title: Analysis of antimicrobial susceptibility and virulence factors in Helicobacter pylori clinical isolates.
abstract: BACKGROUND
  In this study, we evaluated the prevalence of primary resistance of Brazilian H. pylori isolates to metronidazole, clarithromycin, amoxicillin, tetracycline, and furazolidone. In addition, the vacA, iceA, cagA and cagE genotypes of strains isolated from Brazilian patients were determined and associated with clinical data in an effort to correlate these four virulence markers and antibiotic resistance.
  
  
  METHODS
  H. pylori was cultured in 155 H. pylori-positive patients and MICs for metronidazole, clarithromycin, amoxicillin, tetracycline, and furazolidone were determined by the agar dilution method. Genomic DNA was extracted, and allelic variants of vacA, iceA, cagA and cagE were identified by the polymerase chain reaction.
  
  
  RESULTS
  There was a strong association between the vacA s1/cagA -positive genotype and peptic ulcer disease (OR = 5.42, 95% CI 2.6-11.3, p = 0.0006). Additionally, infection by more virulent strains may protect against GERD, since logistic regression showed a negative association between the more virulent strain, vacA s1/cagA-positive genotype and GERD (OR = 0.26, 95% CI 0.08-0.8, p = 0.03). Resistance to metronidazole was detected in 75 patients (55%), to amoxicillin in 54 individuals (38%), to clarithromycin in 23 patients (16%), to tetracycline in 13 patients (9%), and to furazolidone in 19 individuals (13%). No significant correlation between pathogenicity and resistance or susceptibility was detected when MIC values for each antibiotic were compared with different vacA, iceA, cagA and cagE genotypes.
  
  
  CONCLUSIONS
  The analysis of virulence genes revealed a specific association between H. pylori strains and clinical outcome, furthermore, no significant association was detected among pathogenicity and resistance or susceptibility.
authors.affiliation: Clinical Pharmacology and Gastroenterology Unit, São Francisco University Medical School, Bragança Paulista, SP, Brazil. anita@helicobacter.com.br
authors.forename: Anita Paula Ortiz
authors.initials: AP
authors.lastname: Godoy
authors.forename: Marcelo Lima
authors.initials: ML
authors.lastname: Ribeiro
authors.forename: Yune Helena Borges
authors.initials: YH
authors.lastname: Benvengo
authors.forename: Lea
authors.initials: L
authors.lastname: Vitiello
authors.forename: Maira de Carvalho Bueno
authors.initials: Mde C
authors.lastname: Miranda
authors.forename: Sergio
authors.initials: S
authors.lastname: Mendonça
authors.forename: José
authors.initials: J
authors.lastname: Pedrazzoli
mesh_terms: D000328:Adult; D000704:Analysis of Variance; D000890:Anti-Infective Agents / Q000494:pharmacology*; D000942:Antigens, Bacterial / Q000235:genetics; D001426:Bacterial Proteins / Q000235:genetics; D024881:Drug Resistance, Bacterial; D005260:Female; D005764:Gastroesophageal Reflux; D005838:Genotype; D016480:Helicobacter pylori / Q000187:drug effects* / Q000235:genetics / Q000472:pathogenicity*; D006801:Humans; D008297:Male; D016017:Odds Ratio; D010437:Peptic Ulcer; D014774:Virulence / Q000235:genetics
chemical_list: D000890:Anti-Infective Agents; D000942:Antigens, Bacterial; D001426:Bacterial Proteins; C103937:PicB protein, Helicobacter pylori; C074689:VacA protein, Helicobacter pylori; C080866:cagA protein, Helicobacter pylori; C405087:iceA1 protein, Helicobacter pylori