Pathophysiological Processes and Clinical Manifestations of Giardiasis

Abstract

Giardiasis represents one of the most common parasitic diseases of humans, food-producing animals and pets, and it occurs throughout the World. Infected hosts may present with a broad spectrum of symptoms ranging from asymptomatic carriage to acute or chronic diarrhea. Some hosts may develop post-infectious chronic disorders in the gastrointestinal tract as well as at extraintestinal sites. For unknown reasons, Giardia infection does not cause any sign of overt inflammation in the gut.

Of the 7 distinct genetic Giardia duodenalis “assemblages” described to this day, Assemblages A and B can infect human hosts. Both assemblage A and assemblage B isolates are capable of causing symptomatic diarrheal disease, and the same assemblage has been reported to cause differing lengths of symptomatic infection. Much remains to be learned about the role of parasite genotype in pathogenesis.

The immune or humoral status of the host greatly contributes to the variable manifestations of giardiasis, as both humoral- and cellular-mediated immune responses are involved in parasite clearance as well as in pathophysiology. Infection with Giardia is able to trigger chronic gastrointestinal disorders such as irritable bowel syndrome, and may cause disease at extraintestinal sites, via mechanisms that have yet to be identified.

The pathophysiological mechanisms that occur during G. duodenalis infection are not completely understood. Research findings to date indicate that shortly after colonization of the small intestinal lumen, Giardia trophozoites heighten the rates of enterocyte apoptosis, decrease intestinal barrier function, and these changes lead to diffuse shortening of small intestinal brush border microvilli, maldigestion, and malabsorption, via the activation of CD8+ T-lymphocytes. Infection also increases intestinal chloride secretion, and accelerates small intestinal transit. The combination of these events contributes to the diarrheal disease seen in symptomatic infections.

Several parasitic factors, although still incompletely characterized, have been directly implicated in the pathophysiology of giardiasis. Further identification of these factors is sorely needed as it may also help explain symptom variability. Clearly, the pathogenesis of giardiasis is multifactorial. The identification of host and microbial factors responsible for symptoms in giardiasis offers promising research avenues to better understand a variety of enteric infections and chronic gastrointestinal disorders.