Strongyloides venezuelensis infection susceptibility of seven inbred strains of mice

Amarante, Alessandro Francisco Talamini do; Oliveira-Sequeira, T.C.G.

doi:10.1590/s0102-09352002000300009

Cited by 10 publications

(10 citation statements)

References 24 publications

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“…S. venezuelensis, in particular, has often been employed in different animal models, which may lead to differences in parasitological parameters such as the fecundity of female parasites and the duration of the patent period as a function of the host species or lineage (Tsuji et al 1993;Shi et al 1994;Nakai and Amarante 2001;Amarante and Oliveira-Sequeira 2002;Martins et al 2009). Despite the fact that it is commonly employed, however, there does not appear to be any report of a study that used marmosets as an experimental host of Strongyloides.…”

Section: Introductionmentioning

confidence: 99%

Callithrix penicillata as a nonhuman primate model for strongyloidiasis

2012

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In order to better understand experimental strongyloidiasis in small New World primates, and to evaluate aspects of reinfection and immunosuppression induced by glucocorticoids, nine specimens of Callithrix penicillata (Primates: Cebidae) were administered (by subcutaneous injection, sc) 3000 infective larvae of a strain of Strongyloides venezuelensis (Rhabditida: Strongyloididae) that had been maintained in successive passages through AKR/J mice since 1987. The mean prepatent period was 5.6 ± 0.7 days post-infection (DPI). The mean patent period of infection among the untreated animals (marmosets 1-7) was 123.4 ± 61.4 DPI. Two animals (marmosets 8 and 9) received dexamethasone (2.5 mg/kg, sc) for five consecutive days starting on the 20th day after infection, but this treatment did not alter the course of the infection, and the patent period for these animals was 100.5 ± 58.7 DPI (59 and 142, respectively). Stool examination showed that the highest quantities of parasite eggs were expelled between the 8th and 19th days after inoculation of the larvae. Thereafter, there was a gradual reduction in the number of parasite eggs in feces of all marmosets. During the chronic phase of the infection, before completely negative parasitological findings were obtained, the parasitological examinations were intermittently positive. Reinfection of three of these animals did not result in new positive examinations. However, given the receptiveness of these animals to initial infection with S. venezuelensis and their similarities to human beings, it is proposed that C. penicillata could be used as a nonhuman primate model for experimental strongyloidiasis.

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Section: Introductionmentioning

confidence: 99%

Callithrix penicillata as a nonhuman primate model for strongyloidiasis

2012

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“…Lively, 1996;Carius et al, 2001;Ferrari & Godfray, 2003;Little et al, 2006), but most studies on medically relevant diseases in vertebrates have concentrated on either host variation (e.g. Abel & Dessein, 1997;Amarante & Oliveira-Sequeira, 2002) or pathogen variation (e.g. Appleford & Smith, 1997;Macedo & Pena, 1998;Mackinnon & Read, 1999), but not both.…”

Section: Introductionmentioning

confidence: 99%

Host–parasite interactions for virulence and resistance in a malaria model system

Grech

Watt

Read

2006

Journal of Evolutionary Biology

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A rich body of theory on the evolution of virulence (disease severity) attempts to predict the conditions that cause parasites to harm their hosts, and a central assumption to many of these models is that the relative virulence of pathogen strains is stable across a range of host types. In contrast, a largely nonoverlapping body of theory on coevolution assumes that the fitness effects of parasites on hosts is not stable across host genotype, but instead depends on host genotype by parasite genotype interactions. If such genetic interactions largely determine virulence, it becomes difficult to predict the strength and direction of selection on virulence. In this study, we tested for host‐by‐parasite interactions in a medically relevant vertebrate disease model: the rodent malaria parasite Plasmodium chabaudi in laboratory mice. We found that parasite and particularly host main effects explained most of the variance in virulence (anaemia and weight loss), resistance (parasite burden) and transmission potential. Host‐by‐parasite interactions were of limited influence, but nevertheless had significant effects. This raises the possibility that host heterogeneity may affect the rate of any parasite response to selection on virulence. This study of rodent malaria is one of the first tests for host‐by‐parasite interactions in any vertebrate disease; host‐by‐parasite interactions typical of those assumed in coevolutionary models were present, but were by no means pervasive.

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“…For the experimental infections, infective S. venezuelensis third-stage larvae (L3s) were obtained according to Amarante and Oliveira-Sequeira (2002).…”

Section: Methodsmentioning

confidence: 99%