Rapid reappearance of Plasmodium falciparum after drug treatment among Senegalese adults exposed to moderate seasonal transmission.

Sokhna, Cheikh; Fbk, Faye; Spiegel, André; Dieng, Hamady; Trape, Jean‐François

doi:10.4269/ajtmh.2001.65.167

Cited by 14 publications

(12 citation statements)

References 13 publications

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“…In our study, we utilise field data on malaria infection dynamics after a short treatment course in a holoendemic region of Kenya. The estimated P. falciparum infection rates are extremely high, especially amongst young children, but consistent with the high entomological infection rates measured in this area [29]and with the blood-stage infection rates previously observed by others in similar studies [30], [31]. The prior treatment of patients gives an ideal opportunity to study malaria incidence in the absence of recrudesence from prior infection.…”

Section: Discussionsupporting

confidence: 88%

The Dynamics of Naturally Acquired Immunity to Plasmodium falciparum Infection

et al. 2012

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Severe malaria occurs predominantly in young children and immunity to clinical disease is associated with cumulative exposure in holoendemic settings. The relative contribution of immunity against various stages of the parasite life cycle that results in controlling infection and limiting disease is not well understood. Here we analyse the dynamics of Plasmodium falciparum malaria infection after treatment in a cohort of 197 healthy study participants of different ages in order to model naturally acquired immunity. We find that both delayed time-to-infection and reductions in asymptomatic parasitaemias in older age groups can be explained by immunity that reduces the growth of blood stage as opposed to liver stage parasites. We found that this mechanism would require at least two components – a rapidly acting strain-specific component, as well as a slowly acquired cross-reactive or general immunity to all strains. Analysis and modelling of malaria infection dynamics and naturally acquired immunity with age provides important insights into what mechanisms of immune control may be harnessed by malaria vaccine strategists.

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Section: Discussionsupporting

confidence: 88%

The Dynamics of Naturally Acquired Immunity to Plasmodium falciparum Infection

et al. 2012

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“…However, there is in vitro and in vivo evidence of CQ‐resistant Plasmodium falciparum with consequential high rates (up to 50%) of treatment failure (Pradines et al. 1996; Sokhna et al. 1997, 2001a,b; Brasseur et al.…”

Section: Introductionmentioning

confidence: 99%

Economic evaluation of a policy change from single‐agent treatment for suspected malaria to artesunate‐amodiaquine for microscopically confirmed uncomplicated falciparum malaria in the Oussouye District of south‐western Senegal

Agnamey

Brasseur

Cisse³

et al. 2005

Tropical Med Int Health

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SummarySenegal is changing policy for case management of uncomplicated falciparum malaria, which hitherto is diagnosed clinically and treated with chloroquine or intramuscular quinine. The WHO recommends artemisinin-based combinations for treating falciparum malaria, preferably based on a parasitological diagnosis. There are no economic projections if such a policy were introduced in Senegal. We have conducted a preliminary economic assessment of such a policy change. The study took place in the chloroquine-resistant district of Oussouye in south-western Senegal. We reviewed clinic registers of the district health posts (n ¼ 5) from 1996 to 2001, and piloted artesunate combined with amodiaquine (at 4 and 10 mg/kg/day · 3 days respectively) (AS-AQ) for treating slide-proven falciparum malaria during two rainy seasons (2000 and 2001) at one health centre. These data were used to calculate current direct patient costs (clinic visit, diagnosis, drugs) of malaria treatment and project future costs for the district. The robustness of the model was tested by allowing for different drug failure rates and costs of diagnosis. During 1996-2001, the mean number of primary treatments per year was 7654 for a mean, direct cost of US$17 452 to the community. Clinical diagnosis resulted in overtreatment: 56% and 66% in the wet and dry seasons respectively. Current policy leads to substantial drug wastage and excess direct costs for the community. The direct costs of implementing AS-AQ for slide-proven malaria would be US$8150 (53% less expensive). Studies examining the public health effect and economics of deploying AS-AQ on a wider scale are underway in Senegal.

