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BJO Online First, published on August 1, 2017 as 10.1136/bjophthalmol-2017-310210
1
Eye Clinic, Department of
Biomedical and Clinical Science
"L. Sacco", Luigi Sacco Hospital,
University of Milan, Milan, Italy
2
Save Sight Institute, Sydney Eye
Hospital, University of Sydney,
Sydney, Australia
3
Advanced Eye Center -
Postgraduate Institute of
Medical Education and
Research, Chandigarh, India
4
Fatebenefratelli and
Ophthalmic Hospital, Azienda
SocioSanitaria Territoriale (ASST)
Fatebenefratelli-Sacco, Milano,
Italy
5
Department of Clinical
Sciences, Luigi Sacco Hospital,
Section of Infectious and
Tropical Diseases, University of
Milan, Milan, Italy
6
Department of Clinical
Sciences and Community
Health, University of Milan,
Ophthalmological Unit,
IRCCS-Cà Granda Foundation -
Ospedale Maggiore Policlinico,
Milan, Italy
Correspondence to
Dr Alessandro Invernizzi,
Eye Clinic, Department of
Biomedical and Clinical Science
“Luigi Sacco”, Luigi Sacco
Hospital, University of Milan,
Milan 20157, Italy; ​alessandro.​
invernizzi@​gmail.​com
Received 17 January 2017
Revised 18 June 2017
Accepted 24 June 2017
To cite: Invernizzi A,
Agarwal AK, Ravera V, et al.
Br J Ophthalmol Published
Online First: [please include
Day Month Year].
doi:10.1136/
bjophthalmol-2017-310210
Copyright Article author (or their employer) 2017. Produced by BMJ Publishing Group Ltd under licence.
Clinical science
Comparing optical coherence tomography findings in
different aetiologies of infectious necrotising retinitis
Alessandro Invernizzi,1,2 Aniruddha Kishandutt Agarwal,3 Vittoria Ravera,1
Chiara Mapelli,4 Agostino Riva,5 Giovanni Staurenghi,1 Peter J McCluskey,2
Francesco Viola6
Abstract
Aims To compare optical coherence tomography (OCT)
features of active necrotising infectious retinitis (NIR)
due to toxoplasmosis or herpesviruses and to determine
distinctive OCT signs for these two causes of infectious
retinitis.
Methods OCT scans from eyes with active NIR due to
varicella zoster virus (VZV), herpes simplex virus (HSV),
cytomegalovirus (CMV), and toxoplasmosis (TOXO) were
reviewed. All images were evaluated for the presence
of previously described OCT findings in TOXO-NIR and
compared with the viral group. New OCT findings were
recorded and compared. Retinal and choroidal thickness
were measured at the site of NIR and compared.
Results 10 eyes diagnosed with TOXO-NIR and 13
eyes affected by viral-NIR (9 CMV and 4 VZV) were
analysed. All eyes showed full thickness hyper-reflectivity,
disruption of the retina and a variable degree of
vitritis. Among previously described OCT signs, hyper-
reflective oval deposits and hypo-reflectivity of the
choroid had a higher prevalence in TOXO (p=0.018 and
p<0.0001, respectively). Among the new signs, hyper-
reflective round deposits along the posterior hyaloid,
retrohyaloid hyper-reflective spots and a disruption of
the choroidal architecture were more frequent in TOXO
eyes (all p<0.01). Intra-retinal oedema and hyper-
reflective vertical strips within the outer nuclear layer
were suggestive of a viral aetiology (p=0.045). Retinal
thickness at the site of NIR did not differ between the
two groups. Choroidal thickness was significantly higher
in TOXO eyes (p=0.01).
Conclusions The diagnosis of NIR is largely based on
clinical and laboratory findings. OCT changes may be
useful in differentiating different causes of NIR.
