Academic literature on the topic 'Gametocyt'
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Journal articles on the topic "Gametocyt"
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Gruenberg, Maria, Natalie E. Hofmann, Elma Nate, Stephan Karl, Leanne J. Robinson, Kjerstin Lanke, Thomas A. Smith, Teun Bousema, and Ingrid Felger. "qRT-PCR versus IFA-based Quantification of Male and Female Gametocytes in Low-Density Plasmodium falciparum Infections and Their Relevance for Transmission." Journal of Infectious Diseases 221, no. 4 (August 22, 2019): 598–607. http://dx.doi.org/10.1093/infdis/jiz420.
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Abstract Background Accurate quantification of female and male gametocytes and sex ratios in asymptomatic low-density malaria infections are important for assessing their transmission potential. Gametocytes often escape detection even by molecular methods, therefore ultralow gametocyte densities were quantified in large blood volumes. Methods Female and male gametocytes were quantified in 161 PCR-positive Plasmodium falciparum infections from a cross-sectional survey in Papua New Guinea. Ten-fold concentrated RNA from 800 µL blood was analyzed using female-specific pfs25 and male-specific pfmget or mssp qRT-PCR. Gametocyte sex ratios from qRT-PCR were compared with those from immunofluorescence assays (IFA). Results Gametocytes were identified in 58% (93/161) P. falciparum-positive individuals. Mean gametocyte densities were frequently below 1 female and 1 male gametocyte/µL by qRT-PCR. The mean proportion of males was 0.39 (95% confidence interval, 0.33–0.44) by pfs25/pfmget qRT-PCR; this correlated well with IFA results (Pearsons r2 = 0.91; P < .001). A Poisson model fitted to our data predicted 16% P. falciparum-positive individuals that are likely to transmit, assuming at least 1 female and 1 male gametocyte per 2.5 µL mosquito bloodmeal. Conclusions Based on model estimates of female and male gametocytes per 2.5 µL blood, P. falciparum-positive individuals detected exclusively by ultrasensitive diagnostics are negligible for human-to-mosquito transmission. Estimating the transmission potential of ultralow-density malaria infections informs interventions. Almost all infections with ≥1 female and male gametocyte per 2.5 µL mosquito bloodmeal, and thus with highest likelihood of contributing to human-to-mosquito transmission, were detectable by standard molecular diagnostics.
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NEAL, A. T. "Male gametocyte fecundity and sex ratio of a malaria parasite, Plasmodium mexicanum." Parasitology 138, no. 10 (July 15, 2011): 1203–10. http://dx.doi.org/10.1017/s0031182011000941.
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SUMMARYEvolutionary theory predicts that the sex ratio of Plasmodium gametocytes will be determined by the number of gametes produced per male gametocyte (male fecundity), parasite clonal diversity and any factor that reduces male gametes' ability to find and combine with female gametes. Despite the importance of male gametocyte fecundity for sex ratio theory as applied to malaria parasites, few data are available on gamete production by male gametocytes. In this study, exflagellating gametes, a measure of male fecundity, were counted for 866 gametocytes from 26 natural infections of the lizard malaria parasite, Plasmodium mexicanum. The maximum male fecundity observed was 8, but most gametocytes produced 2–3 gametes, a value consistent with the typical sex ratio observed for P. mexicanum. Male gametocytes in infections with higher gametocytaemia had lower fecundity. Male fecundity was not correlated with gametocyte size, but differed among infections, suggesting genetic variation for fecundity. Fecundity and sex ratio were correlated (more female gametocytes with higher fecundity) as predicted by theory. Results agree with evolutionary theory, but also suggest a possible tradeoff between production time and fecundity, which could explain the low fecundity of this species, the variation among infections, and the correlation with gametocytaemia.
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Ferrer, Patricia, Joel Vega-Rodriguez, Abhai K. Tripathi, Marcelo Jacobs-Lorena, and David J. Sullivan. "Antimalarial Iron Chelator FBS0701 Blocks Transmission by Plasmodium falciparum Gametocyte Activation Inhibition." Antimicrobial Agents and Chemotherapy 59, no. 3 (December 15, 2014): 1418–26. http://dx.doi.org/10.1128/aac.04642-14.
