Colonización-infección por Pseudomonas aeruginosa en pacientes con bronquiectasias y EPOCaspectos clínicos microbiológicos y evolutivos

Abstract

In order to know the epidemiological, clinical, micribiologic and outcome features in Pseudomonas aeruginosa (PA) infected-colonized patients with bronchiectasias (without cystic fibrosis) or chronic obstructive pulmonary disease (COPD), a prospective study was conducted on 39 patients admitted to our center during 1998 for acute respiratory exacerbation in which PA was isolated from their sputum. Clinical, epidemiological and microbiologic parameters, including antiobiotic susceptibility and genetic analysis, were evaluated. Twenty tree patients were clinical and microbiologically followed for one year. Twenty-four patients has bronchiectasias (12% of all cases hospitalized with this diagnosis in 1998) and 15 had COPD. All patients presented severe airflow obstruction (FEV1 <45%). Twenty-two patients (56%) had chronic respiratory failure. Of the 42 strains studied (three patients had 2 strains), 14 were mucoid and 28 nonmucoid phenotype. The resistance rates for amikacin, ticarcillin, imipenem and gentamicin were 0%, 5%, 13.3% and 14.2% respectively. During the follow-up, 74% patients developed resistance to one or more antibiotic. Mortality of 38% in one year was observed. The persistent eradication of PA was only achieved in 20% cases (in 15 patients). It continued in sputum in 66% and reappeared, after had apparently been eradicated, in 13.3%. Only one clone was present in 82% patients, which usually tended to persist. Of 41 cases in which genetic study was performed, 29 (70%) had a solo clone. PA isolated from sputum was the same that the one isolated in stool samples in 90% cases in which PA was founded in both specimens. PA infection-colonization affects patients who have severe chronic respiratory diseases increasing mortality and need for hospitalization. PA tends to remain in spite of antimicrobial treatment. According to our genetic study, the emergence of drug resistance is not usually related to the acquisition of new strains. Most patients do not share the same clones; therefore, except for isolated cases, exposure to a common source is not supported.