oc000153
10.3205/oc000153
urn:nbn:de:0183-oc0001534
Case Report
Spontaneous resolution of acute syphilitic posterior placoid chorioretinitis: reappraisal of the literature and pathogenetic insights
Casalino
Casalino
Giuseppe
G
MD, FEBO
Oftalmico Hospital, ASST Fatebenefratelli Sacco, Piazzale Principessa Clotilde 3, 20121 Milano, ItalyOftalmico Hospital, ASST Fatebenefratelli Sacco, Milano, Italy
peppecasalino@gmail.com
author
Erba
Erba
Stefano
S
Oftalmico Hospital, ASST Fatebenefratelli Sacco, Milano, Italy
stefano.erba@outlook.com
author
Sivagnanavel
Sivagnanavel
Vasuki
V
Royal Eye Unit, Kingston Hospital NHS Foundation Trust, London, UK
vsivagnanavel@nhs.net
author
Lari
Lari
Shervin
S
Royal Eye Unit, Kingston Hospital NHS Foundation Trust, London, UK
shervinlari@gmail.com
author
Scialdone
Scialdone
Antonio
A
Oftalmico Hospital, ASST Fatebenefratelli Sacco, Milano, Italy
ocuscialdo@gmail.com
author
Pavesio
Pavesio
Carlos
C
Moorfields Eye Hospital NHS Foundation Trust, London, UK
cpavesio@aol.com
author
German Medical Science GMS Publishing House
Düsseldorf
610
acute syphilitic posterior placoid chorioretinitis
natural course
pathogenesis
retinal imaging
syphilis
20200504
engl
This is an Open Access article distributed under the terms of the Creative Commons Attribution 4.0 License.
Dieser Artikel ist ein Open-Access-Artikel und steht unter den Lizenzbedingungen der Creative Commons Attribution 4.0 License (Namensnennung).
2193-1496
10
GMS Ophthalmology Cases
GMS Ophthalmol Cases
26
Acute syphilitic posterior placoid chorioretinitis (ASPPC) is a rare clinical manifestation of ocular syphilis. Spontaneous resolution of this condition has been reported in a few cases.The aim of this manuscript is to report an additional case and to discuss the possible pathogenesis of this condition by reviewing the current evidence on this subject.A 45-year-old man presented to us with decreased vision in the right eye secondary to a placoid macular lesion. Fourteen days after presentation, there was a dramatic improvement of the vision, and multimodal retinal imaging showed almost complete spontaneous resolution of the placoid lesion. Syphilis serology turned out positive and a diagnosis of ASPPC was made. The pathogenesis of ASPPC is unclear, and there is contrasting evidence about the role of the cellular immune system. Since this condition may resolve spontaneously before systemic antim<![CDATA[icrobi</PlainText></TextGroup>al treatment, the presence of a placoid macular lesion should raise a high suspicion of ASPPC in order to make a timely diagnosis and to avoid progression of untreated syphilis.</Pgraph></Abstract>
<TextBlock linked="yes" name="Introduction">
<MainHeadline>Introduction</MainHeadline><Pgraph>Syphilis is a sexually transmitted infection caused by the spirochete bacterium <Mark2>Treponema</Mark2> <Mark2>pallidum</Mark2> <TextLink reference="1"></TextLink>. Syphilis is a re-emerging and rising infection in the developed world. In up to one-quarter of patients with syphilis, ocular involvement manifests at any time during the disease course. Ocular syphilis may precede the diagnosis of systemic disease in up to one-half of cases <TextLink reference="2"></TextLink>. Ocular syphilis, known as “the great masquerader”, may affect almost every structure of the eye and has a broad spectrum of presentation, including, among others, interstitial keratitis, optic neuropathy and posterior uveitis, the latter commonly represented by chorioretiniti <TextLink reference="3"></TextLink>, <TextLink reference="4"></TextLink>.</Pgraph><Pgraph>In 1988, de Souza et al. <TextLink reference="5"></TextLink> reported three young patients with “unilateral central chorioretinitis” as manifestation of ocular syphilis. Two years later, Gass et al. <TextLink reference="6"></TextLink> reported six additional similar cases. They concluded that this condition was a separate clinical entity, and coined the term “acute syphilitic posterior placoid chorioretinitis” (ASPPC).