Bacterial Fungal and Parasitic Infections

Slide 1 · Bacterial, Fungal, andParasitic Infections

Liver and biliary tree • morphology and clinical correlations

Dr Abu Suraih Sakhri

MBBS, MD (Pathology)

www.abusuraihsakhri.com

Slide 2 · Learning objectives

Recognize

Major pathogen groups and entry routes

Explain

Abscess, cholangitis, granuloma, and fibrosis

Differentiate

Pyogenic, amebic, schistosomal, and hydatid patterns

Integrate

Morphology, clinical presentation, and organism detection

Slide 3 · Hepatic infections: Four recurring lesions

Suppurative

Ascending cholangitis and bacterial abscess

Granulomatous

Disseminated fungal and mycobacterial infection

Fibrosing

Schistosomal egg-induced portal injury

Cystic / necrotic

Echinococcosis and amebiasis

Slide 4 · Infection reaches the liver by different routes

Biliary ascent

Hematogenous dissemination

Direct extension from adjacent infection

Distinct routes converge on hepatic injury

Slide 5 · Local infection versus systemic disease

Pattern

Typical context

Pathologic consequence

Localized

Obstructed infected bile duct

Cholangitis ± hepatic abscess

Disseminated

Systemic bacterial, fungal or mycobacterial disease

Inflammation ± granulomas

Parasite-associated

Eggs, cysts, or trophozoites

Fibrosis, cysts, or necrosis

Slide 6 · Host reaction helps narrow the pathogen class

Neutrophilic

Suppuration and microabscesses

Granulomatous

Aggregated epithelioid macrophages

Fibrosing

Persistent inflammatory injury and scar

Liquefactive

Extensive enzymatic tissue destruction

Slide 7 · Bacterial involvement: Systemic exemplars

Agent

Associated syndrome

Hepatic context

Staphylococcus aureus

Toxic shock syndrome

Systemic bacterial disease

Salmonella Typhi

Typhoid fever

Systemic bacterial disease

Treponema pallidum

Secondary/tertiary syphilis

Systemic bacterial disease

Bartonella henselae

Cat-scratch disease

Systemic or focal infection

Slide 8 · Staphylococcus aureus: Systemic context

The liver may participate in a generalized bacterial illness.

Toxic shock syndrome is one textbook example of S. Aureus-associated systemic infection.

A clinical infectious syndrome cannot be identified from a nonspecific liver inflammatory pattern alone.

Systemic illness ≠ primary biliary infection

Slide 9 · Typhoid fever: Systemic bacterial infection

Salmonella Typhi is included among bacteria that can involve the liver.

The hepatic component occurs in the context of a systemic disease.

Organism identification and clinical context matter when the biopsy lacks a distinctive signature.

Do not infer the species from nonspecific hepatitis

Slide 10 · Syphilis: Spirochetal infection

Treponema pallidum may involve the liver in secondary or tertiary syphilis.

Infectious-disease histology recognizes plasma-cell-rich inflammation in syphilitic lesions.

Hepatic evaluation must be integrated with systemic findings and organism-directed testing.

Slide 11 · Cat-scratch disease: Bartonella henselae

Bartonella henselae is another example of bacterial hepatic involvement.

Its importance here is recognition of a potential systemic infectious etiology.

A hepatic lesion should be interpreted with exposure and extrahepatic disease history.

Slide 12 · Biliary obstruction creates susceptibility

Impaired bile outflow

Favorable milieu for bacterial multiplication

Infection of the biliary tree

Ascending cholangitis

Slide 13 · Common adult causes of large-duct obstruction

Stones

Choledocholithiasis

Neoplasms

Biliary tree or pancreatic head

Strictures

Postoperative or ischemic

Inflammatory

Primary sclerosing cholangitis

Slide 14 · Ascending cholangitis: Usual microbial source

Entry setting

Biliary obstruction

Common pathogens

Enteric coliforms and enterococci

Principal site

Biliary duct lumen and wall

Extension

Intrahepatic abscess in severe infection

Slide 15 · Cholangitis: Clinicopathologic sequence

Biliary obstruction

Ascending bacterial infection

Fever / abdominal pain / jaundice

Abscess or sepsis if severe

Slide 16 · Clinical pattern of ascending cholangitis

Fever and chills indicate an acute infectious process.

