Background/introduction Progressive multifocal leukoencephalopathy, caused by the John Cunningham (JC) polyomavirus, is the third commonest cause of encephalopathy in HIV-infected patient and almost exclusively occurs in immunosuppressed individuals.
Case report A 33-year-old female presented with a late HIV diagnosis during antenatal period and commenced on combivir, darunavir and ritonavir. Baseline viral load was 168,051 copies/ml and CD4 count was 70/100 ml. She then developed right sided weakness and facial droop. Raltegravir was added at 33 weeks gestation. Power on right side was 4/5 with hyperreflexia and a mild cranial nerve VII palsy. Neurological examination done a week prior to presentation found no abnormalities.
Results Routine bloods were unremarkable. CSF analysis showed white cell count of 4 × 106/L predominantly lymphocytes, protein 0.59 g/L, polyomavirus DNA and JC virus DNA positive. Cryptococcal antigen, india ink stain and toxoplasma serology were negative. Initial MRI head showed multiple abnormal areas with the largest abnormal area seen in the left frontal lobe affecting white matter with extension into grey matter. Progress – weakness worsened over the next 2 weeks, power was 1/5 with expressive dysphasia. She was started on 5 days 1 g methylprednisolone which showed no improvement. Due to foetal distress on CTG, emergency caesarean was done at 36 weeks. Viral load at delivery was <40 copies/ml. Darunavir and ritonavir were stopped due to raised ALT, which resolved.
Discussion/conclusion PML progresses rapidly and prognosis is poor. Currently there are no treatment guidelines for PML and studies using mefloquine and methylprednisolone show inconclusive results.
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