Infectious Diseases of Liver

Advancements in technology have brought about significant improvements in the role of medical imaging when it comes to detecting, characterizing, and managing infectious diseases affecting the liver. One noteworthy development is the utilization of imaging-guided percutaneous drainage, aspiration, or biopsy, which has revolutionized the clinical treatment of patients dealing with focal liver abscesses. By leveraging imaging techniques such as ultrasonography (US), computed tomography (CT), and magnetic resonance (MR) imaging, healthcare providers can now accurately assess infectious liver diseases.

In this detailed comparison, we explore infectious pathologies affecting the liver, shedding light on their origins, routes of transmission, histopathological characteristics, clinical manifestations, laboratory investigations, and imaging findings. We delve into the first-line and medical management strategies, as well as potential surgical and interventional radiology interventions where applicable.

Comparing Various Infectious Disease effecting Liver:

Infectious PathologyEtiologyRoute of SpreadHistopathologyClinical FeaturesLab InvestigationsUSG FeaturesCT FeaturesMRI FindingsManagement
Pyogenic Liver AbscessBacterial infection (e.g., E. coli - most common, Klebsiella)Hematogenous (Portal vein/hepatic artery),
Biliary (Ascending Cholangitis)
1. Microscopic examination of the abscess shows various stages, including suppuration, liquefaction with the presence of fibrinopurulent debris, and fibrosis.
2. The borders are composed of a
- chronic inflammatory infiltrate (consisting of macrophages, lymphocytes, eosinophils, and neutrophils) and
- fibrous cuff (which is over a centimeter thick and gradually merges into the liver parenchyma)
3. Gas formation (more common with Klebsiella infection) can be noted in 20% of liver abscess and can either appear as air-fluid level or in form of bubbles. Should be differentiated from non-septic gas formation after tumor ablation.
4. Transient hepatic changes, thought to be due to inflammation and reduced portal venule flow around abscesses, leads to portal flow reduction and compensatory increased arterial flow. This leads to transient hepatic attenuation or signal intensity difference and needs to be distinguished from tumors causing similar enhancement due to vein stenosis or occlusion.
1. Fever - high grade with rigor
2. Abdominal pain - severe pain in right hypochondrium or vague abdominal pain,
3. Hepatomegaly
1. Complete blood count (CBC) - shows raised TLC count
2. Liver function tests (LFTs) - can be non-specific
3. Pus sample obtained from Image guided intervention like aspiration / drainage can be sent for gram staining, routine culture and sensitivity and various other investigations specific to bacterial etiology
1. Well defined Hypoechoic lesion with or without internal echoes.
2. Gas in hepatic abscess - present in non dependent portion of hepatic abscess causing acoustic shadowing or reverberation artifact and difficulty in proper visualisation of abscess.
1. Well defined hypoattenuating lesion
2. Unilocular with smooth margins
3. Complex with internal septa and irregular contour
4. Gas component can be much easily visualised as compared to Ultrasound
5. Cluster Sign - aggregation of multiple low attenuation liver abscesses forming a larger solitary abscess cavity
6. Contrast enhanced CT
- Peripheral rim enhancement with peri-abscess edema can be seen
- Double target sign - central low attenuation fluid-filled area is surrounded by a high attenuation inner rim (showing early enhancement) and a low attenuation outer ring (showing enhancement in delayed phase)
T1: Hypointense due to necrotic tissue and gas (but can vary depending upon the protein content of the abscess)

T2: Hyperintense signal, Perilesional oedema also manifests as high signal intensity on T2-weighted images

T1 C+ (Gd): enhancement of the capsule, although this may be absent in immunocompromised patients

DWI: High signal within the abscess cavity, and at the periphery

ADC: Low signal within the abscess cavity, and high signal at the periphery

Gas: Appears as area of signal void within the abscess
1. Antibiotics for 4-6 weeks but the actual duration can vary depending upon clinical response and type of infection.
2. Image guided percutaneous aspiration/drainage
3. Surgical management
Amebic Liver AbscessEntamoeba histolytica (amoeba)Fecal-Oral (colonic involvement)
Hepatic involvement occurs due to hematogenous spread via portal vein
1. Anchovy paste material is the chocolate coloured material - occurs due to haemorrhage into the abscess cavity.
2. Gas formation is rarely seen
1. Fever - high grade with rigor
2. Abdominal pain - severe pain in right hypochondrium or vague abdominal pain,
3. Hepatomegaly
4. Extrahepatic pathology can be present:
- pleural effusion
- perihepatic fluid collection (likely after rupture of abscess)
- gastric or colonic involvement
- retroperitoneal extension

1. Serology (antibody detection) - can be negative in acute infection (repeat after 7-10 days if needed)
2. Stool examination (cysts/trophozoites).
3. Pus sample obtained from Image guided intervention can be sent for amoebic serology
1. Well defined Hypoechoic lesion with or without internal echoes.
2. Can show posterior acoustic enhancement
1. Well defined hypoattenuating lesion
2. Unilocular with smooth margins
3. Complex with internal septa and irregular contour

