RESUMO

Little is known about the etiology of progressive macular hypomelanosis, although it has been suggested that Propionibacterium acnes plays an important role. While microbiological culture is commonly employed to identify Propionibacterium acnes, new identification methods have been under investigation, amongst them polymerase chain reaction. To determine the cut-off point for the number of genome copies of Propionibacterium acnes in the lesional skin of patients with progressive macular hypomelanosis as a positive marker, employing quantitative real-time polymerase chain reaction and anaerobic culture, considered gold standard. An observational study with a comparison group, included 35 patients with dermatosis, attended at the Oswaldo Cruz University Hospital, Pernambuco, Brazil, between March and May 2008. Lesional skin was compared to non-lesional skin through positive testing with real-time polymerase chain reaction and culture. The Statistical Package for Social Sciences, version 12.0, was employed for the association analysis with the McNemar test, and the cut-off point with the ROC curve for maximum values. Propionibacterium acnes was most frequently encountered in lesional areas (p 0,025). The cut-off point of Propionibacterium acnes in lesional skin was 1,333 genome copies, with a sensitivity of 87,9% and a specificity of 100,0%. Since Propionibacterium acnes is a saprophyte, identifying the cut-off point may assist in determining its positivity in lesional skin in patients suffering with this dermatosis.

RESUMO

Out of 24 nosocomial strains of Pseudomonas aeruginosa from Recife, Brazil, 15 (62%) were metallo-beta-lactamase producers. Such isolates were resistant to main antipseudomonas drugs, except polymixyn B and aztreonam. The enzyme responsible for the carbapenem-resistance belongs to SPM-1 class, and the gene involved, blaspm-1, is likely plasmid located.

De 24 linhagens hospitalares de Pseudomonas aeruginosa provenientes de Recife, Brasil, 15 (62%) produziram metalo-beta-lactamase. Tais isolados foram resistentes às principais drogas antipseudomonas, exceto polimixina B e aztreonam. A enzima responsável pela resistência aos carbapanêmicos pertence à classe SPM-1 e o gene envolvido, blaspm-1, provavelmente é plasmidial.