Abdominal pain accompanies biliary inflammation or obstruction.

Jaundice reflects impaired bile drainage.

Severe disease may progress to abscess, sepsis, or death.

Slide 17 · Ascending cholangitis may extend into the liver

Infected bile ducts

Spread into intrahepatic branches

Localized hepatic suppuration

Intrahepatic abscesses

Slide 18 · Three routes to bacterial liver abscess

Biliary infection

Bacteremia / hematogenous seeding

Extension from adjacent infected tissue

All may culminate in a hepatic abscess

Slide 19 · Suppurative injury: Abscess as tissue destruction

Schematic — not a histologic specimen

Pathologic interpretation

Localized collection of necrotic, inflamed tissue

Bacterial infection can produce suppurative foci

Larger lesions may require intervention beyond antibiotics

Slide 20 · Liver abscess: Clinical triad

Fever

Systemic inflammation

Right upper quadrant pain

Local hepatic involvement

Tender hepatomegaly

Inflamed, enlarged liver

Slide 21 · Why jaundice may occur with liver abscess

Extrahepatic biliary obstruction

Reduced bile delivery to intestine

Cholestasis / jaundice

Abscess alone does not establish obstruction

Slide 22 · Management concepts in bacterial abscess

Antibiotics

Generally effective for bacterial infection

Drainage

May be necessary with large lesions

Source control

Obstruction or adjacent infection remains relevant

Slide 23 · Extrahepatic sepsis can alter liver histology

Intraabdominal infections may cause reactive hepatic inflammation.

The liver changes can be nonspecific despite a serious extrahepatic infection.

Sepsis can produce ductular reaction with cholestasis.

Slide 24 · Cholangiolar cholestasis in sepsis

Bile plugs in ductular lumen

Simplified schematic; Not a biopsy image

Ductular reaction

Bile plugs within ductules

Cholestatic pattern associated with sepsis

Slide 25 · Septic cholestasis versus obstructive cholangitis

Feature

Sepsis-related hepatic change

Ascending cholangitis

Primary process

Systemic infection

Infected obstructed bile ducts

Characteristic clue

Ductular bile plugs

Fever, pain and jaundice

Complication

Cholestatic dysfunction

Hepatic abscess / sepsis

Slide 26 · Applied case: Obstruction and fever

Hypothetical teaching vignette

A patient with biliary obstruction develops fever, chills, abdominal pain, and jaundice.

What route of infection and principal complication should be considered?

