title: Helicobacter pylori infection in children and adults: a single pathogen but a different pathology.
abstract: BACKGROUND
  The aims of this retrospective study were to ascertain in large series of children and adults: the relationship of the infecting strain to gastric mucosal lesions; and the relationship of the infecting strain to its duodenal localization.
  
  
  METHODS
  We studied 307 and 604 consecutive children and adults. In gastric mucosal samples H. pylori was cultured, genotyped and histologically assessed, while inflammation, activity and intestinal metaplasia were graded. In a subset of 171 patients H. pylori ureaseA (ureA) and cagA genes were amplified (PCR) using mucosal biopsies from the duodenum.
  
  
  RESULTS
  H. pylori infection was diagnosed in 40 children and 308 adults. cagA was identified in 50% and 65.5% of infected children and adults. Antral activity was associated with the density of infecting bacteria (p <.001) and with cagA (p <.01). Intestinal metaplasia was correlated with cagA (p <.001). The ureA gene was found in 56 duodenal samples from 82 H. pylori positive patients. Duodenal H. pylori ureA was significantly more frequent in patients with duodenal diseases than in those without (p <.01), cagA positive strains being mainly involved in the infection of this anatomical area (p <.01).
  
  
  CONCLUSIONS
  A severe H. pylori-associated gastritis is more prevalent when the density of infecting bacteria is high and when cagA positive strains cause the infection. The most virulent cagA positive H. pylori colonizes not only the gastric, but also the duodenal mucosa, which can be directly damaged by the bacteria itself or by its products.
authors.affiliation: Department of Laboratory Medicine, University of Padova, Italy.
authors.forename: Nicoletta
authors.initials: N
authors.lastname: Gallo
authors.forename: Carlo-Federico
authors.initials: CF
authors.lastname: Zambon
authors.forename: Filippo
authors.initials: F
authors.lastname: Navaglia
authors.forename: Daniela
authors.initials: D
authors.lastname: Basso
authors.forename: Graziella
authors.initials: G
authors.lastname: Guariso
authors.forename: Maria
authors.initials: M
authors.lastname: Grazia Piva
authors.forename: Eliana
authors.initials: E
authors.lastname: Greco
authors.forename: Saverio
authors.initials: S
authors.lastname: Mazza
authors.forename: Paola
authors.initials: P
authors.lastname: Fogar
authors.forename: Massimo
authors.initials: M
authors.lastname: Rugge
authors.forename: Francesco
authors.initials: F
authors.lastname: Di Mario
authors.forename: Mario
authors.initials: M
authors.lastname: Plebani
mesh_terms: D000293:Adolescent; D000328:Adult; D000367:Age Factors; D000368:Aged; D000942:Antigens, Bacterial / Q000235:genetics; D001426:Bacterial Proteins / Q000235:genetics; D001483:Base Sequence; D002648:Child; D002675:Child, Preschool; D004279:DNA, Viral / Q000235:genetics; D004386:Duodenum / Q000382:microbiology / Q000473:pathology; D005260:Female; D005753:Gastric Mucosa / Q000382:microbiology / Q000473:pathology; D005756:Gastritis / Q000382:microbiology* / Q000473:pathology*; D005814:Genes, Viral; D005838:Genotype; D016481:Helicobacter Infections / Q000382:microbiology* / Q000473:pathology*; D016480:Helicobacter pylori / Q000201:enzymology / Q000235:genetics* / Q000302:isolation & purification*; D006801:Humans; D007223:Infant; D008297:Male; D008679:Metaplasia; D008875:Middle Aged; D012189:Retrospective Studies; D014510:Urease / Q000235:genetics
chemical_list: D000942:Antigens, Bacterial; D001426:Bacterial Proteins; D004279:DNA, Viral; C080866:cagA protein, Helicobacter pylori; D014510:Urease