REVIEW ARTICLE

Infectious causes of posterior uveitis

Efrem D. Mandelcorn, MD, FRCSC, DBO
ABSTRACT RESUME
The differential diagnosis of posterior infectious uveitis is broad. There are, however, a few common infectious causes of posterior
uveitis that should always be considered. The more common infectious causes of posterior uveitis include syphilis, toxoplasmosis,
tuberculosis, endogenous endophthalmitis, and viral causes (including herpes simplex virus, herpes zoster virus, and cytomega-
lovirus). The clinical features, diagnostic tools, and treatment options for each of these are reviewed in this article.

Le diagnostic differentiel des uveites infectieuses posterieures est large. Il y a cependant quelques causes communes duveite
posterieure quil faudrait toujours considerer. Les causes les plus communes dinfection de luveite posterieure sont la syphilis, la
toxoplasmose, la tuberculose, lendophtalmie endogene   simplex, celui de
et les causes virales (y compris le virus de lherpes
 zoster et le cytomegalovirus). Cet article revoit les caracteristiques cliniques, les outils de diagnostic et les choix de
lherpes
traitement de chacun des sujets.

Posterior uveitis has a broad differential diagnosis. One
can group the various causative factors of posterior uveitis
into infectious, inflammatory, or neoplastic causes. A
good strategy when considering work-up and manage-
ment of posterior uveitis is to assume an infectious cause.
Infections often respond well to antibiotic or antiviral
therapy. Furthermore, if infectious causes are ruled out
early on, one can safely proceed to treat the uveitis with
immunosuppressive therapy in a stepwise approach
including topical, local, or systemic steroids.
With this strategy in mind, what testing should one
consider to rule out infectious uveitis? There is a long list
of possible infections, and it is essential for the ophthal-
mologist to take a comprehensive history and review of
systems to obtain any diagnostic clues related to possible
infection. Any travel history should be considered care-
fully, and endemic infections related to travel should be
included in the differential diagnosis. In general, however,
there are a few common infectious causes of posterior
uveitis that should always be considered and ruled out
because even uncommon presentations of infectious
uveitis are a result of common infections. As a tool to
remember this short list, one may consider the acronym
SSTTEEVE, where each letter represents 1 of these
causes. The first S is for sarcoidosis and, although not
an infectious cause, should be included in the differential
diagnosis of posterior uveitis. The subsequent letters are
Syphilis, Toxoplasmosis, Tuberculosis (TB),
Endogenous Endophthalmitis (bacterial, fungal),
Viral causes including herpes simplex virus (HSV),
herpes zoster virus, and cytomegalovirus (CMV). The final
E represents Etc., to remind the clinician to consider
Presented at Canadian Uveitis Society Meeting, Canadian Ophthalmological
Society, Toronto, Ont., June 28, 2012.
From the Department of Ophthalmology and Vision Sciences, Uni-
versity of Toronto, Toronto, Ont.
other infectious possibilities that are specific to the patients
functional inquiry and clinical history. In this review, we
will examine each of the causes of posterior uveitis in the
acronym SSTTEEVE (Table 1).
SYPHILIS (sStteeve)
Background
Syphilis is caused by the spirochete Treponema pallidum,
an obligate human parasite. It is spread by sexual contact,
blood transfusions, and across the placenta to the fetus.
Spirochetes can rapidly penetrate mucous membranes or
small skin abrasions and migrate to lymphatics. The
incidence of syphilis decreased in the late 1990s, but,
more recently, there are concerns that the number of
reported cases is on the rise.1,2
Classification
Syphilis has 3 clinical stages. In primary syphilis, a
painless chancre can be observed at the site of inoculation.
This often resolves spontaneously after 4 to 6 weeks.
Approximately 6 weeks after primary syphilis, secondary
syphilis presents with fever, malaise, and mucocutaneous
lesions. This is the most infectious stage with the highest
systemic load. Ocular involvement occurs in approximately
10% of cases. Tertiary syphilis is characterized by soft,
tumor-like areas of inflammation known as gummas, as well
as other changes that involve the vasa vasorum of the aorta
and the central nervous system. The stage of latent syphilis
implies serologic evidence of infection, but no signs or
symptoms of active disease. Neurosyphilis can occur at any
Can J Ophthalmol 2013;48:3139
0008-4182/13/$-see front matter & 2013 Canadian Ophthalmological
Society. Published by Elsevier Inc. All rights reserved.
http://dx.doi.org/10.1016/j.jcjo.2012.11.013

