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Locally Acquired Neurocysticercosis -- North Carolina, Massachusetts, and South Carolina, 1989-1991

From October 1989 through November 1991, three persons with neurocysticercosis acquired in the eastern United States (North Carolina, Massachusetts, and South Carolina) were reported to CDC. This report summarizes clinical and epidemiologic information for these cases.

Patient 1. On October 4, 1989, a previously healthy man residing in New Jersey had a syncopal episode while at work. Although physical examination was normal, magnetic resonance imaging (MRI) at a New York City hospital revealed multiple ( greater than 20) cystic lesions throughout the brain. A serum specimen was positive for cysticercosis by immunoblot assay. The patient was asymptomatic on anticonvulsant medication until June 1991, when left-sided hemiparesis and weakness were noted. In July, he was treated with albendazole (10 mg/kg per day for 28 days) administered with dexamethasone. His condition improved, and he remains asymptomatic.

The patient was born and raised on a farm in North Carolina and had moved to New Jersey in July 1989; he had never traveled outside the United States. Although there was no family history of neurologic illness or tapeworm infection, some of the workers who were hired seasonally to assist on the farm had immigrated from countries with endemic cysticercosis.

Patient 2. On August 26, 1990, a 16-month-old girl in Boston had a seizure. Cranial contrast-enhanced computerized axial tomographic (CAT) scan showed ring-enhancing lesions in the left parietal and frontal cortex and a solid right parietal lesion. The immunoblot assay for cysticercosis was positive in both serum and cerebrospinal fluid. Stool examination for ova and parasites showed Giardia. The patient was treated with metronidazole for giardiasis, but no specific anthelminthic medication was given. In November 1989, the lesions were resolving, and the patient remains asymptomatic on anticonvulsants.

The patient had always resided in Boston and had never traveled out of Massachusetts. Her parents had emigrated from the Cape Verde Islands 18 months before her birth. Although no immediate family members had been acutely ill, serum specimens obtained from three of four family members were positive for cysticercosis in the immunoblot assay. Stool specimens obtained from the patient's father contained eggs of Taenia sp. All family members were treated with a taeniacidal dose of niclosamide.

Patient 3. In February 1990, a previously healthy girl in South Carolina developed generalized seizures. A CAT scan revealed a single contrast-enhancing right parietal lesion consistent with a tumor. Biopsy of the lesion showed nonspecific inflammation. In May, follow-up examination by MRI demonstrated a recurrence of the lesion, which was resected. The lesion was identified as a cysticercus (larval cyst) of Taenia solium. The patient remains asymptomatic on anticonvulsant medication.

The patient lived in Laurens County, South Carolina, and had never traveled out of state. To identify the source of the infection and possible additional persons with neurocysticercosis, the Upper Savannah District of the South Carolina Department of Health and Environmental Control conducted interviews and voluntary diagnostic tests among 26 family members and contacts. None of these persons had traveled outside the United States or eaten uncooked pork, and none reported previous tapeworm infections, subcutaneous nodules, seizures, or other neurologic symptoms. Serum specimens from all 26 persons were negative in the immunoblot assay for cysticercosis. One contact, a neighbor who had immigrated from Mexico, was seronegative, and the one stool specimen obtained from him was negative for eggs and proglottids of Taenia sp. However, the health department obtained serum specimens from five of the neighbor's friends who also had immigrated from Mexico and who often stayed in the neighbor's residence (often visited by the patient), of which three were positive for cysticercosis by immunoblot assay. One of the seronegative persons reported a history of tapeworm infection several years previously. All five refused stool examination for intestinal parasites. Reported by: LA Lettau, MD, S Gardner, MD, Dept of Hospital Epidemiology and Infectious Diseases, Greenville Hospital System; J Tennis, MD, S Hollis, F Payne, Upper Savannah District, J Jones, MD, State Epidemiologist, South Carolina Dept of Health and Environmental Control. BA Kruskal, MD, DW Teele, MD, Boston City Hospital; L Moths, MD, Upham's Corner Health Center; A DeMaria, MD, State Epidemiologist, Massachusetts Dept of Public Health. K Spitalny, MD, State Epidemiologist, New Jersey Dept of Health. MW Wittner, MD, J Kaplan, MD, HB Tanowitz, MD, Albert Einstein College of Medicine, New York City; K Rowin, MD, New City, New York. Div of Parasitic Diseases, National Center for Infectious Diseases, CDC.

Editorial Note

Editorial Note: Neurocysticercosis is infection of the central nervous system with the tissue-invading larval stages (cysticerci) of the pork tapeworm T. solium. Cysticercosis is acquired by ingesting tapeworm eggs shed in human feces, not by ingesting pork (Figure 1). Although cysticerci may localize throughout the body, most clinical manifestations are related to their presence in the central nervous system, where they can invade parenchyma, the subarachnoid spaces, and the ventricular system, causing seizures, hydrocephalus, and other neurologic dysfunction (1).

