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Pathological Anatomy · Diseases of the Liver, Biliary System, and Exocrine Pancreas

Infectious and parasitic liver diseases

Infectious and parasitic liver diseases of non-viral etiology represent a broad group of pathological conditions. Unlike viral hepatitis, these diseases are caused by bacteria, pathogenic spirochetes, protozoa, and various helminths. In pathomorphological practice, they are characterized by specific morphological changes in tissues: ranging from focal necroses and massive hemorrhages to the formation of non-caseating granulomas and mechanical obstruction of the biliary tract.

EtiologyDiseases caused by bacteria, spirochetes, protozoa, and helminths
LeptospirosisCauses focal fatty degeneration, necrosis, and intrahepatic cholestasis
AscariasisIn 33% of patients, worms obstruct the common bile duct, causing cholangitis
GranulomasNon-caseating granulomas form in the liver in sarcoidosis and schistosomiasis
5 min readFor medical studentsUpdated Sep 25, 2026
Material prepared by WhiteCoat Pro editorial team based on platform study guidesReviewed by medical editor: Aulov A. A., general practitioner · 09/24/2026

Leptospirosis (Weil's disease)

Leptospirosis, also known in clinical practice as icterohemorrhagic leptospirosis or Weil's disease, is a severe infection with pronounced systemic manifestations.

Etiology and epidemiology: The causative agent is the pathogenic spirochete Leptospira icterohaemorrhagiae. In endemic foci, rats serve as the primary reservoir of infection. Human infection occurs through three routes: via the skin, respiratory tract, or gastrointestinal tract. Occupational risk groups include individuals in contact with contaminated water and soil: sewage treatment plant and irrigation field workers, farmers, and fishermen. The incubation period lasts from 10 to 15 days.

Clinical and morphological picture: The disease is generalized in nature. Patients develop jaundice, conjunctivitis, lymphocytic meningitis, and hemorrhagic diathesis. The infection causes damage to the renal tubular epithelium, as well as focal necrosis of the myocardium and skeletal muscles.

Liver microscopy: Histological examination reveals:

  • Focal fatty degeneration of hepatocytes.
  • Focal tissue necrosis.
  • Signs of intrahepatic cholestasis.
  • Multiple hemorrhages.
  • Increased mitotic activity of hepatocytes.

Prognosis: Mortality in leptospirosis reaches 15%. In the first week, patients die from hemorrhagic consolidation (tissue densification) in the lungs, while at later stages, renal failure becomes the cause of death.

Ascariasis of the hepatobiliary system

Ascariasis is a parasitic intestinal infection caused by the roundworm Ascaris lumbricoides.

Epidemiological features: This helminthiasis is most widespread among the pediatric population. Endemic regions with the highest incidence traditionally include African countries 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, migration and invasion of adult ascarid worms into the common bile duct are observed. This condition inevitably leads to mechanical obstruction of the biliary tract and the subsequent development of severe inflammation—cholangitis.

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Granulomatous liver lesions

Pathologies accompanied by a productive granulomatous reaction deserve special attention. Their key morphological sign is the formation of non-caseating granulomas, i.e., nodules lacking caseous necrosis in the center.

Primary liver diseases: Independent nosologies such as primary biliary cholangitis (PBC) and the parasitic disease schistosomiasis lead to granuloma formation.

Secondary lesions: In most cases, hepatic granulomas reflect generalized systemic processes. The most frequent cause is sarcoidosis. Secondary granulomatous inflammation is also caused by various fungal infections, rickettsioses, and parasitic infestations.

Other factors: In addition to infectious and autoimmune agents, a productive granulomatous reaction in liver tissue can be of allergic or drug-induced genesis.

Briefly: answers to topical questions

What pathomorphological changes develop in extrahepatic organs in leptospirosis?

In leptospirosis, multiple extrahepatic organs are affected due to generalized capillarotoxicosis and hemorrhagic syndrome.