Introduction
Infectious necrotising retinitis has several aetiolo-
gies including bacteria, viruses and parasites, with
herpesvirus and toxoplasmosis being the most
common causative agents.1–3 Prompt and specific
therapy is critical for a good outcome and rapid
identification of the causative agent is essential
to guide specific therapy.2 4 5 The clinical signs of
infectious necrotising retinitis are similar regard-
less of the cause, making the differential diagnosis
challenging. This is particularly true in the case of
immunocompromised patients, who often show
atypical clinical features.6
In the last few years, the advent of spectral
domain optical coherence tomography (SD-OCT)
Invernizzi A, et al. Br J Ophthalmol 2017;0:1–5. doi:10.1136/bjophthalmol-2017-310210
has dramatically changed the management of
several retinal diseases, including uveitis, especially
after the introduction of enhanced depth imaging
(EDI-OCT) technology.7 8 In the infectious retinitis
literature, several publications have focused on the
OCT features of toxoplasmosis,9–11 while the liter-
ature on OCT features of viral retinitis is limited
to case reports or small series.12 13 Specific infective
agents spread differently through ocular tissues,
raising the possibility that OCT findings may vary
according to the causative infective agent.14 15
The aim of this study was to compare OCT scans
collected from patients with active toxoplasmic
necrotising retinitis with images from active viral
necrotising retinitis to determine whether there are
distinctive OCT signs for these two entities.
Methods
Charts and imaging studies of patients diagnosed
with infectious necrotising retinitis due to vari-
cella zoster virus (VZV), herpes simplex virus
(HSV), cytomegalovirus (CMV), and toxoplas-
mosis (TOXO) who were referred to the uveitis
clinics of two tertiary centres in the north of Italy
(Eye Clinic, Luigi Sacco Hospital, University of
Milan, and Ophthalmological Unit, IRCCS-Cà
Granda Foundation – Ospedale Maggiore Poli-
clinico, Milan) between January 2013 and
December 2015 were reviewed. Institutional
Review Board/Ethics Committee approval was
obtained for the protocol before the conduct of
the study. The study adhered to the tenets of the
Declaration of Helsinki.
The criteria for the diagnosis, depending on the
disease, were as follows:
VZV/HSV (acute retinal necrosis (ARN)): VZV/
HSV retinitis was diagnosed by the presence of the
following clinical features: (1) acute panuveitis;
(2) occlusive retinal vasculitis (arteritis and phle-
bitis) with or without retinal haemorrhage; and
(3) peripheral patchy necrotising retinitis (usually
multifocal) with or without retinal breaks and optic
disc swelling.2 16
CMV retinitis: CMV retinitis was diagnosed by
the presence of the following features: (1) typical
retinal clinical features; (2) positive CMV serology;
and (3) patient with systemic immunocompromised
status from HIV infection, malignancy or immuno-
suppressive drug therapy.5 17
Toxoplasma retinitis: Toxoplasmic retinitis was
diagnosed by the presence of the following clinical
features: (1) detection of a solitary focus of active
1
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Clinical science
chorioretinitis adjacent to a chorioretinal scar; and (2) positive
toxoplasmosis serology.18
Vitreous PCR was performed to confirm the diagnosis when
the clinical features were unclear or atypical.
OCT images were obtained at the patient’s first visit, using
the Heidelberg HRA Spectralis OCT (Heidelberg Engineering,
Heidelberg, Germany). Vitreal and retinal OCT features were
identified from 30° or 55° single OCT scans (100 ART mean/b-
scan) passing through the lesions. Choroidal OCT features were
identified from 30° or 55° single EDI-OCT scans (100 ART
mean/b-scan).