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ABSTRACTReducing the transmission of the malarial parasite byAnophelesmosquitoes using drugs or vaccines remains a main focus in the efforts to control malaria. Iron chelators have been studied as potential antimalarial drugs due to their activities against different stages of the parasite. The iron chelator FBS0701 affects the development ofPlasmodium falciparumearly gametocytes and lowers blood-stage parasitemia. Here, we tested the effect of FBS0701 on stage V gametocyte infectivity for mosquitoes. The incubation of stage V gametocytes for up to 3 days with increasing concentrations of FBS0701 resulted in a significant dose-related reduction in mosquito infectivity, as measured by the numbers of oocysts per mosquito. The reduction in mosquito infectivity was due to the inhibition of male and female gametocyte activation. The preincubation of FBS0701 with ferric chloride restored gametocyte infectivity, showing that the inhibitory effect of FBS0701 was quenched by iron. Deferoxamine, another iron chelator, also reduced gametocyte infectivity but to a lesser extent. Finally, the simultaneous administration of drug and gametocytes to mosquitoes without previous incubation did not significantly reduce the numbers of oocysts. These results show the importance of gametocyte iron metabolism as a potential target for new transmission-blocking strategies.
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SILVESTRINI, F., P. ALANO, and J. L. WILLIAMS. "Commitment to the production of male and female gametocytes in the human malaria parasite Plasmodium falciparum." Parasitology 121, no. 5 (November 2000): 465–71. http://dx.doi.org/10.1017/s0031182099006691.
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Commitment to the production of female and male gametocytes was studied in the NF54 line of the human malaria parasite Plasmodium falciparum. The development of sibling parasites derived from individual schizonts was followed, and 2 antisera against the female gametocyte-specific protein Pfg377 and the male gametocyte-specific protein α-tubulin II were used to determine the sex of sibling gametocytes. The experiment showed that individual cohorts of sibling gametocytes were stained in a mutually exclusive fashion by only one or the other antiserum, indicating that individual schizonts committed to yield sexual parasite progeny produce gametocytes of the same sex. This work suggests that in P. falciparum commitment to sexual differentiation occurs prior to schizont maturation, at the same moment when the sex of the resulting gametocytes is determined.
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NEAL, A. T., and J. J. SCHALL. "Gametocyte sex ratio in single-clone infections of the malaria parasite Plasmodium mexicanum." Parasitology 137, no. 13 (July 12, 2010): 1851–59. http://dx.doi.org/10.1017/s0031182010000909.
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SUMMARYSex ratio theory predicts that malaria parasites should bias gametocyte production toward female cells in single-clone infections because they will experience complete inbreeding of parasite gametes within the vector. A higher proportion of male gametocytes is favoured under conditions that reduce success of male gametes at reaching females such as low gametocyte density or attack of the immune system later in the infection. Recent experimental studies reveal genetic variation for gametocyte sex ratio in single-clone infections. We examined these issues with a study of experimental single-clone infections for the lizard malaria parasite Plasmodium mexicanum in its natural host. Gametocyte sex ratios of replicate single-clone infections were determined over a period of 3–4 months. Sex ratios were generally female biased, but not as strongly as expected under simple sex ratio theory. Gametocyte density was not related to sex ratio, and male gametocytes did not become more common later in infections. The apparent surplus of male gametocytes could be explained if male fecundity is low in this parasite, or if rapid clotting of the lizard blood reduces male gamete mobility. There was also a significant clone effect on sex ratio, suggesting genetic variation for some life-history trait, possibly male fecundity.
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Duez, Julien, John P. Holleran, Papa Alioune Ndour, Sasdekumar Loganathan, Pascal Amireault, Olivier Français, Wassim El Nemer, et al. "Splenic Retention of Plasmodium falciparum Gametocytes To Block the Transmission of Malaria." Antimicrobial Agents and Chemotherapy 59, no. 7 (May 4, 2015): 4206–14. http://dx.doi.org/10.1128/aac.05030-14.
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ABSTRACTPlasmodium falciparumis transmitted from humans toAnophelesmosquito vectors via the sexual erythrocytic forms termed gametocytes. Erythrocyte filtration through microsphere layers (microsphiltration) had shown that circulating gametocytes are deformable. Compounds reducing gametocyte deformability would induce their splenic clearance, thus removing them from the blood circulation and blocking malaria transmission. The hand-made, single-sample prototype for microsphiltration was miniaturized to a 96-well microtiter plate format, and gametocyte retention in the microsphere filters was quantified by high-content imaging. The stiffening activity of 40 pharmacological compounds was assessed in microtiter plates, using a small molecule (calyculin) as a positive control. The stiffening activity of calyculin was assessed in spleen-mimetic microfluidic chips and in macrophage-depleted mice. Marked mechanical retention (80% to 90%) of mature gametocytes was obtained in microplates following exposure to calyculin at concentrations with no effect on parasite viability. Of the 40 compounds tested, including 20 antimalarials, only 5 endoperoxides significantly increased gametocyte retention (1.5- to 2.5-fold; 24 h of exposure at 1 μM). Mature gametocytes exposed to calyculin accumulated in microfluidic chips and were cleared from the circulation of macrophage-depleted mice as rapidly as heat-stiffened erythrocytes, thus confirming results obtained using the microsphiltration assay. An automated miniaturized approach to select compounds for their gametocyte-stiffening effect has been established. Stiffening induces gametocyte clearance bothin vitroandin vivo. Based on physiologically validated tools, this screening cascade can identify novel compounds and uncover new targets to block malaria transmission. Innovative applications in hematology are also envisioned.
