To describe a case report of Guillain Barre syndrome (GBS) in a patient with babesiosis.

Limited literature exists on development of GBS following Babesia infection and pathophysiology is unclear.

We present a case report of a 41-year-old Hispanic man with no known history who presented to our hospital with one week of progressive myalgias, dyspnea, dysphagia, perioral/extremity paresthesias, and tetraparesis. He denied any preceding fever, diarrhea, rash, tick bite, travel, cough, or sore throat.

Vitals were stable, and his laboratory work-up revealed mildly elevated liver enzymes, thrombocytopenia. Neurologic exam at presentation revealed significant bulbar/bilateral facial weakness, strength of 1-2/5 in the lower limbs and 2-3/5 in the upper limbs with diffuse areflexia and preserved sensation. Contrast-enhanced MRI brain and cervical/thoracic/lumbar spine was unremarkable. The day next to his admission, IVIG was initiated. Serum tick-borne pathogens' panel revealed positive Babesia microti DNA PCR, and a peripheral blood smear with 2% Babesia microti parasitemia. Antimicrobial treatment with azithromycin, atovaquone, and ceftriaxone was started. CSF evaluation indicated albuminocytologic dissociation with a normal cell count and elevated protein of 142. Course was complicated by worsening respiratory status and intubation. IVIG was administered for 5 days followed by extubation on the 6^th day. Neurologic exam showed a mild improvement in shoulder abduction strength. Nerve conduction studies (NCS) showed temporal dispersion in bilateral lower extremities, indicative of demyelination.

Limited literature exists on GBS following infection with Babesia. Only three such case reports were found, and one of them was in a patient with multi-pathogenic infections (Babesia, Ehrlichia, Arcobacter). Pathophysiology of neurologic complications in babesiosis is attributed to red blood cell cytoadherence or excess cytokine expression in high parasitemia, however our patient only had 2% parasitemia. More robust research is needed to establish causation and understand pathophysiology of GBS in babesiosis.