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Cysticercosis

  • Author: Mossammat M Mansur, MD, MBBS; Chief Editor: Pranatharthi Haran Chandrasekar, MBBS, MD  more...
 
Updated: Oct 05, 2015
 

Background

Cysticercosis (ie, infection caused by eggs of the pork tapeworm) is an increasingly common medical problem in the United States, especially in the Southwest and other areas where large populations migrated from endemic areas and among populations that often travel to these areas.

Cysticercosis is caused by the metacestode, or larval, stage of Taenia solium, the pork tapeworm. The clinical syndromes caused by T solium are categorized as either cysticercosis (cysts in various tissues including the brain) or taeniasis (intestinal tapeworm infection).

Neurocysticercosis refers to CNS infection with T solium. Neurocysticercosis, which is probably the most common parasitic infestation of the CNS, has gained increased recognition in the last two decades because of the development of MRI and CT scanning in the United States and in countries where neuro cysticercosis is endemic.

Neurocysticercosis is further divided into parenchymal and extraparenchymal disease. Parenchymal disease is characterized by infection with cysticerci within the brain parenchyma. Extraparenchymal disease develops when cysticerci migrate to the CSF of the ventricles, cisterns, and subarachnoid space or within the eyes or spinal cord. 

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Pathophysiology

When humans ingest undercooked pork that contains cysticerci of T solium, the scolex evaginates from the cyst and develops into an intestinal tapeworm (taeniasis). The tapeworm grows to a length of up to 10 meters and has hundreds of proglottids. Mature proglottids contain approximately 50,000 eggs each. Free eggs or whole proglottids are released periodically into the stool of the carrier and can survive in the environment for many months.

When pigs ingest the proglottids or eggs, the eggs hatch, penetrate the pigs' intestinal wall, and spread to skeletal muscle, especially the neck, tongue, and trunk. There, the larvae mature into encysted cysticerci over 2-3 months. The cysticerci suppress the host inflammatory response and can survive in tissues for months to years. The life cycle is completed when humans ingest inadequately cooked pork that contains viable cysticerci.

This cycle of cysts in pigs and tapeworms in humans can be broken if a human ingests eggs excreted in the feces of a human carrier of the pork tapeworm. Humans are an accidental host of the larval stage and develop cysticercosis similar to that in pigs. These cysticerci have tropism for neural tissue and migrate to the brain, although they can also be found in skeletal muscle. Thus, cysticercosis is a foodborne infection and can be acquired in the absence of pork consumption.[1]

Humans can be infected with eggs through fecal-oral transmission or possibly through autoinfection. Fecal-oral contamination usually occurs via infected food handlers via ingestion of fruit and vegetables fertilized with contaminated human waste. The eggs are sticky and can often be found under the fingers of tapeworm carriers. Thus, even populations who do not eat pork can develop cysticercosis. The egg-containing feces can contaminate water supplies in endemic areas. If the water is used to irrigate fruits and vegetables, eggs are ingested with the contaminated food. Thus, people who have never visited endemic countries can also develop infection.

Cysticerci are able to survive in the human brain by disarming host defenses. The cysticercus secretes prostaglandins and other compounds (paramyosin, taeniastatin, sulfated polysaccharides) that inhibit or divert complement activation and cytokine production, resulting in only minimal host inflammation around the viable cysticercus. In addition, humoral antibodies do not kill the mature metacestode. Taeniastatin and other poorly defined factors may also interfere with lymphocyte proliferation and macrophage function, inhibiting normal cellular immune defenses. The clinical manifestations commonly result when an inflammatory response develops around a degenerating cysticercus after it has died.

Over a period of years, the parasite may lose its ability to control the host defenses. Consequently, an inflammatory response leads to degeneration of the cysticercus. An inflammatory response that occurs in the CNS parenchyma causes seizures typical of parenchymal neurocysticercosis. As the degeneration continues, the parasite becomes encased in a granuloma, which either resolves or leads to scarring and calcification. In rare cases, patients with numerous parenchymal cysticerci develop a diffuse cerebral edema termed cysticercal encephalitis. Pathologically, cysticercal encephalitis may progress to meningoencephalitis, granulomatous meningitis, focal granulomas or abscess, hydrocephalus, ependymitis, or arteritis.

Approximately 10-20% of patients with neurocysticercosis present with extraparenchymal disease, often with concomitant parenchymal disease. Subarachnoid neurocysticercosis may form in the gyri of the cerebral convexities or in the fissures of the brain, especially the sylvian fissures. These forms of neurocysticercosis are associated with parenchymal inflammation and resemble parenchymal disease in manifestations and pathogenesis.

In severe cases, cysticerci in the sylvian fissures may enlarge to several centimeters in diameter and cause mass effects. Cysticerci can form in the ventricles of the brain, where they can cause hydrocephalus by blocking the outflow of CSF. Obstructive hydrocephalus may also be caused by associated ependymitis. If cysticerci form in the basal cisterns, they can cause basilar arachnoiditis. Arachnoiditis may result in communicating hydrocephalus or vasculitis. Involvement of the arteries may lead to lacunar infarctions or, occasionally, large-vessel strokes.