  • Kidneys — interstitial nephritis, tubular necrosis, and in severe cases, acute renal failure
  • Skeletal muscles — edema, myofibrillar vacuolization, focal necrosis, hemorrhages, histiolymphocytic infiltrates
  • Heart — myocarditis, petechial hemorrhages in the epicardium, pericardial effusion
  • Lungs — hemorrhages, pneumonia
  • Eyes — conjunctivitis, scleritis, hemorrhages, iritis, iridocyclitis, uveitis
  • Adrenal glands — hemorrhages
  • Central nervous system — perivascular inflammation, serous meningitis, meningoencephalitis, hemorrhages, cerebral edema

Erythrocyte hemolysis is also noted.

Which helminthiases, besides ascariasis and schistosomiasis, cause parasitic liver lesions?

In addition to ascariasis and schistosomiasis, the following helminthiases cause parasitic liver lesions.

  • Echinococcosis (Echinococcus granulosus) — hydatid form with the formation of a solitary or multiple cyst with a chitinous membrane, daughter vesicles, and scolices inside.
  • Alveococcosis (Echinococcus multilocularis) — multilocular echinococcosis with infiltrative nodular growth of multiple small vesicles, prone to central necrosis and tumor-like metastasis.
  • Opisthorchiasis (Opisthorchis sinensis) — biliary tract infestation with secondary purulent infection and adenomatous hyperplasia of the bile duct epithelium; regarded as a background condition for cholangiocellular carcinoma.

Hepatic echinococcosis and opisthorchiasis are also listed among the causes of secondary biliary cirrhosis.

Which protozoan microorganisms cause infectious liver lesions?

Sources indicate the following protozoa causing liver lesions.

  • Entamoeba histolytica — can cause amoebic liver abscess as a complication of amoebic dysentery.
  • Plasmodium — malaria parasite; in malaria, hepatomegaly develops, the liver in the acute stage is enlarged, plethoric, and dark gray on cross-section. Microscopy shows Kupffer cell hyperplasia, deposition of hemomelanin and hemosiderin in them; in the chronic course, pronounced liver fibrosis develops.

The dark gray color of the liver in malaria is associated with the malarial pigment hemomelanin, which is formed during the hydrolysis of hemoglobin by the parasite.

How to memorize

The acronym ROVZ helps to remember risk groups in leptospirosis: Fishermen (Rybolovyi), Sewage (Ochastnykh sooruzheniy) and Water body (Vodoemov/poley orosheniya) workers, Farmers (Zemledel'tsy). All of them come into contact with a humid environment where infected rats may live.

Class and exam questions

What are the main causes of death in severe leptospirosis?

The overall mortality rate for Weil's disease is about 15%. If the patient dies in the first week, the cause is most often hemorrhagic consolidation in the lungs. At later stages, damage to the renal tubular epithelium leading to renal failure becomes the critical factor.

What is the primary danger of ascariasis for the liver?

The causative agent of ascariasis, the roundworm Ascaris lumbricoides, primarily affects the intestine. However, in 33% of infected patients, helminth invasion into the common bile duct occurs, causing its obstruction and provoking the development of cholangitis.

Which systemic diseases most commonly cause hepatic granuloma formation?

Secondary granulomatous liver lesions reflect generalized processes. The most frequent cause is sarcoidosis. In addition, the reaction can be triggered by fungal infections, rickettsioses, and parasitic infestations.

What is the key morphological distinction of granulomas in the described diseases?

The main pathomorphological feature of granulomas in primary biliary cholangitis, sarcoidosis, and schistosomiasis is their non-caseating nature. This means that the zone of caseous necrosis is completely absent in the center of the inflammatory nodule.

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What else to study on this topic

  • Morphological picture of tuberculosis liver involvement
  • Pathological anatomy of liver syphilis at different stages
  • Primary biliary cholangitis (PBC): pathogenesis and histology
  • Hepatic schistosomiasis: parasite life cycle and tissue reactions
  • Mechanisms of drug-induced and allergic granulomatosis development

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