Heifers that were treated for clinical mastitis prior to parturition or within 14 d postpartum were reexamined approximately 1 mo after treatment. Clinical examination of the heifers and microbiological examination of quarter milk samples were carried out on both occasions. Of the 1000 heifers included in the study, 10.9% were culled within 28 d after treatment. Udder damage caused by mastitis was the only or main reason for culling in 96% of those heifers. In comparison, 4.5% of nonmastitic heifers from the same herds were culled within 30 d postpartum. Twenty-five percent of those heifers that were not culled at d 28 after treatment had at least one nonfunctional quarter at that time. One thousand one hundred twenty-two quarters that were clinically affected at the time of treatment were reexamined; 22% were nonfunctional, 14% were still affected by clinical mastitis, 12% had subclinical mastitis, 5% had a latent infection with coagulase-positive staphylococci or Streptococcus dysgalactiae, and 46% were bacteriologically negative and had a normal cell count at the time of reexamination. High percentages of nonfunctional quarters were observed among those quarters that were infected with Arcanobacterium pyogenes or with coagulase-positive staphylococci at treatment. When all quarters that were clinically affected at treatment were considered, 40% of quarters were cured and were still in lactation at reexamination. Quarters infected with coagulase-negative staphylococci had a higher cure rate than quarters infected with other organisms. At reexamination, clinical signs of thelitis were observed in many of those quarters that were nonfunctional following the episode of clinical mastitis and also in 25% of lactating quarters in which clinical mastitis persisted.
BackgroundThe aim of this study was to investigate possible cross-infection of Dichelobacter nodosus in Norwegian farms practising co-grazing of sheep and cattle.MethodsThirteen farms practising co-grazing of sheep and cattle were included in this descriptive study: five farms with a history of severe ovine footrot (Group I) and eight farms with free-stall housing of cattle and signs of mild or no footrot in sheep (Group II). Sampling for PCR detection of D. nodosus was performed from animals in all farms, and clinical claw examination of sheep and cattle was performed in Group II. D. nodosus positive samples were analysed by a multiplex PCR method that detects variants of the fimA gene corresponding to D. nodosus serogroups A through I.ResultsD. nodosus serogroup A was identified more frequently in sheep from farms with a history of severe footrot (Group I) versus from Group II, and in most of the farms with a history of severe footrot there was a coexistence of D. nodosus serogroup A in sheep and cattle. In one farm heel horn erosion and dermatitis emerged in cattle after co-grazing with sheep suffering from severe footrot where D. nodosus serogroup A was detected. Six months later heel horn erosion and dermatitis were still diagnosed, and D. nodosus serogroup A was identified. Out of the 16 D. nodosus positive sheep samples from Group II, ten of the samples were positive by the fimA serogrouping PCR. Among these 10 samples all serogroups except G were detected. All the D. nodosus serogroups detected in sheep were also present in the corresponding cattle herds.ConclusionThe clinical findings and the coexistence of the same serogroups in co-grazing sheep and cattle could indicate cross-infection. However, further research including isolation of the bacterial strains, virulence-testing and genetic identification, is needed.
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