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 istransmitted in 108 countries containing 3 billion people andcauses nearly 1 million deaths each year.Worldwide distribution
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 orS. these patients are protected against the lethal complications of malaria. P. vivax cannot enter red cells that lack the Duffy blood group therefore manyWest Africans and African-Americans are protected
1. Tropical Splenomegaly (Hyperreactive Malarial Splenomegaly)o Chronic or repeated malarial infections – splenomegalyo An abnormal immunologic response to repeated infections characterizedby massive splenomegaly, hepatomegaly, marked elevations in serum IgMand malarial antibody, hepatic sinusoidal lymphocytosis2. Quartan Malarial Nephropathyo Chronic or repeated infections with P. malariae may cause solubleimmune-complex injury to the renal glomeruli, resulting in the nephroticsyndrome.3. Burkitts Lymphoma and Epstein-Barr Virus Infectiono Malaria-related immune dysregulation provokes infection with lymphomaviruses
In the thick film, erythrocytes are lysed, releasing all blood stagesof the parasite. This, and the fact that more blood is used in thickfilms, facilitates the diagnosis of low-level parasitaemia. A thin film is essential to confirm the diagnosis, to identify thespecies of parasite and, in P. falciparum infections, to quantify theparasite load Immunochromatographic tests for malaria antigens – mostsensitive in diagnosing falciparum sp. Normochromic, normocytic anemia is usual Reactive lymphocytosis and eosinophilia in the weeks after theacute infection can be seen Severe infections - prolonged PT and aPTT and by severethrombocytopenia
1. P. falciparum – sensitive to chloroquine A chloroquine dose of 600 mg base (= 1,000 mg salt) should be giveninitially, followed by 300 mg base (= 500 mg salt) at 6, 24, and 48hours after the initial dose for a total chloroquine dose of 1,500 mgbase (=2,500 mg salt).2. P. falciparum – resistant to chloroquine Artesunate (4 mg/kg body weight) daily for 3 days and sulfadoxine (25mg/kg body weight) + pyrimethamine (1.25 mg/kg body weight) onDay 0 This is to be accompanied by single dose primaquine (0.75 mg/kgbody weight) on Day 2.
3. P vivax or P. ovale Chloroquine in full therapeutic dose of 25 mg/kg divided over threedays Primaquine 0.25 mg/kg body weight daily for 14 days (for clearing thehypnozoites) – Should not be given in severely G6PD deficientpatients4. 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 dayOR Quinine: 20 mg quinine salt/kg body weight on admission (i.v. infusionin 5% dextrose/dextrose saline over a period of 4 hours) followed bymaintenance 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 thepatient has already received quinine.
1. Short term (<6 weeks) Doxycycline: 100 mg daily. The drug should be started 2 days before travel and continued for 4weeks after leaving the malarious area2. Long term (>6 weeks) Mefloquine: 5 mg/kg body weight (up to 250 mg) weekly and shouldbe administered two weeks before, during and four weeks afterleaving the area.