All OCT images were evaluated by two independent assessors
for the presence of specific OCT findings previously described
in toxoplasma chorioretinitis9 11 (ie, vitritis, hyaloid thickening,
disruption, thickening, hyper-reflectivity of the retina, inter-
ruption of photoreceptor inner/outer segment junction, retinal
pigmented epithelium (RPE) elevation, hyper-reflective oval
deposits within the vitreo-retinal interface, sub-retinal fluid, and
hypo-reflectivity of the choroid). These findings in patients
with toxoplasma retinitis were compared with those observed
in patients with viral retinitis. Any new OCT findings observed
during the analyses were also recorded and compared. A third
independent assessor was asked to grade the image in cases of
disagreement.
Retinal and choroidal thickness were measured twice by
two independent operators at the site of the active lesion on
OCT scans, acquired with or without EDI function, by using
the in-built calliper tool (Heyex Eye Explorer, Heidelberg
Engineering, Heidelberg, Germany). Measurements were then
compared between the two patient groups.
Statistical analysis was performed using GraphPad Prism 6
(GraphPad, CA, USA). Fisher’s exact test was used to compare
the prevalence in the two populations of OCT findings. Student’s
t-test was used to compare the retinal and choroidal thickness
between the two groups. A value of p<0.05 was considered to
be statistically significant.
Results
Ten eyes from 10 patients diagnosed with active toxoplasmic
retinochoroiditis and 13 eyes from 10 patients with active viral
necrotising retinitis were included in the study. In the TOXO
group, five of 10 eyes had atypical clinical findings either due
to previous intravitreal or peribulbar steroid injections or due to
a systemic immunocompromised state. In these cases, vitreous
tap and PCR were performed to confirm the diagnosis. In the
viral retinitis group, nine eyes (seven patients) had CMV retinitis
and the remaining four eyes (three patients) had VZV-related
ARN. CMV retinitis was diagnosed clinically in six of nine eyes.
In three eyes (two subjects) there were typical clinical features
of CMV retinitis, but there was no history of a known immu-
nocompromised status. The CMV aetiology was confirmed by
a vitreous tap and PCR analysis in these patients. In addition,
systemic examinations revealed HIV infection in one subject and
leukaemia in the other as the underlying causes of immunocom-
promisation. VZV aetiology was determined in ARN patients
for concomitant VZV comorbidities or due to HSV1-2 negative
serology.
Detailed demographic data for both the groups (mean age,
gender, immune system status, underlying disease) are presented
in table 1.
On fundus examination seven of 10 eyes in the TOXO group
(five atypical +2/4 first diagnosis) had mild vitritis (trace to +1),
and the remaining three eyes had intense vitreous haze (+2 to+3).
2 Invernizzi A, et al. Br J Ophthalmol 2017;0:1–5. doi:10.1136/bjophthalmol-2017-310210
Table 1 Demographic and clinical features of the patients with
toxoplasmic and viral necrotising retinitis
Demographic/clinical features Toxoplasmic Viral
Subjects (eyes) 10 (10) 10 (13)
Age (mean (range)) 36.6 (14–75) 48.7 (7–65)
Gender (males (%)) 6 (60%) 6 (60%)
Bilateral 0 3 (30%)
Immunocompromised (systemic)* 3 (30%) 8 (80%)
Intravitreal/peri-bulbar steroid injection† 2 (20%) 0
First diagnosis‡ 4 (40%) 13 (100%)
*Patients suffering from a compromised immune status due to an underlying
systemic condition (HIV, immunosuppressive treatment, malignancies).
†Patients who had received local treatment with steroids (intravitreal/periocular) for
any other condition in the 2 weeks before diagnosis of necrotising retinitis.
‡Proven first presentation of the disease (absence of scars along with high IgM
titres on serum samples).
Similarly, in the viral group, the degree of vitritis was trace to +1
in most involved eyes with only two eyes (VZV-related ARN
in immunocompetent patients) showing intense vitritis (+3).
Despite the vitritis, by asking the patients to quickly change their
gaze direction, it was possible to collect good quality OCT scans
encompassing the active lesions in all eyes included in the study.
