Malaria transmission and epidemiology
Malaria transmission and epidemiology
Malaria transmission and epidemiology
Malaria is an acute febrile illness characterized clinically by paroxysms of fever, the consequence of rupture of infected red cells due to asexual reproduction by species of Plasmodium (schizogony). Plasmodium vivax, P. ovale and P. malariae are associated with morbidity but no major mortality, but P. falciparum causes both morbidity and considerable mortality.
Malaria is an acute febrile illness characterized clinically by paroxysms of fever, the consequence of rupture ofinfected red cells due to asexual reproduction by species of Plasmodium (schizogony). Plasmodium vivax, P. ovaleand P. malariae are associated with morbidity but no majormortality, but P. falciparum causes both morbidity andconsiderable mortality. The infection is transmitted bythe bite of the female anopheline mosquito. Distribution and incidence Malaria occurs widely throughout the tropical areas of the world, in the Americas, Africa, Asia and the Pacific area. Falciparum malaria is particularly common in tropical Africa, where it causes at least 1000000 deaths per year, mainly in children. The resurgence of malaria in the Indian subcontinent was led by a rising incidence of vivax malaria in the 1970s, and now falciparum infection is more widespread in the region.Ovale malaria is predominantlya west African disease. Malariae malaria is the least common form .Malaria is imported into temperate regions by tourists, people employed overseas, business travellers and immigrants. The numbers of cases have risen progressively over the past 20 years. Vivax and ovale life cycles are similar, with primary exoerythrocyticschizogony (EES) in hepatocytes leading to infection of the peripheral blood with merozoites. These enter red blood cells (RBCs) and undergo erythrocytic schizogony(ES) every 48 hours; this is benign tertian and ovale tertianmalaria. Some of the sporozoites produce latent forms, the hypnozoites, within liver cells, which produce EES and then ES up to 2 or 3 years after infection, i.e. relapsing malaria.Falciparum malaria has no hypnozoite form, and so the infection is cured when parasites are cleared from the blood by treatment. ES has a periodicity of less than 48hours ('sub tertian'). Malariae parasites also lack the hypnozoite stage but can cause reappearance of parasitaemia(parasites in peripheral RBCs) up to 20 or more years afterinfection. Small numbers of parasites persist in RBCs tocause this. The periodicity of ES is 72 hours (quartanmalaria). Vivax, ovale and malariae parasites invade 1-2% ofRBCs at most. Falciparum parasites invade any proportionof RBCs, accounting for the severity of disease and the high mortality. Host A baby born of an indigenous mother in an endemic falciparum area will be protected against infection during the first year of life by maternal antimalaria IgG crossing the placenta in the last trimester of pregnancy. After the first year the child is fully susceptible. Without chemoprophylax is the child experiences repeated attacks of malaria, and by the age of 4 or 5 years will have acquired protective immunity, which persists as long as they remain in the endemic area. Parasites are often found in the peripheralblood of an asymptomatic child ,so that there is disease immunity without immunity to reinfection; indeed, reinfectionis necessary to maintain antigenic challenge and the immune status. The immunity declines if an individual leaves the endemic area. Maternal immunity declines during pregnancy, particularly in primiparae, with transplacental transfer of IgG. Anaemia, fever and intense parasitizationof the placenta make miscarriage, prematurelabour and low birthweight common, especially in areassuch as West Africa, where there is heavy seasonal transmission with a high risk of infection. Where transmissionis not so intense, effective immunity is not built up and all ages in the exposed population are at risk. Any individual, of any age, from a malaria-free area maycontract severe malaria. Splenectomy enhances susceptibilityto maleria to a considerable degree. Sickle cell trait haemoglobin C trait, and the heterozygous state forglucose-6-phosphate dehydrogenase (G6PD) deficiencyprotect against severe malaria. Vector Climatic factors have a profound influence on the transmission of malaria through effects on survival and reproduction of the mosquito population, and on the development of the parasite in the vector. Mosquito survive up to several months and theirlifespan is not affected by malaria parasites. Ambient