• 1

    White AC Jr, 2000. Neurocysticercosis: updates on epidemiology, pathogenesis, diagnosis, and management. Annu Rev Med 51 :187–206.

  • 2

    Garcia HH, Gonzalez AE, Evans CA, Gilman RH, 2003. Taenia solium cysticercosis. Lancet 362 :547–556.

  • 3

    Carpio A, 2002. Neurocysticercosis: an update. Lancet Infect Dis 2 :751–762.

  • 4

    Sept 3 2002. Hispanic Heritage month 2002. Facts for Features: Public Information Office, US Census Bureau, Washington, DC 20233.

  • 5

    Guzman B, 2001. The Hispanic Population. Census 2000 Brief. Washington, DC: U.S. Department of Commerce.

  • 6

    Staff M, 2002. The US-Mexico Border. US in Focus. Washington, DC: Migration Information Source, Migration Policy Institute.

  • 7

    Alvarez F, 1999. Dawn of a New Majority. Los Angeles: Los Angeles Times.

  • 8

    White AC Jr, Atmar RL, 2002. Infections in Hispanic immigrants. Clin Infect Dis 34 :1627–1632.

  • 9

    Townes JM, Hoffmann CJ, Kohn MA, 2004. Neurocysticercosis in Oregon, 1995–2000. Emerg Infect Dis 10 :508–510.

  • 10

    Sorvillo FJ, Waterman SH, Richards FO, Schantz PM, 1992. Cysticercosis surveillance: locally acquired and travel-related infection and detection of intestinal tapeworm carriers in Los Angeles. Am J Trop Med Hyg 47 :365–371.

    • Search Google Scholar
    • Export Citation
  • 11

    Schantz PM, Moore AC, Muñoz JL, Hartman BJ, Schaefer JA, Aron AM, Persaud D, Sarti E, Wilson M, Flisser A, 1992. Neurocysticercosis in an Orthodox Jewish community in New York City. N Engl J Med 327 :692–695.

    • Search Google Scholar
    • Export Citation
  • 12

    Rosenfeld EA, Byrd SE, Shulman ST, 1996. Neurocysticercosis among children in Chicago. Clin Infect Dis 23 :262–268.

  • 13

    Shandera WX, White AC Jr, Chen J, Diaz P, Armstrong R, 1994. Cysticercosis in Houston, Texas: a report of 112 cases. Medicine (Baltimore) 73 :37–52.

    • Search Google Scholar
    • Export Citation
  • 14

    White AC Jr, 1997. Neurocysticercosis: a common cause of neurologic disease worldwide. Clin Infect Dis 24 :101–113.

  • 15

    El Sahly HM, Adams GJ, Soini H, Teeter L, Musser JM, Graviss EA, 2001. Epidemiologic differences between United States-and foreign-born tuberculosis patients in Houston, Texas. J Infect Dis 183 :461–468.

    • Search Google Scholar
    • Export Citation
  • 16

    Ong S, Talan DA, Moran GJ, Mower W, Newdow M, Tsang VC, Pinner RW, 2002. Neurocysticercosis in radio graphically imaged seizure patients in U.S. emergency departments. Emerg Infect Dis 8 :608–613.

    • Search Google Scholar
    • Export Citation
  • 17

    Richards FO, Schantz PM, Ruiz-Tiben E, Sorvillo FJ, 1985. Cysticercosis in Los Angeles County. JAMA 254 :3444–3448.

  • 18

    Larralde C, Padilla A, Hernandez M, Govezensky T, Sciutto E, Gutierrez G, Tapia-Conyer R, Salvatierra B, Sepulveda J, 1992. Seroepidemiology of cysticerosis in Mexico. Salud Publica Mex 34 :197–210.

    • Search Google Scholar
    • Export Citation
  • 19

    Epidemiologica, 1994–2000. Mexico City, Mexico: Direccian General de Epidemiologica.

