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The Diseases – Malaria, Filariasis and Dengue
Published in Jacques Derek Charlwood, The Ecology of Malaria Vectors, 2019
There are a number of other differences in the parasites that affect their transmissibility. In particular, P. vivax gametocytes take 48 h to mature so they are present in the peripheral blood from the start of an infection whilst P. falciparum gametocytes take 7–10 days to mature (the initial stages being sequestered in the bone marrow). There are a number of factors that may induce gametocyte production. Drugs, such as chloroquine, may enhance production and so may have augmented the rise in cases that occurred at the end of the last century. Anaemia may also boost production but this may just be the effect of long-term infection. Other factors, such as the production of antibodies to mosquito saliva, may also induce gametocyte production – which would help explain the rapid rise in cases seen in places where transmission is seasonal. Once mature, gametocytes of P. falciparum may also be found at highest densities in capillaries close to the skin rather than in the veins. This also increases the likelihood that they will be acquired by feeding mosquitoes.
The malaria parasites
Published in David A Warrell, Herbert M Gilles, Essential Malariology, 2017
Robert E Sinden, Herbert M Gilles
The female anopheline mosquito must take blood meals on a regular basis to support the development of successive batches of eggs. When biting a malaria-infected vertebrate host, she will take up erythrocytes infected with the asexual schizogonie stages and with gametocytes. Gametocytes are the first sexual stages of parasite development and are the gamete-forming cells; they persist as mature forms arrested in G0 of the cell cycle in the peripheral blood of the host. Whereas in most species studied, infectivity of gametocytes is sustained throughout the life of the cell, there are reports that in some mammalian malarial species, e.g. P. cynomolgi, infectivity to the mosquito (or gamete-forming ability) follows a circadian pattern that matches the biting behaviour of the mosquito. Evidence for such ‘behavioural’ strategies is, however, convincing only in the related Leucocytozoidae.
Humoral Immune Responses in Mice and Man to Malarial Parasites
Published in Mary M. Stevenson, Malaria: Host Responses to Infection, 2017
When mosquitoes feed on infected hosts, they ingest gametocytes. Within the midgut of the mosquito, the parasites are released from erythrocytes and develop sequentially into gametes (male and female), zygotes, and ookinetes. In 1976, Gwadz152 and Carter and Chen153 showed that fertilization and further parasite development were prevented within mosquitoes that had fed on chickens immunized with irradiated gametes or gametocytes of P. gallinaceum. In one set of experiments, chickens were immunized with 2.7 × 105 to 2.2 × 107 male gametes, challenged with P. gallinaceum, and then mosquitoes were allowed to feed daily during patent parasitemias.153 A total of 0 to 1 oocysts was found in the midgut of mosquitoes fed on vaccinated birds compared to 2267 oocysts in those fed on control, unvaccinated birds. The process of preventing gamete development is known as transmission blocking immunity and had been demonstrated for P. yoelii,154P. falciparum,155 and P. vivax.156 It is clear that Abs present in the sera of the host mediate transmission blocking immunity within mosquitoes.152,155,157,158
Transmission-Blocking Vaccines: Harnessing Herd Immunity for Malaria Elimination
Published in Expert Review of Vaccines, 2021
Sexual and sporogonic development offers a significant bottleneck in the Plasmodium life cycle, making these stages an attractive target for interventions. After gametocytes are drawn into the mosquito midgut during a bloodmeal, several environmental factors (temperature, pH, xanthurenic acid) stimulate egress from red cells. Each female gametocyte (macrogametocyte) yields a single macrogamete, while male microgametes are activated by intracellular calcium to undergo three rounds of DNA replication followed by endomitosis [9]. Each zygote forms within minutes of mosquito ingestion through fertilization of a single macrogamete by a single microgamete, then progresses through the forms of motile ookinete and finally sessile oocyst on the mosquito midgut. Each infected mosquito midgut will usually harbor fewer than 10–100 oocysts [10], a small number of parasites to target for interventions, albeit many more parasites are ingested in the original bloodmeal.
Diagnosis of clinical malaria in endemic settings
Published in Expert Review of Anti-infective Therapy, 2021
Rosauro Varo, Núria Balanza, Alfredo Mayor, Quique Bassat
Molecular assays are usually too expensive and have limited applicability in the field. At the moment, they are mainly used in research activities and as reference methods of evaluation. Despite the wide availability and variety of assays, they currently show little additional value to cheaper alternatives for the clinical assessment and guiding of management decisions for patients. Their high intrinsic sensitivity, an initially positive trait, can make interpretation of positive results difficult in some situations, as these could arise from parasite DNA persistence after treatment. Similarly, the use of molecular assays that do not distinguish between gametocytes and asexual forms, can lead to challenges in the interpretation of results, as these can arise from the detection of gametocytes (which are not responsible for clinical symptoms). Nonetheless, they also have interesting features and there are current efforts to make NAATs more affordable and field-deployable. LAMP and NASBA technologies are specially promising fields and ongoing work can make POC implementation of molecular diagnostics a reality for malaria in the near future.
Can Plasmodium’s tricks for enhancing its transmission be turned against the parasite? New hopes for vector control
Published in Pathogens and Global Health, 2019
S. Noushin Emami, Melika Hajkazemian, Raimondas Mozūraitis
All malaria parasites require two hosts, the vertebrate host where schizogony occurs within the erythrocytes (human blood stages of parasite), and the mosquito vector where sporogony (mosquito stages of parasite) occurs in the mosquito midgut wall [22]. In the vertebrate host, an infection is initiated when sporozoites are injected with the saliva of an infected mosquito, and parasites replicate asexually, first in the liver, and then in the erythrocytes (reviewed in [23]). Whilst the majority of parasites invading erythrocytes are destined to continue through the asexual cycle, a small fraction can develop into gametocytes, the first sexual stage of the life cycle. In Plasmodium falciparum, the presence of gametocytes in the peripheral blood appears 7–15 days after the initial asexual wave which is long compared to the other human malaria species 1–3 days. The ratio of gametocytes to asexual stages in P. falciparum is usually found at very low levels [24]. Only people carrying gametocytes can be infectious to mosquitoes. Recent studies showed that microscopy is insufficiently sensitive to detect low densities of asexual parasites and gametocyte [25,26]. In most endemic settings, a small proportion of infecting parasites are gametocytes [27].