The recent article by Rabeneck and colleagues [1] questioning the association between chronic diarrhea and intestinal microsporidiosis raises several concerns: Were the Enterocytozoon bieneusi-infected asymptomatic patients more likely to develop diarrhea than the pathogen-negative patients [2]? Why and how was transmission electron microscopy used for quantitation? Was there a difference in the degree of parasite maturation or pattern of mucosal infection between the groups? Was there a difference in the large-bowel burden of E. bieneusi [4] compared with that of the small bowel?

The histopathologic findings are important because mucosal damage generally parallels parasite burden and the severity of diarrhea [3]. Because light microscopy of plastic sections can readily detect all microsporidial stages [3] and more accurately assess parasite burden. Further, despite that electron µgraphs showed "abundant organisms," no light microscopic diagnoses were made prospectively, and only 36% were made retrospectively. This fact is in striking contrast to the observations of others [3].

That none of the infections were correlated with diarrhea is surprising. Support for a pathogenic role for Microsporidia is based on its identification, often as the sole pathogen, in several hundred patients worldwide with characteristic histopathologic and functional abnormalities, including impaired D-xylose absorption and weight loss [3]. Self-limiting acute diarrhea and Microsporidia infection were recently reported in patients with and those without human immunodeficiency virus infection (Presented at the Microsporidiosis and Cryptosporidiosis in Immunodeficient Patients Meeting, Ceske Budejovice, Czech Republic, 1993). Moreover, albendazole therapy for the second intestinal microsporidia, Septata intestinalis, leads to resolution of symptoms, clearance of organisms, and reversal of histopathologic abnormalities, fulfilling three of Koch's postulates [5].

Intestinal microsporidiosis is probably a common infection in humans that can exist latently, and the authors are to be congratulated for unearthing evidence of such a condition. However, based on the available data, their implication that microsporidiosis is not a cause of intestinal disease seems unwarranted.