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Delves, Michael J., Andrea Ruecker, Ursula Straschil, Jöel Lelièvre, Sara Marques, María José López-Barragán, Esperanza Herreros, and Robert E. Sinden. "Male and Female Plasmodium falciparum Mature Gametocytes Show Different Responses to Antimalarial Drugs." Antimicrobial Agents and Chemotherapy 57, no. 7 (April 29, 2013): 3268–74. http://dx.doi.org/10.1128/aac.00325-13.
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ABSTRACTIt is the mature gametocytes ofPlasmodiumthat are solely responsible for parasite transmission from the mammalian host to the mosquito. They are therefore a logical target for transmission-blocking antimalarial interventions, which aim to break the cycle of reinfection and reduce the prevalence of malaria cases. Gametocytes, however, are not a homogeneous cell population. They are sexually dimorphic, and both males and females are required for parasite transmission. Using two bioassays, we explored the effects of 20 antimalarials on the functional viability of both male and female mature gametocytes ofPlasmodium falciparum. We show that mature male gametocytes (as reported by their ability to produce male gametes, i.e., to exflagellate) are sensitive to antifolates, some endoperoxides, methylene blue, and thiostrepton, with submicromolar 50% inhibitory concentrations (IC50s), whereas female gametocytes (as reported by their ability to activate and form gametes expressing the marker Pfs25) are much less sensitive to antimalarial intervention, with only methylene blue and thiostrepton showing any significant activity. These findings show firstly that the antimalarial responses of male and female gametocytes differ and secondly that the mature male gametocyte should be considered a more vulnerable target than the female gametocyte for transmission-blocking drugs. Given the female-biased sex ratio ofPlasmodium falciparum(∼3 to 5 females:1 male), current gametocyte assays without a sex-specific readout are unlikely to identify male-targeted compounds and prioritize them for further development. Both assays reported here are being scaled up to at least medium throughput and will permit identification of key transmission-blocking molecules that have been overlooked by other screening campaigns.
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Koepfli, Cristian, Wang Nguitragool, Anne Cristine Gomes de Almeida, Andrea Kuehn, Andreea Waltmann, Eline Kattenberg, Maria Ome-Kaius, et al. "Identification of the asymptomatic Plasmodium falciparum and Plasmodium vivax gametocyte reservoir under different transmission intensities." PLOS Neglected Tropical Diseases 15, no. 8 (August 27, 2021): e0009672. http://dx.doi.org/10.1371/journal.pntd.0009672.
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Background Understanding epidemiological variables affecting gametocyte carriage and density is essential to design interventions that most effectively reduce malaria human-to-mosquito transmission. Methodology/Principal findings Plasmodium falciparum and P. vivax parasites and gametocytes were quantified by qPCR and RT-qPCR assays using the same methodologies in 5 cross-sectional surveys involving 16,493 individuals in Brazil, Thailand, Papua New Guinea, and Solomon Islands. The proportion of infections with detectable gametocytes per survey ranged from 44–94% for P. falciparum and from 23–72% for P. vivax. Blood-stage parasite density was the most important predictor of the probability to detect gametocytes. In moderate transmission settings (prevalence by qPCR>5%), parasite density decreased with age and the majority of gametocyte carriers were children. In low transmission settings (prevalence<5%), >65% of gametocyte carriers were adults. Per survey, 37–100% of all individuals positive for gametocytes by RT-qPCR were positive by light microscopy for asexual stages or gametocytes (overall: P. falciparum 178/348, P. vivax 235/398). Conclusions/Significance Interventions to reduce human-to-mosquito malaria transmission in moderate-high endemicity settings will have the greatest impact when children are targeted. In contrast, all age groups need to be included in control activities in low endemicity settings to achieve elimination. Detection of infections by light microscopy is a valuable tool to identify asymptomatic blood stage infections that likely contribute most to ongoing transmission at the time of sampling.
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Guinet, F., J. A. Dvorak, H. Fujioka, D. B. Keister, O. Muratova, D. C. Kaslow, M. Aikawa, A. B. Vaidya, and T. E. Wellems. "A developmental defect in Plasmodium falciparum male gametogenesis." Journal of Cell Biology 135, no. 1 (October 1, 1996): 269–78. http://dx.doi.org/10.1083/jcb.135.1.269.
