eMedicine Specialties > Pediatrics: General Medicine > Parasitology
Cysticercosis
Updated: Oct 7, 2009
Introduction
Background
Cysticercosis, a tissue infection that involves larval cysts of the cestode Taenia solium (the human pork tapeworm), results from the ingestion of food (especially vegetables) and water contaminated with human feces that contain T solium eggs.
Although infections with Taenia tapeworm cysts may involve many parts of the body, the most common site of severe symptomatic infection is the CNS.
Cysticercosis life cycle. Image courtesy of the Centers for Disease Control and Prevention.
Neurocysticercosis, the most common parasitic disease of the CNS, is the most common cause of adult-onset epilepsy in many of the countries where the infection is endemic.
Pathophysiology
Cysticercosis, the intermediate form of T solium infection, is predominantly acquired by ingesting food or water contaminated with T solium eggs. Additionally, autoinfection may occur by means of fecal-oral contact and, theoretically, by reverse peristalsis in the small intestines of individuals infected with adult T solium worms.
In the stomach, oncospheres are liberated following digestion of the eggs' coats. Oncospheres invade and cross the intestinal wall, enter the bloodstream, and then migrate to and lodge in tissues throughout the body, where they produce small (0.2-0.5 cm) fluid-filled bladders containing a single juvenile-stage parasite (protoscolex).
Although the cysticerci may infect any organ of the body (most often the eye, skeletal muscle, and CNS), serious disease almost exclusively involves the CNS and heart.
Oncospheres that invade the brain may lodge in the brain parenchyma, subarachnoid space, ventricular space, or spinal cord. Cysticerci develop after 2 months and may or may not stimulate an appreciable inflammatory response.
In the brain parenchyma, cysticerci form a thin capsule of fibrous tissue that thickens with time. After several years, the parasite dies or is killed and is replaced by an astroglial and fibrous tissue granuloma that becomes calcified. The number of cysticerci present ranges from one to several hundred.
Cysts that grow in the sylvian fissure and in the subarachnoid space at the base of the skull may enlarge to 10-15 cm in diameter. Meningeal and spinal cord cysticercosis occurs if the oncospheres enter via the choroid plexus and hatch in the arachnoid membranes along the neural axis.
Cysts that develop in the subarachnoid space may cause an inflammatory response. Subsequent fibrosis of the arachnoid membranes may interfere with normal cerebral spinal fluid (CSF) resorption, resulting in hydrocephalus. Fourth ventricle cysts can create a subacute hydrocephalus via a valve-and-ball mechanism. However, head movement can suddenly increase the intracranial pressure (ICP).
With the exception of massive or obstructive disease, the cystic stages of most tapeworms do not provoke a strong immunologic response while they remain alive and intact. However, once the cysts die, the immune system recognizes them as foreign, and a vigorous immunologic response ensues. Seizures, hydrocephalus, blindness, strokes, meningitis, encephalitis, irreversible brain damage, myositis, and myocarditis may occur. Death may subsequently occur.
Frequency
United States
Cysticercosis is not endemic to the United States, although domestic transmission has been documented from recent immigrants to the United States from highly endemic areas.1 Historically, rates significantly decreased in the 1970s.
Since the 1970s, the number of cases of neurocysticercosis in the United States has increased, mainly because of the large number of immigrants from areas with endemic disease, such as Mexico, Central and South America, Africa, Asia, Spain, and Portugal. Americans without a travel history to such areas have developed neurocysticercosis, mainly because of exposure to a cohabitant with a T solium infection.
Disease is prevalent in areas with low socioeconomic status and poor hygiene and sanitation.
International
An accurate estimation of the prevalence of cysticercosis is difficult because of the high prevalence of asymptomatic individuals. Overall, more than 2 million people are estimated to have adult tapeworm infection, and many more are infected with cysticercoids. Disease is prevalent in areas with poor hygiene and sanitation.
