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An Example from Medicine
Published in Donald Gillies, Causality, Probability, and Medicine, 2019
The first surprise came in 1979 when Warren observed spiral bacteria in a biopsy specimen from a human stomach. Previously it had been thought that the stomach was too acid for any bacteria to exist there. In 1981 Marshall joined Warren to help him investigate the new bacterium. At first it was thought to belong to the Campylobacter genus, but further investigation showed this to be false and that the genus was named Helicobacter pylori.
Gastric Ulcers, from Psychosomatic Disease to Infection
Published in Issues in Mental Health Nursing, 2020
These findings were not really taken seriously until the late 1970s, when J. Robin Warren, a pathologist in Perth, Australia, noted the appearance of spiral bacteria overlaying gastric mucosa, chiefly over inflamed tissue. In 1982, two physicians from Perth, Australia, Dr. Warren and Dr. Barry Marshall, again observed bacteria associated with ulcerated and inflamed regions of human gut and began investigating its role in disease (Chow, 2018; Konturek, 2003). They isolated the bacteria from stomach biopsies and named the organism Helicobacter pylori. After a long trial and error period, Warren and Marshall figured out how to grow H. pylori in culture, which occurred by chance after inadvertently leaving the culture to grow over a long Easter holiday (Chow, 2018). H. pylori is slow growing compared with other bacteria and requires additional days of growing time. Using themselves as test subjects, Marshall and another volunteer ingested a culture of H. pylori and soon developed gastritis, thus definitively establishing a link between the infectious agent and disease. Warren and Marshall published their work in 1982 and were awarded the Nobel Prize in Medicine in 2005 for their outstanding contributions to the field (Chow, 2018).
Risk of inflammatory bowel disease after Campylobacter jejuni and Campylobacter concisus infection: a population-based cohort study
Published in Scandinavian Journal of Gastroenterology, 2019
Hans Linde Nielsen, Michael Dalager-Pedersen, Henrik Nielsen
We used the laboratory information system (wwLab, Autonik AB, Nyköping, Sweden) to identify all patients 15 years or older during the study period, who had a first-time positive stool culture with either C. jejuni, C. coli or C. concisus, as the sole pathogenic enteric bacteria. The index date of stool testing was defined as the date of receipt of the stool sample. Stools were cultured for the standard panel of enteric bacterial pathogens including Campylobacter spp., Salmonella, Vibrio, Shigella spp., Yersinia enterocolitica and C. difficile, but the latter was only diagnosed upon clinical suspicion of C. difficile infection, that is, antibiotic-associated diarrhea, hospital-onset diarrhea or pseudomembranous colitis. In brief, C. jejuni and C. coli were routinely identified by their macroscopic morphology on the mCCDA plate (SSI Diagnostica, Hillerød, Denmark) and a positive wet smear of highly motile spiral bacteria. Differentiation between C. jejuni and C. coli was not done routinely, but C. jejuni constitute approximately 93% of thermophilic Campylobacter spp. in Denmark [22], and we will write C. jejuni only hereafter. Cefoperazone susceptible Campylobacter spp., including C. concisus, were isolated by use of the filter technique on 5% horse blood agar plates, containing 1% yeast extract (SSI Diagnostica, Hillerød, Denmark), incubated at 37 °C in a microaerobic atmosphere with 3% hydrogen, as described elsewhere [14,16]. Patients with rare Campylobacter spp. in stools such as C. curvus, C. ureolyticus and C. upsaliensis were excluded due to the small sample size as reported elsewhere [14,16].