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Asexually replicating populations of Plasmodium parasites, including those from cloned lines, generate both male and female gametes to complete the malaria life cycle through the mosquito. The generation of these sexual forms begins with the induction of gametocytes from haploid asexual stage parasites in the blood of the vertebrate host. The molecular processes that govern the differentiation and development of the sexual forms are largely unknown. Here we describe a defect that affects the development of competent male gametocytes from a mutant clone of P. falciparum (Dd2). Comparison of the Dd2 clone to the predecessor clone from which it was derived (W2'82) shows that the defect is a mutation that arose during the long-term cultivation of asexual stages in vitro. Light and electron microscopic images, and indirect immunofluorescence assays with male-specific anti-alpha-tubulin II antibodies, indicate a global disruption of male development at the gametocyte level with at least a 70-90% reduction in the proportion of mature male gametocytes by the Dd2 clone relative to W2'82. A high prevalence of abnormal gametocyte forms, frequently containing multiple and unusually large vacuoles, is associated with the defect. The reduced production of mature male gametocytes may reflect a problem in processes that commit a gametocyte to male development or a progressive attrition of viable male gametocytes during maturation. The defect is genetically linked to an almost complete absence of male gamete production and of infectivity to mosquitoes. This is the first sex-specific developmental mutation identified and characterized in Plasmodium.
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BUTTERWORTH, ALICE S., TINA S. SKINNER-ADAMS, DON L. GARDINER, and KATHARINE R. TRENHOLME. "Plasmodium falciparumgametocytes: with a view to a kill." Parasitology 140, no. 14 (August 19, 2013): 1718–34. http://dx.doi.org/10.1017/s0031182013001236.
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SUMMARYDrugs that kill or inhibit the sexual stages ofPlasmodiumin order to prevent transmission are important components of malaria control programmes. Reducing gametocyte carriage is central to the control ofPlasmodium falciparumtransmission as infection can result in extended periods of gametocytaemia. Unfortunately the number of drugs with activity against gametocytes is limited. Primaquine is currently the only licensed drug with activity against the sexual stages of malaria parasites and its use is hampered by safety concerns. This shortcoming is likely the result of the technical challenges associated with gametocyte studies together with the focus of previous drug discovery campaigns on asexual parasite stages. However recent emphasis on malaria eradication has resulted in an upsurge of interest in identifying compounds with activity against gametocytes. This review examines the gametocytocidal properties of currently available drugs as well as those in the development pipeline and examines the prospects for discovery of new anti-gametocyte compounds.
Dissertations / Theses on the topic "Gametocyt"
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Crooks, Lucy. "Gametocyte investment in malaria." Thesis, University of Edinburgh, 2004. http://hdl.handle.net/1842/13498.
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Gametocytes, the transmission stage of malaria parasites, are generally rare in infections. I explore whether this may be a parasite adaptation that paradoxically maximises fitness. I present an optimality analysis of gametocyte investment based on a discretely formulated within-host model. I show that low gametocyte investment is predicted as a result of the trade-off that exists between producing gametocytes and increasing parasite numbers. I predict that gametocyte investment should decrease as maximum asexual density occurs later in infections and also as parasite fecundity rises. I address statistical problems with estimating gametocyte investment from blood smears. I also consider the simpler case of estimating parasitaemias and gametocytaemias. Traditional methods of counting parasites in smears can produce biased estimates of parasitaemia, gametocytaemia and gametocyte conversion. I introduce an alternative method of counting based on inverse sampling. This method is unbiased, is consistently precise and the most time-efficient method of counting. I used the inverse sampling method to estimate gametocyte conversion (the observed outcome of investment) in P. chabaudi infections in mice, which had been manipulated to alter the time of maximum asexual density. Gametocyte conversion showed two peaks. The timing of the peaks depended on the time of maximum asexual density. Maximum conversion decreased as the time to maximum asexual density rose as predicted by my optimality analysis. An interesting finding was that gametocyte conversion decreased after reaching a maximum. This result is counter to most life history theory. I suggest this indicates that survival of infections into a chronic phase may be an important component of fitness. Maximum conversion occurred after maximum asexual density. This leads me to propose that contrary to the common view, gametocyte investment may be suppressed at times when there is a high risk of parasite clearance. Understanding the reasons for gametocyte rarity may help to predict how P. falciparum will respond to intervention and suggest new methods of malaria control.
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Hayward, Rhian Elizabeth. "The biology of Plasmodium falciparum gametocytes." Thesis, University of Oxford, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.360296.
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Chatora, Tinashe. "Joint models for nonlinear longitudinal profiles in the presence of informative censoring." Doctoral thesis, University of Cape Town, 2018. http://hdl.handle.net/11427/29564.
