MALARIA

INTRODUCTION Malaria – ‘mal’ ‘aria’ = bad air

Malaria in humans - caused by Plasmodium falciparum, P. vivax, P. ovale, P. malariae

Transmitted by the bite of female anopheles mosquitoes

The most important of the parasitic diseases of humans, it is transmitted in 108 countries containing 3 billion people and causes nearly 1 million deaths each year.

Worldwide distribution

LIFE CYCLE

P. falciparum has influenced human evolution,

with the appearance of protective mutations such as Sickle-cell anemia Thalassaemia G6PD deficiency

P. falciparum does not grow well in red cells that contain haemoglobin F, C or S. these patients are protected against the lethal complications of malaria.

P. vivax cannot enter red cells that lack the Duffy blood group therefore many West Africans and African-Americans are protected

CLINICAL FEATURES

Features of severe malaria

Chronic complications of malaria1. Tropical Splenomegaly (Hyperreactive Malarial

Splenomegaly)o Chronic or repeated malarial infections – splenomegalyo An abnormal immunologic response to repeated infections

characterized by massive splenomegaly, hepatomegaly, marked elevations in serum IgM and malarial antibody, hepatic sinusoidal lymphocytosis

2. Quartan Malarial Nephropathyo Chronic or repeated infections with P. malariae may cause soluble

immune-complex injury to the renal glomeruli, resulting in the nephrotic syndrome.

3. Burkitt's Lymphoma and Epstein-Barr Virus Infectiono Malaria-related immune dysregulation provokes infection with

lymphoma viruses

DIAGNOSIS AND LAB FINDINGS In the thick film, erythrocytes are lysed, releasing all

blood stages of the parasite. This, and the fact that more blood is used in thick films, facilitates the diagnosis of low-level parasitaemia.

A thin film is essential to confirm the diagnosis, to identify the species of parasite and, in P. falciparum infections, to quantify the parasite load

Immunochromatographic tests for malaria antigens – most sensitive in diagnosing falciparum sp.

Normochromic, normocytic anemia is usual

Reactive lymphocytosis and eosinophilia in the weeks after the acute infection can be seen

Severe infections - prolonged PT and aPTT and by severe thrombocytopenia

TREATMENT (Indian recommendations)

1. P. falciparum – sensitive to chloroquine A chloroquine dose of 600 mg base (= 1,000 mg salt) should

be given initially, followed by 300 mg base (= 500 mg salt) at 6, 24, and 48 hours after the initial dose for a total chloroquine dose of 1,500 mg base (=2,500 mg salt).

2. P. falciparum – resistant to chloroquine Artesunate (4 mg/kg body weight) daily for 3 days and

sulfadoxine (25 mg/kg body weight) + pyrimethamine (1.25 mg/kg body weight) on Day 0

This is to be accompanied by single dose primaquine (0.75 mg/kg body weight) on Day 2.

3. P vivax or P. ovale Chloroquine in full therapeutic dose of 25 mg/kg divided over

three days Primaquine 0.25 mg/kg body weight daily for 14 days (for

clearing the hypnozoites) – Should not be given in severely G6PD deficient patients

4. Treatment of severe malaria Artesunate: 2.4 mg/kg body weight i.v. or i.m. given on

admission (time=0), then at 12 hours and 24 hours, then once a day

OR Quinine: 20 mg quinine salt/kg body weight on admission (i.v.

infusion in 5% dextrose/dextrose saline over a period of 4 hours) followed by maintenance dose of 10 mg/kg body weight 8 hourly;

Infusion rate should not exceed 5 mg/kg body weight per hour.

Loading dose of 20 mg/kg body eight should not be given, if the patient has already received quinine.

CHEMOPROPHYLAXIS

1. Short term (<6 weeks) Doxycycline: 100 mg daily. The drug should be started 2 days before travel and

continued for 4 weeks after leaving the malarious area

2. Long term (>6 weeks) Mefloquine: 5 mg/kg body weight (up to 250 mg) weekly and

should be administered two weeks before, during and four weeks after leaving the area.