Abstract

A 60-year-old man presented with an acute, pruritic, erythematous rash associated with marked hypereosinophilia (2.34×10⁹/l (0.04–0.40)). There was eosinophilic infiltration on hepatic, bone marrow and lymph node biopsies, with multiple lung nodules and mild splenomegaly. However, extensive investigation excluded parasitic or bacterial causes, specific allergens or the Fip1L1 mutation seen in myeloproliferative hypereosinophilia. Six months into the illness, he developed an acute, left, complete lower motor neurone facial palsy over hours, and an acute right lower motor neurone facial palsy 2 weeks later, without recovery. Over the subsequent 3 months, he developed complex partial seizures, a transient 72-h non-epileptic encephalopathy and episodic vertigo with ataxia. Further investigation showed bilateral enhancement of the VII nerves and labyrinthis on gadolinium-enhanced MR brain scan, cerebrospinal fluid lymphocytosis and neurophysiological evidence of polyradicolopathy. His eosinophil count fell with corticosteroids, hydroxycarbamide, imatinib and ultimately mepolezumab, but without symptomatic improvement. Repeat lymph node biopsy showed Kaposi's sarcoma, leading to a diagnosis of HIV-1 infection with a modestly reduced CD4 count of 413×10⁶/l (430–1690). Hypereosinophila and eosinophilic folliculitis are recognised features of advanced HIV infection, and transient bilateral facial palsy occasionally occurs at the time of seroconversion. This is the first report of a chronic bilateral facial palsy likely due to primary HIV infection, not occurring during seroconversion and in association with hypereosinophilia. This case emphasises the protean manifestations of HIV infection and the need for routine testing in atypical clinical presentations.