Pregnancy and Susceptibility to Parasites

Henriquez, Fiona L.; Menzies, Fiona M.; Roberts, Craig W.

doi:10.1007/978-3-642-02155-8_9

Cited by 4 publications

(4 citation statements)

References 193 publications

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“…Several pathogens, ranging from T. gondii, P. falciparum , and L. major to HIV and influenza can be transmitted from mother to offspring in utero (Andiman, 2002; Pfaff et al, 2007; Rogerson et al, 2007; Yawn et al, 1971). The mechanisms mediating why some pathogens (e.g., T. gondii and P. falciparum ) but not others (e.g., seasonal influenza viruses) harm the fetus when vertically transmitted are diverse (Henriquez et al, 2010; Klein et al, 2010c). The factors that appear to be most significant determinants of the impact of infection on pregnancy outcome include the timing of infection (i.e., whether exposure occurs during early or late pregnancy), the magnitude of the host inflammatory responses mounted, and whether the pathogen is sequestered in the placenta and causes physical damage (Henriquez et al, 2010).…”

Section: Discussionmentioning

confidence: 99%

“…The mechanisms mediating why some pathogens (e.g., T. gondii and P. falciparum ) but not others (e.g., seasonal influenza viruses) harm the fetus when vertically transmitted are diverse (Henriquez et al, 2010; Klein et al, 2010c). The factors that appear to be most significant determinants of the impact of infection on pregnancy outcome include the timing of infection (i.e., whether exposure occurs during early or late pregnancy), the magnitude of the host inflammatory responses mounted, and whether the pathogen is sequestered in the placenta and causes physical damage (Henriquez et al, 2010). Future studies should systematically evaluate the role of endocrine-immune interactions in the context of congenital transmission of pathogens.…”

Section: Discussionmentioning

confidence: 99%

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Pregnancy and pregnancy-associated hormones alter immune responses and disease pathogenesis

Robinson

Klein

2012

Hormones and Behavior

582

462

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During pregnancy, it is evolutionary advantageous for inflammatory immune responses that might lead to fetal rejection to be reduced and anti-inflammatory responses that promote transfer of maternal antibodies to the fetus to be increased. Hormones modulate the immunological shift that occurs during pregnancy. Estrogens, including estradiol and estriol, progesterone, and glucocorticoids increase over the course of pregnancy and affect transcriptional signaling of inflammatory immune responses at the maternal-fetal interface and systemically. During pregnancy, the reduced activity of natural killer cells, inflammatory macrophages, and helper T cell type 1 (Th1) cells and production of inflammatory cytokines, combined with the higher activity of regulatory T cells and production of anti-inflammatory cytokines, affects disease pathogenesis. The severity of diseases caused by inflammatory responses (e.g., multiple sclerosis) is reduced and the severity of diseases that are mitigated by inflammatory responses (e.g., influenza and malaria) is increased during pregnancy. For some infectious diseases, elevated inflammatory responses that are necessary to control and clear a pathogen have a negative consequence on the outcome of pregnancy. The bidirectional interactions between hormones and the immune system contribute to both the outcome of pregnancy and female susceptibility to disease.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Pregnancy and pregnancy-associated hormones alter immune responses and disease pathogenesis

Robinson

Klein

2012

Hormones and Behavior

582

462

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“…Alternatively, pregnant females may be subject to periparturient immunosuppression, which could increase the prevalence and intensity of infection (Vanzon & Eling ; Henriquez et al . ). If this were the case, pregnant females may simply be consuming more food in general to compensate for infection‐induced malnutrition.…”

