Association of Blastocystis hominis with human disease.

Sheehan et al. (3) and Pikula (Z. P. Pikula, Letter, J. Clin. Microbiol. 25:1581, 1987) bear witness to the fact that Blastocystis hominis is a common inhabitant of the human intestinal tract. These authors, like those they cite, have found B. hominis in some persons in whom they identified none of the commonly recognized pathogens, and in others in association with recognized pathogenic protozoa or bacteria. Surveys cite Blastocystis prevalence rates in the 10 to 15% range. To support "the emerging concept of B. hominis ... causative of human disease" (3), one must first rule out the presence of other known pathogens or disease states. This has not been done. The authors of both of the reports referred to above apparently based their conclusions on the results of examinations of single stool specimens. It has long been known that the examination of a single stool sample reveals only a fraction of the total of Entamoeba histolytica or other protozoan infections. Sawitz and Faust (2) found this figure to be approximately 40% for E. histolytica and that a series of six stool examinations was needed to detect some 95% of infections. Modern techniques may have altered these figures (there are no comparable recent studies), but it is impossible to draw conclusions based on the examination of one or two specimens. We monitored a series of 32 patients found to have B. hominis infections over a period of at least 30 months (1). All had six or more stool examinations performed, and 27 patients were found to have one or more recognized pathogens-E. histolytica, Giardia lamblia, or Dientamoeba fragilis-often undetected in the initial stool examinations. Ail became and remained asymptomatic after appropriate therapy, while retaining B. hominis. The other five patients fulfilled the criteria for irritable bowel syndrome, and B. hominis was considered an incidental finding. It is interesting that of the 23 patients with five or more B. hominis cells per 40x microscopic field tabulated by Sheehan et al. (3) the 4 who had stool examinations performed as part of a routine employee screen were all asymptomatic, whereas most of the others had histories suggestive of possible parasitic infections, inadequately investigated with a single stool examination. Furthermore, the figure of "five or more (B. hominis) per 40x field" used by these authors and others as an index of pathogenicity suggests an unparalleled situation in which an organism becomes pathogenic only when its numbers as measured in the stool specimen reach a critical threshold. Is it not at least equally possible that increased numbers of B. hominis may at times result from disturbance of gastrointestinal function caused by some other infection? Repeated stool examinations are time-consuming and costly, but without them any conclusions as to the pathogenicity of B. hominis cannot be considered valid.