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Malaria is the parasitic disease which affects the most humans, with Plasmodium falciparum malaria being responsible for the majority of severe malaria and malaria related deaths. The asexual form of the parasite causes the signs and symptoms associated with malaria infection. The sexual form of the parasite, also known as a gametocyte, is the stage responsible for infectivity of the human host (patient) to the mosquito vector, and thus ongoing transmission of malaria and the spread of antimalarial drug resistance. Historically malaria therapeutic efficacy studies have focused mainly on the clearance of asexual parasites. However, malaria in a community can only be truly combated if a treatment program is implemented which is able to clear both asexual and sexual parasites effectively. In this thesis focus will be on the modeling of the key features of gametocytemia. Particular emphasis will be on the modeling of the time to gametocyte emergence, the density of gametocytes and the duration of gametocytemia. It is also of interest to investigate the impact of the administered treatment on the aforementioned features. Gametocyte data has several interesting features. Firstly, the distribution of gametocyte data is zero-inflated with a long tail to the right. The observed longitudinal gametocyte profile also has a nonlinear relationship with time. In addition, since most malaria intervention studies are not designed to optimally measure the evolution of the longitudinal gametocyte profile, there are very few observation points in the time period where the gametocyte profile is expected to peak. Gametocyte data collected from malaria intervention studies are also affected by informative censoring, which leads to incomplete gametocyte profiles. An example of informative censoring is when a patient who experiences treatment failure is “rescued", and withdrawn, from the study in order to receive alternative treatment. This patient can be considered to be in worse health as compared to the patients who remain in this study. There are also competing risks of exit from the study, as a patient can either experience treatment failure or be lost to follow-up. The above mentioned features of gametocyte data make it a statistically appealing dataset to analyze. In literature there are several modeling techniques which can be used to analyze individual features of the data. These techniques include standard survival models for modeling the time to gametocyte emergence and the duration of gametocytemia. The longitudinal nonlinear gametocyte profile would typically be modeled using nonlinear mixed effect models. These nonlinear models could then subsequently be extended to accommodate the zero-inflation in the data, by changing the underlying assumption around the distribution of the response variable. However, it is important to note that these standard techniques do not account for informative censoring. Failure to account for informative censoring leads to bias in parameter estimates. Joint modeling techniques can be used to account for informative censoring. The joint models applied in this thesis combined the longitudinal nonlinear gametocyte densities and the time to censoring due to either lost to follow up or treatment failure. The data analyzed in this thesis were collected from a series of clinical trials conducted be- tween 2002 and 2004 in Mozambique and the Mpumulanga province of South Africa. These trials were a part of the South East African Combination Antimalarial Therapy (SEACAT) evaluation of the phased introduction of combination anti-malarial therapy, nested in the Lubombo Spatial Development Initiative. The aim of these studies was primarily to measure the efficacy of sulfadoxine-pyrimethamine (SP) and a combination of artesunate and sulfadoxine-pyrimethamine (ACT), in eliminating asexual parasites in patients. The patients enrolled in the study had uncomplicated malaria, at a time of increasing resistance to sulfadoxine-pyrimethamine (SP) treatment. Blood samples were taken from patients during the course of 6 weeks on days 0, 1, 2, 3, 7, 14, 21, 28 and 42. Analysis of these blood samples provided longitudinal measurements for asexual 1 parasite densities, gametocyte densities, sulfadoxine drug concentrations and pyrimethamine drug concentrations. The gametocyte data collected in this study was initially analyzed using standard survival modeling techniques. Non-parametric Cox regression models and parametric survival models were applied to the data as part of this initial investigation. These models were used to investigate the factors which affected the time to gametocyte emergence. Subsequently, using the subset of the population which experienced gametocytemia, accelerated failure time models were applied to investigate the factors which affected the duration of gametocytemia. It is evident that the findings from the aforementioned duration investigation would only be able to provide valid duration estimates for patients who were detected to have gametocytemia. This work was extended to allow for population level duration estimates by incorporating the prevalence of gametocytemia into the estimation of duration, for generic patients with specific covariate patterns. The prevalence of gametocytemia was modeled using an underlying binomial distribution. The delta method was subsequently used to derive confidence intervals for the population level duration estimates which were associated with specific covariate patterns. An investigation into the factors affecting the early withdrawal of patients from the study was also conducted. Early exit from the study arose either through loss to follow-up (LTFU) or through treatment failure. The longitudinal gametocyte profile was modeled using joint modeling techniques. The resulting joint model used shared random effects to combine a Weibull survival model, describing the cause- specific hazards of patient exit from the study, with a nonlinear zero-adjusted gamma mixed effect model for the longitudinal gametocyte profile. This model was used to impute the incomplete gametocyte profiles, after adjusting for informative censoring. These imputed profiles were then used to estimate the duration of gametocytemia. It was found, in this thesis, that treatment had a very strong effect on the hazard of gametocyte emergence, density of gametocytes and the duration of gametocytemia. Patients who received a combination of sulfadoxine-pyrimethamine and artesunate were found to have significantly lower hazards of gametocyte emergence, lower predicted durations of gametocytemia and lower predicted longitudinal gametocyte densities as compared to patients who received sulfadoxine-pyrimethamine treatment only.
