Epidemiological Bulletin
      Vol. 18, No. 1
March 1997  


Mexico City, Mexico
28-29 January, 1997


Amoebiasis is currently defined as infection with the protozoan parasite Entamoeba histolytica. Normally resident in the large bowel, amoebae occasionally penetrate the intestinal mucosa disseminate to other organs. The factors that trigger invasion are unknown. E. Histolytica is responsible for up to 100,000 deaths per annum, placing it second only to malaria in mortality due to protozoan parasites. It has long been known that many people apparently infected with E. Histolytica never develop symptoms and spontaneously clear the infection. This was interpreted by many workers as indicating a parasite of variable virulence. However, in 1925 Emile Brumpt suggested an alternative explanation, that there were in fact two species, one capable of causing invasive disease and one that never causes disease, which he called E. dispar. Brumpts hypothesis was dismissed by other workers.

In 1970s, data started to accumulate that gave support to Brumpts hypothesis of the existence of two distinct organisms within what was being called E. histolytica. Biochemical, immunological, and genetic data continued to accumulate and in 1993 a formal redescription of E. histolytica was published, separating it form E. dispar.

E. histolytica can cause invasive intestinal and extraintestinal disease, while E. dispar can not. The confirmation of these two distinct species of Entamoeba is perhaps the major recent accomplishment in the field of amoebiasis research. In addition, proteins associated with virulence have been identified, including a lectin that mediates adherence to epithelial cells, a pore-forming peptide that lyses host cells, and secreted proteases that degrade host tissues. All of these virulence proteins, as well as other unique antigens present on the parasite surface are potential targets for anti-amoebic vaccines. Biochemical studies have identified the bacteria-like fermentation enzymes, which are the target of metronidazole, the most potent anti-amoebic drug in tissues, and suggest new targets for anti-amoebic drugs. This consultation was called to evaluate the implications of this recent work.

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  1. E. histolytica was previously defined as a unicellular eukaryote with the following morphology: Trophozoites with a single nucleus, 20-40 m in diameter. Cysts are 10-16 m in diameter, with four nuclei when mature, one nucleus when immature with glycogen in a vacuole and often with chromatoid bodies. The nucleus is vesicular, spherical, with a membrane lined with small chromatin granules and with a small central sphericla karyosome.

  2. Biochemical, immunological and genetic data now indicate that there are two species with the above morphological characteristics -E. histolytica and E. dispar- previously known as pathogenic and nonpathogenic E. histolytica, respectively. Only E. histolytica is capable of causing invasive disease. In the future, the name E. histolytica should only be used in this sense and will be used as such in the rest of this document.

  3. When diagnosis is made by light microscopy, the cysts of the two species (10-16 m in diameter) are indistinguishable and should be reported as E. histolytica/E, dispar.

  4. Trophozoites with ingested red blood cells in fresh stool or other specimens and trophozoites in tissue biopsies are both strongly correlated with the presence of E. histolytica and invasive disease.

  5. In symptomatic individuals, the presence of high tires of specific antibody is also strongly correlated with invasive amoebiasis.

  6. Faecal antigen detection tests are commercially available. Currently, only one test specifically identifies E. histolytica, but other tests based on this and other technologies are under development.

  7. We reaffirm the WHO definition of amoebiasis as infection with E. histolytica (in its new sense) with or without clinical manifestations.

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List of participants

  1. Dr. John Ackers, London School of Hygiene and Tropical Medicine, England (co-chair)

  2. Dr. C. Graham Clark, London School of Hygiene and Tropical Medicine, England (rapporteur)

  3. Dr. Louis S. Diamond, National Institute of Health, U.S.A.

  4. Dr. Michael Duchêne, University of Vienna, Austria (unable to attend)

  5. Dr. Martha Espinosa Cantellano, Centro de Investigación y de Estudios Avanzados del IPN, Mexico

  6. Dr. Terry F.H.G. Jackson, South African medical Research Council, South Africa

  7. Dr. Adolfo Martínez-Palomo, Centro de Investigación y de Estudios Avanzados del IPN, Mexico (co-chair)

  8. Dr. David Mirelman, Weizmann Institute of Science, Israel

  9. Dr. Onofre Muñoz Hernández, Centro Médico Nacional, IMSS, México

  10. Dr. Ruy Pérez Tamayo, Universidad Nacional Autónoma de México, Mexico

  11. Dr. William Petri, University of Virginia, U.S.A.

  12. Dr. Sharon Reed, University of California, San Diego, U.S.A.

  13. Dr. Guillermo Ruíz-Palacios, Instituto Nacional de la Nutrición Salvador Zubirán, Mexico

  14. Dr. John Samuelson, Harvard School of Public Health, U.S.A.

  15. Dr. José Ignacio Santos Preciado, Universidad Nacional Autónoma de México, Mexico

  16. Dr. Egbert Tannich, Bernhard Nocht Institute for Tropical Medicine, Germany

  17. Dr. Tsutomu Takeuchi, Keio University, Japan

  18. Dr. Cecilia Ximénez, Universidad Nacional Autónoma de México, Mexico

Source:Divison of Disease Prevention and Control, Communicable Diseases Program, (HCP/HCT), Division of Tropical Diseases, Schistosomiasis and Intestinal Parasitosis Unit, WHO.

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