Cysticercosis (Cysticercus cellulosae infection)
Essentials of Diagnosis
- Surgical excision of affected tissue, with microscopic identification of the parasite.
- Frequently calcified cysts visible on X-ray or computed tomography (CT) scans.
- Positive serology indicating previous exposure to T solium.
- Fine-needle aspiration of cysts (characteristic cytomorphology).
General Considerations
Cysticercosis is caused by invasion of tissues by the larval forms of T solium. These larvae have been referred to as Cysticercus cellulosea, although this name is not taxonomically correct and can be confusing. In a host infected with adult T solium, eggs or proglottids are passed in the stool. When eggs or proglottids are ingested by either pigs (intermediate hosts) or humans (definitive and intermediate hosts), the eggs hatch in gastric juice. This allows the cysticercus to migrate from the intestine to disseminated sites via efferent mesenteric venules. Autoinfection can also occur in humans, in which eggs produced by the adult intestinal worm hatch and invade the intestinal epithelium.
Clinical Findings
Signs and Symptoms
Symptoms associated with cysticercosis relate to the organ invaded by cysticerci and to the inflammatory reaction that occurs in response to the larva. In the brain, cysticercosis may cause arachnoiditis or chronic meningitis, with associated headache, vertigo, vomiting, and cranial neuropathies. Alternative presentations include obstructive hydrocephalus with ataxia and dementia, intracranial vasculitis with focal neurological signs and neuropsychiatric changes, or mass effect with seizures, headache, or focal neurological deficits. In addition, cord compression with lower limb weakness and loss of bowel and bladder continence may occur. Cysts outside the central nervous system tend to occur within muscle, are most often asymptomatic, and eventually die and calcify; they may be detected incidentally on radiographs. Occasionally, muscle cysts cause pseudohypertrophy, which may be associated with myositis, high fever, and eosinophilia. Cysts may also occur in critical organs (commonly the heart and liver), where they present as mass lesions with pain or obstructive symptoms.
Clinical appearance can therefore range from incidentally noted calcifications to severe neurological compromise. The same patient may have both asymptomatic and symptomatic lesions in different organs.
| Site | Typical manifestations | Examples from text |
|---|---|---|
| Brain and meninges | Inflammation, mass effect, CSF flow obstruction | Arachnoiditis, chronic meningitis, obstructive hydrocephalus, seizures, focal neurological deficits, dementia |
| Spinal cord | Compression and neurological deficits | Cord compression with lower limb weakness and loss of bowel and bladder continence |
| Skeletal muscle | Often asymptomatic; occasionally inflammatory | Incidental calcified cysts, pseudohypertrophy, myositis, high fever, eosinophilia |
| Viscera (heart, liver, other organs) | Mass lesions and obstruction | Pain or obstructive symptoms, such as biliary obstruction in hepatic cysticercosis |
Laboratory Findings
Patients with cysticercosis may have a mild elevation in the leukocyte count, possibly with eosinophilia. In patients with meningitis associated with neurocysticercosis, cerebrospinal fluid examination may show either lymphocytic or eosinophilic pleocytosis, hypoglycorrhachia, and elevated protein. A serological test for T solium has recently been developed, but its performance characteristics remain to be validated. False-positive results have been associated with infections caused by other cestodes. A negative serological test does not exclude the diagnosis of cysticercosis.
Imaging
Living cysts associated with cysticercosis are often multiple and have a characteristic appearance on CT scans or magnetic resonance images, as both enhancing and non-enhancing unilocular cysts. Patients with extra-neurological cysticercosis may have painless subcutaneous nodules, often on the shins, which are calcified and have a characteristic appearance on plain radiographs.
| Diagnostic method | Role | Selected features |
|---|---|---|
| Surgical excision and histology | Definitive identification | Microscopic identification of the larval parasite in excised tissue |
| Fine-needle aspiration | Cytological confirmation | Characteristic cytomorphology of cysticerci |
| Serological testing | Evidence of exposure | Positive results suggest prior exposure to T solium; false positives with other cestodes; a negative test does not exclude disease |
| CT / MRI of brain and spine | Neurocysticercosis evaluation | Multiple enhancing and non-enhancing unilocular cysts; assessment of hydrocephalus and mass effect |
| Plain radiographs | Detection of calcified cysts | Calcified subcutaneous or intramuscular nodules, often on the shins |
Differential Diagnosis
Patients who seek care for infection with T solium most commonly do so because of the neurological symptoms associated with neurocysticercosis. The most common neurological symptoms are mass effect and seizures (related to intraparenchymal lesions), hydrocephalus (related to intraventricular cysts), chronic meningitis (related to subarachnoid cysts), and cord compression (owing to spinal cord cysts). The differential diagnosis of each of these symptoms is beyond the scope of this discussion, but malignancy can present in identical ways and must be ruled out.
Complications
Visceral cysticercosis is also commonly asymptomatic, but it may obstruct local structures (e.g., biliary obstruction in hepatic cysticercosis). Neurocysticercosis may lead to permanent neurological impairment, coma, or death.
Treatment
Therapy for cysticercosis includes surgery when feasible and necessary, in combination with praziquantel or albendazole. Treatment of cysticercosis commonly increases local inflammation, thereby transiently causing a paradoxical worsening of the patient's symptoms. Whether corticosteroids should be used as adjunctive therapy for patients being treated for neurocysticercosis remains debated.
Decisions regarding timing of surgery, choice of antiparasitic drug, and use of anti-inflammatory therapy are typically individualised based on cyst location, burden, and the severity of neurological involvement.
Prognosis
The mortality rate for untreated neurocysticercosis approaches 50%, but treatment decreases this rate to 5-15%.
Prevention & Control
Guidelines for the prevention of cysticercosis are the same as for the prevention of T solium infection. These measures include proper cooking of pork, careful hand hygiene, and adequate sanitation to prevent faecal contamination of food and water.