The pathogenicity of protozoan parasites of humans has been slow to be appreciated. Examples are Trypanosoma cruzi, Giardia lamblia, and Dientamoeba fragilis. Blastocystis hominis is a more recent example, despite a preponderance of evidence for pathogenicity [1-4].

In our study, sera were obtained from 19 patients with symptomatic B. hominis infections. Two patients provided acute-phase sera and convalescent-phase sera. An indirect fluorescent antibody test (IFA) and an enzyme-linked immunosorbent assay (ELISA) were developed to search for antibodies against B. hominis. Both the IFA and ELISA techniques demonstrated specific IgG antibody against B. hominis (Table 1). The average titer was 1/268 by IFA and 1/405 by ELISA. The average titer for 50 normal (blood bank) sera was 1/24 by IFA, and all normal sera were negative by ELISA (1/50 was the threshold dilution). Titers for the two acute-phase sera were as follows: Patient 1, 1/200 by IFA and 1/100 by ELISA; Patient 2, 1/200 by IFA and 1/200 by ELISA. Titers for convalescent-phase sera were as follows: Patient 1, 1/800 by IFA and 1/800 by ELISA; Patient 2, 1/600 by IFA and 1/600 by ELISA. The decided increase in titer for these two patients indicates recent systemic infection with B. hominis. Inflammatory response to B. hominis has been said to be part of the pathology related to this infection [4]. The immune titers reported above are much higher than those reported for giardiasis, even though both parasites are noninvasive.

A recent review [5] of Entamoeba histolytica may be pertinent to B. hominis studies. The species has now been divided into the pathogenic E. histolytica and the more prevalent, nonpathogenic E. dispar. Various tests show stable species differences in 125-kd surface antigen, 27-kd cysteine proteinase, 30-kd nuclear antigen, iron superoxide dismutase, small subunit RNA, and noncoding episomal DNA. Selected phenotypic tests facilitate species differentiation. They are morphologically identical. A similar situation may exist in B. hominis infections. Therefore, pathogenic appraisal should be limited strictly to cases of acute, symptomatic disease. Inclusion of asymptomatic or questionably symptomatic cases serves only to confuse the issue.

We are collecting data on coproantibody response to B. hominis infections. It would be useful to know relative rates of increase and decline in circulating antibody as well as in coproantibody.