Originally received Oct. 2, 2012. Accepted Nov. 26, 2012

Correspondence to Efrem D. Mandelcorn, MD, Toronto Western

Hospital, University Health Network, 399 Bathurst Street, 6 East,
Room 415, Toronto ON M5T 2S8; efrem.mandelcorn@utoronto.ca

CAN J OPHTHALMOL VOL. 48, NO. 1, FEBRUARY 2013 31

Infectious causes of posterior uveitisMandelcorn
Table 1SSTTEEVE
S Sarcoidosis
S Syphilis
T Toxoplasmosis
T Tuberculosis
E Endogenous
E Endophthalmitis
V Viral (HSV, VZV, CMV)
E Etc.
HSV, herpes simplex virus; VZV, varicella zoster
virus; CMV, cytomegalovirus.
stage and is categorized as early (meningitis, stroke, seizures,
brainstem or central nervous system abnormalities, vestibu-
lar or ocular disease) or late (dementia, tabes dorsalis, ataxia,
paresis, bowel or bladder dysfunction). There is a high rate
of neurosyphilis in patients with ocular involvement such
that the U.S. Centers for Disease Control and Prevention
recommended in 2002 to do a lumbar puncture for all
patients with ocular involvement. A lumbar puncture may
indicate an elevation of the white blood cell count (45
white blood cells/mm3), protein (445 mg/dl), and a
positive Venereal Disease Reference Laboratory test.
Regardless of the results, ocular syphilis should be treated
with the neurosyphilis treatment protocol.
Clinical features
Ocular syphilis may present in any ocular structure
with features of anterior uveitis (conjunctivitis, scleritis,
interstitial keratitis, iridocyclitis) or posterior uveitis
(vitritis, chorioretinitis, serous retinal detachment, vascu-
litis), as reported by 1 U.S. academic centre.3 Because the
clinical presentation of ocular syphilis is so varied, ocular
syphilis has been classically regarded as the great
imitator. Because syphilis can present in a multitude of
ways, it should be considered in the differential diagnosis
of every case of uveitis and tested for accordingly. There
are, however, some specific presentations of ocular syphilis
that every clinician should look for when assessing a case
of posterior uveitis.
Fig. 1 Case of acute syphilitic posterior placoid chorioretinitis with a pale yellowish placoid subretinal lesion and coarsely
stippled hyperpigmentation seen well on fundus autofluorescence (B).
32 CAN J OPHTHALMOL VOL. 48, NO. 1, FEBRUARY 2013
In 1990, Gass et al.4 coined the term acute syphilitic
posterior placoid chorioretinitis. These cases have large,
solitary, grey-white or pale yellowish placoid subretinal
lesions with evidence of central fading and a pattern of
coarsely stippled hyperpigmentation. This can be seen
clearly on fundus autofluorescence (Fig. 1). On fluores-
cein angiography, there is early hypofluorescence in the
area of the yellowish opacification that stains late, and a
leopard-spot pattern of nonfluorescence in the faded
portions of the lesions.4
Another typical clinical presentation of syphilitic pos-
terior uveitis is known as syphilitic punctate inner
retinitis. These cases have very distinct inner retinal and
preretinal white spots with associated inner retinitis and
arteriolitis. This finding has been described more com-
monly in homosexual males with syphilis.5
Syphilis may also present with neuroretinitis in
which there is inflammation of the prelaminar optic nerve
vasculature that extends into the retina. Gass suggested
this was more in keeping with a disc vasculitis than a retinal
vasculopathy. The name was subsequently modified from
Leber idiopathic stellate maculopathy to neuroretinitis to
reflect this change in our concept of its pathophysiology.
Optic nerve vasculitis results in leakage of lipid and
protein with exudate that accumulates in the peripapillary
outer plexiform layer. As the serous component of the
exudate reabsorbs over the first few weeks, a lipid-rich
deposit precipitates in the outer plexiform layer of
Henles layer, resulting in a typical macular star appear-
ance.6 This appearance is classically associated with cat
scratch disease.
Diagnostic testing
Diagnostic testing for syphilis can be divided into 2
categories. Nontreponemal tests include Venereal Disease
Research Laboratory (VDRL) and rapid plasma reagin
(RPR). These use cardiolipin-lecithin-cholesterol antigen
to test the reactivity of human IgG and IgM. These are