All eyes, regardless of the aetiology, had full thickness
hyper-reflectivity and disruption of the retinal layers in the
necrotic area, with a variable degree of vitritis and choroidal
thickening on OCT scanning. Among the OCT findings previ-
ously described in toxoplasma retinochoroiditis (table 2), only
the hyper-reflective oval deposits on the inner retinal surface
(figure 1A) and the hypo-reflectivity of the choroid beneath
the affected retina (figure 2A) had a significantly lower prev-
alence in patients affected by viral retinitis (p=0.018 and
p<0.0001, respectively).
In addition to the previously described OCT features, we
describe 10 new OCT features in patients with toxoplasmic
and viral retinitis. Among these newly observed OCT signs
(table 2), both hyper-reflective round shaped deposits along the
posterior hyaloid (figure 1B) and retro-hyaloid hyper-reflec-
tive spots (figure 1C) had a significantly higher prevalence in
patients affected by toxoplasma chorioretinitis (p=0.019 and
p=0.003, respectively).
Both intraretinal oedema (figure 3A) and hyper-reflective
vertical strips within the outer nuclear layer (ONL) (figure 3B)
were present in 38.4% of the eyes affected by viral agents and
were absent in toxoplasma chorioretinitis (both p=0.045). All
the other new retinal OCT signs, including epiretinal membrane,
hyper-reflective bridges within the retina, lacunae in the outer
nuclear layer (ONL) and subretinal fluid, had a similar preva-
lence in the two groups.
The choriocapillaris was altered in most patients in both groups
(p=0.1). Disruption of the choroidal architecture, with reduc-
tion/disappearance of the physiological hyper-reflective septa
(figure 2B), was found in 90% of the toxoplasmic retinochoroid-
itis but was not seen in the viral infected group (p<0.0001). In
seven of 10 toxoplasmic cases, details of the choroid where not
visible underneath the centre of the lesion due to shadowing by
the overlying necrotising retinitis (figure 4A). In these patients
the choroidal architecture was assessed along the edges of the
active focus (figure 4B).
Vitreal and choroidal OCT findings suggestive of toxo-
plasmic retinochoroiditis are summarised in figure 1 and
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Clinical science

Table 2 Optical coherence tomography findings: comparison between toxoplasmic and viral necrotising retinitis
OCT signs Toxoplasmic Viral p
Signs previously described in Toxoplasmic retinitis n (%) n (%) p
V* Vitritis 9 (90) 10 (100) 1
Hyaloid thickening 10 (100) 9 (90) 1
R Retinal disruption 10 (100) 13 (100) 1
Retinal thickening 10 (100) 13 (100) 1
Retinal hyper-reflectivity 10 (100) 13 (100) 1
Interruption of photoreceptors IS/OS 10 (100) 13 (100) 1
RPE elevation 10 (100) 10 (76.9) 0.229
Hyper-reflective oval deposits 6 (60) 1 (7.6) 0.018
Subretinal fluid 2 (20) 5 (38.4) 0.405
C Hypo-reflectivity of the choroid 10 (100) 0 <0.0001
Newly observed signs n (%) n (%) p
V* Hyper-reflective round shaped deposits along the posterior hyaloid 7 (70) 1 (10) 0.019
Retrohyaloid hyper-reflective spots 7 (70) 0 0.003
R Epiretinal membrane 8 (80) 12 (92.3) 0.559
Intraretinal oedema 0 5 (38.4) 0.045
Hyper-reflective vertical strips in ONL 0 5 (38.4) 0.045
Hyper-reflective bridges 2 (20) 6 (46.1) 0.378
Lacunae in ONL 2 (20) 6 (46.1) 0.378
C Choriocapillaris alterations 10 (100) 9 (69.2) 0.104
Choroidal architecture disruption 9 (90) 0 <0.0001
Quantitative parameters mean±SD mean±SD p
Retinal thickness 368±64 316±154 0.39
Choroidal thickness 411±135 254±72 0.01
*3/13subjects affected by viral necrotising retinitis were diagnosed with complete posterior vitreous detachment, thus OCT evaluation of the vitreous was performed on 10 eyes
only.
