Secondary attack rate of COVID-19 in shared households in Slovakia.

OBJECTIVE: The objective of this study was to estimate the secondary attack rate in unvaccinated members of households of two regions in the Slovak Republic for the period November 2020 ‒ April 2021. INTRODUCTION: SARS-CoV-2 infection poses a high risk of transmission in close-contact indoor settings, such as households. The household transmissibility of SARS-CoV-2 varies widely across countries. METHODS: We included 278 households for SARS-CoV-2 transmission analysis. We calculated the secondary attack rate (SAR). We assessed sex, level of disease severity and means of isolation during infection of index cases as determinants of disease transmissibilityRESULTS: The secondary attack rate in 278 households was estimated at 63.7% (95%CI: 58.2‒66.7%). The SARs were different by sex (60.2% in females, 67.5% in males). The highest SAR was observed in the households of asymptomatic cases (77.8%), followed by moderate severity (66.5%), hospital admissions (63.2%) and mild disease (58.2%). CONCLUSION: We found a high household secondary attack rate in two regions of Slovakia in the period when Alpha variant (B.1.1.7) of SARS-CoV-2 was dominant in the country. The results highlight the importance of monitoring transmission dynamics (Tab. 1, Fig. 1, Ref. 12). Text in PDF www.elis.sk Keywords: COVID-19, secondary attack rate, Slovak Republic, households.

Mutation of the CgPDR16 gene attenuates azole tolerance and biofilm production in pathogenic Candida glabrata.

The PDR16 gene encodes the homologue of Sec14p, participating in protein secretion, regulation of lipid synthesis and turnover in vivo and acting as a phosphatidylinositol transfer protein in vitro. This gene is also involved in the regulation of multidrug resistance in Saccharomyces cerevisiae and pathogenic yeasts. Here we report the results of functional analysis of the CgPDR16 gene, whose mutation has been previously shown to enhance fluconazole sensitivity in Candida glabrata mutant cells. We have cloned the CgPDR16 gene, which was able to complement the pdr16Δ mutation in both C. glabrata and S. cerevisiae. Along with fluconazole, the pdr16Δ mutation resulted in increased susceptibility of mutant cells to several azole antifungals without changes in sensitivity to polyene antibiotics, cycloheximide, NQO, 5-fluorocytosine and oxidants inducing the intracellular formation of reactive oxygen species. The susceptibility of the pdr16Δ mutant strain to itraconazole and 5-fluorocytosine was enhanced by CTBT [7-chlorotetrazolo(5,1-c)benzo(1,2,4)triazine] inducing oxidative stress. The pdr16Δ mutation increased the accumulation of rhodamine 6G in mutant cells, decreased the level of itraconazole resistance caused by gain-of-function mutations in the CgPDR1 gene, and reduced cell surface hydrophobicity and biofilm production. These results point to the pleiotropic phenotype of the pdr16Δ mutant and support the role of the CgPDR16 gene in the control of drug susceptibility and virulence in the pathogenic C. glabrata.