Pathophysiology of Giardia

The pathogenesis of Giardia is not completely understood due to the extensive variation seen in disease expression. Clinical presentation ranges from asymptomatic cyst passage to chronic diarrhea, malabsorption, severe weight loss, and malnutrition.¹ In asymptomatic patients, histologic exam of the duodenum often shows minimal changes or no abnormal representations. However, the major structural and functional changes associated with giardiasis when symptoms are present are usually found in the small intestine.² Factors that influence the clinical presentation of the disease range from the host's immune response to the parasite, the parasite load in the small intestine, and the virulence of the infecting strain of Giardia.

There are several proposed mechanisms of disease that involve both mucosal and luminal factors in patients who exhibit abdominal pain, diarrhea, and malabsorption symptoms. Actual invasion of the mucosa by organisms is a rare finding. The intestinal mucosa may be damaged by the trophozoite itself disrupting the epithelial brush border during attachment, or less likely by direct invasion.² In addition, release of toxic substances from the organism itself may damage intestinal epithelium. Absorptive activities may also be blocked due to the trophozoites "blanketing" the intestinal mucosa and causing functional mucosal obstruction.³ Some studies have shown that immunologic mechanisms may also play a role since individuals with decreased gamma globulin levels have a higher prevalence of infection and reinfection.

The luminal factors that could possibly explain the pathogenesis of symptoms are increased number of anaerobic and aerobic bacteria in the small intestine of the infected patient. Malabsorption may be due, in part, to bacterial overgrowth which leads to the deconjugation of bile salts. The bile salts are then taken up by the trophozoites, triggering encystations and stimulating parasite growth.⁴