Malaria is a transmissible human disease characterized by a predominant lesion of the reticulohistiocytic system and erythrocytes, febrile attacks, anemia, enlargement of the liver and spleen.


    • The causative agents are protozoans of the genus Plasmodium.
    • Plasmodium vivax – the causative agent of three-day malaria
    • Plasmodium malarias is the causative agent of four-day malaria.
    • Plasmodium falciparum is the causative agent of tropical malaria.
    • Plasmodium ovale – the causative agent of malaria oval (three-day type)
    • Transfusion of infected blood.

Risk factors. Traveling or living in endemic regions. Epidemiology

    • Malaria is detected everywhere from 45 ° north to 40 “south latitude (but more often in the tropics and subtropics) at an altitude of 0 to 1800 m above sea level
    • In states with a temperate climate, Plasmodium vivax is more often isolated, less often Plasmodium malariae
    • In the tropics, Plasmodium falciparum is the main causative agent, and Plasmodium ovale is isolated only sporadically in African countries.
    • Every year, in 104 endemic states, about 250 million people fall ill
    • Deaths are most commonly seen in infants but have also been reported in non-immunized adults (1–2 million annually)
    • The carriers are mosquitoes of the genus Anopheles. The incidence directly depends on the size of the mosquito population and the number of cases that serve as a reservoir of infection.
    • In connection with the development of the tourism industry, the disease is detected in states that lie outside the natural range.
    • The transmission of an infectious agent in the bulk of cases is horizontal (spread during the epidemic season is likely only through mosquitoes). Genetic Aspects
    • Persons whose erythrocytes do not carry Duffy group Ag have a natural resistance to malaria pathogens (many representatives of the black race)
    • Persons with a congenital deficiency of glucose-so-6-dehydrogenase have natural resistance, because parasites are unable to use the glucose monophosphate shunt as an energy source and under such conditions cannot develop in erythrocytes
    • Individuals with hemoglobinopathies are also resistant to infection, because parasites are unable to multiply in erythrocytes with altered morphology, for example, in patients with sickle cell anemia
    • In tropical malaria caused by Plasmodium falciparum, black-water (hemoglobinuric) fever develops, a complication of malaria that occurs after taking quinine and primaquine. It is more often observed in individuals with increased fragility of erythrocytes as a result of a hereditary defect in glucose-6-phosphate dehydrogenase, similar to Marchiafava-Micheli anemia, and also as a delayed-type hypersusceptibility reaction to quinine.

Clinical picture

    • The incubation period for malaria, depending on the type of pathogen, varies from 8 to 25 days (with a three-day period it can reach 8-14 months).
    • Symptoms – fever, anemia and circulatory disorders (for all forms). Tropical malaria is the most severe.
    • Fever is observed at the moment of release of parasites from destroyed erythrocytes; the intervals between manifestations of seizures depend on the biological cycle of the parasite. The onset is acute, the body temperature can reach 40-41.7 ° C (traditionally, the temperature rise is observed in the daytime), after a few hours it lytically drops to 35-36 ° C.
    • Anemia is a consequence of massive lysis of red blood cells and phagocytosis of affected cells by phagocytes. Black-water fever in tropical malaria is characterized by acute massive hemolysis, hemolytic jaundice, back pain, hemoglobinuria. Much less often, and only in tropical malaria, intravascular hemolysis is observed.
    • Circulatory disorders are caused by an increase in body temperature. Vasodilation leads to a decrease in BCC and blood pressure. Subsequent vasospasm, high vis-

blood bone, blockage of capillaries by erythrocyte residues lead to ischemia of organs and tissues.

    • Acute glomerulonephritis sometimes accompanies tropical (falciparum) malaria; with chronic disease caused by Plasmodium malariae, progressive renal failure may develop. Nephropathology in malaria is due to autoimmune mechanisms.
    • Enlargement of the spleen and thrombocytopenia (often).
    • Lesions of the digestive tract (for example, gangrenous and ulcerative changes in the intestinal mucosa, liver enlargement, fibrous pancreatitis).

Laboratory research

    • Blood test – anemia, leukopenia, thrombocytopenia, an increase in the concentrations of ALT and AST, an increase in the content of direct and indirect bilirubin, a decrease in the concentration of albumin
    • Microscopy of smears for the presence of parasites. For the preparation of smears, capillary and venous blood is used. Smears are stained according to Wright or Romanovsky-Giemsa. Plasmodium species are differentiated by morphological differences. Differential Diagnosis
    • Acute hepatitis
    • Acute hemolytic anemia
    • Acute diarrhea
    • Stroke
    • Pneumonia
    • Acute viral infection
    • Other causes of tropical splenomegaly.


Tactics of conducting

    • Hospitalization is recommended for patients in the acute stage and patients with tropical malaria
    • In severe cases, control the likely development of complications, for example, severe anemia and kidney failure. Drug therapy – the impact on the erythrocyte forms of plasmodium (treatment of malaria).
    • For malaria caused by Plasmodium vivax, Plasmodium ovale, Plasmodium malariae, and Plasmodium falciparum sensitive to chloroquine (chingamine), chloroquine phosphate (chloroquine, chingamine) orally.
    • Adults – at the first dose of 1 g (600 mg of base), then after 6 hours – 500 mg (300 mg of base), on days 2 and 3 – 500 mg 1 r / day.
    • Children – at the first dose of 10 mg / kg (not more than 500 mg), then 5 mg / kg after 6 hours, on days 2 and 3, 5 mg / kg 1 r / day.
    • In uncomplicated malaria caused by Plasmodium falciparum resistant to chloroquine.
    • Oral combination of quinine sulfate and tetracycline or clindamycin or sulfadoxine-pyrimethamine (Fansidar)
    • Adults – quinine sulfate 650 mg 3 times a day for 3-7 days, tetracycline 250 mg 4 times a day for 7 days, clindamycin 450 mg 3 times a day for 3 days, sulfadoxine-pyrimethamine 3 tablets in one dose
    • Children – quinine sulfate 3 r / day for 3-7 days, sulfadoxine pyrimethamine 1/2 tablet (up to 4 years), 1 tablet (4-8 years), 2 tablets (8-12 years) and Pregnant women – quinine sulfate 650 mg 3 r / day for 3-7 days, clindamycin 450 mg orally every 8 hours for 3 days or.
    • Mefloquine or halofantrine. Adults – mefloquine 15 mg / kg orally as a single dose (no more than 1,250 mg), halofantrine 6 tablets (250 mg salt), 2 tablets every 6 hours up to 3 doses.
    • In the complicated (malignant) course of malaria (parasitemia> 5%, neurological disorders or inability to take the product orally) – quinine dihydrochloride 10 mg / kg IV drip for 1-2 hours, then, or

continuous infusion at a rate of 0.02 mg/kg/min, or 10 mg/kg s.c. 8 hours before parasitemia

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