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“…Several studies carried out in low-, medium-, and high-transmission areas have measured the time required for Plasmodium parasites to reappear in the blood of individuals after parasitemia has been cleared with blood-stagespecific antimalarial compounds (14,15,21,30,(44)(45)(46)(47). Interestingly, these and other modeling studies have revealed a discrepancy between the estimated number of infective bites per human per time unit (i.e., the EIR) and the resulting force of infection (FOI; i.e., the rate of new blood-stage infections) (16,33).…”

Section: Induction Of Type I Ifn and Ifn-␥ By A First P Berghei Livementioning

confidence: 99%

Innate Immunity Induced by Plasmodium Liver Infection Inhibits Malaria Reinfections

et al. 2015

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bFollowing transmission through a mosquito bite to the mammalian host, Plasmodium parasites first invade and replicate inside hepatocytes before infecting erythrocytes and causing malaria. The mechanisms limiting Plasmodium reinfections in humans living in regions of malaria endemicity have mainly been explored by studying the resistance induced by the blood stage of infection. However, epidemiologic studies have suggested that in high-transmission areas, preerythrocytic stages also activate host resistance to reinfection. This, along with the recent discovery that liver infections trigger a specific and effective type I interferon (IFN) response, prompted us to hypothesize that this pre-erythrocyte-stage-induced resistance is linked to liver innate immunity. Here, we combined experimental approaches and mathematical modeling to recapitulate field studies and understand the molecular basis behind such resistance. We present a newly established mouse reinfection model and demonstrate that rodent malaria liver-stage infection inhibits reinfection. This protection relies on the activation of innate immunity and involves the type I IFN response and the antimicrobial cytokine gamma IFN (IFN-␥). Importantly, mathematical simulations indicate that the predictions based on our experimental murine reinfection model fit available epidemiological data. Overall, our study revealed that liver-stage-induced innate immunity may contribute to the preerythrocytic resistance observed in humans in regions of malaria hyperendemicity. Malaria accounts for over half a million deaths per year and is thus the most prevalent parasitic human disease worldwide (1). The disease is caused by an intracellular protozoan parasite of the genus Plasmodium that infects multiple hosts, such as Anopheles mosquitoes and humans and other mammalians (2). Infection begins with a bite of a female mosquito that injects a few Plasmodium sporozoites, which represent the mosquito-transmitted parasite form, into the skin of the mammalian host. After migrating through skin cells (3), sporozoites enter the bloodstream and are then rapidly and specifically retained in the liver sinusoids. Sporozoites then cross the sinusoidal barrier (4) and traverse several liver cells until individual parasites invade a final hepatocyte with the formation of a parasitophorous vacuole (5). Inside this vacuolar niche, sporozoites asymptomatically develop and replicate into thousands of erythrocyte-infective parasites, termed merozoites (6). Finally, merozoites are released into the bloodstream and rapidly infect erythrocytes, initiating the blood stage and the clinical phase of infection (7).Malaria reinfections are common, especially in regions of high malaria transmission. Plasmodium parasites present an extraordinarily high rate of polymorphism; consequently, the host can be reinfected by different parasites that repeatedly escape the immune response (8). Therefore, efficient immunity to reinfection in one individual is obtained only after many years of facing recurrent infe...

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Rapid reappearance of Plasmodium falciparum after drug treatment among Senegalese adults exposed to moderate seasonal transmission.

Cited by 14 publications

References 13 publications

The Dynamics of Naturally Acquired Immunity to Plasmodium falciparum Infection

The Dynamics of Naturally Acquired Immunity to Plasmodium falciparum Infection

Economic evaluation of a policy change from single‐agent treatment for suspected malaria to artesunate‐amodiaquine for microscopically confirmed uncomplicated falciparum malaria in the Oussouye District of south‐western Senegal

Innate Immunity Induced by Plasmodium Liver Infection Inhibits Malaria Reinfections

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