ena-STUDY-UMCG-16-04-2020-14:57:55:552-409
Characterization of bacterial strains causing endocarditis in hospitalized patients in Rio de Janeiro, Brazil.
Infective endocarditis (IE) caused is a life-threatening disease, normally caused by gram-positive bacteria. Despite infections caused by gram-negative is relatively rare, most of these cases were caused by multidrug resistance E. coli and K. pnemominiae. Since antibiotic resistance has been increasing worldwide, including Brazil, the treatment of this infection can be a challenge. In addition, endocarditis is a common complication of bacteremia and it was already reported as caused by bacteria from urinary tract infections (UTIs) source, for this reason, the aim of this study was to perform molecular characterization of E. coli and K. pneumoniae isolates from the blood of patients with IE and performed a comparative study with isolates from urine samples of patients with urinary tract infections. Our results showed that there are similarities between K. pneumoniae isolates from IE and UTIs, including the same resistance phenotype and resistance genes, the same virulence genes and plasmids. These isolates that belongs to ST76, ST36, ST101 (K. pneumoniae) and ST69 (E. coli) knowing to be associate with resistance and common in these infections. When we examined the E. coli isolates there are also similarities between the samples from blood and urine. Surprisely, the isolates causing endocarditis are not ESBL or carbapenemase-producing as the majority of cases decribed in the literature. We also investigated the virulence phenotype, testing the ability of these isolates to form biofilms and adhere to epithelial cells. The isolates from endocarditis presented a stronger biofilm formation then the isolates from urine. All the isolates from endocarditis were able to adhere, while three of the isolates from UTIs were not able to adhere to epithelial cells. Interestingly, the K. pneumoniae isolates from urine 648 and from blood KP that were genetically closely related do not present the same results in the biofilm formation and adhere assays. In summary, the molecular analysis showed that K. pneumoniae and E. coli causing endocarditis share similarities with isolates capable to cause infections in other sites. These isolates belong to ST types considerate a treat to healthcare, However, they do not present the same resistance phenotype and virulence genes, even without these abilities were able to cause invasive infections. The isolates that are similar genetically do not present the same virulence phenotype. These results lead to the conclusion that even these, not hypervirulent clones should be under surveillance since the susceptibility of the host can increase the chances of these isolates also cause complicate infections.
Infective endocarditis (IE) caused is a life-threatening disease, normally caused by gram-positive bacteria. Despite infections caused by gram-negative is relatively rare, most of these cases were caused by multidrug resistance E. coli and K. pnemominiae. Since antibiotic resistance has been increasing worldwide, including Brazil, the treatment of this infection can be a challenge. In addition, endocarditis is a common complication of bacteremia and it was already reported as caused by bacteria from urinary tract infections (UTIs) source, for this reason, the aim of this study was to perform molecular characterization of E. coli and K. pneumoniae isolates from the blood of patients with IE and performed a comparative study with isolates from urine samples of patients with urinary tract infections. Our results showed that there are similarities between K. pneumoniae isolates from IE and UTIs, including the same resistance phenotype and resistance genes, the same virulence genes and plasmids. These isolates that belongs to ST76, ST36, ST101 (K. pneumoniae) and ST69 (E. coli) knowing to be associate with resistance and common in these infections. When we examined the E. coli isolates there are also similarities between the samples from blood and urine. Surprisely, the isolates causing endocarditis are not ESBL or carbapenemase-producing as the majority of cases decribed in the literature. We also investigated the virulence phenotype, testing the ability of these isolates to form biofilms and adhere to epithelial cells. The isolates from endocarditis presented a stronger biofilm formation then the isolates from urine. All the isolates from endocarditis were able to adhere, while three of the isolates from UTIs were not able to adhere to epithelial cells. Interestingly, the K. pneumoniae isolates from urine 648 and from blood KP that were genetically closely related do not present the same results in the biofilm formation and adhere assays. In summary, the molecular analysis showed that K. pneumoniae and E. coli causing endocarditis share similarities with isolates capable to cause infections in other sites. These isolates belong to ST types considerate a treat to healthcare, However, they do not present the same resistance phenotype and virulence genes, even without these abilities were able to cause invasive infections. The isolates that are similar genetically do not present the same virulence phenotype. These results lead to the conclusion that even these, not hypervirulent clones should be under surveillance since the susceptibility of the host can increase the chances of these isolates also cause complicate infections.