Section: Discussionmentioning

confidence: 97%

Linking predator–prey interactions with exposure to a trophically transmitted parasite usingPCR‐based analyses

et al. 2012

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Parasite transmission is determined by the rate of contact between a susceptible host and an infective stage and susceptibility to infection given an exposure event. Attempts to measure levels of variation in exposure in natural populations can be especially challenging. The level of exposure to a major class of parasites, trophically transmitted parasites, can be estimated by investigating the host's feeding behaviour. Since the parasites rely on the ingestion of infective intermediate hosts for transmission, the potential for exposure to infection is inherently linked to the definitive host's feeding ecology. Here, we combined epidemiological data and molecular analyses (polymerase chain reaction) of the diet of the definitive host, the white-footed mouse (Peromyscus leucopus), to investigate temporal and individual heterogeneities in exposure to infection. Our results show that the consumption of cricket intermediate hosts accounted for much of the variation in infection; mice that had consumed crickets were four times more likely to become infected than animals that tested negative for cricket DNA. In particular, pregnant female hosts were three times more likely to consume crickets, which corresponded to a threefold increase in infection compared with nonpregnant females. Interestingly, males in breeding condition had a higher rate of infection even though breeding males were just as likely to test positive for cricket consumption as nonbreeding males. These results suggest that while heterogeneity in host diet served as a strong predictor of exposure risk, differential susceptibility to infection may also play a key role, particularly among male hosts. By combining PCR analyses with epidemiological data, we revealed temporal variation in exposure through prey consumption and identified potentially important individual heterogeneities in parasite transmission.

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“…For example, in humans, chimpanzees, and domesticated animals (e.g., dogs), adult females are more susceptible to intestinal macroparasites (e.g., helminths) and/or intracellular microparasites (e.g., protozoans) during pregnancy and lactation than during non reproductive periods (Beasley, Kahn, & Windon, ; Jamieson, Theiler, & Rasmussen, ; Lloyd, Amerasinghe, & Soulsby, ; Vleugels, Brabin, Eling, & Graaf, ). Several authors have indicated that the physiological and endocrine changes that females experience during late pregnancy or early lactation, including an increase in the production of estradiol, progesterone, and glucocorticoids, may temporarily suppress female immune function (Henriquez, Menzies, & Roberts, ; Robinson & Klein, ). In this regard, increased levels of progesterone and estradiol in women during the last trimester of pregnancy are reported to inhibit the production of Th1 lymphocytes and macrophages resulting in greater susceptibility to intracellular pathogens (e.g., Plasmodium spp., Toxoplasma spp.)…”

Section: Introductionmentioning

confidence: 99%

The relative effects of reproductive condition, stress, and seasonality on patterns of parasitism in wild female black howler monkeys (Alouatta pigra)

Martínez-Mota

Garber

Palme

et al. 2017

American J Primatol

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Parasitic infections in wildlife are shaped by host-related traits including individual reproductive condition. It has been argued that female primates are more susceptible to infectious diseases during pregnancy due to short-term changes in immune function that result in reduced ability to combat infections. Likewise, lactation, which is the most energetically expensive state, may affect immunity and infection risk due to tradeoffs between milk production and maintenance of immune function. Here, we examine the degree to which parasite prevalence and parasite richness are affected by female reproductive condition and stress levels in wild female black howler monkeys (Alouatta pigra). Over the course of one year, we collected fresh fecal samples from 15 adult females belonging to seven black howler groups living in Escárcega, Mexico. Fecal samples were used for parasitological analysis and for measuring fecal glucocorticoid metabolites (i.e., stress biomarker). We found that the prevalence of intestinal parasites and parasite richness did not differ among non-pregnant, pregnant, and lactating females. Fecal glucocorticoid metabolite levels increased significantly during pregnancy and during the first month of lactation, and positively predicted the probability of Controrchis biliophilus infection. Parasite prevalence and richness decreased during the months of increased rainfall. We conclude that reproductive physiology has limited consequences on intestinal parasitic infection risk in female black howler monkeys and that seasonal environmental fluctuations have greater effects.

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Pregnancy and Susceptibility to Parasites

Cited by 4 publications

References 193 publications

Pregnancy and pregnancy-associated hormones alter immune responses and disease pathogenesis

Pregnancy and pregnancy-associated hormones alter immune responses and disease pathogenesis

Linking predator–prey interactions with exposure to a trophically transmitted parasite usingPCR‐based analyses

The relative effects of reproductive condition, stress, and seasonality on patterns of parasitism in wild female black howler monkeys (Alouatta pigra)

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