A 38-year-old South African woman presented to a district hospital in Durban, Kwa-Zulu Natal with progressive, painless bilateral visual loss since 10 March 2020. She had associated mild, intermittent headaches which were relieved by simple analgesia. Systemic enquiry was non-contributory.
She was diagnosed with HIV infection in 2006 and began antiretroviral treatment (ART) in 2012. She was switched to second-line ART in 2020 after reports of virological failure secondary to default. She was seen initially at McCord's Provincial Eye Hospital (MPEH) on 10 March 2020 with a history of progressive loss of vision. She was noted to have bilateral panuveitis with macula oedema and disc pallor with non-perfused vessels. She was given topical and sub-Tenon's steroids as well as bilateral bevacizumab (Avastin) injections for the macula oedema, which resolved. Her viral load at presentation was 208,806 copies/mL (15 January 2020), which worsened to 237,000 copies/mL (15 March 2020) after which she was switched to second-line ART as a result of treatment default. Her cluster of differentiation (CD4) count on this presentation was 39 cells/microL.
She was diagnosed with pulmonary tuberculosis (PTB) confirmed by typical chest radiographic changes and initiated on anti-TB treatment on 18 April 2020 after which she noticed worsening of the loss of vision in both eyes. She was then seen at MPEH on 25 May 2020 and was noted to have no perception of light (NPL) in both eyes. Fundus examination was still possible at this stage, which noted resolving macula oedema and disc pallor with non-perfused vessels.
She was admitted to a district hospital in Durban for vision loss in February 2021. She reported compliance to her ART, and on admission her HIV viral load was 136 copies/mL, while her CD4 count was 132 cells/microL. She did not report any history of eye trauma. Her surgical, ophthalmological, and family histories were otherwise unremarkable.
She had sober habits with a history of swimming in rivers. She was previously employed as a domestic worker with no history of toxic exposures and reported to have stayed on a farm and consumed cooked meat.
General examination revealed an obese, middle-aged woman. Her vital signs, including blood pressure, were within normal limits. On examination, her Snellen Visual Acuity (VA) was measured as being 6/60 in the right eye and 1/60 in the left eye with no improvement with pinhole testing. Anterior segment examination revealed bilateral corneal pigmented keratic precipitates with cells in the anterior chamber and anterior vitreous humour and lenticular opacities. Fundus examination revealed bilateral optic disc pallor with striae and exudates at the macula and retinal vasculitis with extensive non-perfused vessels.
The chest radiograph was normal. A computed tomography (CT) scan of the brain illustrated a small focus of nodular irregular thickening of the right retina just adjacent to the insertion of the optic nerve suggestive of an inflammatory lesion, non-benign lesion, haemorrhage or artefact. Clinically correlation was advised. There were no periventricular plaques, calcifications, infarcts, or pathological enhancements (Figures 1-3).
Figure 4 shows tractional retinal detachment on the right eye. Figure 5 depicts the left eye with tractional bands and shows a 'double-walled sign' suggestive of echinococcal cystic cavity, causing traction on the retina.  
A full systemic work-up was performed to exclude systemic echinococcus and other infections. A lumbar puncture was within normal range (Table 1). Liver ultrasound revealed no cystic lesions.
Parasitic serology revealed a cysticercosis ELISA IgG negative value of 0.2, while the Echinococcus ELISA IgG was positive with a value of 1.3.
The full blood count revealed a white cell count of 7.26 x 109 with an eosinophilia of 5.70% (0.41 x 109). Her inflammatory markers, both C-reactive protein (CRP) and ertythrocyte sedimentation rate (ESR), were elevated at 47 mg/L and 93mm/hr, respectively. Non-specific markers in the form of Serum Angiotensin Converting Enzyme (SACE) and Rheumatoid Factor (RF) were weakly positive, at 101 U/L (8-52) and 13.0 IU/mL, respectively. Anti-nuclear antibodies and anti-nuclear factor were negative. Hepatitis screen was negative. Vitamin B12 and folate levels were normal.
Syphilis serology tests were negative (Treponema pallidum haemagglutinin assay, fluorescent treponemal antibody absorption test). Herpes simplex virus (HSV) IgM result was negative. Both cytomegalovirus IgM result and Toxoplasma gondii IgM ELISA result were negative. Anaerobic and aerobic blood cultures showed no growth. The rest of the blood parameters were within normal limits.
She was initiated on topical steroids and given bilateral orbital floor intravitreal steroid injections which resulted in decreased intraocular inflammation and dry maculae.
Optical coherence tomography (OCT) revealed a central pre-injection macula thickness of 445 microm on the right and 446 microm on the left with intraretinal and subretinal fluid (Figure 6). Post-injection central macula thickness was 299 microm with scarring on the right. On the left, central macula thickness was reduced to 232 microm.
At her 2-month clinic visit, she had no light perception and had developed cataracts with posterior synechiae which prevented fundal examination with intraocular pressures of 2 mmHg on the right eye and 3 mmHg on the left eye.
After extensive work-up and ophthalmological expert consultation, she was initiated on long-term albendazole at a dose of 600 mg daily orally. She was continued on her ART for the HIV infection.
She was provided with counselling by the social worker, referred to a society for the blind and a disability grant was initiated.
By the fifth month after presentation, her visual acuity remained unchanged with no light perception bilaterally.