Causes of malaria in human Plasmodium falciparum Plasmodium vivax Plasmodium malariae Plasmodium ovale

Transmission 1. It is transmitted by the bite of female anopheline mosquitoes and occurs throughout the tropics and subtropics. 2. Blood transmission and by injection. 3. trans-placenta

Clinical picture of P. vivax and P. ovale infection P. vivax and P. ovale infection In many cases the illness starts with several days of continued fever before the development of classical bouts of fever on alternate days. Fever starts with a rigor. The patient feels cold and the temperature rises to about 40°C. After half an hour to an hour the hot or flush phase begins. It lasts several hours and gives way to profuse perspiration and a gradual fall in temperature..

The cycle is repeated 48 hours later The cycle is repeated 48 hours later. Gradually the spleen and liver enlarge and may become tender. Anaemia develops slowly. Herpes simplex is common. Relapses are frequent in the first 2 years after leaving the malarious area. The first attack of clinical malaria may occur long after the patient has left the endemic area, and the disease may relapse after treatment with drugs that kill only the erythrocytic stage of the parasite.

Clinical picture of P. malariae infection This is usually associated with mild symptoms and bouts of fever every third day. Parasitaemia may persist for many years with the occasiolnal recrudescence of fever, or without producing any symptoms. P. malariae causes glomerulonephritis and the nephrotic syndrome in children.

Clinical picture of F. Malaria This is the most dangerous of the malarias. The onset is often insidious, with malaise, headache and vomiting, and is often mistaken for influenza. Cough and mild diarrhoea are also common. The fever has no particular pattern. Jaundice is common due to haemolysis and hepatic dysfunction. The liver and spleen enlarge and become tender. Anaemia develops rapidly.

A patient with falciparum malaria, apparently not seriously ill, may develop dangerous complications . Cerebral malaria is the most grave complication and is manifested by either confusion or coma, usually without localising signs. Children die rapidly without any special symptoms other than fever. Immunity is impaired in pregnancy, and abortion from parasitisation of the maternal side of the placenta is frequent. Splenectomy increases the risk of severe malaria.

COMPLICATIONS OF FALCIPARUM MALARIA Coma (cerebral malaria) Hyperpyrexia 3. Convulsions 4. Hypoglycaemia 5. Severe anaemia 6. Acute pulmonary oedema 7. Acute renal failure 8. Spontaneous bleeding and coagulopathy

9. Metabolic acidosis 10. Shock ('algid malaria') 11. Aspiration pneumonia 12. Hyperparasitaemia (e.g. > 10% of circulating erythrocytes parasitised in non-immune patient with severe disease)

Diagnosis 1. Thick and thin blood films should be taken whenever malaria is suspected. Thick film: A. all blood stages of the parasite. B. more blood is used in thick films, Both help in the diagnosis of low-level parasitaemias. 2. thin film: A. is essential to confirm the diagnosis, B. to identify the species of parasite and, C. in P. falciparum infections, to quantify the parasite load (by counting the percentage of infected erythrocytes).

In P. falciparum parasites may be very scanty, especially in patients who have been partially treated. With P. falciparum, only ring forms are normally seen in the early stages. With the other species all stages of the erythrocytic cycle may be found. Gametocytes appear after about 2 weeks. They persist after treatment and are harmless, but are the source for infecting mosquitoes.

2. Immunochromatographic 'dipstick' tests for P 2. Immunochromatographic 'dipstick' tests for P. falciparum antigen are now marketed and provide a useful non-microscopic means of diagnosing this infection. They should be used in parallel with blood film examination but are about 100 times less sensitive than a carefully examined blood film.

Treatment of P. vivax, P. ovale and P. malariae P. vivax, P. ovale and P. malariae infections should be treated with chloroquine: 600 mg chloroquine base followed by 300 mg base in 6 hours, then 150 mg base 12-hourly for 2 more days.

P. falciparum is now resistant to chloroquine almost world-wide, so quinine is the drug of choice. Quinine dihydrochloride or sulphate 600 mg salt (10 mg/kg) 8-hourly by mouth is given until the patient is clinically better and the blood is free of parasites (usually 3-5 days). The dose should be reduced to 12-hourly intervals if quinine toxicity develops. This regimen should be followed by a single dose of sulfadoxine 1.5 g combined with pyrimethamine 75 mg, i.e. 3 tablets of Fansidar. In pregnancy a 7-day course of quinine alone should be given.

If sulphonamide sensitivity is suspected, quinine may be followed by doxycycline 100 mg daily for 7 days.. Mefloquine: Also may be used but may cause neuropsychiatric side-effects.

New treatment

New treatment for resistant P. falciparum malaria

Radical cure of malaria due to P. vivax and P. ovale Relapses can be prevented by taking one of the antimalarial drugs in suppressive doses. Radical cure is achieved in most patients with a course of primaquine (15 mg daily for 14 days), which destroys the hypnozoite phase in the liver. Haemolysis may develop in those who are glucose-6-phosphate dehydrogenase (G6PD)-deficient. Cyanosis due to the formation of methaemoglobin in the red cells is more common but not dangerous.

Prevention 1. Avoiding mosquito bites: A. Long sleeves and trousers B. Repellent creams and sprays C. Screened windows D. the use of a mosquito net

2. Chemoprophylaxis A. Clinical attacks of malaria may be preventable with drugs such as proguanil 1 – 2 tabletes daily.which attack the pre-erythrocytic form, B. and also by drugs such as chloroquine (4-aminoquinolones) 2 tabletes weekly after the parasite has entered the erythrocyte ('suppression') Start 1 W before entering and 4 Ws after leaving the endemic area.