Giardia lamblia (also called intestinalis or duodenale) is a flagellate protozoan with two stages: motile trophozoites (Figure 11.1) and cysts.

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Life cycle

Infection may result from ingesting cysts, which release trophozoites in the upper small intestine, attaching to the mucosa by a ventral disc. Giardia trophozoites undergo significant biological changes to survive outside the host by differentiating into infective cysts, which is promoted by exposure to conjugated bile salts and

Figure 11.1 Giardia lamblia trophozoite. Courtesy of UK Tropical International Health.

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low levels of cholesterol.11,12 A specific proteolytic event caused by a constitutively expressed membrane-associated dipeptidyl peptidase IV is necessary for encystation.13 The incubation period is 1-2 weeks.


Giardia lamblia is one of the most common parasitic infections in humans with a prevalence of 2-5% in industrialized countries, and high transmission rates in day-care center outbreaks among 12-36-month-old children who are not toilet trained.14,15 In developing countries, prevalences of 20-30% occur with up to 60% of children infected at some time during childhood. Since cysts are excreted for prolonged periods, community studies often find higher rates of infection in children without diarrhea than in diarrheal cases.16 Giardia accounts for about 5% of travelers' diarrhea and is more common in children with immunodeficiency, although not HIV infection. The main routes of transmission are water, food and fecal-oral. Infection may occur after the ingestion of only 10-100 cysts and unfiltered water has been a common source of outbreaks in developed countries.

A Brazilian 4-year cohort study of 157 children from an urban slum documented substantial morbidity from giardiasis, with a similar frequency between diarrheal and non-diarrheal cases (9.7% vs. 7.4%), an association with persistent diarrhea (20.6% of episodes) and recurrent or relapsing infections (46%) and poorer nutritional status for those with symptomatic infections.17 A study of a rural Egyptian cohort of 152 infants documented 4.5 episodes per child-year with a mean duration of excretion of 7.2 weeks, and reduced risk in breast-fed infants, particularly for symptomatic illness.18 A Kenyan cohort study of 84 rural children aged 10-28 months reported a 44.7% prevalence, an estimated incidence of 2.8 episodes per year and a duration of 75.3 days per child for giar-diasis.19


Despite intensive investigations, the exact mechanisms by which Giardia causes diarrhea and malabsorption are still unclear. There is evidence of a secretory mechanism, malabsorption, decreased brush-border surface area and interference with intraluminal digestion. Another possible mechanism for diarrhea is small-bowel bacterial overgrowth, but mucosal invasion is uncommon. Duodenal morphology may be normal, but partial or even total villus atrophy may occur, as well as a mucosal inflammatory response with increased intraepithelial lymphocytes. Giardia parasites are able to adhere to the gut mucosa and may cause a direct effect on intestinal function by disrupting the brush border and its enzymatic system.

The effect of giardiasis on intestinal structure and function is quite variable, but animal and in vitro studies have documented villus atrophy, malabsorption, increased paracellular permeability and reduced brush-border enzymes.20,21 Giardia trophozoites are known to produce glycosidase enzymes which may affect the barrier function of mucins secreted by mucosal epithelial cells.22 An Italian study of 61 children with symptomatic giar-diasis documented lactose malabsorption on breath testing, resulting in intolerance to cows' milk but not to yogurt.23 However, a breath hydrogen study in asymptomatic Mexican children with giardiasis did not find significant carbohydrate malabsorption.24 Another study found only modest effects of Giardia treatment on biopsy changes, absorptive studies and bile salt conjugation, suggesting that the parasite's effect was synergistic with other organisms in contributing to tropical enteropathy.25

