Revealing the Hidden Pathogen: The Role of Positron Emission Tomography in Diagnosing Amoebic Liver Abscess in an Immunocompetent Patient

Introduction

Amoebic liver abscess (ALA) is a parasitic infection resulting from Entamoeba histolytica (EH), an intestinal protozoan. Transmission typically occurs through the consumption of food or water contaminated with the cyst form of EH, which is the infective stage. These cysts withstand gastric acidity and travel to the distal ileum, where they excyst to release trophozoites — the active, feeding form of the parasite. In over 90% of infected individuals, trophozoites remain confined to the intestinal lumen, feeding on bacteria and mucosal cells without causing clinical symptoms. However, in less than 1% of cases, the trophozoites invade the intestinal mucosa and spread to the liver via the portal circulation, leading to the formation of liver abscesses. Among the various clinical presentations of amoebiasis, ALA is the most prevalent and carries the highest risk of mortality. It continues to be the leading cause of liver abscess in developing and resource-limited settings.1

Although asymptomatic EH infections occur at similar rates in both genders, invasive amoebiasis, particularly ALA, is significantly more common in males, who are four to nine times more likely to develop the condition than females. This gender disparity has been documented even among travellers from non-endemic regions. The heightened susceptibility in males is believed to be associated with hormonal influences — particularly testosterone — as well as higher rates of alcohol consumption. Once EH trophozoites invade the colonic mucosa, they can reach the liver through the portal venous system. The right lobe of the liver is most frequently affected, likely because it receives the majority of portal blood via the superior mesenteric vein, which drains the caecum — the primary site of trophozoite invasion.2

Each year, EH is responsible for an estimated 40,000 to 100,000 deaths worldwide, making it the second leading cause of mortality among parasitic infections, surpassed only by malaria. Although invasive amoebiasis develops in less than 10% of infected individuals, once the parasite overcomes the host’s innate immune defences, it can lead to serious complications such as amoebic colitis and liver abscesses. At the molecular level, EH employs a key virulence factor known as the Gal/GalNAc lectin to facilitate tissue invasion. This lectin plays a dual role: it enables the parasite to adhere to and invade host tissues and simultaneously triggers an antibody response that can inhibit further adherence, offering some degree of protection against recurrent or severe disease.3

Clinically, amoebiasis presents in two primary forms: intestinal and extraintestinal. The intestinal form, which is the most common, arises when EH invades the colonic mucosa — typically in the caecum or ascending colon. Clinical manifestations range from mild abdominal discomfort to severe ulcerative colitis, characterised by bloody and mucus-laden stools, also known as amoebic dysentery. On the other hand, extraintestinal amoebiasis occurs when the parasite spreads beyond the gastrointestinal tract, affecting other organs. Among these, hepatic amoebiasis (liver abscess) is the most frequent, followed by pulmonary involvement, making the liver and lungs the two most commonly affected sites in extraintestinal disease.4

Case Report

A 26-year-old male patient presented with complaints of high-grade fever with chills and rigours persisting for four days, followed by vomiting containing food particles (non-bilious, non-blood stained) and dull aching, continuous, abdominal pain in the right hypochondrial region. The patient had a recent history of outside food consumption. There were no complaints of loose stools, haematochezia, or malaena. There was no significant past medical history, drug allergies, chronic illnesses or chronic drug use.

On presentation, the patient’s vitals were as follows: he was febrile with a temperature of 101.9°F, blood pressure 110/70 mmHg, pulse rate 114 beats per minute (bpm), and SpO₂ 98% on room air. Physical examination revealed intercostal tenderness in the right hypochondrial region. Bowel sounds were normal, and the rest of the systemic examination was unremarkable. The patient was empirically started on intravenous (IV) levofloxacin 500 mg once daily and ceftriaxone 1 g twice daily, along with other supportive measures.

Initial laboratory investigations indicated an infectious aetiology, as shown by leucocytosis (white blood count [WBC]-13,150) and raised procalcitonin (1.6). Imaging studies, including abdominal ultrasonography (USG), suggested partial gallbladder distension but no liver parenchymal involvement. Chest X-ray was normal. The prothrombin time/international normalised ratio (PT/ INR) was 14.6/1.34. Urine routine was normal. Laboratory investigations are shown in Table 1.

Discussion

The term amoebic liver abscess (ALA) is somewhat misleading, as cavity formation and liquefaction do not result from suppuration but rather from a distinctive type of necrosis. The necrotic tissue appears as though chemically dissolved, leading to the early belief that EH secretes a toxin capable of lysing hepatocytes — hence the species name histolytica. However, it is now understood that proteolytic enzymes released primarily by inflammatory cells, play the central role in hepatic tissue destruction.

