Difference between revisions of "Streptococcal Mastitis - Cattle"

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Latest revision as of 14:12, 22 November 2011

Introduction

Bovine streptococcal mastitis involve colonisation of the udder with the following primary agents: S.agalactiae, S. dysgalactiae and S. uberis.

S. pyogenes, S. zooepidemicus and Enterococcus faecalis can also be involved.

S. agalactiae and S. dysgalactiae are considered to be contagious organisms which prefer to live in the udder and teat skin and spread from cow to cow at milking. S. agalactiae is an obligate intramammary bacteria and its survival outside the udder is limited.

Contagious organisms often cause subclinical infections causing a prolonged mild elevation in somatic cell count.

S. uberis is generally considered to be an environmental organism which lives in dirty environments and sporadically gains entry to the udder often causing serious clinical mastitis.

Signalment

Usually affects dairy cows during the lactating period, but infection during the dry period can persist and cause problems in early lactation.

Clinical signs

In subclinical cases, no gross inflammation or changes in the milk are seen. Chronic forms of the disease lead to progressive fibrosis of the affected quarter.

Clinical cases present acutely, sometimes with systemic signs such as anorexia and pyrexia.

There will be changes in the milk from the affected quarter, including fibrin clots and changes in colour. Changes in the udder may also be apparent: swelling, heat, pain and redness.

Signs can progress to abscessation and sloughing of the affected quarter in very severe cases.

Additionally, teat morphology has a primary role in preventing entry of infection, and changes such as prolapse of the teat canal or wounds might indicate a predisposition for mastitis.

Diagnosis

Subclinical mastitis is diagnosed by evaluating the Somatic Cell Count using a California Milk Test or automated methods. Somatic Cell Counts above 200,000 cells/ml are indicative of mastitis in the sampled quarter.

Bulk milk somatic cell counts can also be evaluated and indicate the prevalence of mastitis in the dairy herd on the day of sampling.

Clinical mastitis is diagnosed on the basis of clinical signs.

To determine the agent involved, sterile milk sampling of the affected quarter or udder and bacterial culture is required. An antibiotic sensitivity test should also be performed to select the best treatment.

Treatment

Intramammary therapy is the mainstay of mastitis treatment and involves instilling antibiotics such as a penicillin or beta-lactam into the affected quarter. The choice of antibiotic should be governed by culture and sensitivity results of milk samples.

In acute clinical cases, parenteral antibiotics might also be beneficial along with supportive therapy and glucocorticoids to reduce inflammation.

If premature agalactia occurs in chronic cases with resistant pathogens, culling might be a practical option.

Control and prevention

Control of mastitis is slightly different depending on if the agent is primarily contagious or environmental.

Control of contagious organisms such as S. agalactiae and S. dysgalactiae involve a control of spread at milking time. The aim is to eliminate reservoirs of infection by identifying subclinical infections using individual somatic cell counts and using an effective Five Point Plan:

  1. Prompt detection and treatment of clinical cases: detection in the parlour by stripping the udder and checking the fore milk. Treatment with a suitable antibiotic and resampling of the udder to check resolution.
  2. Use of a post-milking teat dip: the teat orifice remains open for about an hour after milking and bacteria can be transferred onto the teat skin during milking. A disinfectant should be used to kill bacteria and also aid in maintaining the teat in good condition.
  3. Effective dry cow therapy: using long-acting antibiotics infused into the udder to remove existing subclinical infections during the dry period. A teat sealant is also used to block the teat canal and prevent the entry of bacteria.
  4. Culling of persistent offenders: it might be beneficial to cull animals with 3 or more cases of mastitis in one lactation. Also those animals with persistently high Somatic Cell Counts which do not respond to treatment.
  5. Regular servicing and maintenance of the milking machine: rubber of silicone liners in the cups must be changed frequently, and the vacuum must be tested to ensure it is strong enough and has adequate reserve.

The control of S. agalactiae is particular as it is an obligate mammary parasite and it responds well to intramammary antibiotics. Therefore it can be eliminated from herds through the use of blitz therapy. This involves treatment of all four quarters of all animals during lactation to eliminate S. agalactiae infections. Such treatment has been used effectively in the UK and S. agalactiae infections have fallen significantly sing the 1980s.


Control of environmental organisms such as S. uberis follows certain different guidelines, although many principles can be applied from above.

The most important point is to control the cows' environment and ensure clean, dry and comfortable bedding.

Parlour factors are also vital and teat preparation to ensure they are clean and dry before clusters are applied at milking can help control the spread of environmental pathogens.


Attempts have been made to create vaccines against the Streptococcal agents of mastitis, but no products are available yet.

References

Edmonson, P. (2011) Blitz therapy for the eradication of Streptococcus agalactiae infections in dairy cattle In Practice 33, 33-37

Statham, J. (2011) Single-agent infectious diseases In Practice 33, 210-217

Blowey, R. (2000) The environment and mastitis In Practice 22, 382-394

Kahn, C. (2005) The Merck Veterinary Manual 9th Edition Merck and co