S.aureus) or are contaminants from the environment e.g. E.coli, Pseudomonas and Klebsiella spp. (in sawdust). In all cases, incorrectly-adjusted milking machines and poor hygiene can contribute to the spread of established mastitis and predispose to infections from the environment. In many cases there is evidence to link the reflux of infected milk into teat canals or even the skin of the teats with subsequent cases of mastitis. This is particularly obvious with Mycoplasma mastitis. Streptococci such as S.agalactiae can persist for up to 3 weeks on cloths and S.dysgalactiae and staphylococci can survive for long periods on milkers hands. Outbreaks of Pseudomonas mastitis are often connected with the contamination of water tanks or teat dips with the organism and those of coliform mastitis with sawdust bedding in loose-housed animals. Klebsiella spp. are particularly associated with sawdust. Flies are common vectors of infections especially of A.pyogenes in summer mastitis occurring in any cows or heifers at pasture. Carriers are an important source of disease and sub clinically or chronically affected animals can act as sources of infection for healthy animals in the herd. Carriers of streptococci, staphylococci, coliforms, mycoplasmas and A.pyogenes may all initiate outbreaks of mastitis, particularly if brought into a non-immune herd. The use of intramammary antibiotics and teat siphons may also predispose to certain types of mastitis, particularly to those associated with fungi (especially Candida and other yeasts), Nocardia, atypical mycobacteria and mycoplasmas, all of which may be resistant to the intramammary antibiotic preparations currently available. DIAGNOSIS Based on: Assuming a careful clinical examination diagnosis of "mastitis" is not difficult. However clinical differentiation of the various bacteriological types is at best difficult and usually impossible. Summer mastitis, mycoplasma mastitis, tuberculous mastitis and leptospiral mastitis can be diagnosed clinically. It is also possible to differentiate between very severe ‘peracute* staphylococcal mastitis and very severe ‘peracute* E.coli mastitis in most circumstances which will allow rational therapy. Cell counts and bacteriology are essential in assessing the nature and severity of the problem. Accurate bacteriological results are necessary for the identification and rational treatment and control of mastitis. Samples should be taken after the teat has been washed with disinfectant and water, dried and swabbed with alcohol. Foremilk should be discarded and milk should be taken into a sterile container held at an angle to preclude contamination of the sample with hair etc. TREATMENT LACTATING COW TREATMENT Mild clinical mastitis is usually diagnosed and treated by the farmer using intramammary tubes. On the basis of probably efficacy penicillin/aminoglycoside combinations have as successful a "cure" rate as any other antibiotic; they have short withdrawal times and are cheap. Acute and per-acute cases are best treated by systemic injection. Intramammary treatment with the same antibiotic is appropriate but this would probably be only in the uninfected quarters since frequent stripping out and inflammation makes intramammary treatment of the infected quarter worthless. The immediate main aim of the antibiotic is to halt the septicaemia and hopefully also to kill the bacteria in the udder. Since the problem is so acute, since isolation of the causative organism is too slow, and since differentiation of the two main bacteria responsible is not always possible on clinical grounds, the aim is to use an antibiotic reasonably effective against these two organisms. Antibiotic therapy in acute mastitic cases is probably secondary to fluid therapy in terms of altering the prognosis. Large volumes of fluid given intravenously can be life-saving. DRY COW TREATMENT All quarters in all cows be treated with a "dry-cow" intramammary tube at drying-off. Treatment in the ‘dry* period is
A second infusion after 4 weeks of the dry-period may be valuable if there is a high incidence of infection. TEST DIPS In reducing high cell counts, teat dips and hygiene are extremely important. The teat dips should be iodophors, or glutaraldehyde, or hypochlorites in high concentration. Others such as chlorhexidine and quaternary ammonium compounds give poorer efficacy. |
|