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) occurs in the stomach of the female Anopheles mosquito, producing sporozoites. Upon a mosquito bite, they enter the human bloodstream, initiating tissue and subsequently erythrocytic schizogony.
- Tissue stage: In the liver, sporozoites multiply within hepatocytes. The rupture of a single liver cell releases up to 30,000 merozoites.
- Erythrocytic stage: Merozoites invade erythrocytes, where they hydrolyze hemoglobin to form the malaria pigment — hemomelanin. The cycle lasts 48 hours (for P. falciparum, P. vivax, and P. ovale) or 72 hours (for P. malariae).
Infected erythrocytes express surface proteins (such as PfEMP1-like molecules) that bind to endothelial ICAM-1. This allows parasites to evade splenic clearance while causing sludge syndrome and microvascular thrombosis.
Clinical Forms and Morphology of Malaria
The classic malaria paroxysm is associated with the synchronized rupture of erythrocytes and the release of endogenous pyrogens, leading to severe chills, temperatures spiking to 40–41.5 °C, and subsequent rapid defervescence.
Tropical malaria (P. falciparum) is the most severe form. It is characterized by erythrocyte cytoadherence to the endothelium, leading to parasitic blood stasis, perivascular edema, and ischemia. Specific Dürck's granulomas form in the brain, frequently culminating in cerebral coma and death (especially in children).
Tertiary and quartan malaria induce massive intravascular hemolysis, resulting in suprahepatic jaundice and anemia. Reticuloendothelial organs (liver, spleen, bone marrow) accumulate hemomelanin, turning a dark gray to almost black color. Splenic weight may reach up to 3 kg.
Amebiasis (Amebic Dysentery)
Amebiasis is caused by Entamoeba histolytica and transmitted via the fecal-oral route through ingestion of cysts resistant to gastric acid. Vegetative forms (trophozoites) emerge in the intestine.
Pathogenic strains secrete enzymes (hyaluronidase, cysteine proteinases) that destroy the epithelium of the large intestine (most commonly the cecum and ascending colon).
- Amoebas lyse host cells and invade the submucosa.
- Suppurative-hemorrhagic inflammation develops with tissue necrosis.
- Characteristic ulcers with undermined, slightly overhanging edges are formed.
Clinically, the disease presents as bloody diarrhea (up to 15 times a day) containing mucus and blood, acquiring a pathognomonic "raspberry jelly" appearance.
Prion Encephalopathies
Rare prion-related conditions include:
- Alpers' disease: An extremely rare hereditary encephalopathy of infancy and childhood associated with liver involvement (centrilobular necrosis). In the CNS, neuronal degeneration and gliosis localize predominantly to the occipital cortex and striatum.
- Spongiform myositis: Characterized by vacuoles containing spiral filaments composed of prion proteins (PrP) and apolipoprotein E within muscle fibers, manifesting as slowly progressive weakness and myalgia.