Abstract
Sirs: We read with interest this case report. 1 It raises a number of important issues concerning the diagnosis and management of syphilis.
When exploring a diagnosis of syphilis, serology results are notoriously difficult to interpret in isolation, so a clear history of possible previous treponemal infection is paramount. Yaws, pinta and syphilis should all be considered. This information will aid both diagnosis and contact tracing, which should include children of infected mothers were appropriate. 2
Social and sexual history will also highlight the risk of HIV co-infection. Estimated adult HIV prevalence in South Africa was 16.9% in 2008, with women disproportionately affected. 3 HIV can affect the natural history and treatment of syphilis; 4 moreover, syphilis is an independent risk factor for both HIV acquisition (2- to 4-fold) and transmission (2- to 9-fold), so HIV-testing in this case would have been important. 5
You report that, following treatment, the syphilis serology was negative. We are unclear what this means. Treponemal-specific tests, such as the enzyme immunoassay (EIA) test used in this case, are likely to remain positive for life, even with effective treatment, and non-treponemal tests, such as the rapid plasma reagin, used to monitor the effectiveness of treatment, was negative at baseline and would therefore likely remain so.
As you mention, the Jarisch–Herxheimer (JH) reaction is a rare but potentially fatal complication of cardiovascular syphilis treatment as coronary ostial occlusion or rupture of an aortic aneurysm can result from transient inflammation. The British Association for Sexual Health and HIV recommends examination and investigation for both cardiovascular and indeed neurological sequelae of late syphilis prior to treatment and advocate steroids to reduce the risk of a substantial JH reaction. 2 This is particularly indicated for symptomatic cases. However, recently the utility and cost-effectiveness of a plain chest radiograph to exclude cardiovascular syphilis in asymptomatic patients has been called into question. 6
Your pathological findings of periaortic fibrosis and adhesions were interesting. Necropsy specimens studied previously demonstrated adhesions limited to the anterior wall of the left ventricle at the apex 7 and a full-thickness process, described microscopically due to endarteritis of the vasa vasorum. 8 It would be interesting to see a more detailed histological report especially as areas of giant cells were noted, which have been previously described as near-absent from the syphilitic aorta. 9 Finally, polymerase chain reaction of the histological specimen for Treponema pallidum DNA could have been used to add weight to your diagnosis. 10
As a final point, you suggest that cardiovascular syphilis is poised to re-emerge given the large increase in early syphilis diagnoses between 1999 and 2006. We must, however, consider a number of other factors: not all patients with untreated syphilis will develop symptomatic tertiary disease; in the modern antibiotic era many patients receive treponemocidal drugs for other indications that may alter the disease's natural history and finally that the course of syphilis is altered in HIV-infected patients.