Echinococcus granulosus

Author: MBLOGSTU

Introduction

Infection with Echinococcus is naturally transmitted between humans and animals, making it one of the most significant zoonoses. The clinical and economic importance of the parasite is almost entirely confined to its larval stage (the metacestode), known as a hydatid cyst. Here, the terms “hydatid disease” or “hydatidosis” refer specifically to the metacestode infection, whereas “echinococcosis” applies to the adult stage.

Epidemiology

Cystic echinococcosis (CE) is caused by the larval stage of Echinococcus granulosus and is found in Africa, Europe, Asia, the Middle East, Central and South America, and, in rare cases, North America.

Dogs become infected when they ingest organs containing hydatid cysts from intermediate hosts (sheep, cattle, goats, pigs). The cysts develop into adult tapeworms in dogs which then shed eggs in their feces. These eggs contaminate the ground and can be ingested by herbivores. Humans most often acquire the infection by accidentally consuming soil, water, or food contaminated with these eggs. Notably, the eggs remain viable in soil for up to a year.

The disease is most frequent among individuals involved in sheep rearing because of the role of sheep as intermediate hosts and the frequent access of working dogs to infected offal.

Hydatid Cyst

The larval stage, or hydatid cyst, is the key pathological unit in human infection.

• Structure:
  • Outer layer (Ectocyst): Measures about 22–25 μm in thickness, gives rise to brood capsules with scolices, secretes hydatid fluid, and forms the outer layer.
  • Inner germinal layer (Endocyst): The active layer that produces brood capsules and scolices.
• Characteristic Features:
  • Clear, colorless fluid
  • Specific gravity: 1.005–1.010
  • Slightly acidic
  • Contains sodium chloride, sodium sulfate, sodium phosphate, and sodium and calcium salts of succinic acid
  • Antigenic and highly toxic
  • Contains hydatid sand

Life Cycle

Although the detailed cycle is not fully elaborated here, the typical cycle involves transmission from definitive hosts (dogs) to intermediate hosts (sheep, cattle, etc.), with humans becoming accidental hosts upon ingestion of contaminated material.

Pathogenesis

The damage produced by Echinococcus granulosus is mainly mechanical. Young cysts developing from embryos lodged in vital centers may interfere with normal organ function and may even be fatal. In some cases, a benign cyst remains asymptomatic while in others it produces a significant physical burden.

The severity of the disease depends on the type of cyst and the organ or tissue where it is implanted. In addition, anaphylactic reactions can develop, particularly if a cyst suddenly ruptures.

Clinical Manifestations

Clinical manifestations vary depending on the location of the hydatid cyst.

Hepatic Hydatid (Approximately 66%)

In the liver, hydatid cysts commonly occur in the right lobe (extending towards the inferior surface and into the abdominal cavity) or in the dome. They can grow slowly until they produce:

• No symptoms until the cyst increases in size
• Pressure on bile ducts
• Cyst rupture
• Secondary new cysts form through seeding with hydatid sand or fragments of the germinal layer
• If rupture occurs into the bile ducts, it may lead to intermittent jaundice, fever, and eosinophilia
• Allergic manifestations – potentially up to anaphylactic shock – may occur on sudden rupture

Pulmonary Cysts (Approximately 22%)

Early symptoms include haemoptysis, transient thoracic pain, and shortness of breath. In many cases, a pulmonary cyst may develop into a chronic pulmonary abscess if the rupture is incomplete. Patients may complain of a sudden cough with sputum containing frothy blood, mucus, and hydatid sand.

Brain Cysts (Approximately 1%)

A large brain cyst may lead to increased intracranial tension, resulting in headache, vomiting, blurred vision, and potentially epilepsy.

Renal Cysts (Approximately 3%)

Renal hydatid cysts can cause intermittent pain and haematuria, and hydatid sand may be present in urine.

Osseous Cysts (Approximately 2%)

Osseous cysts lack a fibrous tissue or laminated layer and consist only of the germinal layer. Initially developing in the marrow cavity, they eventually extend into osseous tissues, leading to:

• Erosion of extensive areas of bone
• Destruction of bone trabeculae
• Spontaneous (pathological) fractures

Diagnosis

The diagnosis of cystic echinococcosis relies on clinical history, imaging, and laboratory tests.

Clinical Evaluation

A slowly growing cystic tumor in a patient with a history of close contact with dogs is a major clinical clue.

X-ray Imaging

X-ray imaging is particularly useful (especially for pulmonary cysts and calcified cysts) and may reveal:

• Rounded, solitary or multiple, sharply contoured cysts ranging from 1 to 15 cm in diameter
• Internal daughter cysts producing a “car wheel” appearance
• Thin crescent or ring-shaped calcifications

CT & Ultrasonography

Computed tomography (CT) and ultrasonography can detect uncalcified cysts and are of special value in the follow-up of treated cases.

Aspiration Cytology

Aspiration cytology can demonstrate acid‐fast hooklets using trichrome stain. However, this procedure is risky because it may cause:

• Implantation and formation of new cysts
• Anaphylactic shock

Additional Diagnostic Methods

• Detection of hydatid material in sputum or urine after surgery
• Serological tests (IHA, with ELISA preferred)
• Molecular diagnosis through DNA analysis or PCR
• The Intradermal Test of Casoni – note that this may give false positive results in approximately 18% of cases and can trigger allergic reactions
• High eosinophilia is also an important laboratory finding