associated with a high false-positive rate that includes
endocarditis, monocytosis, Lyme disease, malaria,
measles, TB, chronic liver disease, connective tissue
diseases, malignancy, pregnancy, and blood transfusions.
The test has low sensitivity early and late in the disease.
Treponemal tests include Treponema pallidum particle
agglutination (TP-PA) and fluorescent treponemal
antibody absorption (FTA-Abs). These are more sensitive
and specific but still may have some false-positive results
in cases of rheumatoid arthritis, systemic lupus erythema-
tosus, and biliary disease. Unlike the nontreponemal tests,
these tests cannot provide quantification of disease or
response to therapy. They usually remain positive for life.
Cases of ocular syphilis should also be investigated for
concomitant HIV infection. There is an apparent syner-
gistic effect between both infections whereby syphilis
increases the risk for acquiring and transmitting HIV.
Some estimates have suggested that more than 1000 new
cases of HIV were due to syphilis.7 Furthermore, HIV
increases the risk for neurosyphilis.8
Treatment
Treatment for neurosyphilis is aqueous penicillin G (2-5
million units IV every 4 hours for 10-14 days). Alterna-
tively, one may use penicillin G procaine 2.4 million units
IM daily with 500 mg probenecid orally QID for 10 to
14 days.
TOXOPLASMOSIS (ssTteeve)
Background
Toxoplasma gondii is a single-cell, obligate, intracellular
protozoan and is likely the most common cause of
infectious retinochoroiditis in humans. Up to 70% of the
world population is infected with toxoplasmosis. It
accounts for 30% to 50% of all posterior uveitis in North
America and perhaps 85% of cases in Brazil. It is more
commonly seen in children. It is transmitted either by
maternal transmission during pregnancy (often in the third
trimester) or in the postnatal period by ingestion of raw or
undercooked meat with tissue cysts or from contaminated
fruit, vegetables, or water. Historically, ocular toxoplasmo-
sis was considered a congenital infection, but new evidence
suggests that acquired disease may, in fact, be much more
common. The parasite lies dormant in its host in the form
of a cyst, known as a bradyzoite, thereby escaping the
humoral and cellular immune systems. It occasionally
converts to its active form, known as a tachyzoite, causing
localized inflammation and tissue destruction. This trans-
lates clinically into recurrent episodes of uveitis, retinitis,
and retinal vasculitis.
Clinical features
There are various presentations of toxoplasmosis. The
classic lesion is a focal necrotizing retinochoroiditis
CAN J OPHTHALMOL VOL. 48, NO. 1, FEBRUARY 2013
Infectious causes of posterior uveitisMandelcorn
accompanied by vitreous inflammation. The acute lesion
typically arises from the border of a chorioretinal scar.
These lesions often remain active for up to 16 weeks and
then resolve, leaving a hyperpigmented scar. Other forms
described include large destructive lesions, punctate inner
lesions, and punctate deep lesions. Unlike classic toxo-
plasmosis retinitis, which presents with inner retinal
involvement and intense vitritis, punctate outer retinal
toxoplasmosis often has minimal vitritis because the
lesions are in the deeper retinal layers and there is less
spillover of inflammatory cells into the vitreous cavity.9
This subtype of toxoplasmosis more commonly affects
younger patients. The lesions are in the macular region
and are primarily situated in the outer retinal layers,
which can be nicely seen on optical coherence tomogra-
phy (OCT). Peripapillary toxoplasmosis is another form
and should be considered in the differential diagnosis of
cases of papillitis or neuroretinitis.10 Toxoplasmosis in
immunocompromised patients can be multifocal and may
also expand into large areas of full-thickness retinal
necrosis. These cases need to be differentiated from viral
retinitis that can look similar. These lesions are more
resistant to treatment and have a poorer prognosis.11
OCT findings in acute ocular toxoplasmosis may
include retinal thickening with macular edema or macular
schisis. As the lesion heals, there is often significant retinal
thinning with excavation of the retinal and subretinal
layers including the choriocapillaris. In cases of unknown
pigmented retinal scars, excavation on OCT is a useful
feature to look for that because it suggests a previous
toxoplasmosis infection.
Treatment
The goal of treatment of toxoplasmosis is to stop the
