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

MARCIA F. TORRES, ANA P. T. UETANABARO^*, ALESSANDRA F. COSTA, CELSO A. ALVES, LUIS M. FARIAS^*, EDUARDO A. BAMBIRRA, FRANCISCO J. PENNA, ENIO C. VIEIRA and JACQUES R. NICOLI^*

Departamento de Pediatria, Faculdade de Medicina, *Departamento de Microbiologia, Instituto de Ciências Biológicas, Departamento de Anatomia Patológica, Faculdade de Medicina and Departamento de Bioquímica-Imunologia, Universidade Federal de Minas Gerais, Belo Horizonte MG, Brazil

Corresponding author: Dr J. R. Nicoli (e-mail: jnicoli{at}mono.icb.ufmg.br).

Received 20 Jan. 1999; revised version accepted 25 May 1999.

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 10⁷ to 10⁹ cfu/g, all groups were inoculated intragastrically with 10⁵ 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.

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