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Wiley, Jessica Delia. "Investigating the role of the Apicoplast in Plasmodium falciparum Gametocyte Stages." Diss., Virginia Tech, 2014. http://hdl.handle.net/10919/64150.
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Malaria continues to be a global health burden that affects millions of people worldwide each year. Increasing demand for malaria control and eradication has led research to focus on sexual development of the malaria parasite. Sexual development is initiated when pre-destined intraerythrocytic ring stage parasites leave asexual reproduction and develop into gametocytes. A mosquito vector will ingest mature gametocytes during a blood meal. Sexual reproduction will occur in the midgut, leading to the production of sporozoites that will migrate to the salivary gland. The sporozoites will be injected to another human host during the next blood meal consequently, transmitting malaria. Due to decreased drug susceptibility of mature gametocytes, more investigation of the biology and metabolic requirements of malaria parasites during gametocytogenesis, as well as during the mosquito stages, are urgently needed to reveal novel targets for development of transmission-blocking agents. Furthermore, increasing drug resistance of the parasites to current antimalarials, including slowed clearance rates to artemisinin, requires the discovery of innovative drugs against asexual intraerythrocytic stages with novel mechanisms of action. Here, we have investigated the role of the apicoplast during Plasmodium falciparum gametocytogenesis. In addition, we describe drug-screening studies that have elucidated a novel mode of action of one compound from the Malaria Box, as well as identified new natural product compounds that may be serve as starting molecules for antimalarial development.Ph. D.
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Aylor, Samantha Olivia. "The Effect of Drug Resistance on Plasmodium falciparum Transmission and Gametocyte Development." Scholar Commons, 2013. http://scholarcommons.usf.edu/etd/4630.
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In order to reduce malaria prevalence worldwide, a better understanding of parasite transmission and the effect of drug resistance is needed. The effect of drug resistance on malaria transmission has been examined for some drugs, but not for mitochondrial inhibitors such as atovaquone and the current basis of malaria therapy, artemisinin. Therefore, the goal of this study was to produce gametocytes, the life cycle stage that transmits from mosquito to human, in several different drug resistant patient isolates as well as to determine the effect of drug resistance on gametocyte development and transmission. Previous studies have shown that the mutation that confers resistance to atovaquone, a common antimalarial, occurs de novo after treatment and transmission of this resistance is not seen in the field. Therefore, to determine whether or not the resistance mutation can be transmitted, mosquito-feeding experiments were conducted using atovaquone resistant parasites and resulting oocyst DNA was analyzed. In addition to these atovaquone studies, artemisinin resistant gametocytes were also grown in vitro and drug pressure was added to determine if resistance mechanisms affect gametocyte development. This study is the first examine gametocyte development in these resistant strains and the first to report that transmission of the atovaquone resistant mutation may be possible. However, data is currently inconclusive on the effect of artemisinin resistance on gametocyte development.
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Distiller, G. B. "Nonlinear mixed effects modeling of gametocyte carriage in patients with uncomplicated malaria." Master's thesis, University of Cape Town, 2007. http://hdl.handle.net/11427/4378.
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Snider, Danielle A. "The Gametocytocidal Activity of Whole-Plant Artemisia annua and Artemisia afra Tea-Based Therapies against Plasmodium falciparum in vitro." Digital WPI, 2019. https://digitalcommons.wpi.edu/etd-theses/1346.
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Malaria is one of the deadliest parasitic diseases worldwide, causing 219 million infections and 435 thousand deaths per year. As such, this mosquito-borne illness is a major target for global eradication efforts. One critical arm of the eradication strategy is chemotherapy. For a therapeutic to advance the eradication agenda, it must cure the patient of infection and eliminate transmission stage parasites (called gametocytes) from the blood, thereby breaking the cycle of transmission. Currently, first-line treatments against malaria infection consist of an artemisinin derivative in combination with another antimalarial drug from a different drug class. Although artemisinin and its derivatives are highly efficacious at curing malaria, these drugs are ineffective at preventing disease transmission. However, recent in vivo studies have suggested that whole plant Artemisia annua (the botanical source of artemisinin) delivered as tea can cure patients of infection and eliminate transmission stage parasites from the bloodstream. To validate these in vivo results in vitro, experiments were performed to measure the killing efficacy of A. annua and A. afra tea infusions against three different stages of the parasite life cycle— one stage of the asexual cycle, immature gametocytes, and mature gametocytes. Killing effects were observed using light microscopy and gametocyte gene-specific RT-qPCR analyses. Results suggested that A. annua tea was nearly as effective as artemisinin at killing all three tested stages of the parasite. A. afra tea, which contains low levels of artemisinin, showed comparable killing efficacy against late stage gametocytes, but not against the other two tested stages. These results supported the notion that A. annua tea is an effective antimalarial and also provides evidence that both A. annua and A. afra teas may be a viable therapeutic option for eliminating gametocytes during human infection.
