Parasite and vertebrate host genetic heterogeneity determine the outcome of infection by Schistosoma mansoni

Abstract

Intraspecific variation in Schistosoma mansoni infection and modulation of its expression by vertebrate host genetics was studied by evaluation of some biological parameters of the infection in BALB/c and C57BL/6 mice infected with one Brazilian (BH) and two Venezuelan (YT and SM) laboratory strains of the parasite. Mice infected with 60 cercariae of each parasite strain were euthanized at 5, 6, 8, and 12 weeks. Parameters recorded included the number of adult worms recovered by portal perfusion (infectivity); the number of eggs in the feces, the intestine, and the liver; and the ability of the eggs to cross the intestine, expressed as a quotient of the number of eggs in the intestine versus the feces. Results showed that the parasite appeared to determine the infectivity, the sex ratio, the onset and timing of oviposition, the number of eggs produced, initial egg laying toward the liver, and the ability to cross the intestinal wall. In this sense the BH strain appeared to be the most efficient and the SM strain, the most delayed; the YT strain was intermediate, although closer to the SM strain. On the other hand, the host appeared to influence the susceptibility to infection, the fecundity, and the percentage of eggs distributed in the liver and in the intestine during the chronic stage. In this sense, although they have been shown to be less susceptible to infection than BALB/c mice, C57BL/6 mice permit more eggs to be produced and exhibit similar numbers of eggs in the intestine and the liver at certain time points. It appears from these results that parasite genetics is essential for the outcome of infection with S. mansoni, but some characteristics may be quantitatively modulated by host genetics.

A comparative parasitologic study on Biomphalaria glabrata snail and C3H/He mice infected with human and murine isolates of Schistosoma mansoni derived from Sumidouro, Rio de Janeiro, Brazil

“…Thus, it has been well documented that the mean prepatent period is five-six weeks post infection (Kassim et al 1979). Strains that have been maintained for a long period of time under laboratory conditions had a smaller prepatent period compared to newly isolated strains (Fallon et al 1997, Incani et al 2001, Yoshioka et al 2002.…”

“…It is widely known that Schistosoma mansoni geographical strains exhibit variability related to infectivity, prepatent period, fecal egg excretion, liver or intestinal egg counts and altered response to schistosomicidal drugs in rodent models (Kassim et al 1979, Coelho et al 1997, Incani et al 2001, Yoshioka et al 2002, Bonesso-Sabadini & Dias 2002. However, little attention has been paid to the biological characteristics of sympatric human and murine strains.…”

Susceptibility of two strains of mice to the infection with Schistosoma mansoni: Parasitological and biochemical studies

“…The host genotype seems to influence schistosome fecundity (Jones et al 1989) and the loss of worms from the portal system of infected mice (Cheever et al 1994). Incani et al (2001) reported that the strain of the host appeared to influence the susceptibility to infection, the fecundity, and the percentage of eggs distributed in the liver and in the intestine during the chronic stage of infection.…”

Immunological Mechanisms Underlying the Genetic Predisposition to Severe Staphylococcus aureus Infection in the Mouse Model

“…Because of this, the laboratory mouse has been the experimental model of choice to study pathogenesis of infection, including innate and acquired host defense mechanisms. Inbred mouse strains differ significantly in their degree of susceptibility to infection with various human bacterial (eg, Mycobacterium tuberculosis, 15,16 Salmonella enterica, 17 Streptococcus pyogenes, 18 Streptococcus pneumoniae 19 ), fungal (eg, Histoplasma capsulatum, 20 Aspergillus fumigatus 21 ), protozoan (eg, Leishmania major, 22 Plasmodium berghei, 23 Plasmodium chabaudi 24 ), helminthic (eg, Schistosoma mansoni 25,26 ) as well as viral (eg, respiratory syncytial virus 27,28 ) pathogens. This attribute has been exploited to identify novel loci influencing resistance/susceptibility to infection and to provide new insight on host mechanisms involved in response to those pathogens that ultimately affect the onset, progression, and outcome of the infection.…”