4. Contrast enhanced CT
- Peripheral wall enhancement with peri-abscess edema can be seen (characteristics of the lesion)
T1: Hypointense due to necrotic tissue (but can vary depending upon the protein content of the abscess)

T2: Hyperintense signal, Perilesional oedema also manifests as high signal intensity on T2-weighted images
1. Anti-parasitic drugs for 4-6 weeks but the actual duration can vary depending upon clinical response.
2. Image guided percutaneous aspiration/drainage
3. Surgical management
Hydatid Disease (Echinococcosis)Echinococcus granulosus
Ingestion of eggs, Fecal-Oral route,

1. Consists of three layers
A. Outer Pericyst - compressed and fibrosed liver tissue
B. Endocyst - Inner germinal layer
C. Ectocyst - Thin, translucent interleaved membrane
2. Peripheral calcification can be seen in both viable and non viable cyst
3. Maturation of cyst - development of daughter cyst
Asymptomatic and incidentally detected until cyst grows, abdominal discomfort (right upper quadrant), anaphylaxis (rupture), cholangitis (Biliary Echinococcosis - due to biliary obstruction caused by the daughter vesicles).1. Serology (IgE antibody detection) - positive in only 25% of patients
2. Eosinophilia
3. Concomitant use of IHA (indirect hemagglutination) and ELISA is associated with diagnostic sensitivity rates up to 85%-96%
4. LFTs - Hyperbilirubinemia and increased levels of alkaline phosphatase and gamma glutamyl transferase indicate communication of the cyst into the biliary tract
5. Radioallergosorbent test - confirm the presence of active hydatid disease
Gharbi classification and WHO classification
(See below)
1. Well-defined cystic mass with distinguishable mass.
2. Daughter cysts and coarse wall calcifications can also be noted.
1. Pericyst: T1 Hypointense, T2 Hypointense (fibrous component and calcification)
2. Hydatid Matrix: T1 Hypointense, T2 Hyperintense
3. Daughter Cyst: relatively hyperintense to matrix on T2
4. No enhancement (both cyst content and septa) after contrast administration
5. Some cyst can show intracystic fat content or air fluid level demonstrating a communication bile with biliary channel.
1. Anti-parasitic drugs (prevention),
2. Surgical removal (curative)
3. PAIR (percutaneous aspiration, injection, reaspiration)
TuberculosisMycobacterium tuberculosis1. Hematogenous spread - Miliary tuberculosis (more common)
2. Focal or nodular Tuberculosis
Granulomatous inflammation1. Weight loss,
2. Night sweats
3. Evening rise of temperature
1. USG guided liver SOL biopsy (saline sample) / aspiration is almost always required to establish the diagnosis - ZN stain, Gene expert for TB, AFB Direct Fluorescent Microscopy (DFM), MTB culture and sensitivity and other TB specific test can be conducted to rule out MDR TB and start specific Anti-tubercular regime.
2. Mantoux tuberculin skin test
3. Raised ESR
4. LFTs can be non-specific, however is required at regular interval once Anti-tubercular regime has been started
Imaging findings are generally non-specific including:
- Hepatosplenomegaly
- Tubercular abscesses
- Tuberculoma - well defined, round, hypoechoic lesion
- Tubular and heptobiliary tuberculosis
Multiple well defined hypoattenuating hepatic lesions on both NCCT and CECT, calcifications.1. Caseating granulomas
- T1: low signal
- T2: intermediate and high signal
- T1 C+ (Gd): variable

2. Non caseating granulomas
- T1: intermediate signal
- T2: intermediate signal
- T1 C+ (Gd): increased enhancement on arterial phase images with persistent enhancement in delayed images.
1. Anti-tubercular therapy regimen for abdominal tuberculosis
2. Percutaneous abscess drainage (large abscess)
3. Surgical resection (less favourable due to poor wound healing post surgery)
SchistosomiasisSchistosoma species (e.g., S. mansoni, S. japonicum)Penetration of skin by larvae1. Eggs trapped in liver cause granulomatous response and pre-sinusoidal hypertension
2. Chronic infection can cause cirrhosis and risk for hepatocellular carcinoma
3. Granulomas in the liver, containing macrophages, lymphocytes, neutrophils, and eosinophils, are darkened by heme pigments from schistosomes.
Acute: fever, abdominal pain, diarrhea; Chronic: hepatosplenomegaly, liver fibrosis, portal hypertension1. Serology (antibody detection),
2. Stool examination (eggs)
3. Eosinophilia
4. No role of Imaging in case of acute infections
In case of Chronic infection:

1. Irregular hepatic surface
2. Mosaic pattern: echogenic septa forming polygonal areas of relatively normal liver
3. Bull’s-eye appearance: an anechoic portal vein surrounded by echogenic fibrous tissue (occurs due to Portal veins wall thickening and increased echogenicity)
4. Later stages will show feature of cirrhosis and hepatocellular carcinoma
In case of chronic infection:

