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Mechanisms of epithelial dysfunction in giardiasis
  1. Andre G Buret
  1. Correspondence to:
    Professor A G Buret
    Department of Biological Sciences, University of Calgary, 2500 University Drive N.W. Calgary, Alberta, Canada T2N 1N4; aburet{at}

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A better understanding of the pathophysiological processes of Giardia may lead to understanding the diseases it causes and to identifying new therapeutic agents

Infection with the ubiquitous intestinal parasite Giardia lamblia (synonymous G duodenalis or G intestinalis) may cause acute or chronic diarrhoea, dehydration, abdominal discomfort and weight loss.1–4 Despite the prevalence of this disease, the pathophysiological features underlying intestinal disturbances in giardiasis remain incompletely understood. Giardia causes disease without penetrating the epithelium, invading the surrounding tissues or entering the blood stream. Interestingly, the epithelial abnormalities responsible for intestinal malabsorption and diarrhoea in giardiasis seem to share similarities with those observed in other enteric disorders, such as bacterial enteritis, chronic food anaphylaxis, Crohn’s disease and coeliac disease.5–9 Therefore, a better understanding of these pathophysiological processes may help identify new therapeutic targets for a variety of gastrointestinal diseases. In an attempt to unravel the mechanisms by which Giardia exerts its clinical effects, researchers have relied on a variety of cell systems and animal models. This issue of Gut presents data from an elegant human clinical study by Troeger et al10 (see page 328) that sheds new light on these processes. In view of the limited space available, this commentary only highlights selected mechanisms whereby Giardia-induced epithelial dysfunction may contribute to disease development.


Previous studies using models in vivo and in vitro have established that Giardia causes malabsorption of glucose, sodium and water, and reduced disaccharidase activity, due to loss of epithelial absorptive surface area. …

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  • Competing interests: None.

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