temperatures in the range 20-30C, with a relative humidity of 60% or more,are ideal. In most areas of tropical Africa malaria is transmittedall year round, with upsurges of incidence with thedramatic increase of anopheline numbers during rainyseasons. In Asia transmission is seasonal with the rains.Sporogony will not occur below 16 or above 33C. Thevector species vary considerably in different localities.Anopheles gambiae is one of the most efficient vectorsbecause of its long lifespan and preference for bitinghumans rather than other animals.Additional routes for transmission of malaria are: Transplacental, which is uncommon Transfusion associated, which is uncommon in Europeand North America but common in endemic areas Syringe transmitted, among intravenous drug abusers.Mention should be made of 'airport malaria', which hasbeen documented in a range of temperate countries,including the UK and France. Malaria can occur in peoplewho have never been to an endemic area and who are notat risk as a result of transfusion, shared syringes etc. Suchcases have occurred around airports, and it is thought thatmalarious mosquitoes that have been carried on internationalflights survive in the temperate country and biteindividuals there, infecting them and causing disease.Pathogenesis and pathologyThe pathogenesis of falciparum malaria is complex andincompletely understood. The initial step is adhesion of themerozoite to the erythrocyte membrane. Glycophorin A,the major glycoprotein on erythrocyte membranes, is areceptor for binding specific surface proteins of falciparummerozoites. RBCs deficient in glycophorin A are resistantto invasion. The Duffy blood group antigen is a specificreceptor for invasion by P. vivax merozoites, and theabsence of this antigen among populations from westAfrica explains the absence of vivax infections there.Changes in the parasitized RBC result in sequestrationof RBCs containing mature falciparum trophozoites in thepostcapillary venules. 1 Parasitized cells are less flexiblethan normal cells. In addition, as the parasite matures theRBC becomes deformed and knobs develop on its surface.These knobs are an expression of a parasite-derived adhesion-promoting molecule which binds to molecules such asICAM-1, VCAM-1 and thrombospondin expressed on thevascular endothelium of the postcapillary venule. Thisadhesion phenomenon explains why mature trophozoitesand schizonts are usually absent from peripheral bloodfilms. Maximum numbers of adherent RBCs are found invenules in brain, liver, spleen, kidney and lung. The placentais heavily parasitized with chondroitin sulphate Aserving as a specific receptor for adhesion of infectedRBCs. The trophozoite matures into the schizont and atschizogony the RBC membrane bursts, releasing merozoites,malaria antigen, malaria pigment and RBC cytoplasmicconstituents.The cycle continues, progressivelybuilding up the numbers of parasitized RBCs.How these changes lead to altered consciousness in cerebralmalaria is not clear. CT of the brain in patients withcerebral malaria has not shown oedema, although amongchildren in Kenya intracranial pressure recording hasshown raised pressure. Diffuse irreversible vascularobstruction is also an unlikely cause, in view of the normalcerebral flow and complete recovery without neurologicaldeficit in most survivors. CSF lactate levels are increasedin cerebral malaria, which may indicate some degree ofanaerobic cerebral glycolysis. At the molecular level, highlevels of TNF and other cytokines are found in theblood of patients with the most severe forms of malaria,especially cerebral malaria. The extent to which thesemolecules cause severe malaria is not yet known. It isrecognized that quantitative differences in cytokine production,particularly TNF, are genetically determined, indicatingpossible inherent predisposition to severe disease.Renal damage occurs because of prerenal and renalfactors. Acute tubular necrosis is the usual effect of severemalaria on the kidney. This may occur both with andwithout severe intravascular haemolysis. Vessels in theheart are parasitized but cardiac function is well preserved.Reduced peripheral vascular resistance and dehydrationfrom sweating, vomiting and reduced fluid intake may contributeto hypotension.In cerebral malaria post mortem the brain showsswelling with smallhaemorrhages throughout the whitematter. The spleen is enlarged and has a slate-grey hueover the normal red colour. Centrilobular necrosis is seenin the liver with the accumulation of malaria pigmentin Kiipffer cells. The pulmonary venules contain largenumbers of