Protozoal Infections: Amebiasis and Toxoplasmosis
In amebiasis, the pathological process localizes to the wall of the large intestine, where inflammation, necrosis, and ulceration develop. Intestinal complications (ulcer perforation with peritonitis) and extraintestinal manifestations pose significant hazards. The pathogen can spread via the branches of the portal vein (v. portae) to the liver (in 40% of cases), causing amebic hepatitis and abscesses, or disseminate hematogenously to the lungs.
Toxoplasmosis is a zoonotic infection caused by Toxoplasma gondii. Sexual reproduction of the parasite occurs in felines, while asexual reproduction occurs in intermediate hosts (including humans). Transmission occurs via the alimentary route (the primary route), direct contact, or transplacental spread. Within macrophages, the pathogen undergoes incomplete phagocytosis and schizogony, destroying cells and disseminating throughout the body. During chronicity, true cysts form in the brain and muscles. Congenital infection severity depends on the gestational age at infection:
- First trimester: Severe generalized process, often resulting in fetal demise.
- Second trimester: Microcephaly, gliosis, calcification, microphthalmia with cataracts.
- Third trimester: Subacute meningoencephalitis, retinitis.
Tissue Helminthiases: Trichinosis
The causative agent is Trichinella spiralis. Humans are infected alimentarily by consuming undercooked meat from wild or domestic animals. Pathogenesis includes three stages:
- Intestinal: Release and invasion into the mucosa.
- Migratory: Females release larvae that disseminate via lymphatic and blood pathways.
- Muscular: By the 18th day, larvae invade skeletal muscles and become encysted (can persist for up to 40 years).
The disease progresses through enzymatic-toxic, immunologic (severe allergic reactions, vasculitis), and immunopathologic phases. In severe cases, myocarditis, pneumonia, and meningoencephalitis develop.
Cystic Helminthiases: Echinococcosis and Cysticercosis
Echinococcosis is caused by the larval stages of cestodes (Echinococcus granulosus and E. multilocularis). Definitive hosts are canids, which shed oncospheres. In humans (intermediate hosts), oncospheres penetrate the intestinal wall and settle in the liver or lungs, transforming into larval cysts (hydatid cysts). These cysts grow for decades, compressing surrounding tissues. A fibrous capsule forms around them, which may calcify. Cyst rupture carries the risk of anaphylactic shock and dissemination (secondary echinococcosis).
Cysticercosis is caused by Cysticercus cellulosae—the larval form of the pork tapeworm (Taenia solium). Transmission occurs via the fecal-oral route. Larvae frequently localize to the brain and eyes, causing seizures and vision loss. Pathogenesis includes the stages of the viable parasite, degeneration and death (the most toxic phase accompanied by marked serofibrinous inflammation), and residual changes (calcification).
Tropical Infections: Leprosy
Leprosy (Hansen's disease) is a chronic infection caused by Mycobacterium leprae. It affects the skin, peripheral nerves, and internal organs. The disease has low contagiousness and is transmitted via contact and airborne droplets from an infected individual. Mycobacteria enter through the nasopharynx or broken skin (without forming a primary affect), then migrate into nerve endings, the lymphatic system, and the bloodstream. In the majority of infected individuals, the immune system resolves the process.