Ascending cholangitis; Severe infection can extend to intrahepatic abscesses

Slide 27 · Fungal and mycobacterial infections: Common pattern

Clinical setting

Disseminated infection

Tissue response

Epithelioid granulomas

Morphologic variability

With or without necrosis

Confirmation

Serology, cultures, or organisms in biopsy

Slide 28 · Histoplasma: Pulmonary entry to hepatic spread

Inhalation of microconidia

Pulmonary infection

Dissemination via phagocytes

Possible liver involvement

Slide 29 · Histoplasma survives in host phagocytes

Macrophage uptake

Intracellular survival / replication

Delayed T-cell response

Potential dissemination

Slide 30 · Cell-mediated immunity limits histoplasmosis

Th1 cell response

IFN-γ secretion

Macrophage activation

Intracellular yeast killing

Slide 31 · Hepatic granuloma: An immune containment lesion

± necrosis

Conceptual granuloma — not a micrograph

Aggregated activated epithelioid macrophages

Can contain giant cells and central necrosis

Seen in tuberculosis, histoplasmosis and schistosome infection

Slide 32 · Granulomatous infection need not be necrotizing

Granuloma component

Meaning

Epithelioid macrophages

Activated macrophage aggregation

Multinucleated giant cells

May arise by macrophage fusion

Central necrosis

Possible, but not obligatory

Organism demonstration

Requires directed techniques and context

Slide 33 · Organisms to consider in hepatic granulomas

Histoplasma

Disseminated fungal infection

Mycobacteria

Disseminated bacterial infection

Schistosoma

Host reaction to deposited eggs

Slide 34 · How to establish a fungal or mycobacterial cause

Compatible histology

Microbiologic or serologic evidence

Visualization of organisms in biopsy

Integrated etiologic diagnosis

Slide 35 · Impaired T-cell immunity favors disseminated histoplasmosis

Histoplasma is an intracellular organism that depends on cellular immunity for containment.

Immunocompromised hosts are more vulnerable to disseminated disease.

Fungal liver disease should not be excluded because the primary portal of entry is respiratory.

Slide 36 · Applied case: Granulomas with hepatic involvement

Hypothetical teaching vignette

A patient with disseminated infection has hepatic epithelioid granulomas.

Necrosis is variable. Which etiologies and confirmatory strategies are supported by the textbook?

Histoplasma or mycobacteria; Serology, cultures, and tissue organism detection

Slide 37 · Parasitic infections: Diverse hepatic lesions

Example

Dominant hepatic consequence

Schistosoma spp.

Egg granulomas and portal fibrosis

Echinococcus spp.

Hydatid cyst formation

Entamoeba histolytica

Liquefactive necrosis and abscess

Liver flukes

Biliary disease and increased cancer risk

Slide 38 · Parasite location predicts tissue response

Portal vessels / tracts

Schistosome eggs and fibrosis

Parenchymal cyst

Hydatid disease

Necrotic cavity

Amebic abscess

Biliary system

Clonorchis / Opisthorchis / Fasciola

Slide 39 · Schistosomiasis: An ecological infection

Freshwater snail host

Infectious cercariae in freshwater

Human skin penetration

Vascular migration

Slide 40 · Schistosome migration connects gut and liver

Skin / peripheral vessels

Lungs and systemic circulation

Mesenteric and portal vessels

Eggs enter portal circulation

Slide 41 · The schistosome egg drives much of the injury

Egg lodging in liver

Host inflammatory reaction

Granuloma formation

Progressive portal fibrosis

Slide 42 · Early schistosomiasis: Inflammatory mediators

Th1 response

IFN-γ-associated macrophage activation

Macrophage cytokines

TNF, IL-1, IL-6

Acute effects

Inflammatory and febrile illness

Slide 43 · Chronic schistosomiasis: Profibrotic immunity

Persistent egg antigen

Th2-predominant response

Profibrotic macrophages

Progressive hepatic fibrosis

Slide 44 · Schistosome granuloma: Diagnostic constituents

Egg

Conceptual granuloma — not a micrograph

Egg at lesion center

Macrophages, lymphocytes, neutrophils

Eosinophils are conspicuous in helminth-associated lesions

Slide 45 · Early hepatic schistosomiasis morphology

Minute pale granulomas are scattered through the liver.

The central egg contains a miracidium, which can degenerate and calcify.

Liver macrophages may contain iron-free heme-derived pigment.

