New insights into the phenotypes of atopic dermatitis linked with allergies and asthma in children: An overview.

Atopic dermatitis (AD) is a complex disease with multiple causes and complex mechanistic pathways according to age of onset, severity of the illness, ethnic modifiers, response to therapy and triggers. A group of difficult-to-manage patients characterized by early-onset AD and severe lifelong disease associated with allergic asthma and/or food allergy (FA) has been identified. In this study, we focus on these severe phenotypes, analysing their links with other atopic comorbidities, and taking into account the results from recent cohort studies and meta-analyses. The main hypothesis that is currently proposed to explain the onset of allergic diseases is an epithelial barrier defect. Thus, the atopic march could correspond to an epithelial dysfunction, self-sustained by a secondary allergenic sensitization, explaining the transition from AD to allergic asthma. Furthermore, AD severity seems to be a risk factor for associated FA. Results from population-based, birth and patient cohorts show that early-onset and severe AD, male gender, parental history of asthma, and early and multiple sensitizations are risk factors leading to the atopic march and the development of asthma. The importance of environmental factors should be recognized in these high-risk children and prevention programs adapted accordingly. Effective targeted therapies to restore both barrier function and to control inflammation are necessary; early emollient therapy is an important approach to prevent AD in high-risk children. Clinicians should also keep in mind the specific risk of atopic comorbidities in case of filaggrin loss-of-function mutations and the rare phenotypes of orphan syndromes due to heritable mutations in skin barrier components.

Sensibilidad de Staphylococcus aureus aislados de hemocultivo a 11 antimicrobianos y revisión de la literatura / Susceptibility of Staphylococcus aureus isolated from blood to 11 antimicrobial agents and a review of the literature

Entre noviembre de 1998 y febrero de 2000 se estudió la sensibilidad in vitro, mediante el método E-test®, de 91 aislamientos de Staphylococcus aureus procedentes de hemocultivo frente a 11 agentes antimicrobianos. Cincuenta y dos cepas fueron sensibles a meticilina (SASM) y 39 resistentes (SARM). Todos los SASM fueron sensibles a gentamicina, ciprofloxacino, vancomicina, teicoplanina, rifampicina, ácido fusídico, quinupristina-dalfopristina y linezolid, el 90 por ciento fueron sensibles a eritromicina y el 83 por ciento a mupirocina. Todos los SARM fueron sensibles a vancomicina, teicoplanina, rifampicina y linezolid, el 95 por ciento fueron sensibles a quinupristina-dalfopristina y el 92 por ciento a gentamicina, mupirocina y ácido fusídico. Ningún SARM fue sensible a eritromicina ni a ciprofloxacino. La tasa de aislamientos de SARM sensibles a eritromicina o ciprofloxacino fue baja, mientras que el resto de los antibióticos estudiados continúan siendo efectivos frente a S. aureus. (AU)

[Susceptibility of Staphylococcus aureus isolated from blood to 11 antimicrobial agents and a review of the literature]. / Sensibilidad de Staphylococcus aureus aislados de hemocultivo a 11 antimicrobianos y revisión de la literatura.

From November 1998 to February 2000, a total of 91 strains of Staphylococcus aureus isolated from blood were analyzed for their susceptibility to 11 antimicrobial agents using the E-test method. Fifty-two isolates were methicillin-susceptible (MSSA) and 39 were oxacillin-resistant (MRSA). All the MSSA were susceptible to gentamicin, ciprofloxacin, vancomycin, teicoplanin, rifampicin, fusidic acid, quinupristin-dalfopristin and linezolid; 90% were susceptible to erythromycin and 83% to mupirocin. All the MRSA were susceptible to vancomycin, teicoplanin, rifampicin and linezolid; 95% were susceptible to quinupristin-dalfopristin; and 92% to gentamicin, mupirocin, fusidic acid. None of the MRSA were susceptible to erythromycin or ciprofloxacin. The susceptibility of SARM to erythromycin and ciprofloxacin was low, while the susceptibility to the rest of the antimicrobial agents remained active.

Epidemiological, microbiological, clinical, and prognostic factors of bacteremia caused by high-level vancomycin-resistant Enterococcus species.

A case-control study was performed between 1994 and 1996 in order to study the epidemiological, microbiological, clinical, and prognostic features of high-level vancomycin-resistant enterococcal bacteremia. Seventeen consecutive patients who had clinically significant bacteremia due to vancomycin-resistant enterococci (vanA genotype: 16 Enterococcus faecalis, 1 Enterococcus faecium) were compared with 169 who had vancomycin-susceptible enterococcal bacteremia. The following were selected by multivariate analysis as independent risk factors that influenced the development of high-level vancomycin-resistant enterococcal bacteremia: prior glycopeptide therapy (P=0.049); inclusion in a hemodialysis program (P=0.046); prior therapy with corticosteroids or antineoplastic agents (P=0.029); and prior surgical treatment (P=0.022). The following other factors were selected by univariate analysis: tracheostomy (P=0.002); prolonged hospitalization (P=0.01); and any kind of puncture (P=0.02). The crude associated-mortality rate was 13.4%. Gene amplification of vanA was positive for 17 strains of enterococci. Pulsed-field gel electrophoresis of genomic DNA after SmaI digestion of vanA isolates revealed that one strain predominated (10 isolates), though at least four similar banding patterns were identified (6 isolates). The 16 strains closely related to the outbreak were investigated further. The surgical intensive care unit was the first and most involved service. The hospital outbreak of vanA vancomycin-resistant enterococcal bacteremia occurred between 1994 and 1995 and was caused by Enterococcus faecalis. This is believed to be the first and only such outbreak described in a Spanish hospital thus far.