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- Author or Editor: Leane Oliveira x
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Objective—To determine the association between results of in vitro antimicrobial susceptibility tests and outcomes in cows that received intramammary treatment with pirlimycin hydrochloride for subclinical mastitis associated with gram-positive pathogens.
Animals—132 dairy cows (178 mammary glands with subclinical mastitis caused by 194 pathogen isolates).
Procedures—Cows with positive results for a California mastitis test (CMT) were assigned to receive 50 mg of pirlimycin via intramammary administration into each CMT-positive mammary gland every 24 hours for 2 consecutive days or no treatment. Duplicate milk samples were collected before treatment and approximately 21 days later. Target pathogens included coagulase-negative Staphylococcus spp (n = 118 isolates), Streptococcus spp (28), Staphylococcus aureus (7), and other gram-positive cocci (30). Antimicrobial susceptibilities were determined via broth microdilution.
Results—Overall treatment success rate was 66% (128/194) for both groups. In vitro resistance to pirlimycin ranged from 0% (0/7 isolates of S aureus) to 50% (13/26 isolates of other gram-positive cocci). For the treated group, 62 of 94 (66%) target pathogens were classified as treatment successes and 32 (34%) were classified as failures. Similarly for the control group, 66 of 100 (66%) target pathogens were classified as treatment successes, whereas 34 (34%) were classified as failures.
Conclusions and Clinical Relevance—Many target pathogens from cows with subclinical mastitis were eliminated without treatment, and treatment with pirlimycin did not improve the treatment success rate. Results of in vitro antimicrobial susceptibility tests were not useful as predictors of treatment success following intramammary treatment with pirlimycin.
Objective—To evaluate enterotoxin production, enterotoxin gene distribution, and genetic diversity of Staphylococcus aureus in milk obtained from cows with subclinical mastitis.
Sample—Milk samples obtained from 350 cows (1,354 mammary glands) on 11 Wisconsin dairy farms.
Procedures—Of 252 S aureus isolates obtained from 146 cows, 83 isolates (from 66 cows with subclinical mastitis) were compared genotypically by use of pulsed-field gel electrophoresis and via PCR identification of toxic shock syndrome toxin 1 (TSST-1) and classical S aureus enterotoxin genes (sea, seb, sec, sed, and see).
Results—Among the 83 S aureus isolates, ≥ 1 enterotoxin genes were identified in 8 (9.6%). Enterotoxin gene distribution was as follows: TSST-1, 7 isolates (8.4%); sec, 5 isolates (6.0%); and sed, 2 isolates (2.4%). Enterotoxin genes sea, seb, and see were not identified. Twelve pulsotypes and 5 subtypes were identified among the 83 isolates; 5 of the 12 pulsotypes were represented by only 1 isolate. In cows of 1 herd, only a single S aureus pulsotype was detected; in cows on most other farms, a variety of pulsotypes were identified. One pulsotype was recovered from 4 farms (n = 23 cows) and another from 5 other farms (16). Isolates with an enterotoxin gene were represented by 6 pulsotypes.
Conclusions and Clinical Relevance—S aureus classical enterotoxins and TSST-1 were rarely recovered from milk samples obtained from cows with subclinical mastitis in Wisconsin. Diverse pulsotypes of S aureus were detected within and among farms, indicating that different strains of S aureus cause subclinical mastitis in dairy cows.
Objective—To compare the minimum inhibitory concentration (MIC) of cephapirin and ceftiofur with MICs of their active metabolites (desacetylcephapirin and desfuroylceftiofur) for selected mastitis pathogens.
Sample—488 mastitis pathogen isolates from clinically and subclinically affected cows in commercial dairy herds in Wisconsin.
Procedures—Agar dilution was used to determine MICs for Staphylococcus aureus (n = 98), coagulase-negative staphylococci (99), Streptococcus dysgalactiae (97), Streptococcus uberis (96), and Escherichia coli (98).
Results—All S aureus isolates were susceptible to cephapirin and ceftiofur. Most coagulase-negative staphylococci were susceptible to cephapirin and ceftiofur. For E coli, 50 (51.0%; cephapirin) and 93 (94.95%; ceftiofur) isolates were susceptible to the parent compounds, but 88 (89.8%) were not inhibited at the maximum concentration of desacetylcephapirin. All S dysgalactiae isolates were susceptible to ceftiofur and cephapirin, and consistent MICs were obtained for all compounds. Most S uberis isolates were susceptible to cephapirin and ceftiofur. Of 98 S aureus isolates classified as susceptible to ceftiofur, 42 (42.9%) and 51 (52%) were categorized as intermediate or resistant to desfuroylceftiofur, respectively. For 99 coagulase-negative staphylococci classified as susceptible to ceftiofur, 45 (45.5%) and 17 (17.2%) isolates were categorized as intermediate or resistant to desfuroylceftiofur, respectively. For all staphylococci and streptococci, 100% agreement in cross-classified susceptibility outcomes was detected between cephapirin and desacetylcephapirin. No E coli isolates were classified as susceptible to desacetylcephapirin.
Conclusions and Clinical Relevance—Differences in inhibition between parent compounds and their active metabolites may be responsible for some of the variation between clinical outcomes and results of in vitro susceptibility tests.