Leptospirosis (Weil's Disease)
Leptospirosis, also known in clinical practice as icteric leptospirosis or Weil's disease, is a severe infection with prominent systemic manifestations.
Etiology and Epidemiology: The causative agent is the pathogenic spirochete Leptospira icterohaemorrhagiae. Rats serve as the primary reservoir in endemic foci. Human infection occurs via three routes: through the skin, respiratory tract, or digestive tract. Occupational risk groups include individuals in contact with contaminated water and soil, such as sewage and irrigation workers, farmers, and fishermen. The incubation period ranges from 10 to 15 days.
Clinical and Morphological Features: The disease is generalized. Patients develop jaundice, conjunctivitis, lymphocytic meningitis, and hemorrhagic diathesis. The infection causes renal tubular epithelial damage, as well as focal necrosis of the myocardium and skeletal muscle.
Liver Microscopy: Histological examination reveals:
- Focal fatty change (steatosis) of hepatocytes.
- Focal tissue necrosis.
- Signs of intrahepatic cholestasis.
- Multiple hemorrhages.
- Increased mitotic activity of hepatocytes.
Prognosis: Mortality in leptospirosis reaches 15%. During the first week, patients may die from hemorrhagic pulmonary consolidation, while in later stages, renal failure becomes the cause of death.
Hepatobiliary Ascariasis
Ascariasis is a parasitic intestinal infection caused by the roundworm Ascaris lumbricoides.
Epidemiological Features: This helminthiasis is most prevalent among children. Endemic regions with the highest incidence traditionally include countries in Africa and the Far East.
Pathogenesis and Complications: Although the primary habitat of the parasite is the intestine, the disease poses a serious threat to the liver and biliary tract. In one-third of infected patients, adult ascarids migrate and invade the common bile duct. This condition inevitably leads to mechanical biliary obstruction and the subsequent development of severe inflammation—cholangitis.
Granulomatous Liver Disease
Pathologies accompanied by a productive granulomatous reaction warrant special attention. Their key morphological feature is the formation of non-caseating granulomas, which are nodules lacking caseous necrosis in their center.
Primary Liver Diseases: Granuloma formation is driven by primary conditions such as primary biliary cholangitis (PBC) and the parasitic disease schistosomiasis.
Secondary Involvement: In most cases, hepatic granulomas reflect generalized systemic processes. The most frequent cause is sarcoidosis. Secondary granulomatous inflammation is also triggered by various fungal infections, rickettsial diseases, and parasitic infestations.
Other Factors: Beyond infectious and autoimmune agents, a productive granulomatous reaction in hepatic tissue can be of allergic or drug-induced origin.