Extra-intestinal and long term consequences of Giardia duodenalis infections

Table 1 Main pathophysiological effects of Giardia duodenalis and their mechanisms

Giardia-induced pathophysiological responses	Mechanisms involved or hypothesized to be involved	Selected references
Intestinal epithelial cell apoptosis	Induction of pro-apoptotic factors: Caspase-3, 8 and 9, Inhibition of anti-apoptotic factors: poly (ADP-ribose) polymerase (PARP) cleavage	[10,18,19,21,23]
Halt of enterocyte cell-cycle progression	Nutrient competition (arginine), up-regulation of cell-cycle genes	[25]
Intestinal barrier dysfunction	Disruption of claudin-1 and alpha-actinin by unknown mechanisms, caspase-3 mediated disruption of zonula-occludens (ZO)-1, myosin light chain kinase-mediated disruption of F-actin, and ZO-1	[10,17,19,21,26,27,29,30]
Small intestinal hypermotility	Adaptive immunity, neuronal nitric oxide, mast cell degranulation	[118-120]
Diffuse shortening of brush border microvilli	CD8+ lymphocytes - mediated via parasite secretory/excretory products	[13,16,21,31]
Crypt hyperplasia	Alteration villus/crypt ratio	[21,62,99]
Microbiota composition	Microbiota from infected host may become pathogenic	[14,33]
Increased mucus production	Increased mucus secretion in response to the parasite	[66]
Brush border enzyme activity deficiencies	Loss of surface area (microvilli and villi)	[16,21,98,121,122]
Disaccharidases deficiencies	Loss of surface area (microvilli and villi)	[10,16,99,122]
Electrolyte/nutrient/water malabsorption	Loss of surface area (microvilli and villi)	[10,19,21,62,99,123]
Anion hypersecretion	Unknown mechanisms	[10,19,99]

PARP : Poly adenosine diphosphate ribose polymerase.