Malaria -cause, clinical features, treatment and prevention
Malaria is an infectious disease caused by a parasite called Plasmodium. The disease is estimated to kill approximately one million children worldwide. Four species of the parasite are commonly known to affect man-Plasmodium vivax, P. malariae, P. ovale and P. falciparum. Of the four species, infection with P. vivax is the most common and infection with P. falciparum is the most serious and potentially fatal. The parasite is transmitted from one person to another by the bite of female anapheline mosquito. The organism has a complicated life cycle involving two hosts-insect (mosquito) and man. The gematocytes ingested from an affected person form sporozoites in the mosquito. When injected into another person these sporozoites invade the liver cells (hepatocytes). This phase is known as the pre-erythrocytic phase or hepatic phase. This phase lasts for about 1-2 weeks except for P. malariae in which case it may last for 3-5weeks.
In the liver cells the parasite develops into a schizont containing many merozoits. These merozoits are released into the circulation. These invade the red blood cells. Inside the red blood cells the merozoits develop into trophozoits. The trophozoits mature into schizonts which rupture releasing more merozoites into the blood which invade other red blood cells. The red blood cells are destroyed during the process.
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Some trophozotes develop into male and female gematocytes which are ingested by the mosquitoes. Inside the body of the mosquitoes the gematocytes unite to form zygotes. The zygotes develop into oocysts in the intestine of the mosquitoes. The oocysts grow and ultimately rupture releasing sporozoites which reach the salivary glands of the mosquitoes. When an infected mosquito bites a human being the sporozoites are transmitted and the cycle goes on. Infection may also be acquired congenitally from a pregnant woman to the developing baby and by transfusion of blood from an infected person.
Clinical features: Symptoms may vary depending on the species and the status of the immune system of the affected person. Those devoid of spleen may develop serious disease. Recurrent infections lead to some natural immunity in children who are immune competent. This is species specific. Infants usually present with recurrent attacks of fever, vomiting, jaundice enlargement of spleen, irritability and poor feeding. Older children may complain of headache, backache, pain in muscles, chills and fatigue. Fever may be cyclic occurring every 48 or 72 hours or irregular. The child may appear normal in between the attacks of fever.
Infection of a pregnant woman may result in intrauterine growth retardation or premature delivery. Laboratory findings: The diagnosis can be confirmed by demonstrating the parasite in a smear of blood. Both thin and thick smear are examined to increase the chance of detecting the parasite. Usually one species is involved but occasionally infection with more than one species can occur. Recognition of the species requires some experience.
A rough estimate of the parasitemia (the number of parasites in the blood) can be made by noting the percentage of red blood cells affected. Involvement of more than 10% of red blood cells is associated with increased morbidity and mortality, especially in falciparum malaria. Response to treatment can also be assessed by daily examining the blood smear. If the number of parasites remains same or increases 48 hours after starting treatment it indicates resistance to the drugs. Complications: Falcipatum malaria can cause serious and even fatal complications. These complications are due to obstruction to blood flow at the level of capillaries leading to reduced blood flow to organs (Ischemia).
Impairment of consciousness, coma or convulsion, damage to kidneys, severe bleeding and shock can occur. Hypoglycemia (reduction in blood glucose level) is another complication. Treatment of malaria: Those who appear sick or are not able to take oral medication should be admitted, especially if the infection is due to falciparum. Those with mild disease can be treated as out patients. The specific drug of first choice is chloroquin unless infection in that area is known to be due to chloroquin resistant species.
It is given in a dose of 10 mg / kg of chloroquin once followed by 5mg / kg after 6 hours. Two more doses of 5mg/kg are given after 24 and 48 hours. Supportive treatment is given for fever. Adequate hydration should be maintained by giving plenty of liquids. Frequent feeding is recommended to prevent hypoglycemia. Those who are not able to take oral medication should be treated with intravenous chloroquin or quindine. These patients need to be monitored for cardiac arrhythmias when these drugs are given intravenously. Later treatment can be completed with oral medication. For chloroquin resistant P. falciparum oral treatment consists of quinine plus pyrimethamine sulfadoxine or clindamycin. Drugs which can be used for older children (above 8 years) instead of pyrimethamine –sulfadoxine are tetracycline or doxycycline.
Pyrimethamine –sulfadoxine combination can cause bone marrow depression leading to severe anemia, decreased white blood cells (leucopenia) and decrease in number of platelets (thrombocytopenia). Tetracycline and doxycycline can cause permanent discoloration of teeth and affect growth if given to children below 8 years. Other effective drugs are mefloquin, halofantrine or the combination of atovaquone plus proguanil. Newer drugs like artemether and artesunate are very effective but experience with children is limited. Relapse is common with p. vivax and p. ovale and can be prevented by giving primaquine 0.3/kg/day up to 15 mg for 14 days.
Page last reviewed on 18th May 2010
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