RESUMO
Corynebacterium striatum is part of microbiota of skin and nasal mucosa of humans and has been increasingly reported as the etiologic agent of community-acquired and nosocomial diseases. Antimicrobial multidrug-resistant (MDR) C. striatum strains have been increasingly related to various nosocomial diseases and/or outbreaks worldwide, including fatal invasive infections in immunosuppressed and immunocompetent patients. Although cases of infections by C. striatum still neglected in some countries, the improvement of microbiological techniques and studies led to the increase of survival of patients with C. striatum nosocomial infections at different levels of magnitude. Biofilm formation on abiotic surfaces contributes for the persistence of virulent C. striatum and dissemination of antimicrobial resistance in hospital environment. Besides that, empirical antibiotic therapy can select multi-resistant strains and transfer intra and interspecies genes horizontally. In this study, a worldwide survey of C. striatum human infections and nosocomial outbreaks was accomplished by the analysis of clinical-epidemiological and microbiological features of reported cases from varied countries, during a 44-year period (1976-2020).
Assuntos
Antibacterianos/farmacologia , Infecções por Corynebacterium/microbiologia , Corynebacterium/patogenicidade , Infecção Hospitalar/microbiologia , Farmacorresistência Bacteriana Múltipla , Biofilmes/efeitos dos fármacos , Biofilmes/crescimento & desenvolvimento , Corynebacterium/efeitos dos fármacos , Infecções por Corynebacterium/epidemiologia , Infecção Hospitalar/epidemiologia , Surtos de Doenças/estatística & dados numéricos , Farmacorresistência Bacteriana Múltipla/efeitos dos fármacos , Farmacorresistência Bacteriana Múltipla/genética , Humanos , VirulênciaRESUMO
The interaction of Pseudomonas aeruginosa with plasminogen (Plg) is herein reported. Plg bound similarly to laboratory and clinical P. aeruginosa isolates from blood of septicemic patients and stools of asymptomatic carriers. No difference in Plg capture was detected between the piliated PAK strain and its isogenic nonpiliated mutant. Western immunoblotting results suggested that low molecular weight nonpilus adhesins from the bacterial outer membranes accounted for the Plg capture. Bacteria-bound Plg was converted to bioactive plasmin in the presence of exogenous urokinase-type Plg activator. The presence of surface-bound plasmin enhanced significantly the P. aeruginosa capability to invade fibrin gels and a reconstituted basement membrane matrix. These findings support the concept that Plg capture by P. aeruginosa may represent a mechanism which offers advantages to bacterial invasiveness through tissue barriers.