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Biomedical subjects
Publications and source records attributed to S Hoban.
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Viridans group streptococci (VGS) are commonly isolated from the blood of hospitalized patients. The E test represents a convenient method for determining the MICs for VGS, but for this purpose it has not been well validated against reference methods. In this study, 180 unselected VGS isolates were identified to a species level, and the MICs of penicillin, cefuroxime, cefotaxime, and vancomycin were determined by both agar dilution and the E test. Available data regarding demographic and laboratory variables for each VGS bacteremic episode were collected, the significance of each VGS isolate was assessed, and the associations between and among laboratory and clinical variables were investigated. Among all VGS isolates, 68.3% (median of three runs) were found to be fully susceptible to penicillin by agar dilution. The E test and agar dilution showed average agreements (within +/-1 dilution) of 92.2% for penicillin, 95.7% for cefuroxime 91.3% for cefotaxime, and 86.7% for vancomycin. Agreements over serial E tests and serial agar dilutions were excellent for beta-lactam agents (intraclass correlation coefficients, >0.9) but less impressive for vancomycin. Very major error rates for the E test were </=0.7%, and combined major and minor error rates were within acceptable limits for all antimicrobial agents tested. Lysis-centrifugation culture methods were more often associated with clinically insignificant VGS isolates; otherwise, no associations between clinical and laboratory variables were noted.
Swab inoculation of oxacillin agar screen plates was compared with drop inoculation for detection of methicillin-resistant Staphylococcus aureus. The poor sensitivity of the swab method (59%) was related to heteroresistance of the S. aureus isolates. We recommend the drop method (100% sensitivity) because interpretation of results was significantly easier, making it more reliable.
Utilizing a recently described rapid needle extrusion method for determining the sensitivities of burn wound isolates, we have compiled data on the resistance patterns of over 250 isolates from our burn unit. Major isolate groups were Staphylococcus aureus, Pseudomonas aeruginosa, various Enterobacteriaceae and Enterococci. Excellent correlation was exhibited between the inhibitory zone sizes and the minimal inhibitory concentration for 120 organisms tested. Utilizing the needle extrusion sensitivities to facilitate the selection of the burn creams, a significant reduction in the microbiologic flora of the burn wound was noted. The utilization of this technique in the selection of burn creams deserves controlled trials to assess whether changes in topical therapy might alter clinical outcome.
Eighty-one women were randomly selected for treatment with nalidixic acid (1 g four times a day) or cephalexin (500 mg four times a day) as therapy for 131 episodes of bacteriuria localized using the antibody-coated bacteria (ACB) test. Bladder infections were treated for three days and renal infections for 14 days. Rates of cure were not significantly different between treatment groups in each drug regimen. However, significantly more relapses occurred in the patients with ACB-positive infections treated for 14 days with cephalexin than in those treated for 14 days with nalidixic acid. More early reinfections occurred in the cephalexin-treated group after both three and 14 days of therapy. Resistance to nalidixic acid developed in the infecting bacteria in the urine during therapy with nalidixic acid in 3% of women after three days and in 16% of women after 14 days. Simultaneous resistance appeared in the urine, periurethral area, and fecal flora of these patients.
Antibody-coated bacteria were found in only two of 34 urine sediments from 19 catheterized patients infected with a single epidemic strain of Pseudomonas aeruginosa, whereas 12 of 19 urine sediments from 16 outpatients contained antibody-coated P. aeruginosa. In urine sediments, individual cells and microcolonies of the epidemic strain of P. aeruginosa were enclosed in ruthenium red (polysaccharide)-positive material. This strain was extremely mucoid when grown in a liquid medium for enhancement of mucoid formation. Renal infections was present in some patients, as determined by the bladder washout test and by titers of antibody in serum, and antibody was present in the urine but not coating P. aeruginosa. We conclude that the mucoid layer interfered with antibody coating of the epidemic strain of P. aeruginosa.
The site of urinary infection in 51 adult women was determined by the bladder-washout technique (BW). Of the 37 patients with proved upper-tract infection shown by BW, 16 had upper-tract symptoms, three had lower-tract symptoms, and 18 were asymptomatic; 31 had antibody-coated bacteria (ACB), and six had no ACB. Of 14 patients with proved lower-tract infection shown by BW, three had upper-tract symptoms, five had lower-tract symptoms, and six were asymptomatic; none had ACB. All 31 women whose infecting bacteria were coated with antibody proved to have an upper-tract infection shown by BW. A subset of the population of adult women with upper-tract infection have organisms emanating from their ureters at BW localization, which are not coated with antibody. Physicians must be cautious in interpreting results that are negative for ACB.
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The incidence of trimethoprim-resistant Enterobacteriaceae has not increased since the introduction of the combination trimethoprim-sulfamethoxazole (TMP-SMX) into the clinical use at our centre in 1973. Using the minimum inhibitory concentration (MIC) as the index of trimethoprim resistance, this ranged from 1.6 to 800 mug/ml; for the majority of isolates it lay between 1.6 and 12.5 mug/ml. About half of these trimethoprim-resistant organisms were sensitive to sulfonamide. In vitro data suggest that organisms resistant to sulfonamide as well as to trimethoprim, where the MIC for the former drug is 3.1 mug/ml or less, will be susceptible to the combination. More resistant organisms, i.e., those for which the MIC of trimethoprim is 6.2 mug/ml or more, often appear quite resistent to the combination. There is no evidence that previous therapy with TMP-SMX is a significant predisposing factor to infection with these organisms, although there is a significant correlation between previous TMP-SMX therapy and infection with organisms with a high level of trimethoprim resistance. Organisms harbouring R-factor resistance or thymine-dependent mutants were not encountered during the course of this study.