Slide 46 · Pipestem fibrosis: Portal expansion

Portal-tract widening: Schematic, not histology

Expanded fibrotic portal tracts

Relative preservation of intervening parenchyma

Portal vein narrowing and obliteration

Slide 47 · Why pipestem fibrosis differs from cirrhosis

Feature

Hepatosplenic schistosomiasis

Established cirrhosis

Fibrosis

Marked portal-tract widening

Fibrous septa surround nodules

Regenerative nodules

Typically absent in pipestem lesion

Present

Portal pressure

May become markedly elevated

Often elevated

Slide 48 · Presinusoidal obstruction produces portal hypertension

Portal tract fibrosis

Narrowing of portal venous flow

Presinusoidal resistance

Portal hypertension

Slide 49 · Consequences of schistosomal portal hypertension

Congestive splenomegaly

Back-pressure in portal system

Esophageal varices

Portosystemic collateral formation

Ascites

Portal circulatory disturbance

Slide 50 · Schistosomiasis can affect more than the liver

Eggs shunted to the lung can cause granulomatous pulmonary arteritis.

Advanced pulmonary vascular disease may lead to cor pulmonale.

Hepatosplenic disease is associated with certain glomerulopathies.

Slide 51 · Applied case: Portal hypertension without nodules

Hypothetical teaching vignette

A patient from an endemic region has portal hypertension and markedly expanded fibrotic portal tracts without regenerative nodules.

Which infection and morphologic label fit this pattern?

Chronic hepatosplenic schistosomiasis — pipestem fibrosis

Slide 52 · Echinococcus: Hydatid disease transmission

Canid definitive host sheds eggs

Human ingests contaminated food

Oncosphere invades intestinal wall

Larvae seed visceral organs

Slide 53 · Hydatid cysts: Why the liver is involved

Larvae cross intestinal wall

Hematogenous delivery

Cyst development in liver

Expansion or compression

Slide 54 · Hydatid cyst: Layered architecture

Host capsule

Laminated wall

Germinative layer

Simplified cyst anatomy — not a specimen image

Inner germinative layer

Outer laminated, non-nucleated layer

External host fibrous and inflammatory capsule

Slide 55 · Daughter cysts and hydatid sand

Simplified cyst anatomy — not a specimen image

Daughter cysts can form inside the mother cyst.

Brood capsules arise from the germinative lining.

Degenerating scolices yield sediment termed hydatid sand.

Slide 56 · Calcification provides an imaging clue

Wall calcification

Can occur as the cyst degenerates

Imaging consequence

May assist radiologic recognition

Interpretive limitation

Pattern must be placed in clinical context

Slide 57 · Large hydatid cysts may cause obstruction

Many infections remain clinically silent.

Expanding hepatic cysts can cause abdominal pain.

Large cysts may compress nearby biliary or other structures.

Slide 58 · Hydatid cyst rupture or spill is hazardous

Cyst content spill

Immediate hypersensitivity / anaphylaxis

Potential parasite dissemination

Caution during surgical manipulation

Slide 59 · Amebiasis: Fecal–oral acquisition

Ingestion of Entamoeba histolytica cysts

Colonic colonization and trophozoites

Tissue invasion

Potential portal dissemination

Slide 60 · Colonic invasion precedes hepatic amebiasis

Mucosal attachment

Epithelial death / crypt invasion

Flask-shaped ulcer

Access to splanchnic vessels

Slide 61 · Amebic liver abscess: Portal spread

Invasive colonic amebiasis

Entry to portal circulation

Liver tissue destruction

Necrotic abscess cavity

Slide 62 · Amebic abscess: Necrosis dominates

Schematic — not a histologic specimen

Pathologic interpretation

Extensive liquefactive tissue necrosis

Relatively limited inflammatory reaction at the margin

Shaggy fibrinous lining may be present

Slide 63 · Amebic disease may outlast intestinal symptoms

Hepatic abscess can persist after the acute intestinal illness resolves.

Large cavities can form; Extension to contiguous thoracic organs is possible.

The differential includes bacterial suppurative abscess, but tissue responses differ.