Cysticerci may be located in the spinal subarachnoid space and the spinal cord medulla. Medullary cysticerci may cause cord compression or other symptoms related to their location. Ocular cysticercosis is generally intravitreal or subretinal. Skeletal muscle cysticerci are common but usually cause only minor local symptoms unless they are present in overwhelming numbers. Subcutaneous cysticerci manifest as painless, palpable, cystic lesions. CNS parenchymal cysticerci may be present in patients with suspected extraparenchymal or extra-CNS disease.

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Epidemiology

Frequency

United States

Approximately 1,000 new cases of cysticercosis are reported annually in the United States. Most occur among Latin American immigrants in locations such as California, Arizona, and Texas. Less frequently, cysticercosis is observed in immigrants from other areas, including India, Asia, and Africa. A small number of cases of cysticercosis develop in people born in the United States who have traveled to areas in which the infection is endemic. These travelers are often the children of immigrants. Locally acquired infection is rare and is associated with contact with a tapeworm carrier. All tapeworm carriers acquire infection from areas of endemic disease.

In a mortality study using data from the National Center for Health Statistics from 1990 to 2002; 62% of patients with cysticercosis had emigrated from Mexico.[2]

International

An estimated 50-100 million people are infected with cysticercosis worldwide. This is probably an underestimate since many infections go undiagnosed. Neurocysticercosis is one of the leading causes of adult-onset seizures worldwide. CT scanning and MRI of the brain have greatly improved the diagnosis of neurocysticercosis.

Areas of endemic disease include Central and South America, India, China, Southeast Asia, and sub-Saharan Africa.[3] Studies in Latin America and India have noted adult-onset seizures in approximately 2% of the population, with as many as half due to neurocysticercosis. In Latin America, the seroprevalence rate ranges from 4.9-24%. In India, the estimated prevalence is similar. Rural China and Korea have lower infection rates. The seroprevalence in certain rural South American communities is as high as 10-25%.[4]

Mortality/Morbidity

Neurocysticercosis is one of the leading causes of adult-onset seizures and is estimated to cause as many as 50% of adult-onset seizure cases in developing countries where T solium is endemic. Neurocysticercosis was found to be responsible for 10% of newly onset seizures in one Los Angeles, California, emergency department.[5] Overall, among patients who presented to emergency departments with newly onset seizure, neurocysticercosis was found to be responsible for 2.1-5.7% of cases.[6]

A total of 221 deaths were attributed to cysticercosis in the United States from 1990-2002.[2]

Although some patients die of status epilepticus in areas with poor access to medical care, mortality due to parenchymal disease is rare. With modern medical and surgical care, mortality due to extraparenchymal disease is also unusual. However, without aggressive surgical management, hydrocephalus is potentially life-threatening. Even with shunting procedures, subarachnoid cysticercosis is associated with a high 10-year fatality rate.

Race

Immigrants from countries where T solium is endemic are more likely to be infected. While most of these immigrants are Hispanic and some are Asian, prevalence rates appear to be related more to exposure than to genetic predisposition.

Sex

Cysticercal encephalitis, a severe form of cysticercosis, is more common in children and young females. The cause is unknown.

No other sex predisposition has been noted.

Age

Patients with cysticercosis are typically aged 10-40 years. However, cases have been described in every age group.

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Contributor Information and Disclosures
Author

Mossammat M Mansur, MD, MBBS Attending Physician, Nassau ID Physicians

Mossammat M Mansur, MD, MBBS is a member of the following medical societies: Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Coauthor(s)

Martin Montes, MD Fellow, Department of Medicine, Section of Infectious Disease, Baylor College of Medicine; Research Associate, Instituto de Medicina Tropical ‘Alexander von Humboldt’, Universidad Peruana Cayetano Heredia, Perú

Disclosure: Nothing to disclose.

Linda S Yancey, MD Consulting Staff, West Houston Infectious Diseases

Linda S Yancey, MD is a member of the following medical societies: American College of Physicians, American Medical Association, Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

John W King, MD Professor of Medicine, Chief, Section of Infectious Diseases, Director, Viral Therapeutics Clinics for Hepatitis, Louisiana State University Health Sciences Center; Consultant in Infectious Diseases, Overton Brooks Veterans Affairs Medical Center

John W King, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians, American Federation for Medical Research, Association of Subspecialty Professors, American Society for Microbiology, Infectious Diseases Society of America, Sigma Xi

Disclosure: Nothing to disclose.

Chief Editor

Pranatharthi Haran Chandrasekar, MBBS, MD Professor, Chief of Infectious Disease, Program Director of Infectious Disease Fellowship, Department of Internal Medicine, Wayne State University School of Medicine

Pranatharthi Haran Chandrasekar, MBBS, MD is a member of the following medical societies: American College of Physicians, American Society for Microbiology, International Immunocompromised Host Society, Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Additional Contributors

David Hall Shepp, MD Program Director, Fellowship in Infectious Diseases, Department of Medicine, North Shore University Hospital; Associate Professor, New York University School of Medicine

David Hall Shepp, MD is a member of the following medical societies: Infectious Diseases Society of America

Disclosure: Received salary from Gilead Sciences for management position.

Acknowledgements

The authors and editors would like to acknowledge Dr. Martin Montes, Dr. Clinton White Jr., and Dr. Thomas P. Giordano, who were the original authors of this article. They would also like to acknowledge the prior contributions of Dr. John W King to the development and writing of this article.

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Nonenhanced CT scan of the brain demonstrates the multiple calcified lesions of inactive parenchymal neurocysticercosis.
 
 
 
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