Immunopathology of giardiasis

Abstract

G. lamblia continues to be the most common human intestinal protozoan parasite worldwide and still poses a major health problem to infants and young children particularly those in the developing world, to travellers in endemic areas, to immunodeficient individuals and communities exposed to waterborne outbreaks. Despite the availability of effective anti-giardial drugs, it is unlikely that these will eradicate the parasite from the environment particularly as there is increasing evidence that there are domestic and wild animal reservoirs of human infection and that giardiasis is likely to be a zoonosis. Understanding the interaction between Giardia and the host immune system may have important implications not only for the biological control of this parasite in the environment but for improving our understanding of the mechanism(s) by which it causes intestinal disease. Despite the fact that Giardia is essentially a luminal pathogen in the gut it does evoke both systemic and local immune responses. Current evidence emphasises the importance of secretory antibody for clearance of the pathogen, although other cell-mediated effector mechanisms are also likely to be involved. The relationship between serum and secretory antibody responses is not clear, particularly as to whether the presence of anti-Giardia antibodies in serum is in any way indicative of the development of protective immunity. The possibility that cell-mediated immune responses in the mucosa could account for the structural and functional abnormalities sometimes observed in human and experimental giardiasis in animals is an intriguing possibility and awaits further experimental verification. The apparent delay in the development of protective immunity despite continuing exposure to the parasite represents a major challenge for clinicians and biologists. It may relate to there being many antigenically diverse strains of the parasite, possibly due to the ability of a single strain to vary its surface antigens. Passage of the parasite through other mammalian hosts and exposure to bacterial endosymbionts and RNA viruses may also result in phenotypic changes sufficient to nullify a previous immune response to the parasite. These challenging questions await further investigation.