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Protozool., 24:43744 1. 18. Thomas, J. R., McConville, M. J., Thomas-Oates, J. E., Homans, S. W., Ferguson, M. A. J., Gorin, P. A. J., Greis, K. D. & Turco, S. J. 1992. Refined structure of the lipophosphoglycan of Leishmania don- ovani. J. Biol. Chem., 267:6829-6833. Received 10-22-92. 12-8-92; accepted 12-15-92 J. Euk. MicrobioL. 40(3), 1993, pp. 340-344 zyxwvutsrqpon 0 1993 by the Society of zyxwvutsrqp Protozoologists A Redescription of Entamoeba histolytica Schaudinn, 1903 (Emended Walker, 1911) Separating It from Entarnoeba &par Brumpt, 1925l LOUIS S. DIAMOND2 and C. GRAHAM CLARK Laboratory of Parasitic Diseases. Building 4/ROOm 126, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892 ABSTRACT. Explaining the low incidence of invasive disease (1 0%) in humans infected with Entamoeba histolytica has occupied the attention of generations of both clinical and nonclinical investigators. One possible explanation would be the existence of two morphologically identical species-one an invasive pathogen, the other noninvasive. This was first proposed by Brumpt in 1925, but his explanation was virtually ignored until 1978 when the first of several publications appeared suggestingthat E. histolytica did indeed consist of two species. We have reexamined Brumpt’s claim in light of recent biochemical, immunological and genetic studies and conclude that the data derived from these investigations provide unequivocal evidence supporting his hypothesis. With this in mind, we redescribe the invasive parasite retaining the name Entamoeba histolytica Schaudinn, 1903 (Emended Walker, 191 I), and set it apart from the noninvasive parasite described by Brumpt, Entamoeba dispar Brumpt, 1925. Supplementary key words. Amebiasis, antibodies, diagnosis, genes, isoenzyme analysis, speciation. TUDENTS of Entamoeba histolytica and the diseases it S causes have for generations faced one vexing question over- riding all others: how can we account for the well documented fact that only a few of those humans infected with the parasite develop invasive disease? A modem estimate is that less than 10% (36 million) of those infected with E. histolytzca (480 mil- lion) develop clinical symptoms, of which at least 40,000 die annually [55]. Three major hypotheses have been advanced to explain this phenomenon and can be summarized as follows: 1) E . histolytica is a single pathogenic species which in all human hosts produces intestinal lesions that may or may not give rise to recognizable clinical symptoms; 2) E. histolytzca is normally a commensal residing in the human colon which on occasion, for reasons poorly understood, converts into an invasive patho- gen; 3) E. histolytica is comprised of two morphologically iden- tical species, one an invasive pathogen exhibiting varying de- grees of virulence and the other a noninvasive pathogen having the capacity of producing at most superficial erosion of the I This paper is dedicated to the memory of the late Ralph A. Neal * To whom correspondence should be addressed. who made major contributions to the study of these organisms. colonic mucosa. Recent studies have provided evidence that the third hypothesis is the correct one, That humans can be infected by two morphologically identical species of Entamoeba producing quadrinucleate cysts measuring 10 pm or greater in diameter was proposed first by Brumpt in 1925 [5]. He distinguished the two species on the basis of their pathogenicity in humans and in experimentally infected kittens. The invasive pathogen was identified as Entamoeba dysenteriae (Councilman and Lafleur) Craig, 1905, which according to Do- bell [lo] is a synonym for Entamoeba histolytzca Schaudinn, 1903 (Emend. Walker, 191 I). For the noninvasive ameba, Brumpt created the name Entamoeba dispar. Simic [40-42] provided additional convincing evidence for the existence of the two species. He serially passed several ameba1 isolates in healthy volunteers and kittens, a very sensitive model, and be- tween kittens and humans. Neither the kittens nor humans de- veloped symptoms attributable to the presence of the amebae. Because Brumpt was unable to distinguish morphologically between his two proposed species, and because there was a growing body of evidence obtained from experimental human and animal studies that amebae obtained from symptomless camers could produce disease [19, 24, 25, 571, his explanation gained little support. It regained favor only after Sargeaunt and