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Brief or Lively debate

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Conflicting information: was there a 'lively debate' or a 'brief debate' in the 1990s as to whether Blastocystis causes symptoms in humans? —Preceding unsigned comment added by JohnBurton (talk • contribs) 23:28, 16 October 2007 (UTC)[reply]


Hmmm....maybe it was a brief and lively debate :) I couldn't find the reference to the lively debate. Gastro guy 03:16, 17 October 2007 (UTC)[reply]


"Some researchers believe the debate has been resolved . . " No; most do! During the past two years (2008 -2009), more than a dozen articles have appeared (many of them in Parasitology Research) confirming the subtype-dependent differences in the pathogenicity of B. hominus. (There are at least 7 distinct genotypes.) Recent in-vitro host-Blastocystis interaction studies of phenotypic characteristics indicate that Blastocystis subtypes 3, 5, and 7 correlate well with the pathogenic form of this diseases. Transmission electron microscopy has revealed that these sub-types have polymorphic amoeboid forms containing a large central vacuole that is completely filled with tiny electron-dense granules. On days 1- 3 of the life cycle, they undergo a pre-cystic stage characterized by the presence of an immature cell wall which acts as a intermediary stage between the vacuolar and cystic stage. At the cystic stage, they undergo shedding in an irregular pattern, producing variable sequential changes in the encystation in a patient’s stools collected over a time period. Thus patients with chronic symptomatic Blastocystis hominis infection due to pathogenic subtypes experience day-to-days changes in their symptoms because of the organisms’ shedding behavior.

In addition, clinical and experimental studies have shown that these subtypes have the potential to modulate the host immune response. The central vacuole functions as a reservoir for cysteine proteases, and these cysteine proteases activate interleukin-8 (IL-8) gene expression in human colonic epithelial T84 cells. We also know the cysteine protease activativation of receptor-2 plays a role in the presence of abdominal pain and diffuse symptoms in Blastocystis infection, even in the absence of any endoscopic findings (Sohail, M. R., and P. R. Fischer. 2005. Blastocystis hominis and travelers. Travel Medicine Infectious Diseases. 333-38). AndB. hominis WR1 proteases can degrade human secretory immunoglobulin A (Puthia, M. K., A. Vaithilingam, J. Lu, and K. S. Tan. 2005. Degradation of human secretory immunoglobulin A by Blastocystis. Parasitology Research. 97386-389) and induce contact-independent apoptosis, F-actin rearrangement, and barrier function disruption in IEC-6 cells (Puthia, M. K., S. W. Sio, J. Lu, and K. S. Tan. 2006. Blastocystis ratti induces contact-independent apoptosis, F-actin rearrangement, and barrier function disruption in IEC-6 cells. Infection and Immunity. 744114-4123.).

Further, there is clinical evidence that Blastocystis hominis is involved in the etiology of chronic urticaria. Proteases in the central vacuole of these pathogenic sub-types also induce the activation of specific clones of Th2 lymphocytes, the release of related proinflammatory cytokines, and the consequent IgE production. Dr. Karen L. Greenberg 00:58, 4 August 2009 (UTC)[reply]

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The coherency of this chapter and/or the references should be verified.--Wickey-nl (talk) 15:12, 1 February 2009 (UTC)[reply]


Type of diarrhea

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Is that disease causes chronic/persisting or just quickly self-resolving diarrhea? Clarification is needed.

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