  • 20

    Sarti E, 2002. Epidemiology of Taenia solium taeniasis and cysticercosis in Mexico. Singh G, Prabhakar S, eds. Taenia solium Cysticercosis: From Basic to Clinical Science. Wallingford, United Kingdom: CAB International, 83–90.

  • 21

    Dixon HBF, Lipscomb FM, 1961. Cysticercosis: An analysis and follow-up of 450 cases. London: Her Majesty’s Stationary Service.

  • 22

    Stringer JL, Marks LM, White AC Jr, Robinson P, 2003. Epileptogenic activity of granulomas associated with murine cysticercosis. Exp Neurol 183 :532–536.

    • Search Google Scholar
    • Export Citation
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 

 

 

 

EPIDEMIOLOGY OF NEUROCYSTICERCOSIS IN HOUSTON, TEXAS

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  • 1 Infectious Disease Section, Department of Medicine and Department of Pathology, Baylor College of Medicine and Ben Taub General Hospital, Houston, Texas; Division of Parasitic Diseases, Centers for Disease Control and Prevention, Atlanta, Georgia

We identified 114 patients with neurocysticercosis admitted to Ben Taub General Hospital in Houston, Texas between January 1994 and June 1997. Most of these patients were born in Mexico (78%) or Central America (16%), but 6% were born in the United States. Review of neurology clinic records identified 54 patients diagnosed with neurocysticercosis, representing 2% of all neurology clinic patients and 16% of all Hispanics diagnosed with seizures. Forty-one patients were interviewed and all reported significant risk factors for infection, including ingestion of undercooked pork, pig husbandry, immigration from and frequent travel to villages in disease-endemic areas, or personal/ family history of taeniasis. Among Mexican immigrants, most were born in rural areas in Central (31%) or north central Mexico (38%). Significantly fewer of the patients were from the border states (15%). The median period from immigration to diagnosis was 58 months, but it was 28 months for the 13 patients who had not left the United States after immigration. Although neurocysticercosis is being diagnosed with increasing frequency in the United States, acquisition of infection is still strongly associated with pig husbandry in rural Latin America, with little evidence of local transmission. Even among urban immigrants to the United States and United States–born cases, there is close ongoing contact with disease-endemic villages.

INTRODUCTION

Neurocysticercosis, which is caused by infection of the human central nervous system with the parasite Taenia solium, is recognized as an important global public health problem.13 Although commonly considered a disease of the developing world, neurocysticercosis has been increasingly diagnosed in the United States. Improvements in neuroimaging (computed tomography and magnetic resonance imaging) and increased immigration from disease-endemic areas are the main factors linked to this increase.

According to the 2000 United States Census, there were 35.3 million persons born in Latin America living in the United States.4 This represents an increase of 13 million (58%) over the previous decade.4 Immigrants to the United States of Mexican origin now number more than 20 million.5 There is also significant travel between disease-endemic areas in Mexico and U.S. border states, with more than 300 million two-way crossings along the United States-Mexico border each year.6 Houston, Texas has also experienced a dramatic increase in the number of immigrants from developing countries. The 2000 census documented that Hispanics now comprise 37% of Houston’s population and are the largest minority group within the city.5 While Mexicans represent the largest single nationality (58.5%) within the Hispanic community, there are also large subpopulations from Central American countries, particularly El Salvador.

As the number of immigrants entering the United States has increased,7,8 so has the incidence of neurocysticercosis. Large neurocysticercosis case-series have been reported in California, Texas, Oregon, Chicago, and New York.913 In the 1990s, we estimated that over more than 1,000 neurocysticercosis cases were diagnosed in the United States each year,13 and it is likely that the incidence has subsequently increased. This represents an important public health problem. The heterogeneous and diverse population of Houston provides an ideal background in which to study the risk factors associated with neurocysticercosis infection in the United States.

