Emergence of antimicrobial-resistant shigellosis in Oregon.

Ampicillin and trimethoprim-sulfamethoxazole (TMP-SMZ) are currently considered acceptable empirical therapy for shigellosis in developed countries. However, there are few recently reported studies on antimicrobial resistance among shigellae isolated in the United States. We examined the epidemiology of shigellosis and the antimicrobial susceptibility of Shigella species isolated in Oregon from July 1995 through June 1998. Of 430 isolates, 410 were identified to the species level: Shigella sonnei accounted for 55% of isolates, and Shigella flexneri, for 40%. The overall annual incidence of shigellosis was 4.4 cases per 100,000 population. Children aged <5 years (annual incidence, 19.6 cases per 100,000 population) and Hispanics (annual incidence, 28.4 cases per 100,000 population) were at highest risk. Of 369 isolates tested, 59% were resistant to TMP-SMZ, 63% were resistant to ampicillin, 1% were resistant to cefixime, and 0.3% were resistant to nalidixic acid; none of the isolates were resistant to ciprofloxacin. Thirteen percent of the isolates had multidrug resistance to ampicillin, chloramphenicol, streptomycin, sulfisoxazole, and tetracycline. Infections due to multidrug-resistant shigellae are endemic in Oregon. Neither ampicillin nor TMP-SMZ should be considered appropriate empirical therapy for shigellosis any longer; when antibiotics are indicated, a quinolone or cefixime should be used.

Helicobacter pylori infection and urinary excretion of 8-hydroxy-2-deoxyguanosine, an oxidative DNA adduct.

To assess whether Helicobacter pylori-related inflammation increases oxidative DNA damage, we evaluated the association between H. pylori infection and urinary excretion of an adduct of oxidative DNA damage, 8-hydroxy-2-deoxyguanosine (8ohdG). Subjects included 555 healthy persons, ages 20-39, within the Kaiser Permanente Medical Care Program in Northern California. We tested sera for antibodies to H. pylori by ELISA; collected demographic, dietary, smoking, and alcohol data by questionnaire; and assayed 24-h urine samples for 8ohdG with a newly developed ELISA kit. Two hundred eighty-one subjects provided adequate 24-h urine samples for 8ohdG and creatinine assays and had detectable levels of 8ohdG. After adjusting for 24-h urinary creatinine (Ucr) and demographic factors, persons without H. pylori infection had significantly higher amounts of 24-h urinary 8ohdG than infected persons (geometric mean, 18.04 microg 8ohdG/Ucr g versus 14.36 microg 8ohdG/Ucr g, respectively; P = 0.008). Excretion of 8ohdG was higher in whites and Hispanics (17.44 and 18.09 microl/Ucr g) than in blacks (13.21 microg/Ucr g; P < 0.001). Gender was not significantly associated with 8ohdG excretion (16.18 microg/Ucr g for males versus 16.01 microg/Ucr g for females; P = 0.883). Of the dietary factors evaluated, vitamin C negatively correlated (P < 0.001) and carbohydrate intake positively correlated with 8ohdG excretion (P = 0.003). Infection with H. pylori was strongly associated with decreased 8ohdG excretion in the urine. This unexpected finding suggests either that DNA repair is deficient in infected subjects, that inflammation destroys the adduct, or that urinary 8ohdG is not an accurate measure of gastric damage.

Seroprevalence of CagA-positive strains among Helicobacter pylori-infected, healthy young adults.

Helicobacter pylori is categorized into two phenotypes on the basis of the presence or absence of the CagA protein. CagA protein-positive H. pylori are more closely associated with peptic ulcer disease and cancer. Whether CagA-positive strains are similarly represented among racial or ethnic groups in northern California was investigated. Sera from 152 H. pylori-infected healthy young adults were tested by ELISA for IgG against CagA. CagA antibodies were detected in 79.4% of blacks, 63.8% of Hispanics, and 50% of whites. After adjusting for demographic factors, blacks had significantly more infections with CagA-positive H. pylori than did whites (odds ratio [OR] = 5.0; 95% confidence interval [CI] = 1.6-15.3) or Hispanics (OR = 5.5, 95% CI = 1.9-16.0). Also, there was a higher prevalence of CagA in persons born in developing countries than in persons born in industrialized nations (OR = 3.5, 95% CI = 1.3-9.4). This suggests either a genetic predisposition of racial or ethnic groups to infection with particular H. pylori phenotypes or transmission of H. pylori within relatively segregated population groups.

Increased risk of Helicobacter pylori associated with birth in wartime and post-war Japan.

BACKGROUND: Helicobacter pylori infection is now widely recognized as a cause of stomach cancer. We assessed trends in H. pylori infection in Japan, a population with high rates of gastric malignancy. METHODS: Using an enzyme-linked immunosorbent assay (ELISA), we tested sera collected between 1980 and 1993 from Tokyo University Hospital patients for anti-H. pylori IgG. Patients ranged in age from 0 to 94 years. Helicobacter pylori prevalence was then assessed for age and/or birth cohort effects. RESULTS: Of 1207 sera, 470 (38.9%) were positive for H. pylori IgG. By univariate analysis, both older age and birth in an earlier decade were associated with an increased risk of infection. Age-specific prevalence of H. pylori by birth cohort suggested increases in infection during the decades from 1900 to 1959, and age-specific decreases since 1960. In multivariate analysis, H. pylori infection increased with age and was most prevalent among those born in the 1940s and 1950s. CONCLUSION: Relative to other birth cohorts, people born in the 1940s and 1950s have a higher prevalence of H. pylori. This increased prevalence of infection among those born in wartime Japan likely attests to the impact of compromised living conditions on acquisition of H. pylori, and may portend continued high rates of gastric cancer in forthcoming years.

Biologic sex as a risk factor for Helicobacter pylori infection in healthy young adults.

Diseases associated with Helicobacter pylori infection, such as peptic ulcer disease and gastric cancer, afflict men more frequently than women. No study, however, has demonstrated any difference in sex-specific rates of H. pylori infection. In a healthy population undergoing multiphasic health evaluations in 1992-1993 as members of the Kaiser Permanente Medical Care Program of Northern California, adults aged 20-39 years were screened for antibodies to H. pylori infection using a serum enzyme-linked immunosorbent assay and were surveyed with regard to their demographic characteristics and health practices. Among 556 African-American, Hispanic, and white men and women, male sex was a significant risk factor for infection. Other risk factors included African-American race and Hispanic ethnicity, increasing age, living with children, birth in a developing country, and lower levels of income and education. Men consistently had a higher prevalence of antibodies across all strata of race/ethnicity, age, education, and income, and in multivariate analysis male sex remained significantly associated with infection (odds ratio = 2.0, 95% confidence interval 1.2-3.1). African-American race, Hispanic ethnicity, increasing age, lower levels of education, and birth in a developing country were also associated with infection in multivariate analysis. Data from previously reported seroprevalence studies support a tendency for men to have a higher risk of infection. The higher prevalence of infection among young males as observed in Northern California may account in part for the increased incidence of H. pylori-related diseases among men in later decades of life.