C, choroid; IS/OS, inner segment/outer segment; OCT, optical coherence tomography; ONL, outer nuclear layer; R, retina; RPE, retinal pigmented epithelium; V, vitreous.

figure 2, respectively. Retinal OCT signs suggestive for viral aeti-
ology are summarised in figure 3.
Mean retinal thickness of active lesions did not differ among
the two groups (p=0.39). Choroidal thickness beneath active
retinitis was significantly higher (p=0.01) in toxoplasmic retino-
choroiditis compared with viral retinitis (table 2).
Assessment of choriocapillaris alteration (in three cases) and
the distinction between epiretinal membrane and thickened
posterior hyaloid tightly attached to the retinal surface (four
cases) were the only OCT signs that required adjudication by
the third grader.
Discussion
SD-OCT is widely considered to be an extremely useful tool for
the diagnosis and management of several diseases affecting the
posterior segment of the eye.7 The results of the current study
suggest an adjunctive role for SD-OCT in the differential diag-
nosis of necrotising retinitis.
Necrotic retina has been previously described on OCT imaging
as disrupted and hyper-reflective in its entire thickness in both
viral13 and toxoplasma retinitis.9 These features were identified
in our patients regardless of the aetiology, confirming them as
characteristic but non-specific abnormalities in necrotising reti-
nitis. Additionally, most of the OCT signs previously reported in
patients with toxoplasmic retinochoroiditis9 were identified in
the patients with viral necrotising retinitis in the present study.
Earlier studies of OCT changes in patients with toxoplasmosis
were not trying to differentiate toxoplasmosis from other types
of retinitis, and most of the OCT signs are those of non-spe-
cific retinal necrosis rather than being specific for a particular
Invernizzi A, et al. Br J Ophthalmol 2017;0:1–5. doi:10.1136/bjophthalmol-2017-310210
aetiology. In fact, some OCT signs had already been reported in
other retinal necrotising disorders.13
In the current study, five OCT signs were identified that
suggest toxoplasmic retinochoroiditis. Oval deposits lying on
the retinal surface had been previously described in toxoplasmic
posterior uveitis.9 This OCT sign is likely related to a specific
inflammatory reaction pattern induced by the parasite, and was
identified in more than half of the toxoplasma cases compared
with a single patient with viral retinitis in the current study.
Hypo-reflectivity of the choroid beneath the necrotic retinal
focus strongly suggests toxoplasmic retinochoroiditis and was
present in all involved eyes in this study. The low reflectivity
beneath the necrotic retina is most likely due to increased absorp-
tion and reflectance of the OCT signal from the necrotic retina9
and an alteration of the physiological choroidal structure.19 As
necrosis involves all retinal layers regardless of the aetiology, it
is not clear why the necrotising focus blocks the OCT signal far
more in toxoplasmosis than in viral retinitis (figure 2A and C).
It may be that differences in the tissue damage induced by these
entities results in chemical alterations within the retinal layers
that changes their physical properties and alters signal transmis-
sion. The changes in choroidal architecture can be explained by
the anatomical location of the pathogen within ocular tissues
and its pattern of spread during active infection. Toxoplasma
gondii targets the retina and spreads to the choroid resulting in a
granulomatous retinochoroiditis,20 whereas herpesviruses target
the retina only.15 All the patients with toxoplasmic retinochoroid-
itis had a reduction in the number of the hyper-reflective septa
corresponding to the choroidal vessels walls in the affected areas
(figures 2B and 4B), similar to that reported within choroidal
3
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Clinical science

Figure 1 Vitreal optical coherence tomography (OCT) findings. Three

vitreous OCT findings are associated with toxoplasmic retinochoroiditis.
