Prevalence, clinical expression, invasiveness and outcome of Staphylococcus aureus containing Panton-Valentine leukocidin in children treated in a university hospital of Lithuania.

Background: There is a high prevalence of Staphylococcus aureus virulence factor Panton-Valentine leukocidin (PVL) in North-East parts of Europe. The aim was to evaluate data regarding the PVL occurrences in Lithuania, determine the relationship with Methicillin resistant Staphylococcus aureus (MRSA), association with demographic and clinical conditions, invasiveness and severity of the disease in children treated in hospital Kauno klinikos (KK).Methods: We performed a prospective case-cohort single-center study on paediatric patients hospitalized from 2012 to 2015 to KK. We compared characteristics in PVL positive [SA-PVL(+)] and PVL negative [SA-PVL(-)] groups among non-invasive and invasive infections. Logistic regression was performed to detect PVL predicting factors and Cox regression was presented to define factors associated with admission to intensive care unit (ICU).Results: PVL was detected in 51.5%, MRSA in 7.0% and MRSA-PVL(+) in 4.8% of cases. In general, PVL was associated with older age comparing with SA-PVL(-) (median 8.5 vs. 4.0 years, p < .001). Skin and soft tissue infections were presented in 87.9% of all SA-PVL(+) cases. Invasive infections (44.7% vs. 12.1%, p < .001) and co-morbidities (20.5% vs. 2.9%, p < .001) were associated with SA-PVL(-) infections compared to SA-PVL(+), but ICU admission number was higher in invasive SA-PVL(+) cases comparing to invasive SA-PVL(-) cases (41.2% vs. 10.2%, p = .007).Conclusions: There was a high prevalence of pvl gene in patients treated in KK. SA-PVL(+) infections were associated with SSTI and were not common in invasive infections, but the invasive infections caused by SA-PVL(+) were related to severe disease progression and admission to ICU.

Outcome of protease inhibitor substitution with nevirapine in HIV-1 infected children.

BACKGROUND: Protease inhibitors (PIs) have been associated with metabolic complications. There is a trend to switch to simpler therapy to improve these disturbances. We report a case-series describing the effects in metabolic abnormalities in seven HIV-infected children, previously treated with protease inhibitor (PI) after switching to nevirapine. METHODS: Seven children with stable PI-containing regimen and a long lasting HIV-1 RNA < 50 copies/ml were switched to nevirapine. All patients were naïve to non nucleoside reverse transcriptase inhibitor. PIs were switched to nevirapine. Preentry nucleoside reverse transcriptase inhibitors were maintained. The substitution of PIs with nevirapine was made when the patient showed hyperlipidemia or lipodystrophy or the physician and/or the patient's willingness to simplify. Clinical, laboratory data and anthropometric parameters were assessed every 3 months. Dual-energy X-Ray absorptiometry scans (DXA) was performed at baseline and at 12 months. RESULTS: Seven HIV-infected children were enrolled. Median age: 130 months (99,177). Median baseline CD4%: 32%. All had HIV-1 RNA < 50 copies/ml. Median length of preentry PI-therapy was 47 months (28, 91). Median age at the beginning of nevirapine was 120 months (99,177). Median decrease in cholesterol in 7.2 mmol/L was observed (P = 0.09), from baseline to 12 months. HDL-cholesterol increased in 5.1 mmol/L (P = 0.03) throughout the study period. No significant changes were observed in DXA with regard to body fat, but changes in total body bone mineral content and lean body content were significant. CD4% remained stable. All patients but one maintained viral load < 50 copies/ml at 12 months. The patient with virologic failure referred bad adherence. Children referred to take medication more easily. CONCLUSION: PI substitution with nevirapine improved lipid profile in our patients, although this strategy did not show significant changes in body fat or lipodystrophy.