Presence of high numbers of transcriptionally active Helicobacter pylori in vomitus from Bangladeshi patients suffering from acute gastroenteritis.
BACKGROUND
Helicobacter pylori is one of the most prevalent human bacterial pathogens; however, its transmission pathways remain unknown. New infections of H. pylori during outbreaks of gastroenteritis have been suggested previously, and to explore this transmission route further H. pylori was quantified in vomitus and diarrheal stool of patients suffering from acute gastroenteritis in Dhaka, Bangladesh.


METHODS
Vomitus and stool samples from 28 patients seeking care at the International Centre for Diarrhoeal Disease Research hospital were analyzed for presence of H. pylori and other pathogens using quantitative culturing, real-time polymerase chain reaction (PCR), and H. pylori stool antigen test. Bacterial gene expression was analyzed using reverse transcriptase real-time PCR.


RESULTS
The results of real-time PCR show that 23 (88%) of the 26 vomitus samples and 17 (74%) of the 23 stool samples were H. pylori positive, while stool antigen test show that 14 (67%) of the 21 stool samples were H. pylori positive. H. pylori could not be isolated by culture. Analysis using quantitative culture and real-time PCR to detect Vibrio cholerae showed strong correlation between these methods, and validating real-time PCR. Analysis of H. pylori virulence gene transcription in vomitus, diarrheal stool, antral and duodenal biopsy specimens, and in vitro cultures showed that cagA, flaA, and ureA were highly transcribed in vomitus, biopsy specimens, and cultures, whereas hpaA and vacA were expressed at lower levels. No H. pylori gene expression was detected in diarrheal stool.


CONCLUSIONS
We conclude that high numbers of transcriptionally active H. pylori are shed in vomitus, which indicates that new infections may be disseminated through vomiting.
Janzon
Anders
A
Department of Microbiology and Immunology, Institute of Biomedicine, Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden. anders.janzon@microbio.gu.se
Bhuiyan
Taufiq
T
Lundgren
Anna
A
Qadri
Firdausi
F
Svennerholm
Ann-Mari
AM
Sjöling
Asa
A
D000208:Acute Disease / Q000453:epidemiology; D000293:Adolescent; D000328:Adult; D000368:Aged; D000942:Antigens, Bacterial / Q000235:genetics; D001426:Bacterial Proteins / Q000235:genetics; D001459:Bangladesh / Q000453:epidemiology; D002648:Child; D005243:Feces / Q000382:microbiology; D005260:Female; D005759:Gastroenteritis / Q000453:epidemiology / Q000382:microbiology*; D016481:Helicobacter Infections / Q000453:epidemiology / Q000382:microbiology*; D016480:Helicobacter pylori / Q000235:genetics* / Q000302:isolation & purification*; D006801:Humans; D006836:Hydro-Lyases / Q000235:genetics; D008297:Male; D008875:Middle Aged; D010088:Oxidoreductases / Q000235:genetics; D014839:Vomiting / Q000453:epidemiology / Q000382:microbiology*; D055815:Young Adult
D000942:Antigens, Bacterial; D001426:Bacterial Proteins; C417241:FlaA1 protein, Helicobacter pylori; C080866:cagA protein, Helicobacter pylori; D010088:Oxidoreductases; D006836:Hydro-Lyases