Establish the susceptibility pattern of Gram-negative bacteria causing infections in ICU patients, MYSTIC Program Brazil 2003. Gram-negative bacteria (n = 1,550) causing nosocomial infections were collected at 20 Brazilian centers. The central laboratory confirmed the identification and performed the susceptibility tests by Etest methodology (AB Biodisk, Solna, Sweden) for meropenem, imipenem, ciprofloxacin, ceftazidime, cefepime, cefotaxime, piperacillin/tazobactam, gentamicin, and tobramycin. Interpretation criteria used were according to National Committee for Clinical Laboratory Standards (NCCLS). Pseudomonas aeruginosa (30.3%) was the most frequent isolate, followed by E. coli (18.6%), Klebsiella pneumoniae (16.9%), Acitenobacter baumannii (8.8%), and Enterobacter cloacae (7.1%). Pseudomonas aeruginosa (n=470) isolates presented susceptibility rates of 64% to meropenem, 63.8% to piperacillin/tazobactam, 63.4% to amikacin, 58.7% to imipenem. Acitenobacter baumannii presented susceptibility rates to meropenem of 97.1%, and 73% to tobramycin. E. coli and K. pneumoniae were highly susceptible to both carbapenems. Carbapenem resistance among the Enterobacteriaceae is still rare in the region. Acitenobacter baumannii and P. aeruginosa presented elevated resistance rates to all antimicrobials. Since they play an important role in nosocomial infections in this environment, the use of empirical combination therapy to treat these pathogens may be justified.
The ability of some typical enteropathogenic Escherichia coli (EPEC) strains to adhere to, invade, and increase interleukin-8 (IL-8) production in intestinal epithelial cells in vitro has been demonstrated. However, few studies regarding these aspects have been performed with atypical EPEC (aEPEC) strains, which are emerging enteropathogens in Brazil. In this study, we evaluated a selected aEPEC strain (1711-4) of serotype O51:H40, the most prevalent aEPEC serotype in Brazil, in regard to its ability to adhere to and invade Caco-2 and T84 cells and to elicit IL-8 production in Caco-2 cells. The role of flagella in aEPEC 1711-4 adhesion, invasion, and IL-8 production was investigated by performing the same experiments with an isogenic aEPEC mutant unable to produce flagellin (FliC), the flagellum protein subunit. We demonstrated that this mutant (fliC mutant) had a marked decrease in the ability to adhere to T84 cells and invade both T84 and Caco-2 cells in gentamicin protection assays and by transmission electron microscopy. In addition, the aEPEC 1711-4 fliC mutant had a reduced ability to stimulate IL-8 production by Caco-2 cells in early (3-h) but not in late (24-h) infections. Our findings demonstrate that flagella of aEPEC 1711-4 are required for efficient adhesion, invasion, and early but not late IL-8 production in intestinal epithelial cells in vitro.Typical enteropathogenic Escherichia coli (tEPEC) strains are a well-known cause of diarrhea in infants in developing countries (14, 27, 45) whereas atypical EPEC (aEPEC) strains are emerging enteropathogens (1,3,10,14,27,28,33,36,45). tEPEC and aEPEC produce a histopathological lesion on enterocytes that is known as the attaching and effacing (AE) lesion. This lesion is characterized by effacement of microvilli, intimate adherence between the bacterium and the cell membrane, and actin accumulation underneath adherent bacteria, forming a pedestal-like structure. Intimate adherence is mediated by intimin (an outer membrane bacterial adhesin) and its receptor Tir (translocated intimin receptor), which is translocated into the host cell by a type III secretion system (19). The proteins involved in the establishment of AE lesions are encoded on the chromosomal pathogenicity island called the locus of enterocyte effacement (LEE) (24). A functional LEE region is also found in enterohemorrhagic E. coli (EHEC) and probably plays a significant role in disease since patients with hemolytic uremic syndrome develop a strong antibody response to various LEE-encoded proteins, although the major virulence factors in EHEC are the Shiga toxins (19). In addition, only tEPEC strains possess the EPEC adherence factor plasmid, which encodes localized adhesion on cultured epithelial cells mediated by the bundle-forming pilus (Bfp) and a transcriptional activator (Per) that upregulates the expression of the bfp operon and the LEE genes (19,27).It has been shown that tEPEC flagella mediate adhesion and microcolony formation on cultured enterocytes, and they are also implicated in t...
kIn Enterobacteriaceae, the bla NDM genes have been found in many different genetic contexts, and a wide diversity of plasmid scaffolds bearing those genes has been found. In August 2013, we identified NDM-1-producing Escherichia coli and Enterobacter hormaechei strains from a single rectal swab sample from a patient hospitalized in Rio de Janeiro, Brazil, who had no history of travel abroad. Complete DNA sequencing using the Illumina platform and annotation of the two plasmids harboring the bla NDM-1 gene, one from each strain, showed that they belonged to incompatibility groups IncFII K and IncX3 and harbored a novel transposon named Tn3000. Similar genetic structures have been identified among other isolates in Brazil but also on plasmids from other continents. Our findings suggest that the bla NDM-1 gene may be transmitted by Tn3000 in different parts of the world.
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