Varicella Outbreak in an Indian Couple Living in Germany Caused by VZV Clade VI Acquired during a Trip to The Netherlands

Varicella-zoster virus (VZV), the cause of varicella and zoster, is divided into five major clades and four provisional clades, the latter of which have been rarely reported worldwide to date. We present a varicella outbreak by the provisional clade VI within an Indian couple in Germany returning from a trip to Amsterdam. To the best of our knowledge, this is the first case of varicella by the VZV clade VI described in Germany, but the disease was acquired in The Netherlands

The influence of gastric atrophy on Helicobacter pylori antibiotics resistance in therapy-naïve patients

Background: Antibiotic susceptibility of Helicobacter pylori to antibiotics may vary among different niches of the stomach. The progression of chronic H. pylori gastritis to atrophy changes intragastric physiology that may influence selection of resistant strains. Aim: To study the antibiotic resistance of H. pylori taking the severity of atrophic gastritis in antrum and corpus into account. Methods: Helicobacter pylori-positive patients (n = 110, m = 32, mean age 52.6 ± 13.9 years) without prior H. pylori eradication undergoing upper gastrointestinal (GI) endoscopy for dyspeptic symptoms were included in a prospective study. Patients were stratified into three groups depending on the grade of atrophy: no atrophy (OLGA Stage 0), mild atrophy (OLGA Stage I–II) and moderate/severe atrophy (OLGA Stage III–IV). Two biopsies each from the antrum and the corpus and one from the angulus were taken and assessed according to the updated Sydney system. H. pylori strains were isolated from antrum and corpus biopsies and tested for antibiotic susceptibility (AST) for amoxicillin, clarithromycin, metronidazole, levofloxacin, tetracycline, and rifampicin by the agar dilution methods. A Chi-square test of independence with a 95% confidence interval was used to detect differences in the proportion of patients with susceptible and resistant H. pylori strains. Results: Among 110 patients, primary clarithromycin resistance (R) was 30.0%, both in the antrum and corpus; metronidazole resistance accounted for 36.4 and 34.5% in the antrum and corpus; and levofloxacin was 19.1 and 22.7% in the antrum and corpus, respectively. Resistance rates to amoxicillin, tetracycline, and rifampicin were below 5%. Dual antibiotic resistance rate was 21.8%, and triple resistance rate was 9.1%. There was a significant difference in the resistance rate distribution in antrum (p < 0.0001) and corpus (p < 0.0001). With increasing severity of atrophy according to OLGA stages, there was a significant increase in clarithromycin-R and metronidazole-R. Conclusion: In treatment-naïve patients, antibiotic resistance and heteroresistance were related to the severity of atrophy. The high clarithromycin resistance in atrophic gastritis suggests that H. pylori antibiotic susceptibility testing should always be performed in this condition before selecting the eradication regimen

Intra- and Interpatient Variability of the hsp65 and 16S-23S Intergenic Gene Region in Mycobacterium abscessus Strains from Patients with Cystic Fibrosis

To establish the exact pathogenic role of Mycobacterium abscessus in cystic fibrosis (CF), molecular tests are required for accurate identification. Forty-eight M. abscessus isolates from seven patients with CF were analyzed by sequence analysis for sequence variants within the hsp65 gene and the 16S-23S intergenic sequence (ITS). We detected two different hsp65 genes and correspondingly two ITS sequevars belonging to M. abscessus type I and type II

Prostaglandin E₂ from <i>Candida albicans</i> Stimulates the Growth of <i>Staphylococcus aureus</i> in Mixed Biofilms

<div><p>Background</p><p>Previous studies showed that <i>Staphylococcus aureus</i> and <i>Candida albicans</i> interact synergistically in dual species biofilms resulting in enhanced mortality in animal models.</p><p>Methodology/Principal Findings</p><p>The aim of the current study was to test possible candidate molecules which might mediate this synergistic interaction in an <i>in vitro</i> model of mixed biofilms, such as farnesol, tyrosol and prostaglandin (PG) E₂. In mono-microbial and dual biofilms of <i>C</i>.<i>albicans</i> wild type strains PGE₂ levels between 25 and 250 pg/mL were measured. Similar concentrations of purified PGE₂ significantly enhanced <i>S</i>.<i>aureus</i> biofilm formation in a mode comparable to that observed in dual species biofilms. Supernatants of the null mutant deficient in PGE₂ production did not stimulate the proliferation of <i>S</i>.<i>aureus</i> and the addition of the cyclooxygenase inhibitor indomethacin blocked the <i>S</i>.<i>aureus</i> biofilm formation in a dose-dependent manner. Additionally, <i>S</i>. <i>aureus</i> biofilm formation was boosted by low and inhibited by high farnesol concentrations. Supernatants of the farnesol-deficient <i>C</i>. <i>albicans</i> ATCC10231 strain significantly enhanced the biofilm formation of <i>S</i>. <i>aureus</i> but at a lower level than the farnesol producer SC5314. However, <i>C</i>. <i>albicans</i> ATCC10231 also produced PGE₂ but amounts were significantly lower compared to SC5314.</p><p>Conclusion/Significance</p><p>In conclision, we identified <i>C</i>. <i>albicans</i> PGE₂ as a key molecule stimulating the growth and biofilm formation of <i>S</i>. <i>aureus</i> in dual <i>S</i>. <i>aureus/C</i>. <i>albicans</i> biofilms, although <i>C</i>. <i>albicans</i> derived farnesol, but not tyrosol, may also contribute to this effect but to a lesser extent.</p></div

Effect of farnesol on the growth of <i>S</i>. <i>aureus</i> 19552 in mono-microbial biofilms.