1. Features similar to USG
2. Turtle back sign: calcified septa and fibrosis resembling a turtle carapace, considered pathognomonic
3. Periportal fibrosis: low-attenuation rings surrounding the portal vein branches through out liver
Not much role in establishment of diagnosisAnthelminthic drugs (
praziquantel)
Viral Hepatitis (Acute and Chronic Forms)1. Various hepatitis viruses (A, B, C, D, E) and
2. Other viruses (e.g., herpes, yellow fever, rubella, Coxsackie, adenovirus).
Varies by virus; can be fecal-oral, bloodborne, sexual, perinatal, or via skin penetration by larvae in the case of schistosomiasis.1. Acute Viral Hepatitis:
- Necrosis of random isolated liver cells or small cell clusters.
- Diffuse liver cell injury.
- Reactive changes in Kupffer cells and sinusoidal lining cells.
- Inflammatory infiltrate in portal tracts.
- Evidence of hepatocytic regeneration during recovery.
- Confluent necrosis may lead to bridging necrosis in severe cases.
2. Chronic Hepatitis:
- Variable morphologic features.
- Inflammatory infiltrate limited to portal tracts in mild cases.
- Progressive disease marked by piecemeal necrosis, fibrous septum formation, and hepatocyte regeneration leading to cirrhosis.
- Fatigue, jaundice, dark urine, pale stool
- Range from asymptomatic to fulminant acute infections.
- Subclinical persistent infections.
- Rapidly progressive chronic liver disease with cirrhosis (common to HBV and HCV).
1. Diagnosis based on serologic, virologic, and clinical findings.
2. Specific tests for viral identification and liver function tests (elevated liver enzymes).
3. Additional tests based on the specific virus.
1. Nonspecific findings in acute hepatitis, which may include hepatomegaly and a "starry night" pattern.
2. Chronic hepatitis can manifest as coarsened hepatic echotexture and increased parenchymal echogenicity.
1. Nonspecific findings in acute viral hepatitis, including hepatomegaly and periportal edema.
2. Heterogeneous enhancement and regions of low attenuation may be present.
1. In acute hepatitis, periportal edema appears as high-signal-intensity areas on T2-weighted images.
2. Involved areas may show decreased signal intensity on T1-weighted images and increased signal intensity on T2-weighted images.
1. Early detection and diagnosis are essential.
2. Supportive care and monitoring in mild cases.
3. Specific antiviral therapy in chronic cases.
4. Management of complications, such as cirrhosis and hepatocellular carcinoma (Techniques like transarterial chemoembolization, ablation therapies)
5. Liver Transplant
CandidiasisCandida speciesHematogenous1. Typical pattern: Microabscesses with yeast or pseudohyphal forms in the centre, surrounded by necrosis and polymorphonuclear infiltrate.
2. Healing stage: Smaller microabscesses and increased fibrous tissue.
3. Can also form granulomas within liver.
--1. Wheel-within-a-wheel" appearance with central hypoechoic area of necrosis and surrounded by an echogenic zone. Peripheral hypoechoic area represents fibrosis.
2. Bull's-eye configuration with central echogenic nidus surrounded by a hypoechoic rim.
3. Uniformly hypoechoic nodule (most common presentation but less specific).
4. Echogenic foci with variable posterior acoustic shadowing (indicating early resolution).
1. Fungal microabscesses appear as multiple round, discrete areas of low attenuation, typically 2 to 20 mm.
2. Enhancement after intravenous contrast administration, usually central, but peripheral enhancement may occur.
1. Untreated nodules:
- Rounded lesions <1 cm,
- Minimally hypointense on T1-weighted and gadolinium-enhanced images,
- Markedly hyperintense on T2-weighted images.

2. Subacute presentation after treatment:
- Mildly to moderately hyperintense on T1- and T2-weighted images, enhancement on gadolinium-enhanced images.
- Dark ring is present around the lesion in all sequences.

3. Completely treated lesions:
- Minimally hypointense on T1-weighted images,
- Isointense to mildly hyperintense on T2-weighted images,
- Moderately hypointense on early gadolinium-enhanced images with minimally hypointense on delayed gadolinium-enhanced images.
Antifungal therapy, source control

Ultrasonographic Classification for Hydatid cyst:

Gharbi TypeWHO TypeCyst MorphologyViabilityManagement
ICE 1Unilocular anechoic lesion with double line signActive< 5 cm - Albendazole
> 5 cm - Albendazole + PAIRS
IIICE 2Multiseptated rosette like honeycomb cystActiveAlbendazole + Surgery
IICE 3ACyst with detached membranes (water-lily sign)Transitional< 5 cm - Albendazole
> 5 cm - Albendazole + PAIRS
IIICE 3BCyst with daughter cysts in solid matrixTransitionalAlbendazole + Surgery
IVCE 41. Cyst with heterogenous hypoechoic/hyperechoic contents resembling ball of wool
2. No daughter cysts
InactiveFollow up
VCE 5Solid plus calcified wallInactiveFollow up
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