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We adapted the EQ-5D-3L questionnaire and visual analog scale to assess health-related quality of life (HRQOL) and persistent symptoms in 79 patients with laboratory-confirmed dengue in Morelos, Mexico. The lowest HRQOLs were 0.53 and 38.1 (febrile phase). Patients recovered baseline HRQOL in ≈2 months.

Background and Aims: Resistance to antibiotics is common in patients with Helicobacter pylori infection in more than one anatomic stomach site. We assessed whether the antibiotic resistance varies according to virulence factors of the bacteria as well as to the age and gender of individuals infected in two anatomic sites., Methods: H. pylori strains were isolated from an antral and corpus biopsy from 90 patients with gastric ambulatory who had not received any previous therapy. Susceptibility to metronidazole and clarithromycin was assessed by E-test, and vacA and cagA genotypes were determined by polymerase chain reaction., Results: Dual resistance to metronidazole and clarithromycin was 3.3% in antrum and 4.4% in the corpus; heteroresistance was 19% and 5.5% for metronidazole and clarithromycin, respectively. Clarithromycin resistance significantly increased with age. Women showed a twofold increased risk for metronidazole-resistant strains in antrum (odds ratio = 2.85, 95% confidence interval 1.09 to 7.42). Virulence factors were not associated with antimicrobial resistance., Conclusion: Prevalence of resistance to clarithromycin may be increasing in this country. Antimicrobial susceptibility tests from different biopsy sites deserve attention.

Eradication of Helicobacter pylori infection in Mexico is of great importance due to the elevated seroprevalence, however, there is yet very little information about antibiotic resistance rates in H. pylori isolates in our country. We analyzed susceptibility to three antimicrobials used in therapy of 49 H. pylori strains isolated from patients with active chronic gastritis, active chronic gastritis with lymphoid follicles, intestinal metaplasia and gastric cancer. All isolated strains were susceptible to amoxicillin, 28 (58%) were resistant to metronidazole and 2 (4%) were resistant to both clarithromycin and metronidazole. Sequence analysis of the 23S rRNA of the two clarithromycin-resistant strains showed the A2142G mutation in one and A2143G and T2182C mutations in the other. Metronidazole resistance was associated with cagA negative strains with a frequency of 82% (9/11). No significant correlation was found between vacA s/m alleles and metronidazole resistance.

Up to 28-fold differences in vacA expression in Helicobacter pylori strains grown in vitro were demonstrated by real time quantitative RT-PCR. These large differences in expression were unrelated to putative -35 and -10 motifs or to other untranslated sequences upstream of the ATG start site. The lack of correlation between promoter sequences and the vacA expression levels suggest the potential existence of a bacterial strain-specific factor, as earlier proposed by others on the basis of reporter gene fusions.

One hundred eighty-four clinical isolates of Klebsiella pneumoniae were recovered from August 1996 to October 1997 at the Pediatric Hospital of the Instituto Mexicano del Seguro Social in Mexico City, Mexico. Most of the isolates were collected from the neonatal intensive care unit and infant wards, which are located on the same floor of the hospital. Isolates were genotypically compared by pulsed-field gel electrophoresis with XbaI restriction of chromosomal DNA. Of 184 clinical isolates, 91 belonged to cluster A and comprised three subtypes (A1, A2, and A3), while 93 isolates, comprising two minor clones, B (10 isolates) and C (7 isolates), and 76 unique patterns, were considered unrelated isolates (URI). Susceptibility patterns were indistinguishable in both groups. Fifty extended-spectrum beta-lactamase-producing isolates, including 34 from clone A and 16 from URI, were examined for further studies. Molecular and genetic analysis showed that 47 of 50 clinical isolates expressed the SHV-5 beta-lactamase. This enzyme, in combination with TEM-1, was encoded in a >or=170-kb conjugative plasmid. Results indicate that dissemination of this resistance was due to clonal and horizontal spread.