Summary Background Limited information exists regarding risk factors for reinfection after cure of Helicobacter pylori infection. Aim To determine the 2‐year reinfection rate of H. pylori in a cohort of urban Alaska Natives. Methods Participants over 18 years of age undergoing oesophagogastroduodenoscopy had 13 C urea breath test, culture, CLOtest and histology performed. Those diagnosed with H. pylori who tested urea breath test‐negative at 8 weeks after treatment were followed prospectively at 4 months, 6 months, 1 year and 2 years. Subjects experiencing H. pylori reinfection as defined by a positive urea breath test were compared with those who did not become reinfected using univariable and multivariable analysis. Risk of reinfection over time was estimated by the Kaplan–Meier method. Results Helicobacter pylori reinfection occurred in 14 of 98 subjects successfully treated. The cumulative reinfection rate was 5.1% (95% CI: 0.7%–9.5%) at 4 months, 7.2% (2.0–12.3%) at 6 months, 10.3% (4.2–16.3%) at 1‐year and 14.5% (7.5–21.6%) at 2 years. In multivariable analysis, a history of previous peptic ulcer disease or presence of ulcer at time of study oesophagogastroduodenoscopy were the only risk factors associated with reinfection ( P = 0.01). Conclusions Based on the findings from our study, subjects with a history of or current peptic ulcer disease should be followed, after successful treatment for H. pylori , with periodic urea breath test to detect reinfection, as reinfection would put them at high risk for ulcer recurrence.
ABSTRACT A commercially available rapid fluorescent in situ hybridization (FISH) test, (seaFAST H. pylori Combi-Kit; SeaPro Theranostics International, Lelystad, The Netherlands) was used to simultaneously detect the presence of Helicobacter pylori and determine clarithromycin susceptibility in paraffin-embedded biopsy sections. The FISH method was found to be 97% sensitive, 94% specific for the detection of H. pylori and comparable to agar dilution for the detection of resistance to clarithromycin.
Abstract Objective: We investigated a large outbreak of community-onset methicillin-resistant Staphylococcus aureus (MRSA) infections in southwestern Alaska to determine the extent of these infections and whether MRSA isolates were likely community acquired. Design: Retrospective cohort study. Setting: Rural southwestern Alaska. Patients: All patients with a history of culture-confirmed S. aureus infection from March 1, 1999, through August 10, 2000. Results: More than 80% of culture-confirmed S. aureus infections were methicillin resistant, and 84% of MRSA infections involved skin or soft tissue; invasive disease was rare. Most (77%) of the patients with MRSA skin infections had communityacquired MRSA (no hospitalization, surgery, dialysis, indwelling line or catheter, or admission to a long-term-care facility in the 12 months before infection). Patients with MRSA skin infections were more likely to have received a prescription for an antimicrobial agent in the 180 days before infection than were patients with methicillin-susceptible S. aureus skin infections. Conclusions: Our findings indicate that the epidemiology of MRSA in rural southwestern Alaska has changed and suggest that the emergence of community-onset MRSA in this region was not related to spread of a hospital organism. Treatment guidelines were developed recommending that beta-lactam antimicrobial agents not be used as a first-line therapy for suspected S. aureus infections.
The International Circumpolar Surveillance (ICS) program is a population-based surveillance network for invasive bacterial diseases throughout Arctic countries and territories. The ICS quality control program for
We read with interest of three Neisseria meningitidis strains recovered in Germany that reacted with commercial (Oxoid, Wesel, Germany) serogroup Y and serogroup W135 antisera (3). The molecular basis of this dual antigenic specificity has been determined to be due to a single amino acid change at position 310 in the EX7E motif of the capsule polymerase enzyme synG (also referred to as siaDY) (from glycine to serine) or synF (siaDW-135) (from proline to serine) (2). Both studies confirmed our earlier report of such unusual strains causing invasive meningococcal disease (IMD) (10).