replication of the organism and limit inflammation within
the eye. Many different medications are used, and no
consensus exists as to which medication should be used as
first line. One recent study concluded no significant
difference between pyrimethamine and sulfadiazine versus
trimethoprim/sulfamethoxazole.12 Azithromycin and clin-
damycin may also be considered for their effects on
prevention of protozoal protein synthesis. Atovaquone
may also be highly effective for its effect on inhibition of
protozoal mitochondrial electron transport chain.13 Con-
comitant use of corticosteroids will limit intraocular
inflammation and should be considered within a few
days of initiation of antibiotics.
There are data that demonstrate efficacy of local
therapy for toxoplasmosis. Intravitreal clindamycin (1.0-
1.5 mg/0.1 ml) in combination with dexamethasone (400
mg/0.1 ml) is a suitable alternative for patients who are
intolerant of or unresponsive to systemic medications.14
Figure 2 demonstrates a case of a pregnant patient in her
second trimester with acute toxoplasmosis treated with
intravitreal clindamycin and dexamethasone to avoid any
systemic exposure, with good therapeutic response.
33
Infectious causes of posterior uveitisMandelcorn
Fig. 2 Two cases (A, C) of pregnant patients with acute toxoplasmosis retinitis. Both were treated with intravitreal clindamycin
and dexamethasone, with good response to therapy, to avoid systemic toxicity (B, D).
Consensus guidelines state that treatment of ocular
toxoplasmosis should be undertaken in cases of peripa-
pillary (85%), maculopapillary bundle (88%), and paraf-
oveal (94%) lesions with marked (66%) or severe (81%)
vitreous reaction.15 In this report, the choice of therapeu-
tic agent varied from pyrimethamine (69%), sulfadiazine
(55%), clindamycin (45%), sulfamethoxazole and tri-
methoprim (Bactrim; 32%), and prednisone (82%).
Prophylaxis should be considered in cases of recurrent
toxoplasmosis uveitis. One study compared patients with
recurrent disease and grouped them as Bactrim every
3 days versus no prophylactic treatment. The Bactrim
group had fewer recurrences (7%) than the control group
(24%), which suggests that prophylaxis should be con-
sidered in recurrent cases.16
TUBERCULOSIS (sstTeeve)
Background
Mycobacterium TB is a non-spore forming, non-motile
bacillus that spreads in airborne droplets which can
remain suspended in the air for several hours. Over
90% of infected persons never develop the disease; 5%
develop the disease in the first few years, and the
remaining 5% develop it later because of weakened
immunity. In this small proportion of patients, a few
bacilli survive but remain dormant. These patients have
latent TB, which is asymptomatic with no radiographic
findings.
34 CAN J OPHTHALMOL VOL. 48, NO. 1, FEBRUARY 2013
Clinical features
Like syphilitic uveitis, TB uveitis can involve any ocular
structure including any variation of anterior, intermediate,
or posterior uveitis. In the posterior segment, TB may
manifest as choroidal tubercles or tuberculomas, subretinal
abscess, serpiginous choroiditis (SC), or retinal vasculitis.
Choroidal tubercles are small yellow nodules with
indistinct borders that may become pigmented as they
heal and scar. They suggest hematogenous spread of TB.
Tuberculomas are larger, solitary, tumor-like masses that
may grow vertically or spread diffusely in the choroid.
They may have overlying hemorrhage, exudate, or sub-
retinal fluid.17 When there is multiplication of the
organism within the granuloma and secondary liquefac-
tion and necrosis, a subretinal abscess may form.
TB-related retinal vasculitis is associated with vitritis
and sometimes neuroretinitis. Periphlebitis with capillary
nonperfusion often leads to neovascularization, vitreous
hemorrhage, and retinal detachment (Fig. 3). Retinal
vasculitis associated with Eales disease is linked to TB as
some studies have detected TB organisms by polymerase
chain reaction (PCR) in the vitreous fluid of patients with
Eales disease, suggesting that the organism may be
inciting a hypersensitivity reaction.
In serpiginous-like choroiditis (SLC), TB may incite a
hypersensitivity in the choroid or retinal pigment epithe-
lium (RPE), resulting in multifocal plaquelike choroiditis
that is discrete and noncontiguous. This may progress
into a more contiguous lesion with an active advancing
edge similar to what is observed in SC (Fig. 4). In contrast