(A) Hyper-reflective oval deposits on the inner retinal surface (black
arrowhead) (previously described as characteristic OCT feature of
toxoplasmic retinochoroiditis). (B) Hyper-reflective round-shaped
deposits along the posterior hyaloid (white arrows) often with mirror
image deposits on the retinal surface (double head white arrows in
the magnified square 2). (C) Retrohyaloid hyper-reflective dots (white
arrowheads), better seen in the magnified square 3. These findings
were identifiable in immunocompromised (A, C) and immunocompetent
(B) patients. OCT scans from an immunocompromised patient (D) Figure 2 Choroidal enhanced depth imaging optical coherence
and an immunocompetent (E, F) patient diagnosed with viral retinitis. tomography (OCT) findings. Two choroidal OCT findings are associated
Regardless of the immune status of the patient the scans show a lack with toxoplasmic retinochoroiditis: (A) Hypo-reflectivity of the choroid
of oval deposits. Notably, the posterior hyaloid appears thickened (black arrows) beneath the necrotic focus (previously described as
with some hyper-reflective tracts (black arrows) but no round-shaped a characteristic OCT feature of toxoplasmic retinochoroiditis); and (B)
deposits. A variable degree of vitritis (white asterisk) is visible in all choroidal architecture disruption consisting of absence of the hyper-
cases. reflective septa within the choroid (black arrowheads). OCT scans from
patients with viral retinitis (C, D) demonstrate that viral induced retinal
granulomas visualised by EDI-OCT,21 and diffuse thickening of necrosis does not obscure the underlying choroid. Although some
the whole choroidal layer, likely reflecting the ongoing granu- degree of choriocapillaris alteration is present (white arrowheads), the
lomatous choroiditis. Such alterations were absent in the viral choroidal architecture is largely preserved. Choroidal thickness beneath
retinal necrosis (figure 2D) thus suggesting toxoplasmic aetiology. active lesions (white callipers) was significantly higher in toxoplasmic
Choroidal thickness beneath the active focus was also signifi- retinitis compared with viral retinitis.
cantly greater in toxoplasmic retinochoroiditis compared with
viral retinitis. The choriocapillaris was hypo-reflective, with loss frequently in patients with viral retinitis. Cystic spaces within
of its physiological dotted pattern in both groups. These findings the retina were previously described in a large cohort of patients
have been previously described in other cases of posterior uveitis with intraocular toxoplasmosis. In this study, cystoid degenera-
and can represent a sign of hypo-perfusion/inflammation of the tion was identified in 15% of the patients and cystoid macular
choriocapillaris.22 This is not surprising since both herpesviruses oedema (CME) in 7.5%.10 Our study confirms that cystoid
and toxoplasma can affect the choriocapillaris and RPE.23 degeneration is common in toxoplasmic retinochoroiditis, but a
Hyper-reflective round-shaped deposits along the posterior similar percentage of patients with viral retinitis had lacunae in
hyaloid and hyper-reflective dots (likely cells) floating in the
retro-hyaloid space also suggested toxoplasmic retinochoroid-
itis and were almost undetectable in viral-related retinitis. It is
tempting to speculate that these OCT signs could be part of a
specific immune response to toxoplasma infection, as is hypoth-
esised for the oval preretinal deposits.9 Most of the hyper-reflec-
tive deposits along the posterior hyaloid had a corresponding
deposit on the underlying retinal surface, suggesting a common
pathogenesis. In addition, both patient groups included immu-
nocompromised and immunocompetent patients who had a
variable degree of vitritis. Similar findings were identified within Figure 3 Retinal optical coherence tomography (OCT) findings
each group regardless of the immune status of the patients that suggest viral necrotising retinitis. Two retinal OCT findings are
(figure 1). This suggests the pattern of vitreal OCT findings to associated with viral necrotising retinitis: (A) Intra-retinal oedema
be more related to the aetiology than the amount of vitreous (white asterisk) involving the outer nuclear layer, characterised by mid
inflammation. reflective cystoid spaces; and (B) hyper-reflective vertical strips within
Intra-retinal oedema (intra-retinal cystic spaces or lacunae the outer nuclear layer (black arrowheads) commonly located at the
in the ONL) and vertical strips within the ONL were seen more margins of full thickness retinal lesions.