Here we report three other IMD cases caused by similar meningococcal strains in patients residing in an urban area of Alaska. These strains were collected by the Arctic Investigation Program, located in Anchorage, AK, which began statewide surveillance for IMD in 2000. The three cases of IMD reported here were identified through the interlaboratory quality control program implemented as part of the International Circumpolar Surveillance system established in 1999 to monitor infectious diseases of concern in the Arctic (11). Case 1 occurred in July 2006 in a 25-year-old female, while cases 2 and 3 occurred in August and October of 2008 in a male and a female infant less than 12 months old, respectively. There was no known epidemiological link between these cases. In all three cases the N. meningitidis strains were recovered from blood cultures. The serogroup of the isolates was determined by PCR (1, 7) and agglutination with specific rabbit antisera (BD Difco, Sparks, MD). Serotypes, serosubtypes, and PorB and PorA VR genotypes as well as multilocus sequence types (MLST) were determined using established methods as previously described (6). Sequencing of the siaD genes was accomplished by methods previously described (10).
All three isolates were identified as serogroup Y by genogrouping using PCR but agglutinated in both anti-Y and anti-W135 antisera. The antigenic and genetic characteristics of these three isolates are summarized in Table Table11.
TABLE 1.
Phenotypic and genetic characterization of Y/W135:2c:P1.5 Neisseria meningitidis strainsa from Alaska
It is striking to note that all three isolates have the same mutations in their capsule polymerase enzyme that involved incorporation of the amino acid serine into position 310 in the EX7E motif, which apparently allows the isolates to assemble both glucose and galactose, together with sialic acid, into their capsular polysaccharide structure (2, 10). In addition, it is interesting to note that these three IMD isolates in Alaska have all the antigenic and genetic features characteristic of serogroup Y N. meningitidis strains (5, 8, 9).
Therefore, it is tempting to speculate that these unusual N. meningitidis strains may be derived from serogroup Y strains by acquiring a mutation in their capsule polymerase enzyme (G310S) to allow expression of this unique antigenic specificity. The emergence of these strains was coincident with the increase in serogroup Y strains in both the United States (4) and Canada (8), which may favor the argument that they were derived from serogroup Y meningococci.
In summary, surveillance of meningococcal disease with tests that can correctly identify these unusual isolates (2, 10) and MLST may help to determine the genetic background and molecular epidemiology of this group of meningococci.
Helicobacter pylori infection is more common in Alaska Native persons than in the general U.S. population, with seroprevalence to H. pylori approaching 75%. Previous studies in Alaska have demonstrated elevated proportions of antimicrobial resistance among H. pylori isolates. We analyzed H. pylori data from the Centers for Disease Control and Prevention's sentinel surveillance in Alaska from January 2000 to December 2008 to determine the proportion of culture-positive biopsy specimens with antimicrobial resistance from Alaska Native persons undergoing endoscopy. The aim of the present study was to monitor antimicrobial resistance of H. pylori isolates over time and by region in Alaska Native persons. Susceptibility testing of H. pylori isolates to metronidazole, clarithromycin, amoxicillin, and tetracycline was performed using agar dilution. Susceptibility testing for levofloxacin was performed by Etest. Overall, 45% (532/1,181) of persons undergoing upper endoscopy were culture positive for H. pylori. Metronidazole resistance was demonstrated in isolates from 222/531 (42%) persons, clarithromycin resistance in 159/531 (30%) persons, amoxicillin resistance in 10/531 (2%) persons, and levofloxacin resistance in 30/155 (19%) persons; no tetracycline resistance was documented. The prevalence of metronidazole, clarithromycin, and levofloxacin resistance varied by region. Female patients were more likely than male patients to demonstrate metronidazole (P < 0.05) and clarithromycin (P < 0.05) resistance. No substantial change in the proportion of persons with resistant isolates was observed over time. Resistance to metronidazole, clarithromycin, and levofloxacin is more common among H. pylori isolates from Alaska Native persons than those from elsewhere in the United States.
The relationship between prior fluoroquinolone use and levofloxacin resistance in Helicobacter pylori infection is unknown. Among 125 enrolled patients, 8.8% had H. pylori isolates that were resistant to levofloxacin. Levofloxacin resistance was associated with any prior fluoroquinolone use over the previous 10 years and with the total number of fluoroquinolone courses prescribed (P<.001).
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