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Pathological Case of the Month
Robert E. Garola, MD;
David L. Zwick, MD
From the Department of Pathology/Laboratory Medicine, The Children's Mercy Hospital, Kansas City, Mo.
Arch Pediatr Adolesc Med. 1999;153:767-768.
A 13-YEAR-OLD Mexican girl was evaluated for a weeklong history of recurrent tonicoclonic seizure activity. The only observation from a medical examination was a small lymph node in the left anterior region of the neck. The girl was alert and afebrile, and findings were normal for complete blood cell count; prothrombin and activated partial thromboplastin times; electrolytes, serum urea nitrogen, creatinine, and glucose levels; and urinalysis. A radiograph of the chest was unremarkable, but a magnetic resonance image of the brain showed a single, small, ring-enhancing lesion surrounded by edema in the subcortical zone of the high left parietal region.
A computed tomography–guided, stereotactic, left frontal craniotomy was performed, and a fairly well-demarcated, hard, ball-like structure was resected. Inspection of the specimen under dissecting microscope demonstrated gray-white brain tissue 1.0 cm in diameter surrounding a smooth, ovoid, yellow-white mass measuring 0.6 cm in diameter. The mass was solid, and cutting the surface revealed 3 variably thick concentric zones: a peripheral zone of translucent pale yellow, a middle zone of translucent pale gray, and a central opaque, sharply demarcated, yellow necrotic zone (Figure 1).
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Figure.
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Diagnosis and Discussion: Neurocysticercosis
Figure 1. Top, Cut surface of the nodule demonstrating a central necrotic collapsed cyst surrounding a necrotic scolex. Bottom, Necrotic cestodal larva surrounded by purulent debris.
Cysticercosis is a larval cestodiasis caused by the larval form (mastocestode) of Taenia solium. The life cycle of T solium includes humans as intermediate hosts. Acquisition of the disease by humans results from ingesting T solium eggs that are shed in human feces.
Infection of humans by T solium (pork tapeworm) occurs by eating undercooked pork containing the larval form, which causes mostly asymptomatic intestinal tapeworm infection, or by ingesting eggs shed in human feces, causing a systemic or multisystemic infection known as cysticercosis. The eggs of T solium from which the cysts may originate may be acquired in 3 fecal ways: (1) through oral contact with contaminated, egg-bearing fecal material, (2) person-to-person oral transmission by uncleansed hands from persons contaminated by the eggs, and (3) autoinfection. Neurocysticercosis is infection of the central nervous system by the larval stage of T solium. In endemic countries, approximately 50% of the population affected by this infection are children younger than 12 years, and adolescents between 12 and 20 years account for 6% of the affected population.1 In the United States, persons 19 years or younger account for approximately 25% of the cases reported.2 The prognosis of neurocysticercosis varies from benign to severe.
The mature adult worm of T solium is a helminth of the class Cestoidea, morphologically characterized by a head (scolex) and body segments (proglottids). The scolex has suckers and hooks that are used to attach to the intestinal tract of the host. The proglottids, when mature, contain testes and ovaries that act as independent reproductive entities. Humans are definitive hosts of the adult stage and intermediate hosts of the larval stage. The encysted larva contains motile, 6-hooked larvae that can transverse the host's gut and lodge itself into different organs of the host. Then, the larvae encyst and are subjected to a series of metamorphogenic changes. In the central nervous system, the larvae are localized either in the brain parenchyma or in the spinal cord, forming cysts or nodules of variable size (1.0-2.5 cm in largest diameter).3 When the larvae localize in the arachnoid tissue, they form multiple confluent cysts up to 12 cm in largest diameter that invade the ventricular system and sylvian fissure and are able to obstruct the cerebrospinal fluid flow.
Before 1987, only 15 cases of locally acquired cysticercosis were reported in the United States. From 1988 to 1990, 10 cases of locally acquired cysticercosis were reported in Los Angeles County alone.4 Cysticercosis is found in both urban and rural inhabitants of the United States who have never traveled outside the country.5
AUTHOR INFORMATION
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Accepted for publication March 25, 1996.
Corresponding author: Robert E. Garola, MS, Pathology Laboratory, The Children's Mercy Hospital, 2401 Gillham Rd, Kansas City, MO 64108.
REFERENCES
1. Thomson AJ. Neurocysticercosis-experience at the teaching hospitals of the University of Cape Town. S Afr Med J. 1993;83:332-334.
PUBMED
2. Ehnert KL, Roberto RR, Barrett L, Sorvillo FS, Rutherford GW III. Cysticercosis: First 12 Months of Reporting in California. Vol 26. Washington, DC: Pan American Health Organization; 1992:165-172.
3. Ghariani S, Gille M, Matthijs P, Delbecq J, Depre A. Cysticercose cérébrale traitée par albendazole: évolution de l'imagerie par resonance magnetique cérébrale. Rev Neurol. 1994;150:709-712.
PUBMED
4. Sorvillo FJ, Waterman SH, Richards FO, Shantz PM. Cystocercosis surveillance. Am J Trop Med Hyg. 1992;47:365-371.
5. US Department of Health and Human Services. Locally acquired neurocysticercosis—North Carolina, Massachusetts and South Carolina, 1989-1991. MMWR Morb Mortal Wkly Rep. 1992;41:1-4.
SECTION EDITOR: ENID GILBERT-BARNESS, MD
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