</Pgraph><Pgraph>ASPPC is defined by the presence of one or more placoid, yellowish, outer retinal lesions, typically involving the posterior pole and the mid-periphery of the retina near the temporal vascular arcade <TextLink reference="6"></TextLink>. ASPPC may have a unilateral or bilateral involvement with a presenting visual acuity ranging from 20/20 to no light perception <TextLink reference="7"></TextLink>. The advent of multimodal imaging (MMI) of the retina, especially of spectral domain optical coherence tomography (SD-OCT), has made it possible to report pathognomonic features of ASPPC, which include punctate hyperreflectivity in the choroid, disruption and loss of the ellipsoid zone, nodular irregularity of the retinal pigment epithelium, and transient localized subretinal fluid <TextLink reference="8"></TextLink>, <TextLink reference="9"></TextLink>.</Pgraph><Pgraph>Since patients with ASPPC usually receive prompt antim<TextGroup><PlainText>icrobia</PlainText></TextGroup>l treatment after serologic results, little is known about the natural course of the disease. To the best of our knowledge, only 5 cases of ASPPC with spontaneous improvement have been reported <TextLink reference="10"></TextLink>, <TextLink reference="11"></TextLink>, <TextLink reference="12"></TextLink>, <TextLink reference="13"></TextLink>. We report the natural course and the multimodal retinal imaging features of an additional case, and discuss the pathogenetic implications and the importance of early recognition of this rare clinical entity.</Pgraph></TextBlock>
<TextBlock linked="yes" name="Case presentation">
<MainHeadline>Case presentation</MainHeadline><Pgraph>A 45-year-old man with no relevant past medical history presented to the eye casualty service complaining of sudden onset central ‘white ring’ and decreased vision in the right eye (RE) over the past seven days. Best-corrected visual acuity (BCVA) was 6/12 in the right eye and 6/6 in the left eye (LE). Intraocular pressure was <TextGroup><PlainText>14 mmHg</PlainText></TextGroup> in both eyes. Examination of the RE showed no cells in the right anterior chamber and 1+ vitreous cells; fundus examination revealed a yellow placoid lesion involving the macular area with no signs of vasculitis or retinal necrosis. Examination of the LE was unremarkable.</Pgraph><Pgraph>MMI of the retina including colour fundus photograph, fundus autofluorescence, SD-OCT, fluorescein angiography and indocyanine green angiography are presented in Figure 1 <ImgLink imgNo="1" imgType="figure"/>, Figure 2 <ImgLink imgNo="2" imgType="figure"/>, and Figure 3 <ImgLink imgNo="3" imgType="figure"/>.</Pgraph><Pgraph>The medical history was carefully reviewed; the patient admitted to be addicted to poppers and cocaine, and reported promiscuous homosexual activity over the last months. He denied intravenous drug use and any systemic symptoms such as headache, skin rash, nausea, weight loss, cough, or night sweats. A complete laboratory work-up was ordered, including TB QuantiFERON-TB testing, syphilis serology and human immunodeficiency virus (HIV) antibodies. Seven days after presentation, the patient reported spontaneous improvement in the vision of the RE, and BCVA improved to 6/9 in the RE and was stable in the LE. Full blood count, liver function test, kidney function, angiotensin-converting enzyme level were within normal range, HIV antibodies were negative. However, results for QuantiFERON-TB testing and syphilis had not been available yet. MMI revealed spontaneous improvement of the placoid lesion (Figure 2 <ImgLink imgNo="2" imgType="figure"/>, Figure 3 <ImgLink imgNo="3" imgType="figure"/>).</Pgraph><Pgraph>Two weeks after presentation, BCVA further improved to 6/6 in the RE and MMI showed signs of early resolution of the placoid lesion. Laboratory results returned negative for QuantiFERON-TB testing, and positive for venereal disease research laboratory test and fluorescent treponemal antibody testing. Therefore, a definite diagnosis of ASPPC was made, and the patient was promptly referred to the Infectious Disease Department for systemic treatment with penicillin.</Pgraph></TextBlock>
<TextBlock linked="yes" name="Discussion">
