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Dynamics of intramammary infection in the sheep caused by coagulase-negative staphylococci and its influence on udder tissue and milk composition
  1. A. R. Burriel, DVM, MSc, PhD, MRCVS1,1
  1. 1 Department of Farm Animal and Equine Medicine and Surgery, Royal Veterinary College, Boltons Park, Potters Bar EN6 INB

Abstract

Over an entire lactation 891 milk samples were collected from 99 ewes in a well-managed dairy flock. Coagulase-negative staphylococci were isolated from 53 (5.9 per cent) of the samples, with 13 (6.6 per cent) of the glands giving coagulasenegative staphylococci in two or more consecutive samples. When a somatic cell count threshold of 6 x 105/ml of milk was adopted as an indication of inflammation, 30 of the milk samples collected during early and mid-lactation, which contained coagulase-negative staphylococci, were considered to come from glands suffering subclinical mastitis. In five glands subclinical mastitis persisted for the entire lactation. A comparison of somatic cell counts measured with the fossomatic or Coulter counters suggested that the former gave the most reliable values, particularly in late lactation. After the experimental infection of 20 glands of meat breeds with coagulase-negative staphylococci, five glands remained infected for all 49 days of observation and seven glands excreted bacteria intermittently. Irrespective of the presence of coagulase- negative staphylococci in the sample, the composition of the milk from the challenged glands was significantly modified (P<0.0001 for the infected, and P<0.01 for the uninfected glands). Fat and protein concentrations were increased and lactose decreased, suggesting that although coagulase-negative staphylococci could not always be isolated, they persisted in many of the challenged glands and continued to influence the physiology of the gland. This possibility was supported by the presence of severe damage to the udder tissue of glands in which bacteria had been shown to be present for long periods.

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      Footnotes

      • The author's present address is PSC1, Box 1878, APO AE, 09009, USA

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