The life cycle of a malaria parasite
The life cycle of the malaria parasite is completed in two hosts- the vector mosquitoes (the definitive host) in which the sexual cycle takes place the human host in which the asexual cycle occurs. When the female mosquito takes an infective blood meal it ingests both asexual and sexual forms of the parasite. Asexual forms are digested in the mosquito’s stomach but the mature sexual forms gametocytes survive, The male and female gametocytes undergo further development and form micro (male) and macro (ferrule) gametes. A male gamete fertilizes a female gamete and the resultant structure (zygote. which later on develops into oOkinete) penetrates the stomach wall. There it develops into obcyst in which, within 7-11 days. depending on the temperature, the infective forms named sporozoites to develop. The Ocyst ruptures. the sporozoites are released into We body cavity of the mosquito and eventually appear in its salivary glands. When such a mosquito bites man. sporozoites are injected together with saliva and circulate in the bloodstream for less than an hour. by which time some of them have invaded liver cells in which develop pre-erythrocytic forms. These normally rupture in 6-15 days and release thousands of merozoites. Some of the merozoites arc phagocytosed. others enter erythrocytes. and the erythrocytic phase begins. The erythrocytic phase of the life cycle of the malaria parasite continues until drugs, death of hosts or parasites. or immunity of the host prevents the parasite’s further development. P. falciparurn and P. malariae have no persistent tissue phase (hepatic form) but. recrudescence of fever may result from a multiplication in the red cells of the parasites. which have not been eliminated by treatment or immune process. In P. vivax and P . ovale hepatic forms (hypnozoites) persist. Thus liberating merozoites into the bloodstream causing relapses of these infections. However, the trigger which stimulates its growth and division of the nucleus has yet to be found. The previous hypothesis of a cyclical secondary maturation (cxo-erythrocytic form) and re-invasion of tissue schizonts has now been challenged and there is more evidence of a dormant tissue stage (hypnozoites) in the hepatic cells for P. vivax and P. ovale. As regards P. malaria parasite, some recent evidence indicates that their relapse may originate from erythrocytic forms remaining in the body for a considerable time. P, vivax and. P. ovale may continue to relapse for about 2-3 years and P. malaria may persist for 10-20 years or more.
In all species of the malaria parasite, some of the erythrocytic merozoites that invade the bloodstream do not divide but differentiate into male and female gametocytes. During the asexual erythrocytic phase of development, the parasite takes at first the form of a ring, and later of a trophozoite in which malaria pigment (haemozoin) appears. Later still, the chromatin divides, becomes surrounded by pieces of cytoplasm and the mature parasite at this stage is known as a schizont. When the schizont ruptures, merozoites are released and reinvasion of erythrocytes takes place. The number of parasitized erythrocytes in P. ovate and P. malaria parasite infections rarely exceeds 1%, but in P. falciparum, more hepatic merozoites are produced initially than in the other species. and this results in 2% or more of circulating red blood cells becoming parasitized in a very short time. Severe clinical manifestations, sometimes leading to death, thus occur. It must also be remembered that severe malaria can occur when fewer than 2% of erythrocytes are parasitized with P. falciparum. In some very severe infections, up to 35% of the patient’s erythrocytes may be parasitized with P. falciparum.
Malaria Parasite resistance
In practice, drug resistance is most commonly related to the effect of blood schizonticides on falciparum malaria parasite, and the response of P. falciparum to antimalarials varies. The foci of P. falciparum resistant to dihydrofolate reductase inhibitors, such as proguanil and pyrimethamine are widespread throughout the malarious areas of the world, particularly in Africa. Similarly, the distribution of P. falciparum ‘resistant to 4-arninoquinolines arc also widespread (certain regions in South-East Asia, South America and East Africa); this has posed a serious problem in most of the countries of SEA Region necessitating considerable changes in malaria chemotherapy for malaria parasite.
In addition to the above in vitro testing, ‘the introduction of simplified in vivo testing covering an adequate follow-up period is now being considered.
Quinine-resistant P. falciparum malaria may also be encountered in areas where a high degree of resistance to chloroquine has become established. Reduced sensitivity of P. falciparum to quinine has already been reported from one of the countries of the South-East Asia Region.
Host Factors. Under this will be discussed the human host (intermediate host) and the Anopheles mosquito, the definitive host.
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Human host. Immunity in malaria are of two types— natural or innate immunity and acquired immunity.
Natural/innate immunity: Genetic characters of human RBCs have been found to influence their susceptibility to invasion by malaria parasites. Duffy blood group is absent amongst the indigenous population of Africa and in American. blacks where vivax malaria is unknown; and Duffy negative RBCs are susceptible to P. falciparum; Haemoglobin S (Sickle cell haemoglobin) appears to provide protection particularly to very young children against the lethal effects of P. falciparum; this accounts for the frequency of this abnormal haemoglobin in Africa. Haemoglobin S is widespread in the Indian subcontinent and is considered to be predominant among the tribal and scheduled__caste groups; according to some investigators, the severity of infection may be reduced by its presence. There is evidence that the present f of beta-thalassemia in Africa may afford some protection against falciparum malaria. However, in the Indian subcontinent, the direct evidence of this abnormal haemoglobin to malaria has not been demonstrated ‘convincingly. An interesting association has been described between the incidence of G-6-PD deficiency and falciparum malaria, and it is claimed that G-6-PO deficiency has a protective effect against severe falciparum malaria.
Acquired immunity: (i) Active: Unless an acute malaria infection causes death, the parasite encounters an immune response in the host in which a gradual reduction of parasitaemia commences. This is observed in P. vivax infection in which milder clinical symptoms are seen during relapse’s following a few acute attacks. As a result of this partial immunity, a low level of parasitaemia and low-grade sym s result; this condition is known as premunition. The efficacy of acquired immunity generally .ecreases with time. Without reinfection (booster inoculation) immunity in P. falciparum infection lasts a few months after radical cure. In vivax malaria immunity may last longer (4-7 years) and it is not so strictly homologous as in case of P. falciparum. With increasing age acquired immunity disappears first for P. vivax than for P. malaria and last P. falciparum. Participation of the T cell in protective immunity to malaria has been established. Cell-mediated reactions in which T cells are involved include their helper function (T helper cells) in antibody synthesis by B cells. cytotoxic T cells (Tc) and production of mediators which recruit and activate other cells including those of monocyte-macrophage series (classical cell-mediated immunity), Malaria infection provides a potent stimulus for the synthesis of immunoglobulins¬ig,G and IgM. Elevation of IgM is especially marked in the malaria-related tropical splenomegaly syndrome. Studies with monoclonal antibodies have emphasized the protective role of antibody acting independently on cells and in particular the functional importance of immunoglobulin directed against antigens present on merozoite surface. (ii) Passive: In_holoendemic areas, although infection of the placenta is frequent, congenital malaria is rare because of the placental transfer of specific 1gG antibodies from the maternal blood across the placenta. Such passively acquired immunity is transient, and after the first year of life, many young children have high parasitaemia and severe malaria. In the early months of life antibodies, decay and their titre become low.