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.

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.

The fungal flora of the coat of 172 healthy pet cats was examined qualitatively. Fungi were isolated from 136 (79%) of the 172 cats. Fifteen genera were isolated; 13 are commonly regarded as saprophytes, and 2 (Microsporum and Trichophyton) are commonly regarded as pathogens. Aspergillus, Alternaria, Penicillium, and Cladosporium spp were the most frequently isolated saprophytes. Dermatophytic fungi, including Microsporum gypseum (n = 1), M vanbreuseghemii (n = 1), and Trichophyton rubrum (n = 14), were recovered from 16 cats. Microsporum canis was not isolated from any cat during this study.

During the United States Department of Agriculture (USDA) National Animal Health Monitoring System’s (NAHMS) 2007‐2008 beef study, 567 producers from 24 US States were offered the opportunity to collect fecal samples from weaned beef calves and have them evaluated for the presence of parasite eggs (Phase 1). Participating producers were provided with instructions and materials for sample collection. Up to 20 fresh fecal samples were collected from each of the 99 participating operations. Fresh fecal samples were submitted to one of 3 randomly assigned laboratories for evaluation. Upon arrival at the laboratories, all samples were processed for the enumeration of strongyle, Nematodirus, and Trichuris eggs using the modified Wisconsin technique. The presence or absence of coccidian oocysts and tapeworm eggs was also noted. In submissions where the strongyle eggs per gram exceeded 30, aliquots from 2 to 6 animals were pooled for DNA extraction. Extracted DNA was subjected to genus level polymerase chain reaction (PCR) identification for the presence of Ostertagia, Cooperia, Haemonchus, Oesophagostomum, and Trichostrongylus. In this study, 85.6% of the samples had strongyle type, Nematodirus, and Trichuris eggs. Among the samples evaluated, 91% had Cooperia, 79% Ostertagia, 53% Haemonchus, 38% Oesophagostomum, 18% Nematodirus, 7% Trichuris, and 3% Trichostrongylus. The prevalence of coccidia and tapeworm eggs was 59.9% and 13.7%, respectively.

An ELISA, using purified flagellin of Borrelia burgdorferi as the solid-phase antigen, was used to measure antibody concentrations to B burgdorferi in dairy cattle in Wisconsin. Serum obtained from 5,060 cows in 160 randomly selected herds in the state were tested. Serum from an additional 2,600 cattle in Barron County, Wis, a county with a high annual incidence of B burgdorferi infections in human beings, was also tested. Only 7% of the cows that were tested, but 66% of the herds that were tested, were seropositive for B burgdorferi. Sixteen percent of the herds had a prevalence of 15% seropositive cows, whereas 50% of the herds had a prevalence of 1 to 14% seropositive cows. Seropositive herds were concentrated in the west-central part of Wisconsin. An association existed between the geographic location of seropositive herds and counties in which B burgdorferi infection of human beings was acquired (P < 0.05) as well as the geographic location of seropositive herds and the geographic distribution of Ixodes scapularis (P < 0.05). Barron County, in which B burgdorferi infection is endemic, had a significantly (P < 0.05) higher percentage of seropositive cows (17%) than did the state of Wisconsin (7%).

Results of an ELISA, indirect fluorescent antibody (IFA) test, and immunoblot analysis (western blotting) for antibody to Borrelia burgdorferi in a sample of 216 lactating dairy cows were compared. The microscopic microtitration agglutination test for antibody to 6 serovars of Leptospira interrogans was also performed to evaluate possible cross-reactivity between B burgdorferi and L interrogans. Using western blotting as the standard test against which the ELISA and IFA test were compared, the ELISA had greater sensitivity (50% in summer and 38% in spring) with similar specificity (83 and 82%), compared with the IFA test (sensitivity, 6 and 5%; specificity, 90 and 83%). In addition, seropositivity to B burgdorferi, using the ELISA, was not found to be associated with seropositivity to L interrogans serovars. A matched case-control study evaluating the association between clinical lameness and antibody to B burgdorferi was performed in lactating dairy cows of 17 Minnesota and Wisconsin herds. Sera from case and control cows matched by herd, parity, and stage of lactation were evaluated, using an ELISA for B burgdorferi antibody during 2 seasons. High B burgdorferi antibody values were associated with clinical lameness in dairy cows (P = 0.006 in summer and P = 0.04 in spring).