MATERIALS AND METHODS

The current study was conducted at Ben Taub General Hospital, a 575-bed urban teaching hospital that provides care for indigent patients in Harris County, Texas, including Houston. The hospital provides neuroimaging studies for a population of approximately 300,000, including approximately 100,000 immigrants (primarily from Mexico and Central America). Approximately 30 new cases of neurocysticercosis are diagnosed at Ben Taub General Hospital each year.13,14

Patients diagnosed with neurocysticercosis were identified by a computer search of discharge diagnosis for hospitalized patients, by review of patient records of the neurology clinic, and by review of head computed tomography reports. All patient charts at the neurology clinic were reviewed for major symptom, diagnosis, and Hispanic surname. Inpatient records were examined for birthplace and clinical manifestations. Among these patients, we were able to contact 41 who agreed to a detailed interview concerning immigration and travel history, birthplace, and risk factors for infection. Distribution of birthplaces of Mexican immigrants was compared with a population-based database of all tuberculosis patients of Mexican origin diagnosed in Houston.15 The study was reviewed and approved by the Baylor Institutional Review Board and a waiver of consent was granted. Data were analyzed using Epi-Info version 6.02 and Epi-Map version 1.0 (Centers for Disease Control and Prevention, Atlanta, GA) and Excel® 97 (Microsoft, Redmond, WA).

RESULTS

A computer search of discharge diagnoses and head computed tomography reports between January 1994 and June 1997 identified 114 neurocysticercosis patients. Data on country of birth were available for 71 of the 114 patients. Of those 71 patients, 55 (78%) were born in Mexico, 11 (16%) were born in Central America, and 4 (6%) were born in the United States (Table 1). Seizures (75%) were the predominant clinical manifestation, followed by hydrocephalus (25%) and headaches (15%) (Table 1).

A total of 1,090 (37%) of 2,947 patients with active neurology clinic charts were Hispanic. Seizure disorder was diagnosed in 813 (28%) patients. Fifty-four (2%) of these patients had a diagnosis of neurocysticercosis, all were Hispanic. The percentage of seizures in Hispanics attributable to neurocysticercosis was approximately 16% (Table 2).

Among the 41 patients who were interviewed, 26 (63%) were born in Mexico, 9 (22%) were born in Central America and 6 (15%) were born in the United States. Among the Central American patients, 7 were from El Salvador and 1 each were from Guatemala and Costa Rica.

Among the Mexican immigrants, 38% of the patients originated from north central Mexico (including the states of Guanajuato, Zacatecas, Aguascalientes, San Luis Potosi, and Queretaro) (Figure 1). Thirty-one percent of the patients were from central Mexican states (Hidalgo, Mexico, Districto Federal, Puebla, Morelos, and Tlaxcala). Fifteen percent were from the northern border states (Tamaulipas, Neuvo Leon, Chihuahua, and Coahuila) and 12% were from the west central states (Jalisco, Colima, Michoacan, and Guerrero). One patient was from the northwestern region, but there were none from the southeast region. Neurocysticercosis patients were more likely to be from north central and central Mexico than tuberculosis patients (P < 0.01 and P < 0.05, respectively), seen in Houston. In contrast, fewer neurocysticercosis patients were from northern border states (P < 0.01) (Table 3). Few patients in either group were from northwestern or southern states, suggesting that immigrants to Houston infrequently came from these areas.

Six (14.6%) United States-born patients were surveyed for risk factors for neurocysticercosis. All six reported frequent travel to rural Mexico or Central America. All had visited relatives and friends who raised pigs. Three of the six reported a family history of taeniasis, and four patients reported a history of tapeworms. Only one patient did not report either personal or family history of tapeworms (Table 4).

Among the 35 immigrants interviewed, all ingested pork. Twenty-nine (83%) raised pigs prior to immigrating to the United States and 15 (43%) of those reported pigs living in their home. Fifteen (43%) had a personal history of taeniasis. Of the seven patients who did not raise pigs, five reported a history of taeniasis. Nineteen (54%) patients recalled a family history of taeniasis, 16 (46%) of these in a sibling or parent. Twenty-two (63%) of the patients reported traveling back to their country of origin within the past five years (Table 5).

The median time from immigration to the United States and diagnosis was 58 months. For the three patients who had remained in the United States continuously since immigration, the median time to diagnosis was 28 months (Table 6).

