Post-contrast images showed there was peripherally an avid ring of enhancement along the cysts. There was also an irregular rim with effacement of the roots along the peripheral aspect, and likely there was enhancement of the roots in this location as well (Figure 1). Hematological evaluation and biochemical parameters were normal. The clinical diagnosis was arachnoid cyst or arachnoiditis or possibly spinal tumors, and surgery was believed to be warranted because of the patient’s progressive neurological symptoms. A lumbar
laminectomy L1 to L4 was performed and the underlying dura mater was opened. Beneath were grossly abnormally thickened arachnoid and a round thick fluid-filled Olaparib manufacturer sac that was directly compressing the conus medullaris and the cauda equina. This was carefully removed and sent for pathology. Histological examination was compatible with neurocysticercosis (NCC;
Figure 2). The serum was positive for anticysticercus antibodies by enzyme-linked immunosorbent assay (ELISA), using glycoproteins purified from Taenia solium cyst fluid as antigens. Examination of stools was negative for the presence of parasites, proglottids, and ova. The patient underwent full craniospinal axis MRI evaluation, which demonstrated no evidence of other cysticercosis lesions. She recovered from the surgery uneventfully, and at a 3-month follow-up visit she complained of mild residual left leg numbness and weakness in the legs after prolonged standing. She had subjective decrease in light touch sensation on the left Quizartinib lower leg compared with the right and strength was slightly diminished on the left compared with the right leg that had normal strength. To further evaluate where the infection was acquired from, we analyzed cytochrome c oxidase l (cox1) of mitochondrial DNA (mtDNA) using the formalin-fixed Erastin ic50 and paraffin-embedded histological specimen prepared from the patient and stored in the pathology department in tissue blocks.1 Comparing with the GenBank database, the sequence was completely identical to the cox1 sequence of T solium from Korea and China (data not shown).1 NCC is a neurologic
infestation caused by the larval form of T solium. Taenia solium has a complex life cycle that requires two hosts. Humans are the only known definitive hosts for the adult cestode, whereas pigs are the natural intermediate host and humans may become accidental intermediate hosts for the larval form or cysticercus.2 Humans acquire the intestinal tapeworm T solium by eating raw pork. They acquire NCC by ingesting T solium eggs through fecal oral contamination. In the United States, NCC has become an increasingly important emerging infection. This has largely been driven by the influx of immigrants from endemic regions.3 Despite an increasing number of NCC cases overall, the number of spinal NCC cases remains very low.4 The incidence of spinal NCC among travelers is extremely rare.