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in Cure & Care

Malaria Diary

25

Malaria is a disease that has persisted in India for centuries, so much so that even Ancient Indian medical literature like the Charaka Samhita addressed it.

  • In the 1930s, people from every walk of life were afflicted by malaria.
  • In 1935, the economic loss caused because of the loss of working days due to malaria, was estimated to be a staggering Rs. 10,000 million per year. Then, the annual incidence of malaria was around 75 million cases, with 0.8 million people paying for it with their lives.
  • Thus came in the National Malaria Control Programme, in April 1953. The programme was successful indeed – within five years, the malaria cases dropped significantly to two million.
  • Encouraged by this, the Government of India enlarged the scope of the combat, ushering in the National Malaria Eradication Programme of 1958.
  • By 1961 the incidences dropped to a thankful 50,000 cases a year.
  • But since then the programme suffered repeated setbacks due to technical, operational and administrative reasons. There was a rise in the number of cases.

Malaria has now staged a dramatic comeback in India after its near eradication in the early and mid sixties.

What Causes Malaria?

Four species of the plasmodium parasite can infect humans; the most serious forms of the disease being caused by Plasmodium falciparum. The types of malaria caused by Plasmodium vivax, Plasmodium ovale and Plasmodium malariae are generally not fatal.

The natural ecology of malaria involves malaria parasites infecting successively two types of hosts: humans and female anopheles mosquitoes.

In humans, the parasites grow and multiply first in the liver cells and then in the Red Blood Cells (RBCs) of the blood. In the blood, successive broods of parasites grow inside the RBCs and destroy them, releasing daughter parasites (merozoites) that continue the cycle by invading other RBCs.

Drained of Blood

Anaemia is caused when RBCs are destroyed by the parasite, and is a common manifestation of all types of malaria.

  • It is more common and poses more problems for pregnant women and for children.
  • In developing countries of the tropics, pre-existing anaemia, most commonly due to malnutrition and helminthiasis (parasitic infection in children), compounds the problem.
  • In falciparum malaria, one of the deadliest forms, which is becoming increasingly resistant to anti-malarial drugs, anaemia can develop rapidly due to acute haemolysis.
  • The degree of anaemia correlates with parasitemia, a condition in which parasites are present in the blood.
  • It is also associated with high serum bilirubin (the bile pigment in the red blood cells), and creatinine (a component in our blood dependent on muscle mass which is flushed out by the kidneys) levels.
  • Pregnancy, secondary bacterial infections and bleeding disorders like disseminated intravascular coagulation can aggravate the anaemia.
  • Children may have severe anaemia even with low parasitemia and in such cases the reticuloendothelial cells (the immune system) exhibit abundant malarial pigments.
  • Thus, anaemia in malaria is multi- factorial. The causes include obligatory destruction of RBCs at merogony (asexual division of parasites), accelerated destruction of non-parasitised RBCs, bone marrow dysfunction that can persist for weeks, shortened RBCs survival and increased clearance from the spleen.
  • Massive gastrointestinal haemorrhage can also contribute to the anaemia of malaria.

Repercussions

  • Treatment with antimalarials, especially Chloroquine may lead to nausea and vomiting.
  • Some patients have gastrointestinal haemorrhage and may vomit blood (haematemesis).
  • Enlargement of the liver and spleen can also occur, which can be deduced through examination.
  • Jaundice is common in falciparum malaria. Most often it is caused by haemolysis (rupturing of RBCs, releasing the haemoglobin into the surrounding) and accordingly, there is elevation of the unconjugated bilirubin levels.

However, liver dysfunction may also be seen in cases of severe falciparum malaria. Such patients have:

  • Conjugated hyperbilirubinemia.
  • Marked elevations of enzymes like aspartate aminotransferase and alanine aminotransferase and prolongation of prothrombin.
  • Massive haemolysis.
  • Disseminated intravascular coagulation.

Occasionally malaria patients become comatose due to cerebral malaria and with a setting of jaundice, may mimic viral hepatitis with fulminant hepatic failure (the severe impairment of liver functions in the absence of pre-existing liver disease). The enlarged spleen may rupture, presenting as severe abdominal pain, requiring emergency surgery.

It Can Be Treated

These findings alone do not imply severe liver dysfunction in malaria. Clinical signs of liver failure are never due to malaria and in such cases, other associated hepatic diseases, like viral hepatitis, should be considered. The mild elevation in serum bilirubin and enzyme levels usually return to normal within three to five days of effective antimalarial treatment. No other specific treatment is needed.

To sum it up, malaria can present the gastroenterologist with multiple challenges of anaemia, jaundice, enlarged liver and spleen – at times even as an emergency, i.e, in cases of encephalopathy (a brain disease) and rupture of the spleen. It is necessary to identify the exact condition, as malaria can be completely treated.

 

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