Cerebral gnathostomiasis

A previously well, 42‐year‐old man presented to an Australian hospital with a 4‐day history of sudden onset, bilateral, occipital headache, 4 weeks after returning from a holiday in Thailand. He had consumed duck blood while travelling in Asia, but had eaten no raw or undercooked meat or seafood. His physical examination was normal with no evidence of neurological dysfunction and he had no rash or skin swellings. Blood tests revealed a peripheral blood eosinophilia of 4.89 × 10⁹/L (reference interval [RI], < 0.6 × 10⁹/L) but were otherwise normal. Computed tomography of the brain was unremarkable. Cerebrospinal fluid examination showed 30 × 10⁶/L red blood cells (RI, < 5 × 10⁶/L) and 1120 × 10⁶/L white blood cells, 80% of which were eosinophils (RI, < 5 × 10⁶/L). Magnetic resonance imaging (MRI) of the brain demonstrated non‐specific T2 hyperintensities in the subcortical white matter (Supporting Information) and normal T1‐weighted post gadolinium images (Box 1, A). However, susceptibility‐weighted images showed serpiginous tracts in both occipital lobes (Box 1, B). Cerebral gnathostomiasis was suspected and daily oral prednisolone at a dose of 60 mg was prescribed. His headache improved and he was discharged home. Four days later, he re‐presented with right‐sided upper limb weakness and mixed dysphasia. Repeat MRI showed significant progression of the tracts (Box 1, C). His corticosteroid therapy was increased to 8 mg dexamethasone three times daily, but antihelminthic agents were not prescribed as there was concern that dying larvae might migrate further or lead to cerebral oedema. His corticosteroids were subsequently weaned, and his neurological deficits gradually improved over one month. Blood that had been sent to Thailand for serological testing during his first hospital admission returned a positive result for gnathostomiasis. Sixteen months after his initial presentation, he had made an excellent neurological and functional recovery, with only a subtle short term memory deficit. Repeat MRI performed at this time revealed persistent, but stable, changes with no new tract formation (Box 1, D).