Knowledge, attitudes, and practices regarding coccidioidomycosis among healthcare providers in four counties in Washington State, 2017.

Coccidioidomycosis is an emerging infection in Washington State. The epidemiology of the disease in Washington is poorly understood at present; underrecognition and underreporting of coccidioidomycosis is suspected based on reports of only severe disease. We sought to characterize healthcare provider knowledge, attitudes, and practices regarding coccidioidomycosis awareness, diagnosis, and treatment in south-central Washington. We conducted a cross-sectional survey of actively practicing healthcare providers in four counties in south-central Washington, an area recently described as endemic for Coccidioides. Survey results were used to assess awareness of reporting requirements, confidence in ability to diagnose and treat, confidence that knowledge is current, calculated knowledge score, and consideration of risk in patient population. The majority of respondents were unaware of the reporting requirement for coccidioidomycosis in Washington and further unaware that the disease had been reported in the state. Less than a third of survey respondents reported confidence in their ability to diagnose coccidioidomycosis and confidence that their knowledge is current. The majority of respondents never or rarely consider a diagnosis of coccidioidomycosis, and <25% of respondents indicated a working knowledge of serologic tests for the infection. The average knowledge score for respondents was 65%. Previous education, training, or practice regarding coccidioidomycosis was the only identified predictor of confidence and consideration of risk. These data indicate the substantial need for education and training among healthcare providers in south-central Washington and support the concern that a small proportion of existing cases of coccidioidomycosis are reported to the health department.

Importance of case age in the purported association between phylogenetics and hemolytic uremic syndrome in Escherichia coli O157:H7 infections.

Escherichia coli O157:H7 is the largest cause of hemolytic uremic syndrome (HUS). Previous studies proposed that HUS risk varies across the E. coli O157:H7 phylogenetic tree (hypervirulent clade 8), but the role of age in the association is unknown. We determined phylogenetic lineage of E. coli O157:H7 isolates from 1160 culture-confirmed E. coli O157:H7 cases reported in Washington State, 2004-2015. Using generalised estimating equations, we tested the association between phylogenetic lineage and HUS. Age was evaluated as an effect modifier. Among 1082 E. coli O157:H7 cases with both phylogenetic lineage and HUS status (HUS n = 76), stratified analysis suggested effect modification by age. Lineages IIa and IIb, relative to Ib, did not appear associated with HUS in children 0-9-years-old. For cases 10-59-years-old, lineages IIa and IIb appeared to confer increased risk of HUS, relative to lineage Ib. The association reversed in ⩾60-year-olds. Results were similar for clade 8. Phylogenetic lineage appears to be associated with HUS risk only among those ⩾10-years-old. Among children <10, the age group most frequently affected, lineage does not explain progression to HUS. However, lineage frequency varied across age groups, suggesting differences in exposure and/or early disease manifestation.

Triclosan antagonizes fluconazole activity against Candida albicans.

Triclosan is a broad-spectrum antimicrobial compound commonly used in oral hygiene products. Investigation of its activity against Candida albicans showed that triclosan was fungicidal at concentrations of 16 mg/L. However, at subinhibitory concentrations (0.5-2 mg/L), triclosan antagonized the activity of fluconazole. Although triclosan induced CDR1 expression in C. albicans, antagonism was still observed in cdr1Δ and cdr2Δ strains. Triclosan did not affect fluconazole uptake or alter total membrane sterol content, but did induce the expression of FAS1 and FAS2, indicating that its mode of action may involve inhibition of fatty acid synthesis, as it does in prokaryotes. However, FAS2 mutants did not exhibit increased susceptibility to triclosan, and overexpression of both FAS1 and FAS2 alleles did not alter triclosan susceptibility. Unexpectedly, the antagonistic effect was specific for C. albicans under hypha-inducing conditions and was absent in the non-filamentous efg1Δ strain. This antagonism may be due to the membranotropic activity of triclosan and the unique composition of hyphal membranes.