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Meaden, Cora S. J. "Genetic determinants of gametocyte sex ratio in the human malaria parasite Plasmodium falciparum." Thesis, University of Glasgow, 2013. http://theses.gla.ac.uk/4700/.
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The aim of this study was to investigate the genetic basis of variation in gametocyte sex ratio in the human malaria parasite, Plasmodium falciparum. The gametocyte sex ratio was measured in progeny clones from the 3D7 x HB3 experimental genetic cross and found to be remarkably stable across replicates of different parasite clones. Significant differences in the sex ratio were observed between the parents of the cross. Progeny clones fell into two classes of sex ratio, one similar to that seen in parent 3D7 and the other like parent HB3, suggesting a single gene of major effect controlling sex ratio. Using a genetic map of the progeny and parental clones, QTL analysis revealed two highly significant loci, the first on chromosome 10 (LOD score = 8.8), and the second on chromosome 14 (LOD = 4.0), linked to gametocyte sex ratio. The locus on chromosome 10, spanning approximately 35kb, contained ten genes. This locus, named PfROS1 (Plasmodium falciparum Ratio of Sex 1), explained 95% of the variation in sex ratio. The second locus on chromosome 14, PfROS2 (Plasmodium falciparum Ratio of Sex 2), explained a small proportion of gametocyte sex ratio variation when combined with PfROS1, the two loci explained 99% of the variation in gametocyte sex ratio observed. As PfROS1 explains such a high percentage of the variation observed in the gametocyte sex ratio it represents a single controlling locus to define the sex ratio of gametocytes produced. This is the first report of a genomic locus influencing gametocyte sex ratio in any Plasmodium species. In addition, changes in the sex ratio of clones 3D7 and HB3, over the course of 16 days of gametocyte culture were investigated. The number of gametocytes, and especially male gametocytes, was observed to fall markedly in the last few days of culture, when the majority of gametocytes were stage V (mature). Fluctuations in temperature during the culture process were found to influence sex ratio, suggesting the loss of males was due to exflagellation of mature gametocytes. Parasite clone and day of culture were also significant explanatory variables in influencing sex ratio.
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Chen, Hong, Stefanie Wiedmer, Sacha Hanig, Rolf Entzeroth, and Michael Kurth. "Development of Eimeria nieschulzi (Coccidia, Apicomplexa) Gamonts and Oocysts in Primary Fetal Rat Cells." Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2014. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-127190.
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The in vitro production of gametocytes and oocysts of the apicomplexan parasite genus Eimeria is still a challenge in coccidiosis research. Until today, an in vitro development of gametocytes or oocysts had only been shown in some Eimeria species. For several mammalian Eimeria species, partial developments could be achieved in different cell types, but a development up to gametocytes or oocysts is still lacking. This study compares several permanent cell lines with primary fetal cells of the black rat (Rattus norvegicus) concerning the qualitative in vitro development of the rat parasite Eimeria nieschulzi. With the help of transgenic parasites, the developmental progress was documented. The selected Eimeria nieschulzi strain constitutively expresses the yellow fluorescent protein and a macrogamont specific upregulated red tandem dimer tomato. In the majority of all investigated host cells the development stopped at the second merozoite stage. In a mixed culture of cells derived from inner fetal organs the development of schizont generations I-IV, macrogamonts, and oocysts were observed in crypt-like organoid structures. Microgamonts and microgametes could not be observed and oocysts did not sporulate under air supply. By immunohistology, we could confirm that wild-type E. nieschulzi stages can be found in the crypts of the small intestine. The results of this study may be helpful for characterization of native host cells and for development of an in vitro cultivation system for Eimeria species.
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Elsideg, Ahmed Mohammed Abdelrhaman Watcharapong Piyaphanee. "Emergence and clearance of gametocytes in complicated plasmodium falciparum Malaria /." Abstract, 2008. http://mulinet3.li.mahidol.ac.th/thesis/2551/cd414/5038615.pdf.
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Thematic Paper (M.C.T.M.(Clinical Tropical Medicine)--Mahidol University, 2008.LICL has E-Thesis 0038 ; please contact computer services. LIRV has E-Thesis 0038 ; please contact circulation services.
Books on the topic "Gametocyt"
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Gametes - The Oocyte (Cambridge Reviews in Human Reproduction). Cambridge University Press, 1995.
