Treatment of malaria

Diagnostics and severity assessment

The basis of malaria diagnostics is proper microscopic examination of the blood. To accurately identify the Plasmodium species, thin blood smear microscopy (Romanowsky-Giemsa staining) is necessary, as this method clearly stains the erythrocyte membrane and cytoplasm. The "thick drop" preparation is used exclusively for rapidly finding the malaria parasite, but determining the specific species from it is impossible.

The severity of the condition directly correlates with the level of parasitemia. A criterion for an extremely unfavorable prognosis and the development of malignant falciparum malaria caused by Plasmodium falciparum is a level of 100,000 parasites or more per 1 µL of blood (which corresponds to an infection of more than 5% of all erythrocytes).

During the patient examination, a repeat complete blood count (CBC) with reticulocytes and platelets, a biochemical blood test (bilirubin, AST, ALT, creatinine, urea, ALP), and a urinalysis must be ordered. It is important to perform differential diagnosis with viral hepatitis, as malaria is frequently complicated by hemolytic jaundice.

Clinical and laboratory features

Different Plasmodium species produce specific clinical presentations, which directly affect management tactics:

• Malaria caused by Plasmodium vivax: Characterized by an acute onset and marked intoxication. Initial fever lasts the first 6 days without a clear periodicity, after which typical malarial paroxysms (chills, fever, sweats) become established, repeating every other day. Hepatosplenomegaly develops. The CBC shows a normal or decreased leukocyte count, and by the end of the 2nd–3rd week of the illness, anemia (decreased hemoglobin) develops.
• Malaria caused by Plasmodium falciparum: Prone to a severe course with the development of life-threatening complications.
• Malaria caused by Plasmodium malariae: Can remain latent for a long time (parasites may not be detected for years after leaving an endemic focus) and lead to severe kidney damage, up to chronic glomerulonephritis with marked proteinuria and anasarca.

The development of hemolytic jaundice in malaria is confirmed laboratory-wise: predominantly unconjugated bilirubin rises in the blood, hemoglobin drops, erythrocytes (anisocytosis and poikilocytosis appear), color index and serum iron fall. Urinary urobilin levels are significantly elevated.

Vivax malaria treatment regimen

Treatment of infection caused by Plasmodium vivax proceeds in two mandatory stages. If the patient takes only suppressive drugs and ignores the second stage, relapses will inevitably occur.

1. Suppressive therapy: Aims to eliminate erythrocytic forms. The drug of choice is chloroquine (Delagil).
2. Day 1: 1.0 g, followed by another 0.5 g 6 hours later.
3. Days 2 and 3: 0.5 g daily.

1. Radical therapy: Prescribed strictly after an effective course of suppressive therapy to eradicate dormant tissue forms. Primaquine is used.
2. Dosage: 45 mg (27 mg base) per day, which is equivalent to 3 tablets.
3. Course: 14 days.

Severe Plasmodium falciparum therapy

Patients with severe Plasmodium falciparum infection are subject to immediate hospitalization strictly in an intensive care unit (ICU). Severe cases are accompanied by complications such as cerebral malaria (with the development of stage I encephalopathy, confusion, disorientation, and severe lethargy), acute renal injury (marked decrease in urine output), and hemolytic jaundice.

Aetiotropic therapy is carried out in two stages:

1. Stage I (until the resolution of the critical condition): Quinine dihydrochloride is administered intravenously slowly (no more than 20 drops per minute). The dose is 10-20 mg/kg (maximum up to 2.0 g per day). The drug must be diluted in 500 ml of a 5% glucose solution and administered 2-3 times a day.
2. Stage II (after haemodynamic stabilisation): Switching to oral forms is carried out. Mefloquine is frequently used according to the regimen: 0.5 g three times within one day.

Pathogenetic and symptomatic therapy plays a crucial role in the ICU and includes detoxicating therapy, correction of hypoglycaemia (characteristic of severe malaria and quinine treatment), oxygen therapy, administration of glucocorticoids (e.g. dexamethasone) and diuretics (Lasix, osmotic diuretics) to prevent cerebral oedema and manage acute kidney injury. Continuous monitoring of the blood acid-base balance is also essential.

Chemoprophylaxis

The approach to malaria prophylaxis has changed significantly in recent years. The traditional drug Delagil (chloroquine) is currently recognised as ineffective for the prophylaxis of Plasmodium falciparum infection. This is due to the universal spread of resistant strains of the pathogen.

The drug of choice for non-immune individuals travelling to high-endemic regions is mefloquine.

Class and exam questions

What else to study on this topic

• Mechanism of development of malarial encephalopathy and coma
• Acute kidney injury in malaria: pathogenesis and criteria
• Features of nephrotic syndrome in Plasmodium malariae infection
• Differential diagnosis of malaria and viral hepatitis

Other topics in the "Vector-borne infections" section

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