A Danish study of 29 children with chronic diarrhea from giardiasis documented enteropathy in 20, vitamin B12 malabsorption in nine, folate malabsorption in only five, no evidence of small-bowel bacterial overgrowth (SBBO) or iron malabsorption and more severe manifestations in those who acquired giardiasis overseas.26 A study of 210 urban Nepali children found no association between helminth infection and growth or intestinal permeability, but the eight children with giar-diasis had significantly higher mean permeability ratios (L : M ratio 0.43) than for either helminth infected (0.27) or uninfected (0.25).27 A Canadian study in a mouse model showed that Giardia trophozoites increase small-intestinal permeability, mediated by a myosin light chain kinase-dependent cytoskeletal effect on tight junctions.28 This disrupted enterocyte barrier function was T-cell independent and did not affect the stomach or colon. It is still unclear whether it is these effects or other mechanisms that cause the T-cell-dependent shortening of the brush-border microvilli with reduced disaccharidases and impaired absorptive function.

The immune response to Giardia involves both humoral and cellular mechanisms.29 Humans produce IgG, IgM, IgA and IgE responses including cytotoxic antibodies and an important intestinal IgA response to acute infection. Nevertheless, there is still no direct evidence that antibodies control infection. A Gambian study of six children with giardiasis, persistent diarrhea and malnutrition who failed to clear infection after treatment had raised only Giardia-specific IgM antibodies, so poor serum and secretory IgA response may be a marker for ineffective parasite clearance.30 Children with agammaglobulinemia, but not HIV-infected children, are susceptible to giardiasis and it is difficult to eradicate. Breast feeding provides protection from symptomatic disease, but not from infection.31

An association between giardiasis and allergy has been suggested based on the hypothesis that increased antigen penetration through damaged intestinal mucosa enhances sensitization to food antigens. One study documented allergy symptoms in 70% of children with giardiasis who had mean IgE levels of 1194 IU/ml compared to 43% and 822 IU/ml, respectively, for controls.32 The giardiasis group also had higher levels of specific serum IgE antibodies to food allergens compared both to controls and to other parasitic infections, whereas IgE responses to house dust mite were similar.

Clinical features

The clinical manifestations of Giardia infection vary from asymptomatic passage of cysts to chronic diarrhea with malabsorption and weight loss. The usual clinical syndrome is characterized by watery diarrhea, foul-smelling stools, bloating and abdominal cramps. Only about half of patients develop symptoms following ingestion of cysts, with 15% passing cysts asymptomatically and the remainder showing no trace of infection. Although older children may be asymptomatic, infection early in life usually causes acute symptoms with watery diarrhea, anorexia, abdominal distension and foul stools which persist untreated and may result in malabsorption. The course of giardiasis is frequently prolonged and, although many eventually resolve without treatment, some go on to syndromes of chronic diarrhea or frequent relapses. The severity of disease may be determined by strain-dependent virulence factors in the parasite, as well as age, nutritional status and immunocompetence of the host.33 Young children are more likely to be severely affected, with failure to thrive, hypokalemia and malabsorption (fat, vitamins A and B12, protein and lactose). Children in the developing world with chronic diarrhea and malnutrition often have giardiasis, but it is not always clear how much Giardia is contributing to the illness, since they are often co-infected with other enteric pathogens. The results of a small Venezuelan trial suggested that the therapeutic control of giardiasis could be important in programs to combat anemia in children living in settings with high prevalence.34


The diagnosis of giardiasis relies upon stool microscopy finding trophozoites or cysts. The sensitivity of a single stool is only 50-70% but increases to 90% if three stools are examined. Commercial assays for Giardia antigen are more sensitive and use polyclonal or monoclonal antibody directed against cyst or trophozoite antigens, usually as an enzyme-linked immunosorbent assay (ELISA) or immunofluorescent assay. These antigen detection assays are most useful for population screening such as children at day-care centers. Duodenal aspirates or biopsies are invasive, so are not justified exclusively to diagnose giardiasis, but when done for other reasons are reliable, particularly in the immunocompromised subject.


Giardia is waterborne and cysts are highly resistant to chlorine and ozone, so filtration provides the best protection against transmission through tap water.35 Hygiene measures to prevent fecal-oral transmission need to focus on young children. The drug treatment of choice for symptomatic disease (not just cyst excretors) is tinidazole (see p.183).

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