Malaria: Life cycle and pathogenesis
Malaria is a vector-borne disease caused by protozoa of the genus Plasmodium. The parasite's life cycle is strictly divided between two hosts. The sexual stage (sporogony), which results in the formation of sporozoites, takes place in the midgut of the female Anopheles mosquito. Upon a mosquito bite, they enter the human bloodstream, initiating tissue and subsequently erythrocytic schizogony.
- Tissue stage: In the liver, sporozoites replicate within hepatocytes. The destruction of a single liver cell releases up to 30,000 merozoites.
- Erythrocytic stage: Merozoites penetrate erythrocytes, where they hydrolyze hemoglobin to form the malaria pigment — hemomelanin. The cycle lasts 48 hours (for falciparum, tertian, and ovale malaria) or 72 hours (for quartan malaria).
Infected erythrocytes produce sequesterin proteins that bind to the endothelium via ICAM-1 molecules. This allows the parasites to evade destruction in the spleen while causing sludge syndrome and microthrombosis in capillaries.
Clinical forms and morphology of malaria
The classical malaria attack is associated with the mass release of parasites from erythrocytes and a surge of endopyrogens. Rigors develop, body temperature rises to 40–41.5 °C, and then drops sharply.
Falciparum malaria (P. falciparum) is the most severe form. It is characterized by erythrocyte adhesion to the endothelium, leading to parasitic blood stasis, perivascular edema, and ischemia. Specific Dürck's granulomas form in the brain. This frequently leads to cerebral coma and death (especially in children).
Tertian and quartan malaria cause massive intravascular hemolysis, leading to suprahepatic jaundice and anemia. Organs of the reticuloendothelial system (liver, spleen, bone marrow) accumulate hemomelanin and acquire a dark gray, almost black color. Spleen weight can reach up to 3 kg.
Amebiasis (amebic dysentery)
Amebiasis is caused by Entamoeba histolytica and is transmitted by the fecal-oral route. Infection occurs through the ingestion of cysts that are resistant to the acidic environment of the stomach. Vegetative forms—trophozoites—emerge from them in the intestine.
Pathogenic strains release enzymes (hyaluronidase, cysteine proteinases) that destroy the epithelium of the large intestine (most often the cecum and ascending colon).
- Amebae lyse cells and invade the submucosa.
- Suppurative-hemorrhagic inflammation with tissue necrosis develops.
- Characteristic ulcers with undermined, slightly overhanging edges are formed.
Clinically, the disease manifests as bloody diarrhea (up to 15 times a day), with the stool containing mucus and blood, acquiring the pathognomonic appearance of "raspberry jelly".
Prion encephalopathies
The material also mentions rare prion diseases:
- Alpers' disease: An extremely rare hereditary encephalopathy of childhood and adolescence. It is combined with liver damage (centrilobular necrosis). In the central nervous system, neuronal dystrophy and gliosis are localized predominantly in the occipital cortex and striatum.
- Spongiform myositis: Characterized by the presence in muscle cells of vacuoles with spiral filaments consisting of prion proteins (PrP) and apolipoprotein E. It manifests as slowly progressive weakness and myalgia.
Briefly: answers to topical questions
Which pathogen causes parainfluenza?
Parainfluenza is caused by pneumotropic RNA-containing parainfluenza viruses (human paramyxoviruses, Human Parainfluenza virus), which belong to types 1 through 4 (serotype 3 is of the greatest clinical significance). The main pathogen belongs to the group of acute respiratory viral infections and infects the respiratory epithelium of the airways.
What are the main routes of transmission of parainfluenza?
The main mechanism of transmission of parainfluenza is aerogenic, and the main route of transmission is airborne. In addition, respiratory viruses can be transmitted by contact via surfaces and infected objects.
What are the main morphological changes in the respiratory tract in parainfluenza?
The main morphological changes in parainfluenza are associated with the predominant involvement of the larynx, where acute laryngitis develops with edema of the mucosa and submucosa. In young children, this leads to the development of acute stenosing laryngotracheitis (croup). Microscopically, viral damage leads to the formation of giant multinucleated cells (syncytia) in the bronchial and alveolar epithelium, as well as the development of hemorrhagic exudate in the alveolar lumens upon transition to hemorrhagic pneumonia.
What target cells does the parainfluenza virus infect in the respiratory tract?
The parainfluenza virus exhibits a pronounced tropism for the respiratory epithelium and binds to the receptors of the respiratory tract mucosal epithelium and alveolar epithelium. The pathogen binds to the surface of epithelial cells in the area where ICAM-1 adhesion molecules are localized.
What respiratory complications are typical for parainfluenza?
The main characteristic respiratory complication of parainfluenza is false croup with progressive respiratory failure. The development of primary viral hemorrhagic pneumonia and the addition of a secondary bacterial infection, which worsens the course of the disease, are also possible.
What does the macroscopic appearance of the laryngeal and tracheal mucosa look like in parainfluenza?
The provided methodological materials do not give a detailed description of the macroscopic picture of the laryngeal and tracheal mucosa specifically for parainfluenza (noting the development of pronounced laryngitis with edema of the mucosa and submucosa, as well as the picture of catarrhal subglottic laryngitis without fibrinous membranes).
What microscopic changes are found in the bronchial epithelium in parainfluenza?
Microscopically, paramyxovirus infection in the bronchial and alveolar epithelium reveals a characteristic cytopathic effect—the formation of giant multinucleated cells (syncytia) arising from the fusion of neighboring infected cells.
To memorize the appearance of stool in amebiasis: The ameba loves sweets—stool in the form of "raspberry jelly." The ulcers have "undermined" edges, as if the ameba has tunneled underneath.
Class and exam questions
Why do organs turn black in malaria?
Plasmodia break down hemoglobin, forming the pigment hemomelanin. It is phagocytosed by macrophages of the liver, spleen, and bone marrow, giving the tissues a dark gray or black color.
Who possesses natural resistance to malaria?
People with glucose-6-phosphate dehydrogenase deficiency, carriers of various hemoglobinopathies, and representatives of the Negroid race lacking the Duffy blood group antigen.
What are Dürck's granulomas?
These are microscopic accumulations of proliferating macrophages and oligodendrogliocytes in brain tissue. They occur in response to ischemia and neuronal death in severe falciparum malaria.
What else to study on this topic
- The mechanism of sequestration of infected erythrocytes and the role of ICAM-1 molecules.
- Features of tissue schizogony in hepatocytes.
- Pathogenesis of infectious-toxic shock in malaria.
- Morphological differences between ulcers in amebiasis and other colitides.
- Occupational risk groups for prion infections.
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