Giardiasis pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Yazan Daaboul, M.D.; Serge Korjian M.D.


Giardia is usually transmitted via the fecal-oral route through personal contact and contaminated water and food. Giardia is a zoonotic infection that may also transmitted from animals to humans. Major reservoir hosts include beavers, dogs, cats, horses, and cattle. Following transmission, Giardia colonizes the human intestine and attaches to the epithelium by a ventral adhesive disc. The mechanism of pathogenesis of Giardia is thought to include increased pro-apoptotic processes, subsequent loss of intestinal epithelial barrier, hypersecretion of electrolytes, and increased exposure to luminal antigens to subepithelial host immune cells. It is thought lymphocyte activation, particularly CD8+ T-cells, results in local inflammation, as well as diffuse shortening of microvilli (without villous atrophy). Dysfunctional microvilli are then unable to absorb luminal nutrients, resulting in the development and worsening of clinical manifestations of giardiasis.



  • Giardia is usually transmitted via the fecal-oral route through personal contact and contaminated water and food.
  • Giardia is also thought to be a zoonotic infection (unconfirmed association) that may also transmitted from animals to humans. Major reservoir hosts include beavers, dogs, cats, horses, and cattle.


  • Following transmission, Giardia colonizes the human intestine.
  • Giardia attaches to the epithelium by a ventral adhesive disc.

Increased Apoptosis

  • It is thought that Giardia induces caspase-mediated enterocytic apopotosis and results in the impairment of cellular tight junction integrity.[1][2][3]
  • The following mechanisms are altered among patients with giardiasis:
  • Increased concentration of reactive oxygen species
  • Reduced concentration of nitric oxide, which normally inhibits growth of Giardia
  • Down-regulation of anti-apoptotic proteins (e.g. Bcl-2)
  • Up-regulation of pro-apoptotic proteins (e.g. Bax)

Loss of Epithelial Barrier

  • Enterocyte apoptosis results in the loss of the intestinal epithelial barrier and subsequent increased permeability.[4][5][6][3]
  • Accordingly, subepithelial host immune cells are more likely to be activated by antigens located in the intestinal lumen.
  • The increased susceptibility of subepithelial immune activation, particularly CD8+ T-cells, results in local inflammation and the retraction of the of the microvilli of the small intestine (shortening of the intestinal brush border).

Brush Border Damage

  • Despite the absence of villus atrophy, giardiasis-mediated immune cell activation results in intestinal malabsorption through the process of diffuse microvilli shortening, whereby microvilli are unable to absorb nutrients in the intestinal lumen.[6][7][8][9][3]
  • In addition, electrolytes are hypersecreted (e.g. chloride hypersecretion), resulting in fluid accumulation in the intestinal lumen and development of clinical manifestations (i.e. watery diarrhea).[6][3]


  1. Chin AC, Teoh DA, Scott KG, Meddings JB, Macnaughton WK, Buret AG (2002). "Strain-dependent induction of enterocyte apoptosis by Giardia lamblia disrupts epithelial barrier function in a caspase-3-dependent manner". Infect Immun. 70 (7): 3673–80. PMC 128105. PMID 12065509.
  2. Roxström-Lindquist K, Palm D, Reiner D, Ringqvist E, Svärd SG (2006). "Giardia immunity--an update". Trends Parasitol. 22 (1): 26–31. doi:10.1016/ PMID 16303332.
  3. 3.0 3.1 3.2 3.3 Buret AG (2008). "Pathophysiology of enteric infections with Giardia duodenalius". Parasite. 15 (3): 261–5. PMID 18814692.
  4. Abreu MT, Palladino AA, Arnold ET, Kwon RS, McRoberts JA (2000). "Modulation of barrier function during Fas-mediated apoptosis in human intestinal epithelial cells". Gastroenterology. 119 (6): 1524–36. PMID 11113074.
  5. Sun Z, Wang X, Wallen R, Deng X, Du X, Hallberg E; et al. (1998). "The influence of apoptosis on intestinal barrier integrity in rats". Scand J Gastroenterol. 33 (4): 415–22. PMID 9605264.
  6. 6.0 6.1 6.2 Troeger H, Epple HJ, Schneider T, Wahnschaffe U, Ullrich R, Burchard GD; et al. (2007). "Effect of chronic Giardia lamblia infection on epithelial transport and barrier function in human duodenum". Gut. 56 (3): 328–35. doi:10.1136/gut.2006.100198. PMC 1856804. PMID 16935925.
  7. Eckmann L, Gillin FD (2001). "Microbes and microbial toxins: paradigms for microbial-mucosal interactions I. Pathophysiological aspects of enteric infections with the lumen-dwelling protozoan pathogen Giardia lamblia". Am J Physiol Gastrointest Liver Physiol. 280 (1): G1–6. PMID 11123191.
  8. Müller N, von Allmen N (2005). "Recent insights into the mucosal reactions associated with Giardia lamblia infections". Int J Parasitol. 35 (13): 1339–47. doi:10.1016/j.ijpara.2005.07.008. PMID 16182298.
  9. Belosevic M, Faubert GM, MacLean JD (1989). "Disaccharidase activity in the small intestine of gerbils (Meriones unguiculatus) during primary and challenge infections with Giardia lamblia". Gut. 30 (9): 1213–9. PMC 1434240. PMID 2806988.

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