Slide 64 · Pyogenic and amebic liver abscesses: Contrast

Characteristic

Bacterial/pyogenic

Amebic

Mechanism

Bacterial seeding or ascending biliary infection

Portal dissemination of trophozoites

Dominant reaction

Suppurative inflammation

Liquefactive necrosis; Scant marginal infiltrate

Clinical overlap

Fever, right upper quadrant pain

Hepatic abscess may follow colitis

Slide 65 · Visceral leishmaniasis: Hepatic component

Systemic syndrome

Fever, weight loss, hepatosplenomegaly

Cellular location

Parasites within phagocytic cells

Late hepatic outcome

Increasing hepatic fibrosis

Slide 66 · Leishmania and the mononuclear phagocyte system

Sandfly transmission

Intracellular infection of macrophages

Dissemination through phagocyte system

Liver and spleen enlargement

Slide 67 · Malaria: Hepatic phase is part of the life cycle

Infected female Anopheles mosquito

Parasite deposited in host

Pre-erythrocytic liver stage

Subsequent erythrocytic infection

Slide 68 · Other parasites named in the hepatic differential

Strongyloides

Helminthic infection listed in hepatobiliary section

Cryptosporidium

Protozoal infection listed in hepatobiliary section

Fasciola hepatica

Liver fluke

Opisthorchis / Clonorchis

Liver flukes associated with biliary disease

Slide 69 · Liver flukes are a biliary cancer risk context

Chronic fluke infection

Persistent biliary tract injury

Increased cholangiocarcinoma risk

Association highlighted for Opisthorchis and Clonorchis

Slide 70 · Hepatobiliary infection can affect different compartments

Compartment

Examples

Major lesion

Bile ducts

Ascending bacteria; Liver flukes

Cholangitis or chronic biliary injury

Portal tracts

Schistosome eggs

Granulomas and fibrosis

Parenchyma

Bacteria; Entamoeba

Abscess and tissue necrosis

Mononuclear phagocytes

Histoplasma; Leishmania

Granulomatous or systemic disease

Slide 71 · An integrated pattern-based diagnostic approach

Define lesion pattern

Locate affected compartment

Check host and exposure context

Seek organism-specific evidence

Slide 72 · Microbiologic confirmation remains essential

Fungal / mycobacterial

Serology, blood culture, or biopsy organisms

Parasite-associated

Organism or characteristic tissue lesion

Bacterial obstruction

Clinical syndrome and biliary source

Any pattern

Interpret tests with clinical context

Slide 73 · Three high-yield clinicopathologic distinctions

Observation

Strongest concept

Fever + obstructive jaundice

Consider ascending cholangitis

Granulomas ± necrosis

Consider disseminated fungal / mycobacterial disease

Portal fibrosis without regenerative nodules

Consider schistosomal pipestem fibrosis

Laminated cyst with daughter cysts

Consider hydatid disease

Slide 74 · Applied case: Choose the dominant lesion

Hypothetical teaching vignette

A liver specimen contains a laminated cyst wall, germinative lining, and daughter cysts.

Which organism group is implicated, and why must spillage be avoided?

Echinococcus; Cyst contents can cause anaphylaxis or disseminate parasites

Slide 75 · Integrated review: Organism → lesion → consequence

Cause

Dominant lesion

Clinical consequence

Ascending bacteria

Cholangitis / abscess

Sepsis; Jaundice

Histoplasma / mycobacteria

Granuloma

Systemic disseminated infection

Schistosoma

Egg granulomas / portal fibrosis

Portal hypertension

Echinococcus

Hydatid cyst

Mass effect / spill risk

Entamoeba

Liquefactive abscess

Persistent hepatic disease

Slide 76 · Core references and scope

Robbins, Cotran & Kumar. Pathologic Basis of Disease. 11th ed. 2026. Chapter 18: Liver and Gallbladder, pp. 762–763.

Related primary-text sections: Chapter 8 (infectious response; histoplasmosis; schistosomiasis; echinococcosis; malaria; leishmaniasis).

Additional related text within source: Chapter 17 (amebiasis), Chapter 18 (large bile duct obstruction, portal hypertension, cholangiocarcinoma).