Minimum inhibitory concentrations of cephalosporin compounds and their active metabolites for selected mastitis pathogens
2013
Cortinhas, Cristina S. | Oliveira, Leane | Hulland, Carol A. | Santos, Marcos V. | Ruegg, Pamela L.
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.
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