Etiology

Humans can be the definitive host (parasite sexual reproduction) as well as the intermediate host (parasite asexual reproduction) of Taenia solium, the pork tapeworm. Infection with the invasive intermediate stage (cysticercus) is called cysticercosis. Unlike Taenia saginata, the intermediate stage of T. solium is invasive with a tropism for the central nervous system (CNS) in humans, causing neurocysticercosis. The risk of cysticercosis may be the same for individuals who eat or do not eat pork, since humans acquire the intermediate form by ingestion of food or water contaminated with the eggs of T. solium. By contrast, consumption of infected undercooked pork produces intestinal infection with the adult worm (Chapter 294). Individuals harboring an adult worm may infect themselves with the eggs by the fecal-oral route. Reverse peristalsis in the small intestine has also been implicated as a means of autoinfection. In the small intestine, the egg releases an oncosphere that crosses the gut wall and spreads hematogenously to many tissues, primarily brain and muscle. Wherever the eggs lodge, they produce small (0.2-0.5 cm) fluid-filled bladders containing a single protoscolex, the juvenile-stage parasite.

Epidemiology

The pork tapeworm is distributed worldwide wherever pigs are raised. Intense transmission occurs in Central and South America, India, Indonesia, Korea, and China as well as some areas of Africa. In these areas, 20-50% of cases of epilepsy may be due to cysticercosis. Most cases of cysticercosis in the USA are imported; transmission is uncommon but occurs.

Pathogenesis

Living, intact cystic stages usually do not provoke a strong immunologic response. Intact cysts can be associated with disease when the initial parasite invasion of the brain is massive or when they obstruct the flow of cerebrospinal fluid (CSF). Most cysts remain viable for 5-10 yr and then begin to degenerate, followed by a vigorous host response. The natural history of cysts is to resolve by complete resorption or calcification.

Clinical Manifestations

Seizures are the presenting finding in ~70% of cases, although any cognitive or neurologic abnormality ranging from psychosis to stroke may be a manifestation of cysticercosis. It is useful to classify neurocysticercosis as parenchymal, intraventricular, meningeal, spinal, or ocular on the basis of anatomic location, clinical presentation, and radiologic appearance. Prognosis and management vary with location.

Parenchymal neurocysticercosis produces seizures as well as focal neurologic deficits. The seizures are generalized in 80% of cases but frequently begin as simple or complex partial seizures. Rarely, cerebral infarction can result from obstruction of small terminal arteries or vasculitis. With extensive frontal lobe disease, symptoms of intellectual deterioration with dementia or parkinsonism may obfuscate diagnosis until focal signs appear. A fulminant encephalitis-like presentation also occurs, most frequently in children who have had a massive initial infection. Intraventricular neurocysticercosis (5-10% of all cases) is associated with hydrocephalus and acute, subacute, or intermittent signs of increased intracranial pressure without localizing signs. The 4th ventricle is the most common site for obstruction and symptoms; cysts in the lateral ventricles are less likely to cause obstruction. Meningeal neurocysticercosis is associated with signs of meningeal irritation and also increased intracranial pressure that results from edema, inflammation, or the presence of a cyst obstructing flow of CSF. Chronic basilar meningitis is associated with many forms of neurocysticercosis, but predominantly meningeal presentations. Racemose neurocysticercosis is a meningeal form of disease in which large, lobulated cysts appear in the basal cisterns. Spinal neurocysticercosis

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