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A case of gastric phycomycosis in Malaysia

Ahluwalia HS, Lie Kian Joe, Arulambalam TR

Southeast Asian J. Trop. Med. Public Health, 1973 Jun;4(2):280.
PMID: 4749089
Matched MeSH terms: Stomach Diseases/microbiology*
Role of vacuolating cytotoxin A in Helicobacter pylori infection and its impact on gastric pathogenesis

Ansari S, Yamaoka Y

Expert Rev Anti Infect Ther, 2020 10;18(10):987-996.
PMID: 32536287 DOI: 10.1080/14787210.2020.1782739

Introduction Helicobacter pylori causes, via the influence of several virulence factors, persistent infection of the stomach, which leads to severe complications. Vacuolating cytotoxin A (VacA) is observed in almost all clinical strains of H. pylori; however, only some strains produce the toxigenic and pathogenic VacA, which is influenced by the gene sequence variations. VacA exerts its action by causing cell vacuolation and apoptosis. We performed a PubMed search to review the latest literatures published in English language. Areas covered Articles regarding H. pylori VacA and its genotypes, architecture, internalization, and role in gastric infection and pathogenicity are reviewed. We included the search for recently published literature until January 2020. Expert opinion H. pylori VacA plays a crucial role in severe gastric pathogenicity. In addition, VacA mediated in vivo bacterial survival leads to persistent infection and an enhanced bacterial evasion from the action of antibiotics and the innate host defense system, which leads to drug evasion. VacA as a co-stimulator for the CagA phosphorylation may exert a synergistic effect playing an important role in the CagA-mediated pathogenicity.

Matched MeSH terms: Stomach Diseases/microbiology
Fulltext Culturable bacterial microbiota of the stomach of Helicobacter pylori positive and negative gastric disease patients

Khosravi Y, Dieye Y, Poh BH, Ng CG, Loke MF, Goh KL, et al.

ScientificWorldJournal, 2014;2014:610421.
PMID: 25105162 DOI: 10.1155/2014/610421

Human stomach is the only known natural habitat of Helicobacter pylori (Hp), a major bacterial pathogen that causes different gastroduodenal diseases. Despite this, the impact of Hp on the diversity and the composition of the gastric microbiota has been poorly studied. In this study, we have analyzed the culturable gastric microbiota of 215 Malaysian patients, including 131 Hp positive and 84 Hp negative individuals that were affected by different gastric diseases. Non-Hp bacteria isolated from biopsy samples were identified by matrix assisted laser desorption ionization-time of flight mass spectrometry based biotyping and 16SrRNA sequencing. The presence of Hp did not significantly modify the diversity of the gastric microbiota. However, correlation was observed between the isolation of Streptococci and peptic ulcer disease. In addition, as a first report, Burkholderia pseudomallei was also isolated from the gastric samples of the local population. This study suggested that there may be geographical variations in the diversity of the human gastric microbiome. Geographically linked diversity in the gastric microbiome and possible interactions between Hp and other bacterial species from stomach microbiota in pathogenesis are proposed for further investigations.

Matched MeSH terms: Stomach Diseases/microbiology
Dual role of Helicobacter and Campylobacter species in IBD: a systematic review and meta-analysis

Castaño-Rodríguez N, Kaakoush NO, Lee WS, Mitchell HM

Gut, 2017 02;66(2):235-249.
PMID: 26508508 DOI: 10.1136/gutjnl-2015-310545

OBJECTIVE: To conduct a comprehensive global systematic review and meta-analysis on the association between Helicobacter pylori infection and IBD. As bacterial antigen cross-reactivity has been postulated to be involved in this association, published data on enterohepatic Helicobacter spp (EHS) and Campylobacter spp and IBD was also analysed.
DESIGN: Electronic databases were searched up to July 2015 for all case-control studies on H. pylori infection/EHS/Campylobacter spp and IBD. Pooled ORs (P-OR) and 95% CIs were obtained using the random effects model. Heterogeneity, sensitivity and stratified analyses were performed.
RESULTS: Analyses comprising patients with Crohn's disease (CD), UC and IBD unclassified (IBDU), showed a consistent negative association between gastric H. pylori infection and IBD (P-OR: 0.43, p value <1e-10). This association appears to be stronger in patients with CD (P-OR: 0.38, p value <1e-10) and IBDU (P-OR: 0.43, p value=0.008) than UC (P-OR: 0.53, p value <1e-10). Stratification by age, ethnicity and medications showed significant results. In contrast to gastric H. pylori, non H. pylori-EHS (P-OR: 2.62, p value=0.001) and Campylobacter spp, in particular C. concisus (P-OR: 3.76, p value=0.006) and C. showae (P-OR: 2.39, p value=0.027), increase IBD risk.
CONCLUSIONS: H. pylori infection is negatively associated with IBD regardless of ethnicity, age, H. pylori detection methods and previous use of aminosalicylates and corticosteroids. Antibiotics influenced the magnitude of this association. Closely related bacteria including EHS and Campylobacter spp increase the risk of IBD. These results infer that H. pylori might exert an immunomodulatory effect in IBD.

Matched MeSH terms: Stomach Diseases/microbiology
Fulltext Variant of Helicobacter pylori CagA proteins induce different magnitude of morphological changes in gastric epithelial cells

Alfizah H, Ramelah M

Malays J Pathol, 2012 Jun;34(1):29-34.
PMID: 22870595 MyJurnal

Infection with Helicobacter pylori cagA-positive strains is associated with gastroduodenal diseases. The CagA protein is injected into gastric epithelial cells and supposedly induces morphological changes termed the 'hummingbird phenotype', which is associated with scattering and increased cell motility. The molecular mechanisms leading to the CagA-dependent morphological changes are only partially known. The present study was carried out to investigate the effect of CagA variants on the magnitude of gastric epithelial cell morphological changes. Recombinant 3' terminal domains of cagA were cloned and expressed in a gastric epithelial cell line and the hummingbird phenotype was quantified by microscopy. The 3' region of the cagA gene of Malaysian H. pylori isolates showed six sub-genotypes that differed in the structural organization of the EPIYA repeat sequences. The percentage of hummingbird cells induced by CagA increased with duration of transfection. The hummingbird phenotype was observed to be more pronounced when CagA with 4 EPIYA motifs rather than 3 or 2 EPIYA motifs was produced. The activity of different CagA variants in the induction of the hummingbird phenotype in gastric epithelial cells depends at least in part on EPIYA motif variability. The difference in CagA genotypes might influence the potential of individual CagAs to cause morphological changes in host cells. Depending on the relative exposure of cells to CagA genotypes, this may contribute to the various disease outcomes caused by H. pylori infection in different individuals.

Matched MeSH terms: Stomach Diseases/microbiology