Genotypical variation of Campylobacter pylori from gastric mucosa.

In a previous study, the recurrence of the Campylobacter pylori infection after apparently successful antibacterial therapy was determined to be due to recrudescence rather than reinfection. Although the DNA patterns of pre- and posttreatment isolates were very similar, we detected minor differences between the two patterns in about one third of the patients. These differences were not artifacts, but originated in the coexistence in the stomach of (sub)populations of bacteria with slightly different chromosomal DNAs, plasmids, or both. The presence of such (sub)populations was probably caused by mutation in vivo, as mutation in vitro was demonstrated in one patient after the original isolate was subcultured 10 times. Minor differences were not correlated with a difference in susceptibility to the antibiotic(s) that was used. An additional conclusion of this investigation was that the results of plasmid analysis should be interpreted very carefully when this method is used as an epidemiologic marker in the investigation of C. pylori infections.

Patient-to-patient transmission of Campylobacter pylori infection by fiberoptic gastroduodenoscopy and biopsy.

Three instances of subclinical reinfection with Campylobacter pylori were observed in two successfully treated patients during follow-up of C. pylori gastritis. The reinfections occurred 1 month and 21 months (patient 1) and 32 months (patient 2) after the completion of antibacterial treatment. Sequential measurement by ELISA of serum IgG antibody levels to the microorganism showed a significant increase in two of the three instances of reinfection. Patient-to-patient transmission was proved by restriction enzyme analysis of bacterial DNA. Between patients the endoscope had been mechanically cleaned using a detergent and treated with 70% ethanol. The risk of gastroscopic cross-infection with C. pylori was estimated by retrospective analysis of the data of 281 negative examinations (107 in 47 initially negative patients and 174 in 37 cured patients). The frequency in uninfected patients of documented endoscopic transmission of C. pylori infection was 1.1% in this study, corresponding with three iatrogenic acquisitions of manifest infection for every 1000 gastroduodenoscopies in our clinic.

Rapidly decreased serum IgG to Campylobacter pylori following elimination of Campylobacter in histological chronic biopsy Campylobacter-positive gastritis.

The anaerobic bacterium Campylobacter pylori (Cp) is thought to be associated with chronic gastritis. This paper presents clinical data underpinning this view. Five patients with histological chronic gastritis as determined by diagnostic endoscopy, which was associated with Cp as determined by positive biopsy cultures, all possessed statistically raised serum IgG ELISA titers to Cp during a longitudinal period of observation of 15 months. Treatment with the antibiotics amoxycillin (clamoxyl) or colloidal bismuth subcitrate (denol) eliminated Cp within one month. Associated with this, serum IgG ELISA titers were found to decrease sharply and rapidly. Tagamet and spiramycin had little effect. Although the data are preliminary, they support the assumed Cp involvement in chronic gastritis and suggest that specific serum IgG ELISA titers to Cp are useful parameters in monitoring disease status, exceeding bacteriological culture of biopsy specimens in speed and convenience.

Application of whole-cell DNA restriction endonuclease profiles to the epidemiology of Clostridium difficile-induced diarrhea.

Two patients in one hospital room acquired pseudomembranous colitis, one shortly after the other. The DNA restriction patterns of isolates from the patients and of four isolates from the environment were indistinguishable from one another and differed from isolates of other patients. Restriction endonuclease digest analysis appears to be a useful method for studying the epidemiology of Clostridium difficile.