parasitized RBCs. Pulmonary oedema of theARDS type occurs but the cause is not understood. Theplacenta is usually heavily parasitized.The anaemia of malaria has several causes, which includerupture of parasitized RBCs in schizogony; sequestrationof RBCs in tissue venules; destruction of parasitized andnon-parasitized RBCs in the reticuloendothelial system(especially the spleen); haemolysis due to the presence ofmalaria antigen, antibodies and complement on RBCs;and marrow suppression. Abnormalities of coagulation are usual, with low platelet counts due to peripheralconsumption and consumption of clotting factors.Disseminated intravascular coagulation does occur in afew patients with severe malaria but is probably not a major factor in pathogenesis in most severely ill patients. Clinical features Vivax and ovale After an incubation period of about 13 days (vivax) or18 days (ovale), prodromal symptoms begin with headache, fever, shivering without rigors, and generalaches. These last for up to 3 days before the first paroxysm of coldness, then extreme heat, then defervescence with a profuse sweat. Forty-eight hours later the full paroxysm occurs, with a feeling of extreme coldness and a rigor beginning inthe late afternoon. Headache, nausea and vomiting areusually present. The temperature is high, the pulse rapidand low in volume, and the skin is cold. This phase lasts for 45 minutes to 1 hour. When the rigor ceases, peripheral dilatation occurs; the patient feels very hot andt hirsty. The pulse is rapid and of full volume. The skin is hot and dry. This lasts about 1 hour and defervescence follows, with a profuse sweat. The symptoms settle completely and the patient will usually sleep. The following day there may be a little weakness. One day later the malaria paroxysm recurs. Daily paroxysms occur when parasite broods are undergoing schizogony on successive days. Untreated, the paroxysms continue for 6 weeks and die out spontaneously, only to recur 2-3 months later. By the time symptoms have been present for a week the spleen is usually palpable and there may be mild anaemia. Rupture of the enlarged spleen is reported in vivax malaria. incubation period is usually about 28 days. Nonspecific prodromal symptoms last for 2-3 days before the onset of the first paroxysm, which is accompanied by arigor. The periodicity of symptoms is every 72 hours. The spleen is enlarged when symptoms have been present for7-10 days. Falciparum malaria The incubation period is about 12 days, range 9-17 days. Headache, anorexia, nausea, vomiting, weakness and fever are prominent symptoms. The periodicity of symptoms is less than 48 hours, andperiodicity is an unreliable clinical feature, being present in only 30% of cases. The patient feels ill all the time, with exacerbation ofsymptoms at the time of paroxysms, which are similar to those described above but usually more severe. Convulsions occur in children. Vomiting and diarrhea are sometimes prominent features in the history. Herpes simplex vesicles may appear on the lips during the illness. Complications Complicated malaria occurs in falciparum infections. Altered consciousness in the presence of falciparum malaria must be taken as a clinical indication of cerebral malaria. Neck rigidity is not a feature, although mild neck stiffness may be present. Raised intracranial pressure is not seen and focal neurological signs are uncommon. Generalized convulsions occur in children and adults. Hypoglycaemia occurs in children, pregnant women with severe malaria and, less often, in adults with severe infection. Jaundice may be a prominent physical sign in some patients with severe malaria. Haemolysis can cause this, but tender hepatomegaly and abnormalities of liver function suggest liver involvement. Some degree of uraemia is common, but this resolves after treatment. Uraemia with oliguria indicates renal involvement. Pulmonary oedema can result from over hydration, but can also occur in the patient whose infection is coming under control. Blackwater fever, due to acute massive intravascular haemolysis, became less common after chloroquine replaced quinine for prophylaxis and treatment of malaria, suggesting that quinine itself contributed to pathogenesis. It does, however, occur in people who have not taken quinine. The urine is black, the haemoglobinfalls rapidly and jaundice appears. Hypotension and tachycardia are usual, and renal failure may follow. Gram-negative septicaemia has been reported in patients with severe malaria and may be responsible for hypotension.
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