Intragastric infection of conventional and germfree mice with Giardia lamblia

The effects of experimental infection with Giardia lamblia were studied in 30-day old conventional and germfree CFW mice (7 animals in each group) of both sexes. Cysts were observed in the feces of both groups 6 to 7 days after intragastric infection of each animal with about 2.5 x 10 5 G. lamblia trophozoites. Fecal cyst level was statisticaly higher in germfree mice (abouth 10 5 cysts/g feces) when compared with the conventional group (about 10 4 cysts/g feces). The peak of infection in the conventional group apparently occurred on the 10th day after infection as indicated by an increase of fecal weight and by histopathological examination. Intense infiltration of the lamina propria and high reactional hyperplasia of the lymphoiud component were observed in the conventional group. There was no infiltration or hyperplasia in germfree infected mice and fecal weight was relatively constant throughout the experiment. These results suggest that, as is the case for other intestinal pathogenic protozoa, the intestinal microflora is indispensable for the expression of the pathogenicity but not for the multiplication of G. lamblia

The acute phase of experimental infection with Trypanosoma cruzi is more severe in mice monoassociated with strict anaerobic bacteria

The influence of some components of the normal human intestinal flora on the acute phase of experimental infection with strain CL of Trypanosoma cruzi was studied in 30-day old germfree or gnotobiotic CFW (LOB) mice monassociated with Bacteroids fragilis, Peptostreptococcus sp or Clostridium sp by intragastrical inoculation of 10 6 bacteria 10 days before the intraperitoneal infections with 5 x 10 3 trypomastigotes/ g body weight. Significantly earlier parasitemia peak and mortality were observed in Bacteroides fragilis and Clostridium-associated mice (16.75 ñ 0.96 and 15.00 ñ 1.15 days, respectively) when compared with germfree animals (18.83 ñ 1.17 days). More precocious mortlity (10.40 ñ 2.06 days) and , curiouslyy, much lower blood parasitemia were observed in Peptostreptococcus-associated mice than in other gnobiotic mice. The extent of cardiac tissue parasitism decreased in the following order: germfree, B. fragilis-associated, Clostridium-associated and Peptostreptococcus associated animals. The levels of inflammatory reaction decreased in the following order: germfree, Peptostreptococcus-associated , Clostridium-associated, and B. fragilis-associated mice. These results show that the acute phase of experimental infection with T. cruzi was more severe in mice associated with strict anaerobic bacteria when compared with germfree animals. This suggests that a normal intestinal flora may be another factor, in addition to nutritional and genetic factors, responsible for the different susceptibility of organisms of the same species infected with T. cruzi

Effect of an essential fatty acid deficient diet on experimental infection with Trypanosoma cruzi in germefree and conventional mice

1) To investigate the possible role of essential fatty acid deficiency in host cell/parasite interaction, weanling germefree (GF) and conventional (CV) CFW mice maintained on an essential fatty acid-deficient (-) or a control (+) diet for 110 days were infected with Trypanosoma cruzi. 2) Blood parasitemia indicated that the disease was milder in the animals maintained on the essential fatty acid-deficient diet than in the GF and CV controls (maximum parasitemia: GF+33,300,GF-26,200,CV+17,100 and CV-6,400 trypomastigotes?ml blood). 3) Survival 30 days a after infection was 12% for GF+,28% for GF-,37% for CV+ and 65% for CV- mice. 4) Linoleic and arachidonic acid levels were significantly lower in animals kept on the essential fatty acid-deficient diet (GF-:28.0 ñ 9.3, 23.4 ñ 8.6; CV-:37.6 ñ 5.8, 19.9 ñ 3.6) than in controls (GF+: 164 ñ 48.8, 162.6 ñ 45.8; CV+: 147.1 ñ 26.5, 107.5 ñ 23.6) confirming the deficiency. Before the infection, succinic dehydrogenase levels were higher in liver of all CV mice *4.52 ug phosphate/mg fresh tissue) than in GF mice (0.84 ug phosphate/mg fresh tissue) whereas the opposite was true for 5'-nucleotidase levels in brain and liver, respectively (GF:2.84 and 3.18 ug phosphate/mg fresh tissue: CV:1.25 and 1.54 ug phosphate?mg fresh tissue). The disease was milder in deficient than in control animals in both the GF and CV groups on the basis of parasitemia and survival, indicating that fatty acid-deficient mice are partially protected against Chagas'disease. The mechanism underlying this phenomen requires further investigation

Immune responses of germfree mice to experimental infection with trypanosoma cruzi

1. The immune responses to Trypanosoma cruzi infection of germfree mice were compared to the reponses of infected conventional mice. Two groups (40 animals in each group) of 2-month old female CFW germfree and vonventional mice were used. The IgM and IgG which bound to the surface of T. cruzi epimastigotes determined by ELISA were significantly lower in germfree than in conventional mice (1/3 and 1/5 for IgM and IgG, respectively). 2. After infection there was a three-fold increase in the circulating levels of these immunoglobulins in germfree but not in conventional mice. twenty-one days after T. cruzi inoculation, both IgG and IgM levels were similar in germfree and conventional animals. 3. Footpad swelling after T. cruzi-antigen inoculation was initially four-fold more intense in germfree than in conventional mice. 4. These results suggest that the reduced humoral immune response of germfree mice during ythe initiation of experimental Chagas' disease may be responsible for the more severe parasitism when compared to conventional mice