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Giardia: both a harmless commensal and a devastating pathogen
Herbert L. DuPont
University of Texas School of Public Health and Medical School, St. Luke’s Episcopal Hospital, Baylor College of Medicine, and the Kelsey Research Foundation, Houston, Texas, USA.
Address correspondence to: Herbert L. DuPont, 1200 Herman Pressler, Suite 733, Houston, Texas 77030, USA. Phone: 713.500.9366; Fax: 713.500.9359; E-mail: Herbert.L.Dupont@uth.tmc.edu.
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Published May 24, 2013 - More info
J Clin Invest. 2013;123(6):2352–2354. https://doi.org/10.1172/JCI69932.
© 2013 The American Society for Clinical Investigation
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Abstract
Authors
Luther A. Bartelt, James Roche, Glynis Kolling, David Bolick, Francisco Noronha, Caitlin Naylor, Paul Hoffman, Cirle Warren, Steven Singer, Richard Guerrant
Giardia lamblia (synonymous with G. intestinalis and G. duodenalis), referred to herein as Giardia, was first detected in 1681 by Antonie van Leeuwenhoek when looking at his own stools and was later described in 1859 by Lambl (1). Finding the organism as frequently in patients without symptoms as in those with diarrheal illness has led many over the years to conclude that the organism is not a pathogen. Giardia can be identified in stools of 2% to 5% of presumably healthy people living in industrialized countries like the United States and in 20% to 30% of people in developing regions (2). It is found in water sources and infects many animal species. The organism can be classified into at least 8 different genotypes called assemblages in humans and animals, with assemblages A and B being the most important in human infection. Each year in the United States, we identify approximately 20,000 people with Giardia infection, but the actual prevalence is estimated to be much higher.
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The two faces of Giardia infection
In rural areas of the developing world, Giardia is ubiquitous and infects nearly all children, although most remain free of symptoms (3). In these endemic areas, infants experience an acute clinical disease only when first exposed to the protozoan, but quickly recover from infection without adverse long-term effects (4). Self-limiting diarrhea from a Giardia infection is common in young children newly attending day care centers (5, 6) and in international travelers (7) to endemic areas when first exposed to the protozoa. After initial exposure in otherwise healthy people, symptomatic infection occurs rarely. Risk factors for first symptomatic infection in young children were shown in one study carried out in rural Egypt to include young age, poverty, low education level, in-home storage of drinking water, and unhygienic treatment of girls related to gender discrimination (8). A proportion of infected people, mainly underweight children with preexistent malnutrition, suffer from persistent infection with chronic diarrhea and dramatic health impairments (9), including worsening of nutrition (10), growth retardation, and cognitive impairment (11). In severe cases of giardiasis, during infection Giardia trophozoites attach to the epithelium of the proximal small bowel aided by their ventral adhesive discs, evade host defenses possibly by undergoing genetic variation (12), and produce local alterations of villus structure and cellular apoptosis. The most devastating effects of Giardia infection are related to damage of the absorptive small bowel mucosa, together with abnormal intestinal immunity that favors chronic infection (13, 14). While there is little evidence that preexistent malnutrition in young children makes them more susceptible to Giardia infection, once they are infected, persistent symptoms and health consequences are more likely to develop (15). Patients with hypogammaglobulinemia are particularly susceptible to chronic Giardia infection (16). However, Giardia is not a common opportunistic infection in patients with HIV infection or in those with cancer or cancer chemotherapy–induced immunosuppression, suggesting that not all forms of immunosuppression predispose to the infection. The likely explanation for increased symptomatic Giardia infection in infants with first exposure compared with older children and adults is the presence of an immature adaptive immune system in infants (17), particularly in those with preexistent nutritional deficits.
Long-term follow-up studies in children and adults with Giardia infection are needed to understand the relationship between infection and growth and learning defects, persistent abdominal symptoms (18), postinfectious functional bowel disease, and chronic fatigue (19). These chronic illnesses may result from low-level Giardia infections undetected by microscopic examination of stools (10), making their study and identification with previous Giardia infection more difficult.
What determines whether Giardia is a harmless commensal or a devastating pathogen? The difference may relate in part to the virulence of various Giardia strains, and more studies are needed to define these differences between Giardia strains and assemblages, many of which are derived from animal sources (20). In the rural developing world, a majority of young children are surrounded by animals that live in and roam about their homes and that may be sources of Giardia infection (21). A more likely explanation for the two faces of Giardia is the variation in host immune makeup and level of nutrition, although undoubtedly, future studies will reveal that host genetic factors also play an important role. Figure 1 outlines the host and microbial factors that are important in the pathophysiology of asymptomatic and symptomatic giardiasis.
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