<MainHeadline>Discussion</MainHeadline><Pgraph>ASPPC is a rare clinical manifestation of ocular syphilis. Although the pathophysiology of ASPPC is not completely understood, timing and characteristics of SD-OCT findings may be the reflection of the sequence of disease events <TextLink reference="9"></TextLink>. It has been suggested that circulating <Mark2>T</Mark2>. <Mark2>pallidum</Mark2> organisms may enter the choroidal circulation, giving the choroidal hyperreflective pinpoint lesions seen on SD-OCT; subsequent access to the outer retina may give a variable amount of subretinal fluid and impaired photoreceptor function expressed by disruption of EZ seen on SD-OCT <TextLink reference="9"></TextLink>.</Pgraph><Pgraph>However, the role played by the cellular immune system in the pathogenesis of this condition remains controversial. While it was initially suggested that ASPPC is secondary to immunocompromised status such as in HIV-positive patients <TextLink reference="5"></TextLink>, <TextLink reference="6"></TextLink>, <TextLink reference="14"></TextLink>, it was later described in both immunocompetent and immunocompromised individuals <TextLink reference="7"></TextLink>, <TextLink reference="9"></TextLink>, <TextLink reference="15"></TextLink>.</Pgraph><Pgraph>Of note, no differences have been found in terms of clinical characteristics and long-term visual outcome in HIV-positive versus HIV-negative patients with ASPPC <TextLink reference="7"></TextLink>.</Pgraph><Pgraph>To the best of our knowledge, spontaneous resolution of ASPPC before initiation of systemic antimicrobial treatment has been reported in 5 cases <TextLink reference="10"></TextLink>, <TextLink reference="11"></TextLink>, <TextLink reference="12"></TextLink>, <TextLink reference="13"></TextLink>. The first cases were described in 2015 by Ji et al. <TextLink reference="10"></TextLink>, who reported two HIV-negative patients with ASPPC which spontaneously improved 10 days (for the first case) and 3 weeks (for the second case) after presentation. In the same year, Aranda et al. <TextLink reference="11"></TextLink> reported an HIV-positive patient on anti-retroviral therapy for 4 years and CD4+ <TextGroup><PlainText>T-c</PlainText></TextGroup>ell count of 204 cells/µL presenting with ASPPPC; spontaneous resolution of ASPPC was observed 10 days after presentation <TextLink reference="11"></TextLink>. One year later, Franco et al. <TextLink reference="12"></TextLink> reported an additional case of ASPPC in an HIV-negative patient with complete spontaneous recovery and no signs of reactivation until the patient was started on antimicrobial treatment, 45 days after presentation.</Pgraph><Pgraph>The spontaneous improvement observed in our case is in line with these previous reports <TextLink reference="10"></TextLink>, <TextLink reference="11"></TextLink>, <TextLink reference="12"></TextLink> and may suggest that ASPPC is the result of the host’s cellular immune response which may be able to locally control the spirochete infection. Some authors have speculated that the immune privilege of the eye may contribute to the spontaneous resolution of ASPPC.</Pgraph><Pgraph>Alternatively, spontaneous resolution of initial ASPPC can be explained as the disease entering prolonged latency. Indeed it is known that syphilis is characterized by episodes of active disease that are interrupted by periods of latency because of the host’s cellular immune response <TextLink reference="1"></TextLink>, <TextLink reference="12"></TextLink>. Therefore the placoid lesions may disappear in the same way the mucocutaneous syphilitic lesions disappear without treatment during the latent stage of the disease. The latter hypothesis has been supported by Baek et al. <TextLink reference="13"></TextLink> who reported an HIV-negative patient presenting with ASPPC which spontaneously improved <TextGroup><PlainText>7 d</PlainText></TextGroup>ays after presentation, but unlike the aforementioned cases <TextLink reference="10"></TextLink>, <TextLink reference="11"></TextLink>, <TextLink reference="12"></TextLink> did not receive systemic antimicrobial treatment and returned 9 months later with progression to posterior uveitis <TextLink reference="13"></TextLink>.</Pgraph><Pgraph>Of note, in 2014 Armstrong et al. <TextLink reference="16"></TextLink> had reported spontaneous evolution of unilateral ASPPC to panuveitis in a patient with HIV co-infection. In their case, panuveitis developed 6 weeks after the initial diagnosis of ASPPC, without spontaneous resolution of the lesion.