Teaching Case

A 19-year-old man presented to the emergency department with seizures and febricula. His laboratory examinations showed leukocytosis and neutrophilia. No respiratory or digestive symptoms were noted. Emergency cranial CT and a chest X-ray were performed.
Thereafter, a body CT and cranial MRI were done in order to complete the study.

Cranial CT showed a rounded hypodense lesion with mild peripheral enhancement in the parietal region in the convexity, without significant mass effect and no displacement of midline shift (Fig. 1).

Emergency chest X-ray showed multiple and bilateral pulmonary nodules (Fig. 2).

The imaging study was completed with body CT and cerebral MRI.

Body CT demonstrated multiple hypodense pulmonary nodules, most of them peripheric (Fig. 3). In the left hepatic lobe, there was a well-defined heterogeneous low density lesion with peripheral focal areas of calcification.
Additional thoracic US was performed to confirm the cystic nature of the nodules. It showed several hypoechoic lesions with posterior enhancement in the lung parenchyma (Fig. 4).
Cerebral MRI shows a single rounded lesion in the left parietal region. The lesion was hypointense on T1- and hyperintense on T2-weighted images with mild peripheric post-contrast enhancement. A moderate perilesional oedema was demonstrated (Fig. 5).
These findings strongly suggested the diagnosis of disseminated hydatid disease and it was confirmed by serological tests for Echinococcus granulosus.

Hydatid cysts (HCs) result from infection by the Echinococcus worm, and can result in cyst formation anywhere in the body [1-7]. The liver acts as the first line of defence and is therefore the most frequently involved organ. Secondary involvement due to haematogenous dissemination may be seen in almost any anatomic location [1].
The diagnosis of hydatid disease is generally based on the identification of a cystic sign by imaging and detecting specific antibodies against the parasite by immunological tests. [3]

The imaging method used depends on the involved organ and the growth stage of the cyst. US most clearly demonstrates the hydatid sands in purely cystic lesions, as well as floating membranes, daughter cysts, and vesicles. CT is best for detecting calcification and revealing the internal cystic structure posterior to calcification. MR imaging is especially helpful in detecting HCs of the central nervous system [2, 5].

The lung is the second most common site of haematogenous spread in adults and probably the most common site in children. Pulmonary HCs have a predilection for the right posterior lung segments, with half of the cases manifesting in the lower lobes. Multiple cysts occurs in 30% of cases. Concurrent involvement of the liver and lungs is seen in approximately 6% of all patients with HCs. Pulmonary HCs may vary from 1 to 20 cm in diameter [1-3].

Cerebral HCs is extremely rare, accounting for only 2% of all intracranial masses. It is more common in children than in adults.
In brain hydatidosis, symptoms and signs of intracranial hypertension are currently encountered, followed by hemiparesis, epilepsy, mental changes and skull deformities [6].
HCs are mostly supratentorial and located in the territories of the middle cerebral artery but can be seen anywhere within the brain. The parietal lobe is most frequently involved.
Generally it appears unilocular and is isointense or isoattenuating relative to cerebrospinal fluid. Fine peripheral enhancement can be seen in the fibrous capsule. The presence of a hypointense rim, especially on T2- weighted MR images, is characteristic of HCs of the brain. Cerebral HCs is generally solitary but may be multiple when it ruptures spontaneously or due to trauma or surgery. [2, 4]

Medical therapy with benzimidazoles is valuable in disseminated disease, as in our case, including secondary lung or pleural hydatidosis, poor surgical risk patients and when there is intraoperative spillage of hydatid fluid [3].