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 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
 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
1. Tropical Splenomegaly (Hyperreactive Malarial Splenomegaly)
o Chronic or repeated malarial infections – splenomegaly
o 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 Nephropathy
o 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 Infection
o Malaria-related immune dysregulation provokes infection with lymphoma
viruses
 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
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.
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.

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Malaria

  • 1.
  • 2.  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
  • 3.
  • 4.  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
  • 5.
  • 6.
  • 7. 1. Tropical Splenomegaly (Hyperreactive Malarial Splenomegaly) o Chronic or repeated malarial infections – splenomegaly o 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 Nephropathy o 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 Infection o Malaria-related immune dysregulation provokes infection with lymphoma viruses
  • 8.  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
  • 9. 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.
  • 10. 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.
  • 11. 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.