DISCUSSION

Our study shows that neurocysticercosis is a common cause of neurologic disease in Hispanic immigrants in Houston, Texas. Among the patients identified by discharge diagnosis, most (60%) were from Mexico. Most of the immigrants were from rural areas and reported a history of significant exposure to pig husbandry. Most also reported a personal or family history of taeniasis. All six United States–born patients had a history of frequent travel to rural pig-rearing areas in Mexico or Central America and five had a personal or family history of taeniasis.

Neurocysticercosis is increasingly being recognized as a significant health problem in the United States. It accounted for 2% of all Neurology Clinic visits in our series and 16% of the seizures in Hispanics visiting our Neurology Clinic. A prospective study at 11 University-affiliated geographically diverse, urban emergency departments in the United States from July 1996 to September 1998 reported that 2.1% of the patients coming to emergency rooms with seizures had neurocysticercosis.16 The investigators estimated that neurocysticercosis is the cause of seizures in 13.5% of Hispanic patients, a proportion very similar to our finding. Sorvillo and others studied reported cases of cysticercosis in Los Angeles County (the only jurisdiction in the United States where neurocysticercosis is a reportable disease).10 They documented 138 cases in the three years from 1988 to 1990, with most patients being Mexican immigrants. However, 6.5% of the cases were travel-associated and 7.2% were autochthonous. Similarly, a review of hospital discharge diagnoses from Oregon identified 61 patients with neurocysticerocis.9 While 72% were born in Mexico, 18% were born in the United States. Thus, the majority of neurocysticercosis patients are immigrants from Latin America.

We noted a close association between rural pork husbandry in Latin America and neurocysticercsis in the United States. All immigrants in our study ate pork prior to immigration, 83% raised pigs, and many noted that the pigs lived inside their houses. While pork consumption per se does not lead to cysticercosis, it is associated with development of taeniasis, which in turn poses risks for cysticercosis. Indeed, most of our patients had a family history of taeniasis and many reported symptoms consistent with prior taeniasis. This is in contrast to findings from most clinical series, in which cysticercosis patients in the United States are only rarely found to harbor tapeworms.10,11,13

Travel to disease-endemic villages was quite common, even after immigration. Also, all the United States–born cases reported significant risk factors for acquisition of neurocysticercosis, including annual travel to disease-endemic villages in rural Mexico or Central America, exposure to pigs, and a personal or family history of taeniasis. This highlights the close relationship between urban immigrant populations in the United States and rural pig-rearing environments in developing countries.

Several studies have documented autochthonous cases of neurocysticercosis in the United States. For example, 12 United States–born patients without a history of travel outside the United States were noted among cases reported from Los Angeles.10,17 Similarly, local transmission has been documented in New York, Chicago, and Oregon.9,11,12 The source of these local infections was presumed to be through close contact with tapeworm carriers. In contrast, no confirmed cases of domestically acquired neurocysticercosis were identified in our series. This may reflect a selection bias in other series (cases born in the United States are more likely to be reported or brought to the attention of public health authorities). Alternatively, some of the cases we noted with risk factors for acquisition abroad may have been infected in the United States.

While the association between cysticercosis and immigrants is well recognized, no data from the United States address the question of regional variations in disease-endemic areas. Most (94%) of our immigrant patients were born in Mexico or El Salvador. The distribution of Central American nations is a reflection of the local immigrant population in Houston, where a large proportion of Central Americans are from El Salvador. This suggests a fairly uniform distribution of the disease in Central America. In contrast, we noted significant regional variations among the Mexican immigrants. Immigrants from Mexico to the United States are largely from the border region of Mexico with the United States and north central and west central Mexico.18 A similar distribution was also noted in a database of tuberculosis patients of Mexican origin diagnosed in Houston. A national seroepidemiologic survey in Mexico indicated that the states with high seroprevalence of antibodies to T. solium antigens include Jalisco, Guanajuato, Zacatecas, Guerrero, and Distrito Federal, which lie mainly in north central and west central Mexico.19,20 In our study, a large percentage of the patients also originated from the north central and central regions (Figure 1). However, the northern border states, which account for a significant portion of immigrants, have a low seroprevalence of cysticercosis, with few patients from this region in our study. The southern and northwestern states comprise only a small proportion of immigrants to Houston. Thus, it is not surprising that we noted only one patient from these regions. Surprisingly, we did not have a single patient from Jalisco. Jalisco is a common birthplace of immigrants and an area with a high reported seroprevalence of cysticercosis.1820 It is possible that Houston immigrants are mainly from urban regions of Jalisco (e.g., Guadalajara). Overall, the birthplace of neurocysticercosis patients in the United States reflects both the patterns of immigration and the level of endemicity.