4 Invernizzi A, et al. Br J Ophthalmol 2017;0:1–5. doi:10.1136/bjophthalmol-2017-310210
 Downloaded from http://bjo.bmj.com/ on August 1, 2017 - Published by group.bmj.com
Figure 4 Enhanced depth imaging optical coherence tomography
(EDI-OCT) findings that suggest toxoplasmic retinochoroiditis. EDI-
OCT scan encompassing a toxoplasmic lesion (A) clearly shows the
shadowing induced by active retinitis on the underlying choroid
(black arrows). This hypo-reflectivity prevents a good evaluation of
the choroidal structure. To bypass this problem an OCT scan at the
edge of the lesion can be performed (B). In this image the shadowing
effect is reduced and the choroidal structure under the active retinitis
is visible. The choroid appears thickened (black arrowheads) with
disruption of its normal vascular pattern compared to the unaffected
tissue aside (black asterisk). These choroidal changes are characteristic
OCT features of toxoplasmic retinochoroiditis and are not seen in viral
retinitis.
the ONL. No involved eyes with toxoplasmic retinochoroiditis
developed CME but 35% of eyes with viral retinitis had CME
on OCT. Vertical hyper-reflective strips within the ONL were
only seen in eyes with viral necrotising retinitis. It is possible that
such hyper-reflective change is related to swelling of the retinal
Muller cells infected by the virus as it spreads from the RPE to
the inner retinal layers.15 24
The present study has some important limitations as a result
of the retrospective nature of the analysis, the small sample size,
and the inclusion of different herpesviruses (ie, CMV, VZV) in
the viral retinitis group. Additionally, the small sample size did
not allow separate analysis of the immunocompromised patients,
who may have different OCT changes.
Necrotising retinitis is a sight threatening condition that
requires prompt identification of the causative agent to start
specific treatment. Although the diagnosis is based on clinical
and laboratory findings, OCT may represent a helpful tool in
the differential diagnosis between toxoplasmic and viral aeti-
ology. Despite its limitations, the current study identified several
OCT signs suggestive of either a toxoplasma or viral aetiology
in patients with necrotising retinitis that may be clinically useful,
especially in challenging cases.
Contributors AI: designed the work, acquired, analysed and interpreted the data,
drafted the work, revised and gave final approval. AA: analysed and interpreted
Invernizzi A, et al. Br J Ophthalmol 2017;0:1–5. doi:10.1136/bjophthalmol-2017-310210
Clinical science
the data, drafted the work, revised and gave final approval. VR, CM, AR: acquired,
analysed and interpreted the data, revised and gave final approval. GS, FV, PMC:
interpreted the data, revised and gave final approval.
Competing interests GS has financial relations with OCT manufacturers
including: Heidelberg Engineering, Zeiss, Nidek, Canon, Optovue.
Ethics approval Local IRB.
Provenance and peer review Not commissioned; externally peer reviewed.
© Article author(s) (or their employer(s) unless otherwise stated in the text of the
article) 2017. All rights reserved. No commercial use is permitted unless otherwise
expressly granted.
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Comparing optical coherence tomography

findings in different aetiologies of infectious
necrotising retinitis
Alessandro Invernizzi, Aniruddha Kishandutt Agarwal, Vittoria Ravera,
Chiara Mapelli, Agostino Riva, Giovanni Staurenghi, Peter J McCluskey
and Francesco Viola

Br J Ophthalmol published online August 1, 2017

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References This article cites 23 articles, 5 of which you can access for free at:
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