Cysticercosis is widely endemic in rural areas of Latin America, Asia, and Africa. During the 1980s, however, neurocysticercosis has been increasingly recognized in the United States through improved brain imaging by CAT and MRI. Most cases have been diagnosed in the western states among immigrants from areas with endemic cysticercosis (2-4). In addition, from 1988 through 1990, 7.3% of 138 cases reported to the Los Angeles Department of Health Services were acquired locally (i.e., in patients born in the United States who had not traveled to foreign countries with endemic cysticercosis). Epidemiologic investigation of these cases identified as possible sources of infection household contact with persons who had imported tapeworm infections (5).

Because none of the patients in this report had traveled outside the United States, they could not have acquired their infections in areas of known endemic cysticercosis. Moreover, because T. solium cysticercosis is virtually unknown in swine in the United States (6), transmission through the pig-human cycle was unlikely. The highly variable and usually prolonged (i.e., greater than 1 year) incubation period of neurocysticercosis has complicated attempts to identify sources for individual infections; however, the investigations suggest two of these patients may have been infected from household (fecal-oral) exposure to persons with imported tapeworm infections. This explanation is supported by the demonstration of Taenia sp. eggs in the stools of the father of patient 2 and the history of previous tapeworm infection and demonstration of antibodies to T. solium in the immigrants who were household contacts of patient 3. Although the source of infection for patient 1 is less clear, infection may have been associated with exposure to migrant laborers employed for seasonal farm work; in 1987, a survey for intestinal parasites in migrant workers in North Carolina determined that Taenia sp. were present in stool specimens obtained from 3% of persons of Central American origin (S. Ciesielski, Ph.D., J.R. Seed, Ph.D., University of North Carolina School of Public Health, personal communication, 1991).

In the United States, sewage disposal systems are adequate to prevent transmission of helminths that require a period of soil incubation to become infective. Thus, helminth infections among immigrant populations in the United States are not considered a major public health problem. However, in contrast to most helminth parasites, the eggs of T. solium are immediately infectious when passed in the stool and may be transmitted directly by person-to-person contact. Intestinal T. solium infections may persist for many years, and substantial numbers of infective eggs can be passed in the host's stools; eggs have been recovered from fingernail dirt, skin, and clothes of carriers (7).

Patients with cysticercosis and their household and other personal contacts should be screened for tapeworm infection since treatment with a single dose of niclosamide or praziquantel will eradicate the tapeworm (8) and remove a potential source of transmission. Consideration should be given to screening persons at high risk for T. solium infections for intestinal parasites if those persons are to be employed as food handlers or housekeepers. Persons having household or other close contact (i.e., contact that exposes them to inadvertent infection through the fecal-oral route) with a person with a documented tapeworm should be screened for cysticercosis by medical history and serologic testing; if such an assessment suggests cysticercosis, neurologic examination and brain scan is advised.

Clinical manifestations of neurocysticercosis are varied, nonspecific, and related to the number and location of lesions (1). A heightened index of suspicion is a critical first step in establishing the diagnosis; the most sensitive and specific diagnostic tool is brain imaging by CAT or MRI. The diagnosis can be confirmed serologically using the recently developed enzyme-linked immunoelectrotransfer blot (9) that is 100% specific and highly sensitive for persons with multiple intracranial lesions. Although the assay is less sensitive for infected persons having solitary cysts, serologic testing may obviate the need for invasive biopsy. While cysts often resolve without anthelminthic treatment, praziquantel or albendazole is effective in persons with serious clinical manifestations and viable cysts (10).

In most states--including the eastern United States--cysticercosis is not a reportable condition. However, the cases described in this report suggest local transmission has occurred in diverse locations in the United States. Cases of cysticercosis may be reported to CDC's Division of Parasitic Diseases, National Center for Infectious Diseases, through state and local health departments.


  1. Nash TE, Neva FA. Recent advances in the diagnosis and treatment of cerebral cysticercosis. New Engl J Med 1984;311:1492-6.

  2. Earnest MP, Reller LB, Filley CM, Grek AJ. Neurocysticercosis in the United States: 35 cases and a review. Rev Infect Dis 1987;9:961-78.

  3. Richards FR, Schantz PM, Ruiz-Tiben E, Sorvillo F. Cysticercosis in Los Angeles County. JAMA 1985;254:3444-8.

  4. California Department of Health. Cysticercosis in California. California Morbidity 1991;nos. 23, 24.

  5. Sorvillo FJ, Waterman SH, Richards FO, Schantz PM. Cysticercosis surveillance: locally acquired and travel-related infections in Los Angeles County. Am J Trop Med Hyg (in press).

  6. Schantz PM, McAuley J. Current status of foodborne parasitic zoonoses in the United States. Southeast Asian J Trop Med Public Health (in press).

  7. Schantz PM, Sarti-Gutierrez E. Diagnostic methods and epidemiologic surveillance of Taenia solium infection. Acta Leiden 1989;57:153-63.

  8. Anonymous. Drugs for parasitic infections. Med Lett Drugs Ther 1986;28:9-18.

  9. Wilson M, Bryan RT, Fried JA, et al. Clinical evaluation of the cysticercosis enzyme-linked immunoelectrotransfer blot in patients with neurocysticercosis. J Infect Dis 1991;164:1007-9.

  10. Sotelo J, Escobedo F, Penagos, P. Albendazole vs. praziquantel for therapy for neurocysticercosis: a controlled trial. Arch Neurol 1988;45:532-4.

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