Define Malaria. Describe its clinical features, investigations, management and prognosis.

Definition

• Malaria is a protozoal infection caused by Plasmodium species (P.
• Falciparum, P.
• Vivax, ovale, malariae, knowlesi), transmitted by the bite of the female Anopheles mosquito.
• P.
• Falciparum causes the most severe disease.

Life Cycle (in Brief)

Mosquito injects sporozoites → Liver (exo-erythrocytic) stage — vivax/ovale form dormant hypnozoites → Release into blood → RBC (erythrocytic) cycle → RBC rupture → fever paroxysm + release of merozoites → Gametocytes taken up by mosquito

Hypnozoites of vivax/ovale cause later relapses — hence the need for anti-relapse therapy.

Clinical Features

• Uncomplicated malaria — classical paroxysm of cold stage → hot stage → sweating stage, with periodicity (tertian/quartan), plus anaemia and splenomegaly.
• Severe (mostly falciparum) malaria — cerebral malaria (coma, seizures), severe anaemia, hypoglycaemia, acute kidney injury (blackwater fever), respiratory distress/ARDS, shock, metabolic acidosis and DIC.

Investigations

• Peripheral blood smear (thick and thin) — the gold standard; identifies species and parasite density.
• Rapid diagnostic test (RDT) — detects parasite antigen (HRP-2, pLDH).
• Supportive tests — blood glucose, haemoglobin, renal function (to detect severe disease).

Management

• Uncomplicated P. Falciparum — Artemisinin-based Combination Therapy (act) (in India, artesunate + sulfadoxine-pyrimethamine) plus a single dose of primaquine (gametocidal).
• P. Vivax — chloroquine (3 days) plus primaquine × 14 days for radical cure of hypnozoites (check G6PD status first).
• Severe malaria — IV artesunate is the drug of choice; manage complications (hypoglycaemia, seizures, anaemia, fluids).

Plasmodium Species (comparison)

Cerebral Malaria

• A severe falciparum complication — impaired consciousness/coma and seizures with sequestration in cerebral microvasculature.
• Manage the airway, treat seizures and hypoglycaemia, give IV artesunate, and provide intensive supportive care; it carries significant mortality and a risk of neurological sequelae.

Monitoring

• Serial parasitaemia, blood glucose, haemoglobin and urine output.
• Reassess for evolving danger signs — malaria can deteriorate quickly.

Epidemiology

• A major cause of febrile illness in endemic areas; P. Vivax predominates in much of India, P. Falciparum causes most severe disease/deaths.
• Transmission by the female Anopheles mosquito, mainly at dusk/dawn.

Congenital & Transfusion Malaria

Malaria can rarely be transmitted transplacentally (congenital malaria — fever, anaemia, splenomegaly in a neonate) or through blood transfusion; consider it in at-risk neonates.

Prognosis

Uncomplicated malaria treated promptly recovers fully; severe falciparum malaria is a medical emergency with appreciable mortality, so early recognition, IV artesunate and management of complications are essential.

Complications (severe Falciparum)

• Cerebral malaria, severe anaemia, hypoglycaemia, renal failure, ARDS, shock, acidosis, DIC.
• High mortality if untreated — severe malaria is a medical emergency.

Prevention

• Vector control — insecticide-treated bed nets (LLINs), indoor residual spraying, source reduction.
• Chemoprophylaxis for travellers; early diagnosis and prompt treatment; malaria vaccines (RTS,S/R21) in endemic Africa.

WHY Falciparum Is the One That Kills

• The single most important distinction in malaria is understanding why Plasmodium falciparum is lethal while the other species are not.
• Two properties set it apart.
• First, it invades red cells of all ages — whereas P.
• Vivax invades only young reticulocytes and P.
• Malariae only old cells.
• So falciparum can achieve an enormously high parasitaemia (over 5–10%), producing severe anaemia and a massive parasite burden.
• Second — and this is what kills — falciparum-infected red cells express adhesive knobs (PfEMP-1) on their surface, which make them stick to the endothelium of capillaries and venules ('cytoadherence'), and to each other and to uninfected cells ('rosetting').
• The infected cells are therefore sequestered in the microvasculature of the vital organs — and there they obstruct the microcirculation.
• In the brain this causes cerebral malaria (coma, seizures); in the kidney, acute kidney injury; in the lung, ARDS; and everywhere it causes tissue hypoxia with a profound lactic acidosis and hypoglycaemia.
• Understanding sequestration explains why the peripheral parasite count may underestimate the true burden.

WHY the Child Must Be Treated for the Hypoglycaemia and Acidosis Too

• A crucial practical lesson is understanding why killing the parasite is not enough — and why children with severe malaria die of things that an antimalarial cannot fix.
• Artesunate kills parasites brilliantly and rapidly, and it has been shown to reduce mortality.
• But the child is dying of the metabolic consequences of sequestration, which take time to resolve even after the parasites are cleared.
• Three, in particular, must be actively treated.
• Hypoglycaemia is very common in children with severe malaria — caused by the parasite's consumption of glucose, impaired gluconeogenesis, and (in the past) quinine-induced hyperinsulinaemia.
• It causes coma and seizures, it is easily mistaken for cerebral malaria, and it is instantly reversible — so the glucose must BE checked repeatedly.
• Metabolic (lactic) acidosis — manifest as deep, laboured breathing — is the single strongest predictor of death, and it must be corrected by restoring perfusion.
• And severe anaemia (from haemolysis) may require urgent transfusion.
• Meanwhile, over-aggressive fluid resuscitation is harmful (it causes pulmonary oedema).