Malaria is a transmissible protozoal infection caused by pathogenic protozoa of the genus Plasmodium and characterized by a paroxysmal, recurrent course. Specific symptoms are repeated attacks of fever, hepatosplenomegaly, anemia. During feverish attacks in malaria patients, the alternating stages of chills, fever and sweat are clearly traced. The diagnosis is confirmed when malarial plasmodium is detected in a smear or thick drop of blood, as well as the results of serological diagnostics. For etiotropic therapy of malaria, special antiprotozoal drugs (quinine and its analogues) are used.
General information
Malaria (intermittent fever, swamp fever) is a group of human parasitic diseases, the causative agents of which are various types of malarial plasmodium, affecting mainly red blood cells and the reticuloendothelial system. Malaria occurs with febrile paroxysms, hepatolienal and anemic syndrome. Malaria is widespread in the countries of Equatorial Africa, Southeast Asia, Oceania, Central and South America. 350-500 million new invasions and about 1.3-3 million deaths from malaria are registered annually in the world. The high incidence of malaria in the world is explained by the development of plasmodium resistance to specific therapy, and protozoal infection vectors – to the action of insecticides. Due to the increase in migration and tourist flows, imported cases are increasingly common in Europe.
Causes
Malaria is caused by parasitic protozoa belonging to the class of spores, the genus Plasmodium (malarial plasmodia). Human disease is caused by 4 types of plasmodium: P. Vivax (causative agent of three-day malaria), P. Malariae (causative agent of four-day malaria), P.falciparum (causative agent of tropical malaria) and P. Ovale (causative agent of ovale malaria, similar to three-day malaria).
Malarial plasmodia undergo a complex life cycle, including asexual development (schizogony) in the body of an intermediate host – a human and sexual development (sporogony) in the body of the main host – female Anopheles mosquitoes. Infection of mosquitoes occurs when bites of a person with malaria or a parasite carrier. During blood sucking, male and female plasmodium germ cells (micro- and macrogametocytes) enter the mosquito’s stomach; here their fertilization occurs with the formation of a zygote, and then oocysts. As a result of repeated division of the oocyst, it turns into invasive forms of plasmodium – sporozoites, which penetrate into the salivary glands of the mosquito and can stay there for 2 months.
Infection of a person occurs when an invaded female mosquito bites, with whose saliva sporozoites penetrate into the blood of the intermediate host. In the human body, the causative agent undergoes the tissue and erythrocyte phases of its asexual development. The tissue phase (exoerythrocytic schizogony) occurs in hepatocytes and tissue macrophages, where sporozoites are successively transformed into tissue trophozoites, schizonts and merozoites. At the end of this phase, merozoites penetrate into the red blood cells, where the erythrocyte phase of schizogony occurs. In blood cells, merozoites turn into trophozoites, and then into schizonts, from which merozoites are formed again as a result of division. At the end of such a cycle, red blood cells are destroyed, and the released merozoites are introduced into new red blood cells, where the cycle of transformations repeats again. As a result of 3-4 erythrocyte cycles, gametocytes are formed – immature male and female germ cells, the further (sexual) development of which takes place in the body of the female Anopheles mosquito.
Given the peculiarities of the development of plasmodium, it becomes obvious that the main route of transmission of malaria from person to person is transmissible, implemented through bites by female mosquitoes of the genus Anopheles. At the same time, transplacental transmission of infection during pregnancy is possible, as well as parenteral infection with transfusion of donor blood taken from parasite carriers. In endemic foci, children and visitors are more susceptible to malaria. The peak incidence of malaria coincides with the season of mosquito activity and falls on the summer-autumn time.
The paroxysmal nature of febrile attacks in malaria is associated with the erythrocyte phase of the development of malarial plasmodium. The development of fever coincides with the breakdown of red blood cells, the release of merozoites and their metabolic products into the blood. Substances foreign to the body have a general toxic effect, causing a pyrogenic reaction, as well as hyperplasia of the lymphoid and reticuloendothelial elements of the liver and spleen, leading to an increase in these organs. Hemolytic anemia in malaria is a consequence of the breakdown of red blood cells.
Symptoms
During malaria, there is an incubation period, a period of primary acute manifestations, a secondary latent period and a period of relapses. The incubation period for three-day malaria and ovale malaria lasts 1-3 weeks, for four-day malaria – 2-5 weeks, for tropical malaria – about 2 weeks. Typical clinical syndromes for all forms of malaria are febrile, hepatolienal and anemic.
The disease can begin acutely or with short-term prodromal phenomena – malaise, subfebrility, headache. During the first days, the fever has a remitting character, later it becomes intermittent. A typical malaria paroxysm develops on the 3rd-5th day and is characterized by a consistent change of phases: chills, heat and sweat. The attack usually begins in the morning with a terrific chill and an increase in body temperature, which force the patient to go to bed. In this phase, nausea, headaches and muscle pains are noted. The skin becomes pale, “goose-like”, the limbs are cold; acrocyanosis appears.
