Case Presentation:

A 36–year–old Hispanic female immigrant presented with two days of headache and neck pain. She had presented on a prior occasion with similar complaints, and was diagnosed with migraine headaches. She was admitted for presumed bacterial meningitis. A lumbar puncture was performed, revealing 642 white blood cells/mL with 46% eosinophils. The Gram stain and cultures were negative. Magnetic resonance imaging of the brain showed communicating hydrocephalus and a sellar arachnoidocele. She was started on empiric intravenous antibiotics, but continued to complain of headaches. Two repeat lumbar punctures were performed and continued to result in culture–negative eosinophilic meningitis. Stool ova and parasites were negative. She was discharged with presumed ibuprofen induced eosinophilic meningitis. Two weeks later, she re–presented, at which time serum studies for parasites obtained during the initial hospitalization were found to be positive for cysticercosis.

Discussion:

Meningitis is one of the most common diagnoses encountered by the hospitalist. While most causes are due to bacterial or viral etiologies, the hospitalist must be able to recognize the signs and symptoms suggestive of other CNS infections. Cysticercosis, caused by the parasite Taenia solium, is the most common parasitic disease of the central nervous system. Endemic in many foreign countries including Latin America, it is now being recognized as an important health issue in the United States due to rural immigration. The clinical presentation of neurocysticercosis can vary greatly depending on location, host inflammatory response, and stage of the cysticerci. Viable parasites are able to modulate the host’s immune responses, typically delaying onset of symptoms for years. Symptoms begin to occur as the cysticerci age and lose their ability to influence inflammation. Seizures, occurring in 70–90% of patients, are the most common manifestation due to intra–parenchymal cysterci. However, atypical presentations including hydrocephalus, chronic meningitis, and cranial nerve abnormalities are more likely when lesions are extraparenchymal. These atypical presentations can also be secondary to an inflammatory response caused by asymptomatic parenchymal cysterci.

Conclusions:

Diagnosis of neurocysticerosis is difficult due to variable presentations, nonpathognomonic neuroimaging, and unreliable serologic testing. As a result, the diagnosis hinges on a high pretest probability; recurrent meningial–type headaches, immigration status, eosinophilia, and culture–negative CSF meningitis should prompt the hospitalist to consider the diagnosis. All of these symptoms were present in our patient. This case also illustrates the importance of laboratory follow–up as an essential element of the discharge transitions–of–care process. Although the laboratory tests establishing the diagnosis were obtained in the initial hospitalization, it was not until she re–presented that the results of these tests were observed.