Influence of bacteria from the duodenal microbiota of patients with symptomatic giardiasis on the pathogenicity of Giardia duodenalis in gnotoxenic mice

Abstract

Recent studies have shown that the intestinal microbiota is essential for the pathogenicity but not for the multiplication of Giardia duodenalis in the intestinal lumen. The microbial components responsible for this phenomenon are not known. Twenty-eight facultative and three strictly anaerobic micro-organisms were isolated from the dominant duodenal microbiota of five patients with symptomatic giardiasis. The bacterial combinations from each patient were associated with groups (GN) of germ-free mice. Five days after the association, when their faecal populations ranged from 10 7 to 10 9 cfu=g, all groups were inoculated intragastrically with 10 5 viable trophozoites of G. duodenalis strain BT6. Two groups of germ-free (GF) and conventional (CV1) mice were also infected. Gnotobiotic animals were killed 10 days after infection and GF and CV1 animals were killed 10, 20 and 30 days after infection. More marked pathological alterations were detected in CV1 mice when compared with GF animals. Gnotobiotic animals showed intermediate pathological alterations between CV1 and GF mice. The CV1 and GF groups became infected by day 3 and faecal cyst levels were similar in both groups throughout the experiment. Total and G. duodenalis-specific IgA levels in the intestinal fluid and G. duodenalis-specific IgM and IgG levels in the serum increased during the infection and were higher in CV1 animals at all times tested when compared with GF mice. The present results confirm the stimulatory activity of the intestinal microbiota on the pathogenicity of G. duodenalis, and some combinations of microbial components of the dominant duodenal ecosystem from patients with symptomatic giardiasis can partially develop this function. However, none of these combinations was able to stimulate the protozoan pathogenicity in the same manner as the entire intestinal microbiota.

Giardia Alters Commensal Microbial Diversity throughout the Murine Gut

“…Commensal gut microbial communities are known to both limit and exacerbate pathogen colonization (19)(20)(21)(22), and thus the disruption of the gut ecosystem may impact Giardia colonization and consequent symptoms of diarrheal disease. The histopathology of giardiasis has been noted to be less severe in germfree mice than in conventional mice, supporting the idea that commensal microbes can aggravate parasite infection or symptoms (23).…”

The Intersection of Immune Responses, Microbiota, and Pathogenesis in Giardiasis

“…Infected conventional mice showed the greatest signs of intestinal pathology among the three groups, with the reconstituted germ-free mice showing moderate pathology. Interestingly, infected germ-free mice did not develop intestinal pathology as compared to the other groups, suggesting a need for intestinal microbes to stimulate pathology [24]. Parasite genetics may also play a role in infection susceptibility and outcomes.…”

Influence of normal microbiota on some aspects of the immune response during experimental infection with Trypanosoma cruzi in mice

“…Presently available data also indicate that this normal microbiota almost always has a profound influence on host-parasite relationships. As an example, it is well known that the presence of intestinal microbiota is essential for the pathogenicity of some protozoa and helminthes such as Entamoeba histolytica (Phillips & Wolfe, 1959), Nippostrongylus brasiliensis (Wescott & Todd, 1964), Nematospiroides dubius (Wescott, 1968), Trichinella spiralis (Przyjalkowski & Wescott, 1969), Eimeria tenella (Visco & Burns, 1972), Ascaridia galli (Johnson & Reid, 1973), Trichuris suis (Rutter & Beer, 1975), Eimeria falciformes (Owen, 1975), Eimeria ovinoidalis (Gouet et al, 1984) and Giardia duodenalis (Torres et al, 2000). In contrast, this microbiota can reduce the pathological consequences of other infectious diseases as described for experimental infections with Trypanosoma cruzi (Silva et al, 1987), Cryptococcus neoformans (Salkowski et al, 1987), Strongyloides venezuelensis (Martins et al, 2000) and almost all enteropathogenic bacteria (Clostridium difficile, Clostridium perfringens, Escherichia coli, Pseudomonas aeruginosa, Salmonella typhimurium, Shigella flexneri, Vibrio cholerae) (Wilson, 1995).…”