Cysticercosis is endemic throughout Latin American, although it is rare in Chile, Argentina, and Uruguay.
Cysticercosis is absent in Arabic regions of Asia and Africa but is found in areas where pigs live in close proximity to humans. In Europe, cysticercosis is still endemic in Spain, Portugal, and some Eastern European countries but is rare in most other countries.
Mortality/Morbidity
Worldwide, an estimated 50,000 people die from cysticercosis each year because of CNS or cardiac complications.
Race
No racial predilection for cysticercosis is known.
Sex
The prevalence does not differ according to sex.
Age
No known age-based differences in the frequency of cysticercosis have been reported.
Clinical
History
- The clinical presentation of cysticercosis depends on the number, location, and stage of the lesions present, as well as the host immune response.
- In general, the diagnosis of neurocysticercosis should be considered in any individual who is from or has traveled to an area where T solium is endemic and who has new-onset partial seizures (with or without secondary generalization), behavioral disturbances, confusion, stupor, cognitive impairment, or signs of increased intracranial pressure (ICP).
- Seizures are the presenting symptom in more than 70% of cases. The seizures frequently begin as simple or complex partial seizures but become generalized in 80% of cases.
- Parenchymal disease causes seizures and focal neurologic deficits.
- Headache, vertigo, vomiting, papilledema, an altered level of consciousness, and gait disturbances may be present in patients with meningeal cysticercosis.
- Spinal neurocysticercosis can cause spinal cord compression, nerve root pain, transverse myelitis, or meningitis.
- Intraventricular neurocysticercosis (5-10% of all cases) is associated with hydrocephalus and acute, subacute, or intermittent signs of increased ICP without localizing signs.
- The lateral ventricles are less likely to become obstructed, whereas the fourth ventricle most commonly becomes obstructed.
- Hydrocephalus develops from the intense and widespread immune response in the subarachnoid space.
- Ocular cysticercosis may decrease visual acuity because of retinal detachment, iridocyclitis, or floating cysticerci in the vitreous.
- Heavy infections in skeletal or heart muscle may result in myositis or carditis, respectively.
- Rarely, cysticerci may obstruct small terminal arteries or cause a vasculitis, leading to a cerebral infarction.
- Children with an acute infection that is massive may present with signs and symptoms of fulminant encephalitis.
- Intellectual deterioration due to extensive frontal lobe disease may simulate dementia or parkinsonism.
- Chronic basilar meningitis is associated with many forms of neurocysticercosis. In addition to signs of meningeal irritation, increased ICP due to inflammation, edema, or an obstructing cyst may be present.
Physical
- Findings vary depending on the number, location, and local effects of cysticerci, as well as on the host response.
- In general, neurologic deficits, seizures, and subcutaneous or ocular cysts may be present.
- Cysts may be palpable under the skin.
- The features of the history assist in focusing the physical examination.
Causes
- Cysticercosis is caused by the ingestion of T solium eggs. The human is the only definitive host of the adult pork tapeworm, which lives in the human intestinal tract and lays eggs that are shed in human feces. In the normal life cycle of the parasite, eggs shed in human feces are ingested by pigs, which then develop cysticerci in muscle tissue. Human infection with the adult tapeworm develops in people who ingest raw or poorly cooked pork that contains cysticerci. Note that human ingestion of pork does not result in the development of cysticercosis.
- Contamination of water, fruits, and vegetables by human feces that contain eggs is usually the result of poor sanitation.
- Untreated, adult T solium worms may cause autoinfection by means of fecal-oral ingestion and reverse peristalsis, but this is believed to be very uncommon.
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| References |
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Further Reading
Keywords
cysticercosis, neurocysticercosis, giant cysticercosis, cysticercus cellulosae, cysticercus racemosus, adult-onset epilepsy, cysticerci, tapeworm infection, cysticercoids, neurocysticercosis, cysticerci, hydrocephalus, parkinsonism, treatment, diagnosis
