Cysticercosis epidemiology and demographics
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Epidemiology and Demographics
Taenia solium is found worldwide. Because pigs are intermediate hosts of the parasite, completion of the life cycle occurs in regions where humans live in close contact with pigs and eat undercooked pork. Taeniasis and cysticercosis are very rare in Muslim countries. It is important to note that human cysticercosis is acquired by ingesting T. solium eggs shed in the feces of a human T. solium tapeworm carrier, and thus can occur in populations that neither eat pork nor share environments with pigs.
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. 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.
Can infection be spread from person to person?
No. Cysticercosis is not spread from person to person. However, a person infected with the intestinal tapeworm stage of the infection (T. solium) will shed tapeworm eggs in their bowel movements. Tapeworm eggs that are accidentally swallowed by another person can cause infection.
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.