There are few good data on the pre-patent period for neurocysticercosis. In a review of 450 British citizens in the United Kingdom with cysticercosis presumably acquired in India, Dixon and Lipscomb estimated an average pre-patent period of 58 months (range = 1–30 years) with a median of 2–3 years.21 Similarly, we found a median time from immigration to diagnosis of 58 months among our patients. Among those who did not return to Latin America after immigration to the United States, the median time to diagnosis was 28 months, which was similar to the median period of 2–3 years noted by Dixon and Lipscomb.21 This shorter interval suggests that some immigrants may have been infected during subsequent visits. The pre-patent period is consistent with current models of immunopathogenesis, in which viable parasites suppress the host inflammatory response, but disease occurs when the parasite can no longer suppress the host inflammatory response and seizures occur.22

In summary, we have noted that neurocysticercosis is an important neurologic disease among Hispanic immigrants, a group that is growing and becoming more widely dispersed throughout the United States. Clinicians should note, however, that cysticercosis is not uniformly present throughout Latin America. Instead, we noted a close association between pork husbandry in villages in Mexico and Central America and neurologic disease in the United States. Even cases born in the United States often show close contact with rural disease-endemic areas. Thus, exposure to these areas is a more precise risk factor than the country of birth. This study also underscores the increasing interconnection between urban areas in the United States and developing countries and the impact of diseases endemic in developing countries on public health in the United States.

Table 1

Birthplace and clinical manifestations for 114 hospitalized patients diagnosed with neurocysticercosis at Ben Taub General Hospital, Houston, Texas, 1/94–6/97

BirthplaceNo. (%)*SymptomsNo. (%)
* Percentage of the patients for whom the country of birth was known.
Mexico55 (78)Seizures86 (75)
El Salvador7 (10)Hydrocephalus28 (25)
Other Central American country4 (6)Headaches17 (15)
United States4 (6)Confusion8 (7)
India1 (1)Ataxia6 (5)
Country not specified43
Table 2

Records of all active patients at the neurology clinic at Ben Taub General Hospital reviewed for major symptom, diagnosis of neurocysticercosis, and Hispanic surname

No. (%)
Total charts reviewed2,947 (100)
Number with seizure disorders813 (28)
Patients with neurocysticercosis54 (2)
Patients with neurocysticercosis and seizures48 (2)
Estimated % of Hispanic patients with seizures due to neurocysticercosis16
Table 3

Birthplace of Mexican immigrants with neurocysticercosis compared with those with tuberculosis

RegionNeurocysticercosisTuberculosis
* P < 0.05.
P < 0.01.
Texas border states* (Nuevo Leon, Tamaulipas, Chihuahua, Coahuila)4 (15%)217 (42%)
North central status (Aguascalientes, Guanajuato, San Luis Potosi, Queretaro, Zacatecas)10 (38%)113 (22%)
Central states† (Distrito Federal, Mexico, Hidalgo, Puebla, Morelos, Tlaxcala)8 (31%)66 (13%)
Northwestern states (Sonora, Sinaloa, Baja California, Nayarit, Durango)1 (4%)12 (2%)
West central states (Jalisco, Michoacan, Colima, Guerrero)3 (12%)82 (16%)
Southern and southeastern states (Veracruz, Campeche, Chiapas, Yucatan, Tabasco, Quintana Roo, Oaxaca)0 (0%)31 (6%)
Table 4