<p>(<b>a</b>) Pre-cultered 24h old <i>S</i>. <i>aureus</i> biofilms were supplemented with different concentrations of purified farnesol and the number of cfu`s was determined. <i>S</i>. <i>aureus</i> biofilms incubated in farnesol-free medium were used as control. (<b>b</b>) Growth kinetics of <i>S</i>. <i>aureus</i> in dual biofilms with the farnesol-deficient <i>C</i>. <i>albicans</i> strain ATCC10231 (striped) and the farnesol producer <i>C</i>. <i>albicans</i> SC5314 (open bars). Colony forming units (cfu`s) of <i>S</i>. <i>aureus</i> derived from single species biofilms were function as control (solid bars). Shown are the mean cfu`s and the standard deviations of two representative experiments with three replicates each. Asterisks indicate significant (p<0.05) differences compared to controls.</p

PGE₂ synthesis in <i>C</i>.<i>albicans</i> wild type and mutant strains and its effect on <i>S</i>. <i>aureus</i> biofilms.

<p>(<b>a</b>) Time-dependent accumulation of PGE₂ in culture supernatants of the <i>C</i>. <i>albicans</i> SC5314 wt (dashed), the reference strain <i>ura3</i>-/- (open bars), and the null mutant <i>ura3-/-fet31-/-</i> (solid bars) measured by EIA. (<b>b</b>) Effect of cell-free supernatants derived from <i>C</i>. <i>albicans</i> SC5314 wt (striped), from the reference (grey bars) and from the null mutant (solid bars) to the growth of established <i>S</i>. <i>aureus</i> 19552 biofilms (control; open bars) after further 24h of incubation. (<b>c</b>) PGE₂ levels in supernatants of <i>C</i>. <i>albicans</i> ATCC10231 (farnesol nonproducer; open bars) and SC5314 (farnesol producer; solid bars) were compared. Mean and standard deviations derived from two representative experiments with three replicates per test are demonstrated. Significant differences (<i>p</i><0.001) between the two groups were identified by asterisks.</p

PGE₂ stimulates the growth of <i>S</i>. <i>aureus</i> biofilms.

<p>(<b>a</b>) <i>S</i>. <i>aureus</i> 19552 was grown in single species biofilms in the presence of various concentrations of purified PGE_2. The mean number of colony forming units (cfu`s) from untreated <i>S</i>. <i>aureus</i> biofilms were used as control. Asteriks indicate statistically significant (p< 0.05) differences between PGE<sub>2</sub>-treated and untreated biofilms. (<b>b</b>) Cultures of <i>S</i>. <i>aureus</i> 19552 biofilms were supplemented with heat-treated (solid bars) and untreated (open bars) PGE<sub>2</sub> supplemented medium. Shown are the mean number of <i>S</i>. <i>aureus</i> cfu`s normalized to the non-supplemented control as well as the standard deviations derived from two independent experiments and three replicates per experiment. Asterisks indicate significant (p< 0.05) differences between the groups.</p

Growth kinetics of <i>S</i>.<i>aureus</i> in mono-microbial and in dual <i>S</i>. <i>aureus/C</i>. <i>albicans</i> biofilms.

<p>(<b>a</b>) Biofilm thickness of <i>S</i>. <i>aureus</i> 19552 single (open bars) and mixed biofilms with <i>C</i>. <i>albicans</i> 31883 wt (clinical strain; striped) or <i>C</i>. <i>albicans</i> SC5314 wt (laboratory strain; solid bars) at various time points determined by staining with crystal violet. Total biofilm thickness is expressed as mean of the optical density (OD) measured at a wave length of 570 nm. Shown are the means and standard deviations of two independent experiments with 24 replicates each. (<b>b</b>) Quantification of <i>S</i>. <i>aureus</i> 19552 in mono-microbial (circle) and in dual species biofilms together with <i>C</i>. <i>albicans</i> clinical isolate 31883 (triangle) or <i>C</i>. <i>albicans</i> SC5314 laboratory strain (square). Shown are the mean cfu`s of <i>S</i>. <i>aureus</i> derived from two representative experiments with three intra-assay replicates. Asterisks indicate significant (<i>p</i><0.001) differences between mono-microbial and dual species biofilms.</p