After 1-2 hours, the phase of chills is replaced by heat, which coincides with an increase in body temperature to 40-41 ° C. There are hyperemia, hyperthermia, dry skin, injection of sclera, thirst, enlargement of the liver and spleen. There may be excitement, delirium, convulsions, loss of consciousness. At a high level, the temperature can be kept up to 5-8 or more hours, after which profuse sweating occurs, a sharp decrease in body temperature to a normal level, which marks the end of a fever attack with malaria. With three-day malaria, attacks are repeated every 3rd day, with four–day malaria – every 4th day, etc. By the 2nd-3rd week, hemolytic anemia develops, skin subictericity and sclera appear with normal urine and feces coloration.
Timely treatment can stop the development after 1-2 attacks. Without specific therapy, the duration of three-day malaria is about 2 years, tropical – about 1 year, ovale-malaria – 3-4 years. In this case, after 10-14 paroxysms, the infection goes into a latent stage, which can last from several weeks to 1 year or longer. Usually, after 2-3 months of visible well-being, early relapses of malaria develop, which proceed in the same way as acute manifestations of the disease. Late relapses occur after 5-9 months – during this period, seizures have a lighter course.
Complications
Severe, sometimes life-threatening complications of malaria can be malarial coma, malarial algid, rupture of the spleen, brain edema, acute respiratory failure, DIC syndrome, mental disorders. Malarial coma is most often complicated by the course of tropical malaria. The development of coma is associated with impaired microcirculation of the brain as a result of the formation of parasitic blood clots consisting of erythrocytes infected with schizonts. During a malarial coma, periods of somnolence (drowsiness, adynamia), sopor (sudden inhibition, decreased reflexes) and deep coma (lack of consciousness and reflexes) are distinguished. The fatal outcome of this complication occurs in 96-98% of cases.
Malarial algid is accompanied by the development of a collaptoid state with arterial hypotension, thready pulse, hypothermia, decreased tendon reflexes, pallor of the skin, cold sweat. Diarrhea and dehydration phenomena often occur. Signs of rupture of the spleen in malaria occur spontaneously and include dagger abdominal pain with irradiation to the left shoulder and shoulder blade, sharp pallor, cold sweat, decreased blood pressure, tachycardia, thready pulse. According to ultrasound data, free fluid is detected in the abdominal cavity. In the absence of emergency surgery, death from acute blood loss and hypovolemic shock quickly occurs.
Brain edema develops in a malignant, lightning-fast form of three-day malaria, more often in preschool children and adolescents. It occurs at the height of a feverish paroxysm and is characterized by severe headache, convulsions with loss of consciousness, foaming from the mouth and the imminent death of the patient. The development of acute renal failure in malaria is associated with massive intravascular hemolysis of erythrocytes, impaired renal circulation, and intense hemoglobinuria. It is usually the outcome of hemoglobinuria fever. A specific complication of tropical malaria is mental disorders, including psychomotor agitation, delirium, hallucinations, etc.
Diagnosis
The foundation of the clinical diagnosis of malaria is a triad of signs: paroxysmal intermittent fever, recurring every 48 or 72 hours, hepatosplenomegaly, hemolytic anemia. At the same time, it turns out that the patient visited endemic regions, underwent blood transfusions and parenteral interventions during the last 2-3 months.
A specific laboratory method for diagnosing malaria is microscopy of a thick drop of blood, which allows detecting the presence and number of parasites. Qualitative identification of the type of plasmodium and the stage of schizogony is carried out by examining a blood smear for malarial plasmodium. It is better to take blood at the height of a febrile attack. Serological methods – RIF, RFA, RPH – play an auxiliary role in the detection of malaria. In terms of differential diagnosis, the most important exception is in a febrile patient of brucellosis, recurrent typhus, leishmaniasis, sepsis, tuberculosis, meningoencephalitis, hemolytic jaundice, cirrhosis of the liver, leukemia, etc.
Treatment
Patients with suspected malaria are hospitalized in an infectious hospital with the appointment of strict bed rest, copious drinking, infusion therapy, general restorative and symptomatic treatment. If necessary, patients undergo hemosorption and hemodialysis.
Initially, quinine isolated from the bark of the cinchona tree was used for specific chemotherapy of malaria. Currently, a large number of synthetic drugs have been created, but due to the rapid development of resistance of parasites to synthetic drugs, quinine has not yet lost its relevance. Depending on the effect, antimalarial drugs are divided into tissue schizontocides that affect tissue forms of malarial plasmodium (quinocide, primachine) and hematocides that affect erythocytic forms of the pathogen (chloroquine, pyrimethamine, mepacrine, quinine, etc.). They are prescribed in various combinations and according to a certain scheme, depending on the form and severity of the course of malaria. So, with three-day malaria, a 3-day course of treatment with chloroquine is usually carried out, followed by a 10-day intake of primachine or quinocide to destroy tissue forms of the parasite. Other antimalarial therapy regimens are also possible.
Prognosis and prevention
Timely and correct therapy of malaria leads to rapid relief of clinical manifestations. Fatal outcomes during treatment occur in about 1% of cases, as a rule, in complicated forms of tropical malaria.
Prevention of malaria is carried out in two directions: the destruction of mosquitoes-carriers of pathogens and individual protection. The first direction includes the treatment of territories with insecticides. The second is the use of personal protective equipment (creams, lotions, mosquito nets), carrying out specific chemoprophylaxis for people traveling to areas that are disadvantaged by malaria. For the purpose of early detection of patients and parasite carriers, all patients with fever of unknown origin should undergo blood microscopy for malaria.
