A 30-year-old man was presented to a regional hospital in Cape Town, South Africa, with a 3-month history of odynophagia, vomiting, abdominal pain and unilateral vision loss. He reported no respiratory complaints or diarrhoea. He had been diagnosed with HIV and drug-sensitive tuberculosis (TB) six months earlier and was initiated on tenofovir, lamivudine and dolutegravir (as well as the first-line anti-TB treatment). He admitted to interrupting ART and anti-TB treatment because of gastrointestinal symptoms. He gave a history of being diagnosed with ataxia of undetermined cause by a neurologist three months earlier. The workup for his ataxia, which included serum thyroid stimulating hormone, vitamin B12 levels, cerebrospinal fluid analysis, and magnetic resonance imaging (MRI) of his brain and spine, was normal.
On examination, he looked chronically ill with muscle wasting and conjunctival pallor. His vital signs were within normal limits, and his abdominal examination revealed epigastric tenderness but no guarding or organomegaly. On neurological assessment, he was alert and orientated with no neck stiffness. He had cerebellar signs that included truncal ataxia, bilateral intention tremor, dysdiadochokinesis and positive heel-shin tests bilaterally. Examination of visual acuity demonstrated no light perception in the left eye and 6/6 vision in the right eye.
A urine lipoarabinomannan assay (LAM) for TB was negative, and the chest radiograph was unremarkable. Direct ophthalmoscopy demonstrated areas of retinal haemorrhage and necrosis in the left eye. These features were confirmed by an ophthalmologist to be in keeping with CMV retinitis. He had a pancytopenia with neutropenia (Table 1). Vitamin B12, folate and haptoglobin were normal, and the peripheral smear did not demonstrate any features of haemolysis. Renal function and liver enzymes were normal. His CD4 count was 5 cells/muL and his serum CMV viral load was elevated at 1 322 783 IU/mL (Log 6.1). Cerebrospinal fluid (CSF) analysis revealed normal glucose at 2.9 mmol/L, raised protein at 0.76 g/L, no cells and an elevated CMV viral load at 481 617 IU/mL (Log 5.7). CSF microscopy and culture, cryptococcal antigen and GeneXpert Ultra testing were negative. An abdominal ultrasound showed no evidence of opportunistic infections. Gastroscopy demonstrated severe oesophageal candida, pangastritis and a cherry-red papule at the gastroesophageal junction. Biopsy and histology of the lesion showed acute inflammation, focally ulcerated mucosal fragments with intra-nuclear CMV inclusions (Figure 1 and Figure 2). Kaposi's sarcoma was excluded on histology and by a negative HHV-8 immunohistochemical stain.
Our patient was diagnosed with multisystem CMV EOD: retinitis, encephalitis and oesophagitis, with advanced HIV-related immunosuppression. Intravenous (IV) ganciclovir, IV fluconazole and IV pantoprazole were initiated, together with his previous ART. He developed worsening cytopenia on ganciclovir (Table 1) and was transferred to a tertiary referral hospital for further investigation, including neuroimaging, and management. Our patient died three days following his transfer, with the precise cause of death being unknown.