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(Editor), J. G. Grudzinskas, and J. L. Yovich (Editor), eds. Gametes the Oocyte. Cambridge University Press, 1995.
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G, Grudzinskas J., and Yovich John, eds. Gametes: The oocyte. Cambridge: Cambridge University Press, 1995.
Find full textBook chapters on the topic "Gametocyt"
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Gooch, Jan W. "Gametocyte." In Encyclopedic Dictionary of Polymers, 895. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-6247-8_13805.
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Alano, Pietro, and Oliver Billker. "Gametocytes and Gametes." In Molecular Approaches to Malaria, 191–219. Washington, DC, USA: ASM Press, 2014. http://dx.doi.org/10.1128/9781555817558.ch10.
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Saliba, Kathryn Shaw, and Marcelo Jacobs-Lorena. "Production of Plasmodium falciparum Gametocytes In Vitro." In Methods in Molecular Biology, 17–25. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-62703-026-7_2.
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Held, Andreas, and Manuela Held. "Bei Moosen ist der Gametophyt das dominierende Stadium." In Diversität 1 b, 35–37. Berlin, Heidelberg: Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/978-3-662-55084-7_9.
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Ghosh, Anil K., and Marcelo Jacobs-Lorena. "In Vitro Differentiation of Plasmodium falciparum Gametocytes into Ookinetes." In Methods in Molecular Biology, 27–33. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-62703-026-7_3.
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Rogosa, Morrison, Micah I. Krichevsky, and Rita R. Colwell. "Myxospores, Sporocysts, Fruiting Bodies, Spores, Sporozoites, Trophozoites, and Gametocytes." In Springer Series in Microbiology, 63–65. New York, NY: Springer New York, 1986. http://dx.doi.org/10.1007/978-1-4612-4986-3_9.
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Sattabongkot, Jetsumon, Chalermpon Kumpitak, and Kirakorn Kiattibutr. "Membrane Feeding Assay to Determine the Infectiousness of Plasmodium vivax Gametocytes." In Malaria Vaccines, 93–99. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-2815-6_8.
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Kepple, Daniel, Anthony Ford, Ebony Little, Gabrielle Kolesar, Beka R. Abagero, Ashley N. Blackwell, Swarnapali De Silva Indrasekara, Delenasaw Yewhalaw, and Eugenia Lo. "From Genes to Biomarkers: Understanding the Biology of Malaria Gametocytes and Their Detection." In Genetic Polymorphisms - New Insights [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.99364.
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Each year, approximately 230 million malaria cases and 400,00 malaria deaths are reported worldwide. Malaria is a life-threatening disease caused by Plasmodium parasites that are transmitted from one individual to another through the bites of infected female Anopheles mosquitoes. Malaria parasites replicate asexually in the human host, and, in each replication cycle, a portion of the asexual stages develops into sexual gametocytes that permit transmission. The proportion of infections that carries gametocytes and the infectivity of gametocytes are indicators of human-to-mosquito transmission potential. In P. falciparum, gametocytes appear 10–14 days after infection, whereas in P. vivax gametocytes appear simultaneously with asexual schizonts. Such difference in development not only increases the length of time that an individual is infectious, but also increases the likelihood of transmission before treatment. The conversion from asexual parasites to gametocytes is also highly variable between infections. Differences in age, host immune response, parasite genetic composition, density of red blood cells, presence of co-infecting parasite strains, and antimalarial drug use could affect gametocytes production. In P. vivax, the unique ability to produce hypnozoites, a dormant liver stage of the parasite, may allow gametocytes to be produced periodically from relapse and contribute to transmission. In this chapter, we will provide an overview of the biology of Plasmodium gametocytes, existing tools for gametocyte detection, and features of gametocyte genes. The biological insights and genetic findings are essential to developing better detection biomarkers and effective strategies to reduce transmission in malaria-endemic countries.
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"Gametocyte." In Encyclopedia of Genetics, Genomics, Proteomics and Informatics, 733. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6754-9_6414.
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"Gametocyte." In Encyclopedia of Parasitology, 1105. Berlin, Heidelberg: Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/978-3-662-43978-4_1248.
Full textConference papers on the topic "Gametocyt"
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Karl, Stephan, Robert C. Woodward, Timothy M. E. Davis, Tim G. St.Pierre, Urs Häfeli, Wolfgang Schütt, and Maciej Zborowski. "Manufacture and Testing of a High Field Gradient Magnetic Fractionation System for Quantitative Detection of Plasmodium falciparum Gametocytes." In 8TH INTERNATIONAL CONFERENCE ON THE SCIENTIFIC AND CLINICAL APPLICATIONS OF MAGNETIC CARRIERS. AIP, 2010. http://dx.doi.org/10.1063/1.3530002.
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