Epidemiologia molecular, resistência aos antimicrobianos e marcadores genéticos de adaptabilidade em amostras de Pseudomonas aeruginosa obtidas de pacientes com fibrose cística cronicamente infectados: um estudo multicêntrico

• Autor(a) principal: Ferreira, Alex Guerra
• Data de Publicação: 2013
• Outros Autores: [e-mail]
• Tipo de documento: Tese
• Idioma: por
• Título da fonte: Biblioteca Digital de Teses e Dissertações da UERJ
• Texto Completo: http://www.bdtd.uerj.br/handle/1/18811
• topic: Psedomonas aeruginosa; Cystic Fibrosis; Resistance; Epidemiology; Pseudomonas aeruginosa; Fibrose Cística; Resistência; Epidemiologia; CIENCIAS BIOLOGICAS::BIOLOGIA GERAL

Chronic lung infections with Pseudomonas aeruginosa are the major cause of morbidity and mortality in patients with cystic fibrosis (CF). In Brazil, epidemiology and resistance studies of this microorganism has a local feature. Given this, we selected 75 patients with chronic pulmonary infection attended in four reference centers in Brazil: Hospital das Clínicas de Porto Alegre (HCPA), Rio Grande do Sul; Hospital Especializado Octavio Mangabeira (HEOM), Bahia, Instituto Fernandes Figueira (IFF) and Hospital Universitário Pedro Ernesto (HUPE), both of Rio de Janeiro. P. aeruginosa isolates were obtained between May 2009 and June 2011 and submitted to molecular typing by PFGE; determining the antimicrobial susceptibility profile, detection of carbapenem resistance genes by PCR and sequencing of genes mucA and lasR. Molecular typing of 274 samples showed 224 clones. No clones were found circulating between the centers or within the same center. However, samples from two brothers had attended at HEOM belong to the same clone, and were identified clusters of two different patients sharing the same clone in IFF and HCPA. Chronic infection is characterized by the maintenance of a single clone in each patient, but most patients were colonized by intermittent clones. A general analysis of the susceptibility profile showed the highest rates of resistance to amikacin, gentamicin (26%) and cefepime (22%). Comparing the centers, we found that these three antimicrobials were also the least effective at HCPA, but the IFF and HEOM drugs with greater resistance rate were tobramycin and piperacillin / tazobactam, respectively, which indicates the adoption of different treatment protocols between centers. Non mucoid NM isolates (present in the early stages of infection) were significantly more resistant to tobramycin than mucoid (M) (associated with later infection) in IFF and HCPA, but only in the latter M isolates were more resistant to β-lactam antibiotics than NM. About 17% of the samples has been multiresistant and 15 (20%) patients were colonized with at least one sample with this phenotype. The 24 samples from three patients with maintaining the same clone were subjected to sequencing of genes mucA and lasR and of these, of then, 14 (58%) exhibited mutations in at least one gene, which alterations are considered markers of chronic infection. This work stands out because its multicenter feature, the first in FC scope in Brazil, highlighting the need for continued monitoring of this scenario in the country.