Prenatal and lactational transmission of Toxocara canis and Ancylostoma caninum: experimental infection of the bitch before pregnancy

Breeding of five parasite-free and five experimentally infected (6000 Toxocara canis eggs orally and 2500 Ancylostoma caninum larvae subcutaneously) beagle bitches was done so that pairs of bitches (1 uninfected, 1 infected) whelped simultaneously. Pups born to an infected bitch were removed at birth and nursed by the paired uninfected bitch until 4 weeks of age when pups were necropsied to determine the number of parasites they had acquired prenatally from their infected mother. Pups born to the parasite-free bitch were nursed by the infected bitch until necropsied at 4 weeks of age to determine the number of parasites passed via the lactational route. Of 680 ascarids transmitted to pups by either route, 98.5% were transmitted prenatally and 1.5% lactationally. Transmission of 2746 hookworms to 22 pups occurred solely by the lactational route; prenatal transmission of this parasite did not occur in any of the 25 pups born to infected bitches.     

Contrasting effects of heterozygosity on survival and hookworm resistance in California sea lion pups

Low genetic heterozygosity is associated with loss of fitness in many natural populations. However, it remains unclear whether the mechanism is related to general (i.e. inbreeding) or local effects, in particular from a subset of loci lying close to genes under balancing selection. Here we analyse involving heterozygosity-fitness correlations on neonatal survival of California sea lions and on susceptibility to hookworm (Uncinaria spp.) infection, the single most important cause of pup mortality. We show that regardless of differences in hookworm burden, homozygosity is a key predictor of hookworm-related lesions, with no single locus contributing disproportionately. Conversely, the subsequent occurrence of anaemia due to blood loss in infected pups is overwhelmingly associated with homozygosity at one particular locus, all other loci showing no pattern. Our results suggest contrasting genetic mechanisms underlying two pathologies related to the same pathogen. First, relatively inbred pups are less able to expel hookworms and prevent their attachment to the intestinal mucosa, possibly due to a weakened immune response. In contrast, infected pups that are homozygous for a gene near to microsatellite Hg4.2 are strongly predisposed to anaemia. As yet, this gene is unknown, but could plausibly be involved in the blood-coagulation cascade. Taken together, these results suggest that pathogenic burden alone may not be the main factor regulating pathogen-related mortality in natural populations. Our study could have important implications for the conservation of small, isolated or threatened populations, particularly when they are at a risk of facing pathogenic challenges.     

Parasites and human evolution

Our understanding of human evolutionary and population history can be advanced by ecological and evolutionary studies of our parasites. Many parasites flourish only in the presence of very specific human behaviors and in specific habitats, are wholly dependent on us, and have evolved with us for thousands or millions of years. Therefore, by asking when and how we first acquired those parasites, under which environmental and cultural conditions we are the most susceptible, and how the parasites have evolved and adapted to us and we in response to them, we can gain considerable insight into our own evolutionary history. 1 , 2 As examples, the tapeworm life cycle is dependent on our consumption of meat,³ the divergence of body and head lice may have been subsequent to the development of clothing, 4 , 5 and malaria hyperendemicity may be associated with agriculture. 6 Thus, the evolutionary and population histories of these parasites are likely intertwined with critical aspects of human biology and culture. Here I review the mechanics of these and multiple other parasite proxies for human evolutionary history and discuss how they currently complement our fossil, archeological, molecular, linguistic, historical, and ethnographic records. I also highlight potential future applications of this promising model for the field of evolutionary anthropology.     

Suppression of inflammation by helminths: a role for the gut microbiota?

Multiple recent investigations have highlighted the promise of helminth-based therapies for the treatment of inflammatory disorders of the intestinal tract of humans, including inflammatory bowel disease and coeliac disease. However, the mechanisms by which helminths regulate immune responses, leading to the amelioration of symptoms of chronic inflammation are unknown. Given the pivotal roles of the intestinal microbiota in the pathogenesis of these disorders, it has been hypothesized that helminth-induced modifications of the gut commensal flora may be responsible for the therapeutic properties of gastrointestinal parasites. In this article, we review recent progress in the elucidation of host–parasite–microbiota interactions in both animal models of chronic inflammation and humans, and provide a working hypothesis of the role of the gut microbiota in helminth-induced suppression of inflammation.     

Prenatal and lactational transmission of Toxocara canis and Ancylostoma caninum: experimental infection of the bitch at midpregnancy and at parturition

The degree of prenatal transmission and both the degree and longevity of lactogenic transmission of Toxocara canis, and Ancylostoma caninum to pups were studied in Beagle bitches which were experimentally infected with both parasites at either mid-pregnancy or within 48 h following parturition. Pups born to infected bitches were removed at birth and raised by a surrogate parasite-free mother until 4 weeks of age when pups were necropsied to determine prenatal infections. At the beginning of each week of lactation, a new group of four parasite-free pups was placed with each infected bitch. After nursing an infected bitch for 1 week, each group was transferred to an uninfected bitch for at least 3 additional weeks of nursing after which the pups were necropsied to recover and tabulate parasites acquired lactationally from the infected bitch. When bitches were infected at mid-pregnancy, 95.5% of the ascarids were transmitted prenatally to their own off-spring and 4.5% of the asearids were transmitted lactationally to weekly rotated pups. Ascarids were transmitted via the milk during each of 5 weeks of lactation, with transmission of consistently higher numbers during weeks 1–3 than in weeks 4 and 5. Infection of bitches at parturition denied ascarids the prenatal route of transmission but resulted in greater numbers of ascarids being passed through the milk for each of 4 consecutive weeks of lactation. Transmission of hookworms was solely by the lactational route. With mid-pregnancy infections, a significantly higher number of hookworms (63.1 %) were transmitted during the first of 5 weeks of lactation; progressively fewer were passed in subsequent weeks. With infections at parturition, only 27.8% of hookworms were transmitted through the milk during the first week of nursing but large numbers were transferred in weeks 2 (36.9%) and 3 (26.7%). The quantity of parasites transmitted in the milk was not significantly different among weeks 1, 2 and 3.     

The contrasting hidden consequences of parasitism: Effects of a hematophagous nematode (Uncinaria sp.) in the development of a marine mammal swimming behavior

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Hookworm infection,anaemia and genetic variability of the New Zealand sea lion

Hookworms are intestinal blood-feeding nematodes that parasitize and cause high levels of mortality in a wide range of mammals, including otariid pinnipeds. Recently, an empirical study showed that inbreeding (assessed by individual measures of multi-locus heterozygosity) is associated with hookworm-related mortality of California sea lions. If inbreeding increases susceptibility to hookworms, effects would expectedly be stronger in small, fragmented populations. We tested this assumption in the New Zealand sea lion, a threatened otariid that has low levels of genetic variability and high hookworm infection rates. Using a panel of 22 microsatellites, we found that average allelic diversity (5.9) and mean heterozygosity (0.72) were higher than expected for a small population with restricted breeding, and we found no evidence of an association between genetic variability and hookworm resistance. However, similar to what was observed for the California sea lion, homozygosity at a single locus explained the occurrence of anaemia and thrombocytopenia in hookworm-infected pups (generalized linear model, F = 11.81, p < 0.001) and the effect was apparently driven by a particular allele (odds ratio = 34.95%; CI: 7.12–162.41; p < 0.00001). Our study offers further evidence that these haematophagus parasites exert selective pressure on otariid blood-clotting processes.