Malaria

Introduction

The subcontinent, malaria is still continuing as a life-threatening illness, if not recognized early and correct treatment is instituted. Human malaria is caused by:

• Plasmodium falciparum
• Plasmodium vivax
• Plasmodium ovale
• Plasmodium malariae

Clinical Presentation

Intermittent fever on alternate days following an initial period of continuous fever in the case of Pl.vivax and Pl.malariae. Fever may go up to 40o C and usually starts with rigor. After half to one hour, the hot or flush phase begins. It lasts for several hours and gives way to profuse perspiration and gradual fall in temperature. The fever can be of any pattern in falciparum malaria.

• Hepatosplenomegaly
• Anaemia Pl. malariae
• Mild symptoms
• Fever occurs on every 3rd day
• Produces AGN and nephrotic syndrome in children (not commonly seen). Pl. falciparum
• More dangerous
• Malaise, headache and vomiting
• Cough with mild diarrhoea can occur
• No specific pattern for fever and it is not very high. The cold, hot and sweating stages are seldom found
• Jaundice is common due to hepatocellular dysfunction and haemolysis
• Hepatosplenomegaly
• Anaemia due to intravascular haemolysis
• An apparently not seriously ill patient may develop serious complications like cerebral malaria or ARDS
• Pl. falciparum do not multiply in RBC containing haemoglobin, F, C or S. HbS heterozygotes are well protected against the lethal complications. Splenectomised individuals are more susceptible.

Diagnosis

Malaria should be considered in any febrile patient who has recently left an endemic area for malaria or is residing in such area.

​2. Peripheral blood smear (both thick and thin) taken just one hour before the paroxysm may demonstrate the parasite.

​3. Falciparum: parasites are usually scanty in peripheral blood due to the cytoadherence and visceral localization, especially in partially treated patients and patients with cerebral malaria.

• Remember malaria can coexist with other diseases. Hence, exclude: — purulent meningitis — typhoid fever — viral hepatitis — other fevers with hepatosplenomegaly

Treatment

In chloroquine sensitive cases (Pl. vivax)

• Chloroquine base 600 mg (4 tab) stat and followed by 300 mg base (2 tab) after 6 hr
• Then 150 mg base (1 tab) BD × 3 days Total: 12 tablets
• In falciparum malaria (usually chloroquin resistant)
• Quinine dihydrochloride or sulphate 600 mg (10 mg/ kg) thrice daily for 5-7 days PO or as IV infusion in 5% dextrose (or in N saline, if the person is diabetic).
• If quinine toxicity occurs, the dose is reduced to twice daily. Reduce the dose to half in the presence of renal failure
• If quinine is not available or not tolerated

1. Amodiaquine may be used in the same dosage as chloroquine
2. Mefloquine also can be used
3. Quinidine also can be used in the same dosage orally or as slow infusion as Quinine—cardiac toxicity should be looked for when using Quinidine. If not sensitive to sulphonamide, Quinine treatment is followed by the administration of 3 tablets of FANSIDAR as a single dose One tab of FANSIDAR = Sulphadoxine 500 mg + = Pyrimethamine 25 mg If the individual is sensitive to sulphonamide: Quinine is followed by Tetracycline 250 mg Q6h × 7 days or Doxycycline 100 mg BD × 7 days

• Radical cure of malaria due to Pl.vivax and Pl.ovale
• Primaquine 15 mg /day × 14 days
• Primaquine destroys the hypnozoite phase of the parasite in the liver Note: Exclude G6PD deficiency before starting Primaquine, which may precipitate haemolysis in G6PD deficient patients.