The gross morphology of ALA varies according to disease stage and severity. In the early phase, lesions consists of a central area of liquefied necrotic tissue, often described as chocolate-coloured sterile pus. This liquefied material within the abscess contains red blood cells (RBCs), leucocytes, and disintegrated hepatocytes, producing the classic reddish-brown appearance often likened to chocolate sauce or anchovy sauce. This necrotic core is surrounded by a zone of partially liquefied and solid tissue, giving the abscess wall a ragged or shaggy appearance. Notably, a mature fibrous capsule is absent at this stage. The surrounding hepatic tissue is typically congested, compressed, and oedematous, and mass effect may cause pressure on adjacent liver parenchyma or the hepatic capsule. In fatal cases, venous thrombosis and ischaemic infarction are frequently observed.

Clinically, ALA manifests in three forms:

• Subacute mild ALA (~80%) is the most common form. It develops over 2–4 weeks with low-grade symptoms like fever, right upper quadrant pain, and hepatomegaly. Symptoms usually resolve rapidly with medical treatment. A characteristic finding on physical examination is localised tenderness over the right intercostal spaces. Organ dysfunction is minimal or absent.
• Acute aggressive ALA (~13%) is severe and rapidly progressive, presenting with high-grade fever, chills, and pronounced right upper quadrant tenderness due to exquisitely tender hepatomegaly. One of the hallmark features of this form is spontaneous abscess rupture, which may be the initial presentation in up to 57% of cases. Free intraperitoneal rupture frequently results in generalised peritonitis, necessitating hospitalisation, abscess drainage, and carries high mortality. Due to its severity, hospitalisation is required in up to 90% of cases, and around 13% may necessitate intensive care unit (ICU) admission. Misdiagnosis is common, as clinical features overlap with acute cholecystitis, appendicitis, or bowel perforation. Unlike in subacute disease, medical therapy alone is often insufficient. In most cases, abscess drainage — either via needle aspiration or catheter insertion — is required to achieve clinical improvement.
• Chronic indolent ALA (~10%–20%) is prolonged and milder, presenting with dull pain, systemic symptoms like weight loss, and complications like secondary infection. A history of previous medical therapy or even prior needle aspiration is frequently reported. Imaging plays a key role in evaluation.

Imaging plays a critical role in differentiating these clinical forms. Contrast-enhanced CT is particularly valuable, as it differentiates viable hepatic tissue from necrotic areas, allowing better distinction between chronic necrotic masses and active, aggressive abscesses. Acute ALA (Type 1) typically appears as ragged-edged lesions; subacute ALA (Type II) shows rim-enhancing walls with a thin rim of perilesional oedema, producing a “halo sign”; chronic ALA (Type III) demonstrates thick, non-enhancing fibrotic walls.1

ALA has a highly variable presentation, causing diagnostic difficulties. Uncommon manifestations occur due to abscess rupture into neighbouring cavities — pleura, pericardium, peritoneum — or compression of tubular ALA has a highly variable presentation, causing diagnostic difficulties. Uncommon manifestations occur due to abscess rupture into neighbouring cavities — pleura, pericardium, peritoneum — or compression of tubular structures in the hepatic hilum, or distant embolic dissemination.5 The diagnosis of ALA is confirmed by microscopic examination of aspirated pus, which characteristically resembles anchovy sauce. Aspiration is particularly indicated when the abscess exceeds 10 cm, shows a thin rim of liver parenchyma suggesting impending rupture, or demonstrates rapid enlargement.6

The laboratory diagnosis of amoebiasis relies on a combination of parasitological, serological, and molecular methods. Parasitological techniques, such as microscopy and culture, remain foundational, with microscopic detection of EH in stool, tissue, or body fluid samples still considered the diagnostic gold standard. However, microscopy is limited by low sensitivity and specificity, especially in distinguishing EH from non-pathogenic species. Serological tests such as enzyme-linked immunosorbent assay (ELISA), indirect haemagglutination assay (IHA), and latex agglutination are widely used for diagnosing extraintestinal amoebiasis, where stool microscopy often fails. In recent decades, the polymerase chain reaction (PCR) technique has emerged as a highly sensitive and specific tool for detecting EH deoxyribonucleic acid (DNA). In addition, imaging modalities such as USG, CT, magnetic resonance imaging (MRI), and radiography have become valuable adjuncts for diagnosing hepatic and other extraintestinal forms of amoebiasis, aiding in localisation, characterisation, and monitoring of abscesses and other lesions.4

Metronidazole remains the most effective agent, with cure rates approaching 90%.1 It is typically administered IV at 750 mg three times daily for 7–10 days. In severe cases, other agents such as emetine, dehydroemetine, and chloroquine may be considered. The risk of complications increases with larger abscess size and multiplicity of abscesses. Autopsy studies reveal that up to 60% of fatal cases involve multiple abscesses, often measuring 10 to 15 cm. Comparative data from Southeast Asia report a higher incidence of large (> 5–10 cm) and multiple abscesses in approximately 50% of cases, highlighting geographic variation.1