Background: Although several clinical and scientific evidences confirmed B. hominis pathogenicity in
irritable bowel syndrome (IBS), host biochemical risk factors involved in IBS manifestations are still
ambiguous.
Objective: To investigate the interactions between B. hominis genotypes, host biochemical factors, and
microbiota.
Patients and Methods: In a cross-sectional study, 167 stool samples from patients attending the Internal
Medicine Department, of Kafr El-Sheikh University Hospital were examined. Using specific sequencedtagged
site (STS) primers, samples positive for B. hominis were subtyped. Reducing sugar and pH were
assessed in B. hominis-positive samples. The lactate dehydrogenase (LDH) enzyme was measured in both
B. hominis sole infections and blastocystosis coexisting with G. intestinalis. To determine the predominant
co-existing organisms in blastocystosis infections, bacterial and fungal stool cultures were performed.
Furthermore, laboratory-cultivated B. hominis was incubated in vitro with Escherichia (Esch.) coli and
Candida non-albicans to assess possible interactions with models of normal microbiota.
Results: Of 167 cases, thirty-three (19.7%) were microscopically positive, and twenty seven (16.2%)
were molecularly confirmed harboring B. hominis. Genotype 3 was solely detected with higher prevalence
in summer and spring. There was a consistent chemical association of carbohydrate intolerance and acidic
pH with genotype-3 B. hominis that seemed to augment IBS-like manifestations. Predominant overgrowth
of Esch. coli in cultured stool samples was observed. Co-culture of B. hominis with Esch. coli and C. nonalbicans
augmented their growth whereas the parasite was suppressed. Coinfection of B. hominis with G.
intestinalis showed a significant rise in LDH enzyme in stool samples compared with the presence of B.
hominis alone.
Conclusion: Genotype-3 B. hominis is predominant and closely related to IBS-like manifestations.
Blastocystosis appeared to be related to carbohydrate intolerance, fecal acidity, and enhanced effect on
the growth of Esch. coli and C. non-albicans.