Polyneuritis cranialis after acute tularemia infection: A case study

Abstract

A 60-year-old man was referred for multiple cranial neuropathies. Six weeks earlier, a minor left finger laceration was exposed to rabbit blood. Two days later, he developed flulike symptoms and lymphadenopathy. The wound became swollen, and expressed pus was sent for culture. He started an empirical course of cephalexin, but, when the culture was positive for Francisella tularensis, he was initiated on a 20-day course of doxycycline.Over the subsequent 2 weeks he developed worsening cough, dry heaves, and conjunctivitis. He was admitted to a local hospital 1 month only present in 50% and 75% of GBS patients within the first and third week of symptoms, respectively. 10 GBS spectrum disorders exist, such as Miller Fisher syndrome (MFS) and other variants. Polyneuritis cranialis, characterized by manifestations isolated to cranial nerves without limb involvement (as seen in our patient), could be considered a GBS/MFS interface disorder. 11The neurological abnormalities in the patient described were restricted to cranial nerves, which only developed several weeks after the initial ulceroglandular infection. This, along with unremarkable CSF and MRI results, supported an immune-mediated mechanism rather than damage due to direct F tularensis infection. Accordingly, rather than additional antibiotic therapy, he was treated with IVIg with subsequent clinical and electrodiagnostic improvement. The presence of low-titer P/Q-type calcium channel antibodies is of uncertain significance, possibly supporting an autoimmune mechanism.In conclusion, polyneuritis cranialis may be a rare immunemediated manifestation of ulceroglandular tularemia.