</Pgraph><Pgraph>These latter cases may suggest that ASPPC could be an early manifestation of posterior uveitis, and in absence of an adequate host’s immune response, such as in patients with untreated HIV co-infection, progression without spontaneous improvement may be observed.</Pgraph><Pgraph>In addition, there is evidence that immunosuppression may be a major stimulator of ASPPC. Zamani et al. <TextLink reference="17"></TextLink> reported a case of undiagnosed syphilitic chorioretinitis which evolved to multifocal placoid lesions following immunosuppression induced by corticosteroid therapy. Furthermore, Erol et al. <TextLink reference="18"></TextLink> and Song et al. <TextLink reference="19"></TextLink> published cases of ASPPC following local intravitreal triamcinolone injections. However, in contrast to these aforementioned cases <TextLink reference="17"></TextLink>, <TextLink reference="18"></TextLink>, <TextLink reference="19"></TextLink>, Ormaechea et al. <TextLink reference="20"></TextLink> reported a patient with ASPPC who was initially misdiagnosed as having non-infectious uveitis and received corticosteroid as well as methotrexate for 7 months and demonstrated no worsening of the disease.</Pgraph></TextBlock>
<TextBlock linked="yes" name="Conclusions">
<MainHeadline>Conclusions</MainHeadline><Pgraph>There is contrasting evidence about the role of the immune system in the pathogenesis of ASPPC which may be the manifestation of different pathogenetic pathways that ultimately lead to an inflammatory response driven by the presence of the spirochete. Since this condition may resolve spontaneously before antimicrobial treatment, the presence of a placoid macular lesion should raise a high suspicion of ASPPC, as the ophthalmologist may be the first to diagnose syphilis in the patient. Indeed, timely diagnosis and antimicrobial treatment are essential to preventing the progression of syphilis which may include irreversible visual damage <TextLink reference="21"></TextLink>.</Pgraph></TextBlock>
<TextBlock linked="yes" name="Notes">
<MainHeadline>Notes</MainHeadline><SubHeadline>Competing interests</SubHeadline><Pgraph>The authors declare that they have no competing interests.</Pgraph><SubHeadline>Informed consent</SubHeadline><Pgraph>We obtained written informed consent from the patient for publishing the information and images.</Pgraph></TextBlock>
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<Caption><Pgraph><Mark1>Figure 1: Fluorescein angiography (FA) and indocyanine green angiography (ICGA) of acute syphilitic posterior placoid chorioretinitis in the right eye at presentation. (a) Early frame of FA shows hypofluorescence (yellow arrowhead) of the placoid lesion which appears hyperfluorescent in the late frames (b). (c), (d) ICGA shows hypocianescence of the placoid lesion (green arrowhead) throughout the whole examination.</Mark1></Pgraph></Caption>
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<Caption><Pgraph><Mark1>Figure 2: Colour fundus photograph (CFP) and fundus autofluorescence (FAF) changes of acute syphilitic posterior placoid chorioretinitis in the right eye over time. (a) CFP shows a yellow placoid lesion (white arrowhead) at the posterior pole which gradually fades 1 week after presentation (b) and 2 weeks after presentation (c). FAF shows increased AF in correspondence of the placoid lesion at presentation (d) with gradual normalisazion of the AF 1 week after presentation (e) and 2 weeks after presentation (f). </Mark1></Pgraph></Caption>
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<Caption><Pgraph><Mark1>Figure 3: (a) Spectral domain optical coherence tomography (SD-OCT) scan of the right eye at presentation shows disruption of the ellipsoid zone (white asterisks), nodular thickening of the retinal pigment epithelium (yellow arowheads) and punctate hyperreflectivity in the inner choroid (white arrows). SD-OCT scan 1 week after presentation (b) and 2 weeks after presentation (c) show gradual recovery of the ellipsoid zone and retinal pigment epithelium.</Mark1></Pgraph></Caption>
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