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Infectious Diseases · Vector-Borne Infections

Malaria

Malaria

Malaria is a severe infectious disease caused by parasites of the genus Plasmodium. It is characterized by cyclical fever attacks, hepatosplenomegaly, and the development of hemolytic anemia.

EpidemiologyInfection frequently occurs in endemic regions (Africa, Indonesia).
PathogenesisThe causative agent undergoes hepatic and erythrocytic schizogony stages.
DiagnosticsThe gold standard is microscopy of thick and thin blood films.
ComplicationsHigh risk of severe forms when infected with Plasmodium falciparum.
3 min readFor medical studentsUpdated 10.10.2026
Material prepared by WhiteCoat Pro editorial team based on platform study guidesPending instructor review

Clinical Presentation: From Initial Fever to Paroxysms

The disease often begins acutely. In the first days (up to a week), non-immune individuals may experience initial fever—temperature remains constantly at 38–40.5 °C, accompanied by chills and sweating. This is followed by the development of a typical malarial paroxysm, which recurs with strict periodicity (e.g., strictly every other day in Plasmodium vivax infection).

The attack typically starts in the morning hours, lasts from 30 minutes to an hour, and includes three consecutive phases:

  • Severe chills.
  • Fever (temperature rise to 39–40 °C, severe headache).
  • Profuse sweating, leading to a drop in temperature by evening (8–10 hours after the onset of the attack).

During the interparoxysmal period, body temperature normalizes, but the patient retains pronounced weakness (asthenic syndrome). Taking regular antipyretics during the attack generally has no effect.

Pathogenesis: How the Parasite Affects the Body

The development of the malarial parasite in the human body goes through several stages. First, tissue (hepatic) schizogony occurs, followed by erythrocytic schizogony and gametocytogenesis.

Massive erythrocyte destruction during the parasite's developmental cycle leads to hemolytic anemia. The reaction of the reticuloendothelial system to the infection causes hepatosplenomegaly (enlargement of the liver and spleen). In Plasmodium malariae infection, renal tissue may become involved with the development of nephrotic syndrome, while Plasmodium falciparum infection carries the risk of the most severe and complicated forms.

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Laboratory diagnostics

A carefully taken epidemiological history (stay in endemic zones, absence or inefficacy of chemoprophylaxis) plays a key role in making the diagnosis.

The following methods are used to verify the diagnosis:

  1. Microscopy: examination of thin and thick blood films. This allows the detection of plasmodia, identification of their species, and calculation of the level of parasitemia (e.g., number of parasites per 100 leukocytes or per 1 µL of blood).
  2. Rapid diagnostic tests: ParaShigt and ICT systems for detecting specific proteins or lactate dehydrogenase (LDH) of malarial plasmodia in serum.
  3. Hemogram: anemia, leukopenia, lymphomonocytosis, and high erythrocyte sedimentation rate (ESR) values are typical.

Differential diagnosis

Malaria must be differentiated from numerous infections accompanied by fever and hepatosplenomegaly. First of all, influenza (ARVI), typhoid fever, leptospirosis, brucellosis, visceral leishmaniasis, sepsis, and Hodgkin's lymphoma are ruled out.

For example, sepsis also presents with chills and sweats, but it is characterized by neutrophilic leukocytosis with a left shift and the presence of a primary purulent focus. In Hodgkin's lymphoma, fever is combined with skin itching and lymph node enlargement. Typhoid fever can mimic malaria, especially if the patient has abdominal distension, pallor, and a coated tongue, but typhoid lacks the typical periodicity of attacks.

Principles of treatment and prevention

Malaria therapy is divided into suppressive (relief of acute symptoms) and radical. Etiotropic treatment is prescribed strictly taking into account the species of plasmodium confirmed by laboratory tests. It is important to consider the pathogen's possible resistance to standard drugs (e.g., chloroquine resistance in certain regions of Africa).

Adequate pathogenetic and detoxification therapy (intravenous fluid administration) must be performed. Discharge of a convalescent is permitted only after a control thick blood film microscopy, and mandatory dispensary observation is established for recovered patients.

How to memorize

To memorize the classic triad of the malarial paroxysm, use the rule "C-F-S": Chills (onset of the attack) — Fever (peak of fever up to 40 °C) — Sweating (temperature drop and profuse sweating).

Class and exam questions

How does the disease begin in non-immune individuals?

Often with initial fever—a persistently high temperature during the first days (up to a week), which is only later replaced by typical periodic attacks.

What complete blood count changes are typical for malaria?

The hemogram typically reveals anemia, leukopenia, lymphomonocytosis, and a significant increase in the erythrocyte sedimentation rate (ESR).

Why is it important to accurately determine the species of plasmodium?

The species of the causative agent (e.g., Plasmodium vivax or Plasmodium falciparum) determines the severity of the clinical course, the risk of complications, and the tactics of etiotropic treatment.

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What else to study on this topic

  • Mechanisms of development of severe and complicated forms of falciparum malaria.
  • Features of tissue and erythrocytic schizogony in different forms of the disease.
  • Pathogenesis of nephrotic syndrome in Plasmodium malariae infection.
  • Suppressive and radical therapy: drug selection depending on resistance.
  • The concept of the "malaria season" and necessary conditions for the spread of the infection.

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