Risk factors for neurocysticercosis for six patients born in the United States

Risk factorNo. positive/total
Travel to rural Mexico (5) or Central America (1)6/6
Median frequency of travel outside the US1 visit/year
Visited people who raised pigs6/6
Family history of taeniasis3/6
History of taeniasis4/6
Personal or family history of taeniasis5/6
Table 5

Risk factors for neurocysticercosis for 35 immigrant cases

Risk factorNo. positive/total (%)
Ate pork prior to immigration35/35 (100)
Raised pigs prior to immigration29/35 (83)
Pigs lived in house15/35 (43)
History of taeniasis15/35 (43)
Of those not raising pigs, history of taeniasis5/7 (71)
Family history of taeniasis19/35 (54)
History of taeniasis in sibling or parent16/35 (46)
Travel to country of origin in past 5 years22/35 (63)
Range = 1–10 visits
Table 6

Survey results for 41 patients diagnosed with neurocysticercosis at Ben Taub Hospital, Houston, Texas

No. (%)
Birthplace
    Mexico26 (63)
    Central America (El Salvador 7, Guatemala 1, Costa Rica 1)9 (22)
    United States6 (15)
Time from immigration to diagnosis (median)58 months (range = 5–209)
Time from immigration to diagnosis for those in the United States continuously after immigration (median)28 months (range = 2–121)
Figure 1.
Figure 1.

States of birth in Mexico of the cases of neurocysticercosis in Houston, Texas. This figure appears in color at www.ajtmh.org.

Citation: The American Journal of Tropical Medicine and Hygiene Am J Trop Med Hyg 73, 4; 10.4269/ajtmh.2005.73.766

*

Address correspondence to A. Clinton White Jr., Department of Infectious Disease, Baylor College of Medicine, 1 Baylor Plaza, Houston, TX 77030. E-mail: arthurw@bcm.tmc.edu

Authors’ addresses: Yazmin del la Garza, Departamento de Neurologia, Instituto Nacional de Ciencias Medicas y Nuitricion Salvador Zubiran, Mexico City, Mexico. Edward A. Graviss, Department of Pathology, Baylor College of Medicine, 1 Baylor Plaza, Houston, TX 77030, Telephone: 713-798-8097, Fax: 713-798-8895. Naval G. Daver, Kimberley J. Gambarin, Wayne X. Shandera, and A. Clinton White, Jr., Department of Infectious Disease, Baylor College of Medicine, 1 Baylor Plaza, Houston, TX 77030, Telephone: 713-798-6846, Fax: 713-798-0681, E-mail: arthurw@bcm.tmc.edu. Peter M. Schantz, Division of Parasitic Diseases, Centers for Disease Control and Prevention, 4770 Buford Highway, Atlanta, GA 30341, Telephone: 770-488-7767, Fax: 770-488-7761.

Acknowledgments: We thank Jose Luis Molinari for assistance in arranging funding and Richard Armstrong for providing access to Neurology Clinic information.

Financial support: This work was supported in part by a scholarship to Yazmin Del la Garza from the Fundacion Universidad Nacional Autónoma de México.

REFERENCES

  • 1

    White AC Jr, 2000. Neurocysticercosis: updates on epidemiology, pathogenesis, diagnosis, and management. Annu Rev Med 51 :187–206.

  • 2

    Garcia HH, Gonzalez AE, Evans CA, Gilman RH, 2003. Taenia solium cysticercosis. Lancet 362 :547–556.

  • 3

    Carpio A, 2002. Neurocysticercosis: an update. Lancet Infect Dis 2 :751–762.

  • 4

    Sept 3 2002. Hispanic Heritage month 2002. Facts for Features: Public Information Office, US Census Bureau, Washington, DC 20233.

  • 5

    Guzman B, 2001. The Hispanic Population. Census 2000 Brief. Washington, DC: U.S. Department of Commerce.

