Pathophysiology and clinical features

The parasite was first discovered by Anthony van Leeuwenhook in the diarrhoeic stool but he did not consider Giardia as associated with the symptomatic disease (Dobell 1931). Today, there is no question that it causes symptomatic diarrhoeal illness.

The infective dose for giardiasis is low. The incubation period for symptomatic infection is 1-2 weeks but could vary from 1 to 45 days or more. The majority of infected individuals remain asymptomatic, sometimes amounting to 60% (Ortega and Adam 1997). Giardiasis has a range of clinical expression from asymptomatic cyst passage to a syndrome of chronic diarrhoea, malabsorption, and weight loss. This spectrum is likely to be related to virulence of the Giardia strain and the host's immune response to the parasite. Classification of strains relies on antigen, isoenzymes, chromosome, and DNA pattern. However, no tissue invasion is observed and the presence of a toxin has not been demonstrated to date; nor have any specific virulence factors been identified.

Giardia is able to perturb the structure and the function of the intestinal mucosa. At the same time additional factors contribute to diarrhoea and malabsorption (Katelaris and Farthing 1992; Farthing 1993). Changes of the small intestinal architecture from normal to sub-total villous atrophy will be seen in the human infection. The morphological abnormalities are associated with disaccharide activities and contribute to osmotic diarrhoea (Welsh et al. 1984). In animal models impaired solute and electrolyte absorption, together with impaired glucose absorption can be demonstrated. Several explanations for these abnormalities have been proposed. The Giardia trophozoites attach to the enterocytes and a recently identified mannose-binding lectin, which interacts with the mannose residues on the cells, contributes to disruption of microvilli.

It is suggested that the parasite might produce cytopathic substances such as proteinase, which could cleave the proteins in the microvillous membranes (Lev et al. 1986).

There is also increasing evidence that T-cell activation within the intestinal mucosa can produce villous atrophy (Mac Donald and Spencer 1988).

Bacterial overgrowth could contribute to malabsorption by the conjugation of bile salts (Tandon et al. 1977). It has been shown that concentration of pancreatic enzymes are reduced, which may relate to a direct effect of the pancreatic proteins (Katelaris et al. 1991).

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Acute giardiasis has characteristic symptoms with watery diarrhoea often developing into steatorrhea, nausea, abdominal discomfort, bloating, and weight loss. Although giardiasis, to a great extent, is self-limiting in healthy, immunocompetent individuals a proportion of these continue having diarrhoea and steatorrhea. In symptomatic patients with diarrhoea around 50% will have evidence of malabsorption of fat and protein as well as D-xylose, vitamin A, and vitamin B^. Secondary lactase deficiency is well recognized and may take many weeks to recover even after clearance of parasite. Recurrent diarrhoea after treatment for Giardia would rather be lactose intolerance than relapse of infection. Malabsorption in giardiasis is well documented and is also responsible for weight loss as well as failure to thrive. Even when the infection is asymptomatic, malabsorption may occur. Extraintestinal manifestations in unusual cases have been described (Shaw and Stevens 1987; Clyne and Eliopoulus 1989).

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