Dear Editor:

We read with interest the paper by van der Vaart and colleagues [1] entitled “Unilateral solitary choroidal granuloma as presenting sign of secondary syphilis,” and were struck by the similarity of the color fundus images of the two presented cases to the findings in Acute Syphilitic Posterior Placoid Chorioretinopathy (ASPPC) [2]. Our recently reported case series and comprehensive review of the literature concluded that ASPPC lesions, like the two presented, tend to be yellow-white, flat, round or oval-shaped, and often involving the macula [2]. While detailed descriptions of additional imaging studies were not presented by van der Vaart and associates, we have found ancillary imaging to be quite useful in the diagnosis of ASPPC [2]. Fluorescein angiography, for example, tends to show early hypofluorescence with progressive late hyperfluorescence, often with an irregular or ‘leopard skin’ pattern. Indocyanine green typically shows hypofluorescence corresponding to the macular lesion in both the early and late phases, although late hyperfluorescence can be observed as well. In the acute setting, Spectral Domain-Ocular Coherence Tomography (SD-OCT) tends to show some degree of disruption of the outer retinal hyper-reflective bands associated with the external limiting membrane, the photoreceptors, and/or the photoreceptor-retinal pigment epithelium (RPE) junction. Irregular nodularity of the photoreceptor-RPE junction can also be observed. Lastly, enhanced depth imaging (EDI) OCT and B-scan ultrasonography show no thickening of the choroid or scleral in ASPPC, and effectively rule out choroiditis and scleritis as a cause of the lesion. All of these changes typically normalize completely following treatment with neurosyphilis doses of intravenous penicillin for 10 to 14 days. Given the diameter of the lesions presented by van der Vaart and colleagues, one would expect the choroid to be thickened if choroiditis were, in fact, the underlying cause. Perhaps this is what the authors intended when they wrote that the “granulomatous choroidal lesions were singular and rounded in appearance, with height noted also on OCT.” A more detailed description of findings noted on imaging studies performed by the authors would be of interest.

It is noteworthy that both of the patients reported by van der Vaart and associates [1] did quite well following a 2-week treatment with intravenous penicillin, despite the fact that one was infected by the human immunodeficiency virus (HIV; the status of the second patient was not reported). While a number of case reports and small clinic-based series have suggested that HIV co-infection can worsen the severity and/or outcome of ocular syphilis, our experience and review of the literature would not support such a conclusion [3]. In our comprehensive study of ASPPC, for example, we compared the clinical findings at presentation and the visual acuity at last visit in 35 affected eyes in 23 HIV-positive patients to 58 affected eyes in 37 HIV-negative patients, and found no meaningful differences in either severity of clinical presentation or vision outcome [2]. Similarly, Amaratunge and associate reviewed 41 original reports on syphilitic uveitis in the English language literature published from 1984 to June, 2008, including 93 HIV-positive and 50 HIV-negative patients [4]. They found that only one of the 50 HIV-negative patients (2 %) had isolated anterior or intermediate uveitis, compared to 27 of the 93 HIV-positive patients (29 %; p = 0.000023, Fisher’s exact test). Given that isolated anterior or intermediate uveitis tends to be less likely to cause permanent vision loss than posterior or panuveitis, this large retrospective review would seem to similarly suggest that HIV co-infection alone does not put patients at increased risk for a more severe, vision-threatening uveitis at presentation. The notion that HIV co-infection puts patients with syphilitic uveitis at increased risk for a more severe uveitis and/or worse vision outcome is, in our opinion, largely unsubstantiated.