  • 6

    Staff M, 2002. The US-Mexico Border. US in Focus. Washington, DC: Migration Information Source, Migration Policy Institute.

  • 7

    Alvarez F, 1999. Dawn of a New Majority. Los Angeles: Los Angeles Times.

  • 8

    White AC Jr, Atmar RL, 2002. Infections in Hispanic immigrants. Clin Infect Dis 34 :1627–1632.

  • 9

    Townes JM, Hoffmann CJ, Kohn MA, 2004. Neurocysticercosis in Oregon, 1995–2000. Emerg Infect Dis 10 :508–510.

  • 10

    Sorvillo FJ, Waterman SH, Richards FO, Schantz PM, 1992. Cysticercosis surveillance: locally acquired and travel-related infection and detection of intestinal tapeworm carriers in Los Angeles. Am J Trop Med Hyg 47 :365–371.

    • Search Google Scholar
    • Export Citation
  • 11

    Schantz PM, Moore AC, Muñoz JL, Hartman BJ, Schaefer JA, Aron AM, Persaud D, Sarti E, Wilson M, Flisser A, 1992. Neurocysticercosis in an Orthodox Jewish community in New York City. N Engl J Med 327 :692–695.

    • Search Google Scholar
    • Export Citation
  • 12

    Rosenfeld EA, Byrd SE, Shulman ST, 1996. Neurocysticercosis among children in Chicago. Clin Infect Dis 23 :262–268.

  • 13

    Shandera WX, White AC Jr, Chen J, Diaz P, Armstrong R, 1994. Cysticercosis in Houston, Texas: a report of 112 cases. Medicine (Baltimore) 73 :37–52.

    • Search Google Scholar
    • Export Citation
  • 14

    White AC Jr, 1997. Neurocysticercosis: a common cause of neurologic disease worldwide. Clin Infect Dis 24 :101–113.

  • 15

    El Sahly HM, Adams GJ, Soini H, Teeter L, Musser JM, Graviss EA, 2001. Epidemiologic differences between United States-and foreign-born tuberculosis patients in Houston, Texas. J Infect Dis 183 :461–468.

    • Search Google Scholar
    • Export Citation
  • 16

    Ong S, Talan DA, Moran GJ, Mower W, Newdow M, Tsang VC, Pinner RW, 2002. Neurocysticercosis in radio graphically imaged seizure patients in U.S. emergency departments. Emerg Infect Dis 8 :608–613.

    • Search Google Scholar
    • Export Citation
  • 17

    Richards FO, Schantz PM, Ruiz-Tiben E, Sorvillo FJ, 1985. Cysticercosis in Los Angeles County. JAMA 254 :3444–3448.

  • 18

    Larralde C, Padilla A, Hernandez M, Govezensky T, Sciutto E, Gutierrez G, Tapia-Conyer R, Salvatierra B, Sepulveda J, 1992. Seroepidemiology of cysticerosis in Mexico. Salud Publica Mex 34 :197–210.

    • Search Google Scholar
    • Export Citation
  • 19

    Epidemiologica, 1994–2000. Mexico City, Mexico: Direccian General de Epidemiologica.

  • 20

    Sarti E, 2002. Epidemiology of Taenia solium taeniasis and cysticercosis in Mexico. Singh G, Prabhakar S, eds. Taenia solium Cysticercosis: From Basic to Clinical Science. Wallingford, United Kingdom: CAB International, 83–90.

  • 21

    Dixon HBF, Lipscomb FM, 1961. Cysticercosis: An analysis and follow-up of 450 cases. London: Her Majesty’s Stationary Service.

  • 22

    Stringer JL, Marks LM, White AC Jr, Robinson P, 2003. Epileptogenic activity of granulomas associated with murine cysticercosis. Exp Neurol 183 :532–536.

    • Search Google Scholar
    • Export Citation

Author Notes

Reprint requests: A. Clinton White, Jr., Department of Infectious Disease, Baylor College of Medicine, 1 Baylor Plaza, Houston, TX 77030.
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