CYSTICERCUS CELLULOSAE (Cysticercosis)

GEOGRAPHICA DISTRIBUTION

This is common where Taenia solium infection is prevalent especially south and Central America, South and east Africa, India and former Russian Federation countries.

LOCATION IN HOST

Cysticerci may be found in any organ or tissue of the body as they carried by the blood stream on hatching of the onchosphere in the small intestine. Common sites are the brain, skeletal muscles, heart and the eye.

MORPHOLOGY

Cysticercus cellulosae (commonly called ‘bladder worm’) are ovoid white and measure 8*5 mm and are easily visible to the naked eye. Each Cysticercus cellulosae consists of a fluid filled bladder with a small protoscolex invaginated into the lumen. The protoscolex has four suckers and two rows of hooks (Cysticercus bovis of Taenia saginata has no hooks).

TRANSMISSION

Accidental ingestion of Taenia solium eggs which are passed in infected person’s faeces may take place via contaminated green vegetables, fruits or drinking water. Since about 25% of patients with Cysticercosis also harbour adult Taenia solium in small intestine it is possible that autoinfection takes place following regurgitation of segments or eggs into stomach. The eggs need to pass through the stomach, as gastric acid is responsible for the dissolution of the thick wall of the eggs. Infection may take place from anus to fingers to mouth.

PATHOGENESIS

This is related to the organ affected. Generally the cysts are distributed throughout the body roughly in proportion to the weight of the organ. The living cysts cause only mild symptoms unless the path of CSF flow is blocked (cerebral infection). Severe pathology is seen following the death of the cysts due to inflammatory reactions. Allergic manifestations due to leakage of fluid also occur.

CLINICAL FEATURES

The clinical presentation of Cysticercosis depends on the number and location of cysticerci as well as the extent of associated inflammatory responses or scarring.

1. Cerebral Cysticercosis; minors symptoms related to the Central Nervous System are common but the most serious manifestations are epileptiform fits. These seizures may be generalized, focal, or Jacksonian. Hydrocephalus results from obstruction of cerebrospinal fluid (CSF) flow by cysticerci and accompanying inflammation or by CSF outflow obstruction from arachnoiditis. Signs of increased intracranial pressure, including headache, nausea, vomiting, changes in vision, dizziness, ataxia, or confusion, are often evident. Cysticerci in different part of the brain could give rise to motor, sensory and psychological symptoms. The cysticerci may get calcified.

2. Muscle Cysticercosis; this is common site. They could sometimes be felt as nodules. Muscle cysts are usually more elongate than others. These cysts get calcified earlier.

3. Ocular Cysticercosis; The cysts lodged in the eye cause pain and blurring of vision. With time and with encapsulation these cause severe damage to the eye.

4. Cardiac Cysticercosis; in the heart the cysts can be found in the epicardium, myocardium and endorcadium.

DIAGNOSIS

There are different types of diagnostic methods are available. The method which should be employed depends on the organ system which is suspected be affected. Radiological, histological and serological tests are useful.

1. Radiological: X-rays are useful to demonstrate calcified cysts in muscles. CT scan is important to detect the cerebral Cysticercosis.

2. Histological: Palpable cysts in the muscles can be identified by following biopsy.

3. Serological: Several specific serological tests, including PCR are now available.

PREVENTION AND CONTROL

This is same as for Taenia solium. Improvement of sanitary habits and environmental hygiene are important.

TREATMENT

There is no specific treatment. Various drugs such as albendazole and praziquantel have been used. However, praziquantel can evoke an inflammatory response in the central nervous system. Niclosamide (2 g) is also effective but is not widely available.

The management of neurocysticercosis focuses primarily on symptom-based treatment of seizures or hydrocephalus. Seizures can usually be controlled with antiepileptics. If parenchymal lesions resolve without development of calcifications and patients remain free of seizures, antiepileptic therapy can usually be discontinued after 2 years. High-dose Glucocorticoids can be used during treatment or if symptoms worsen. Since glucocorticoids induce first-pass metabolism of praziquantel and may decrease its antiparasitic effect, cimetidine should be coadministered to inhibit praziquantel metabolism.

For patients with hydrocephalus, the emergent reduction of intracranial pressure is the mainstay of therapy. In the case of obstructive hydrocephalus, the preferred approach is removal of the cysticercus via endoscopic surgery. However, this intervention is not always possible. An alternative approach is initially to perform a diverting procedure, such as ventriculoperitoneal shunting. Historically, shunts have usually failed, but low failure rates have recently been attained with treatment with antiparasitic drugs, chronic administration of glucocorticoids, or use of flow-sensitive shunts. Open craniotomy to remove the cysticerci is now required only infrequently. For patients with subarachnoid cysts or giant cysticerci, glucocorticoids are needed to reduce arachnoiditis and accompanying vasculitis.