We would like to thank Dr. A. Goenka for the sincere response to our case report of disseminated cysticercosis and taeniasis in a Japanese traveler. As cited in that report, the occurrence of neurocysticercosis (NCC) among international travelers is quite low, with the most prevalent form a single parenchymal cyst.1 Although a diagnosis of NCC is usually based on detection of specific antibodies against Taenia solium antigens in neuroimaging and/or serological findings, the majority of these cases do not show typical findings and serology is not always useful for a solitary cyst.2 Because our patient was presented with a disseminated form of the disease, a quite rare type of NCC found in international travelers, we were able to make a rapid and accurate diagnosis.
As also mentioned in the case presentation, the patient had stayed with a local host family and was treated with hospitality, including daily meals that often included grilled pork. We agree with Dr. Goenka and speculate that ingestion of pork containing cysticerci was the route through which our patient became a T. solium carrier.
Our primary point of interest in this case was the pathogenesis of disseminated cysticercosis. The patient was considered to initially become a carrier by ingesting pork, which then resulted in cysticerci dissemination as autoinfection by eggs released from the internal tapeworm. A common type of human transmission of T. solium eggs is through fecal–oral contamination from the feces in tapeworm carriers in close proximity to the infected individual.3 However, we think that this mode of infection was not likely in this case, because no one near the patient, including the host family members, were apparently ill or showed evidence of cysticercosis. In addition, contamination in the environment including food and water usually results in exposure to a small number of eggs, which accounts for the high prevalence of cases with a single enhancing lesion in India.4 In consideration of the multiple lesions seen in our patient; autoinfection seems to be the likely transmission route of the eggs. Thus, we speculate that internal autoinfection (regurgitation of gravid proglottides into the stomach) rather than external autoinfection might have been the reason for the disseminated cysticercosis in this case, though we were not able to confirm the actual transmission route.
Finally, we agree that whole-body magnetic resonance imaging (MRI) is a powerful tool for diagnosis and management of disseminated cysticercosis, and think that its widespread use would be very helpful.
Ito A, Takayanagui OM, Sako Y, Sato MO, Odashima NS, Yamasaki H, Nakaya K, Nakao M, 2006. Neurocysticercosis: clinical manifestation, neuroimaging, serology and molecular confirmation of histopathologic specimens. Southeast Asian J Trop Med Public Health 37 (Suppl 3): 74–81.
Garcia HH, Gonzales AE, Tsang VCW, Gilman RH, for the cysticercosis working group in Peru, 2006. Neurocysticercosis: some of the essentials. Pract Neurol 6: 288–297.
Garcia HH, Gonzalez AE, Rodriguez S, Tsang VC, Pretell EJ, Gonzales I, Gilman RH, 2010. Neurocysticercosis: unraveling the nature of the single cysticercal granuloma. Neurology 75: 654–658.