Quinolone-resistant Escherichia coli

Quinolones (nalidixic acid - NAL, norfloxacin - NOR, ciprofloxacin - CIP and gatifloxacin - GAT) were tested against Escherichia coli isolated from urine (385 patient samples) by disk diffusion (DD) and agar dilution (AD) methods. Fifty-three samples (13.8 percent) were classified as resistant to at least one of the quinolones tested. CIP and NOR susceptibilities were the same (91.4 percent) and they were similar to GAT (92.7 percent). Susceptibility to NAL, detected by the disk diffusion method, was used to predict susceptibility to NOR, CIP and GAT by the agar dilution method. The sensitivity and specificity of NAL were 100 percent and 95 percent, respectively. Twelve samples were analyzed for mutations in the quinolone resistance-determining region (QRDR) of the gyrA and parC genes. Sequencing of these genes failed to find any mutations in the quinolone-sensitive isolates. However, three mutations were observed in the isolates resistant to all the quinolones tested - two in gyrA and one in parC. A single mutation in gyrA was found in the strains that were resistant to nalidixic acid but fluoroquinolone-sensitive. These findings support the suggestion that NAL could be used as a marker for susceptibility to fluoroquinolones in routine microbiology laboratories. The overall resistance rate to quinolones in the present study was 13.8 percent, which is higher than that observed in other studies carried out in developed countries. Our findings serve as a warning that resistance to this group of antimicrobial agents is increasing.

Frequency of polymorphisms of genes coding for HIV-1 co-receptors CCR5 and CCR2 in a Brazilian population

Entry of human immunodeficiency type 1 virus (HIV-1) into target cells requires both CD4and one of the chemokine receptors. Viruses predominantly use one, or occasionally both, of the major co-receptors CCR5 and CXCR4, although other receptors, including CCR2B and CCR3, function as minor co-receptors. A 32-nucleotide deletion (delta32) within the beta-chemokine receptor 5 gene (CCR5) has been described in subjects who remain uninfected despite extensive exposition to HIV-1. The heterozygous genotype delays disease progression. This allele is common among Caucasians, but has not been found in people of African or Asian ancestry. A more common transition involving a valine to isoleucine switch in transmembrane domain I of CCR2B (64I), with unknown functional consequences, was found to delay disease progression but not to reduce infection risk. As the Brazilian population consists of a mixture of several ethnic groups, we decided to examine the genotype frequency of these polymorphisms in this country. There were 11.5 percent CCR5 heterozygotes among the HIV-1 infected population and 12.5 percent among uninfected individuals, similar to data from North America and Western Europe. The prevalence of CCR2-64I homozygotes and heterozygotes was 0.06 and 15.2 percent, respectively, also similar to what is known for North America and Western Europe