Guillain Barre Syndrome in a Patient with Babesiosis: A Case Report
Karandeep Singh Bhatti1, Tomer Noff1, Jesse Thon1
1Cooper University Hospital
Objective:

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

Background:

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

Design/Methods:

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.

Results:

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 6th 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.

Conclusions:

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.

10.1212/WNL.0000000000208331