Key result
Pregnancy induced Plasmodium berghei recrudescence in 58% of pre-exposed primiparous mice, which was associated with placental pathology and decreased in incidence during subsequent pregnancies.
Why the study?
Does pregnancy induce malaria recrudescence and placental pathology in mice with chronic P. berghei infection?
Does pregnancy induce malaria recrudescence and placental pathology in mice with chronic P. berghei infection?
Absolute Event Rate: 58% vs 0%
This experimental mouse model demonstrates that pregnancy induces malaria recrudescence with enhanced placental binding, leading to placental pathology and poor pregnancy outcomes that decrease in severity with subsequent pregnancies.
Animal model supports pregnancy as recrudescence trigger with placental effects; hypothesis-generating for human malaria and should not change practice.
Pregnancy-associated malaria (PAM) is associated with placenta pathology and poor pregnancy outcome but the mechanisms that control the malaria parasite expansion in pregnancy are still poorly understood and not amenable for study in human subjects. Here, we used a set of new tools to re-visit an experimental mouse model of pregnancy-induced malaria recrudescence, BALB/c with chronic Plasmodium berghei infection. During pregnancy 60% of the pre-exposed primiparous females showed pregnancy-induced malaria recrudescence and we demonstrated that the recrudescent P. berghei show an unexpected enhancement of the adherence to placenta tissue sections with a marked specificity for CSA. Furthermore, we showed that the intensity of parasitemia in primigravida was quantitatively correlated with the degree of thickening of the placental tissue and up-regulation of inflammation-related genes such as IL10. We also confirmed that the incidence of pregnancy-induced recrudescence, the intensity of the parasitemia peak and the impact on the pregnancy outcome decreased gradually from the first to the third pregnancy. Interestingly, placenta pathology and fetal impairment were also observed at low frequency among non-recrudescent females. Together, the data raise the hypothesis that recrudescent P. berghei displays selected specificity for the placenta tissue enabling on one hand, the triggering of the pathological process underlying PAM and on the other hand, the induction of PAM protection mechanisms that are revealed in subsequent pregnancies. Thus, by exploiting P. berghei pregnancy-induced recrudescence, this experimental system offers a mouse model to study the susceptibility to PAM and the mechanisms of disease protection in multigravida.
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Marinho et al. (2009) studied Pregnancy-associated malaria (n=100). Pregnancy vs. Non-pregnant state was evaluated on Pregnancy-induced malaria recrudescence. Pregnancy induced Plasmodium berghei recrudescence in 58% of pre-exposed primiparous mice, which was associated with placental pathology and decreased in incidence during subsequent pregnancies.
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