Fig. 3 Case of Eales disease with periphlebitis, capillary
nonperfusion, and early peripheral neovascularization.
with classic SC, patients with TB-SLC are from an
endemic TB area, and have vitritis and unilateral multi-
focal lesions that often spare the peripapillary region.
They also demonstrate positive results on TB investiga-
tion (tuberculin skin test or interferon-g release assay).
Patients with classic SC who do not respond to steroids or
immunosuppressive agents should be further evaluated
and treated for TB-SLC.18
Diagnostic testing
Confirming a diagnosis of ocular TB is problematic
because direct evidence of the organism is difficult to
obtain by culture or acid-fast stain. The combination of
Fig. 4 Case of serpiginous-like choroiditis in a patient with
a positive interferon-g release assay test. Note the active
border of choroiditis superior and inferior to the fovea.
CAN J OPHTHALMOL VOL. 48, NO. 1, FEBRUARY 2013
Infectious causes of posterior uveitisMandelcorn
clinical features and direct stain or culture of TB is termed
confirmed ocular TB. Presumed ocular TB refers to clinical
features of TB with a positive test for TB including
tuberculin skin test, a lesion on the chest radiograph, or
evidence of active extrapulmonary TB. Finally, presumed
ocular TB refers to clinical features of TB along with the
exclusion of other uveitic entities and a positive thera-
peutic trial of anti-TB therapy.
Treatment
Systemic anti-TB treatment should be initiated by an
infectious disease specialist and may include isoniazid,
rifampin, pyrazinamide, and ethambutol. The U.S.
Centers for Disease Control and Prevention recommends
the use of 4 agents for initial 2 months followed by a
choice of 2 medications for the next 4 to 7 months.
Concomitant use of low-dose systemic steroids is often
implemented as well.
ENDOGENOUS ENDOPHTHALMITIS (ssttEEve)
Background
Endophthalmitis usually presents with significant
intraocular inflammation and may be caused by bacteria
or fungi. Endophthalmitis can be categorized as exogen-
ous or endogenous. Exogenous endophthalmitis occurs in
healthy patients after surgery, by contiguous spread from
an external ocular infection, or after trauma. Endogenous
endophthalmitis occurs primarily in patients who are
relatively immunocompromised such as patients with
HIV or patients on long-term antibiotics, corticosteroids,
or immunosuppressive agents. Patients with indwelling
intravenous catheters or hyperalimentation, or intrave-
nous drug users are similarly at risk.
In cases of endogenous endophthalmitis, spread of
infection to the eye occurs after bacteremia or fungemia.
The most commonly encountered type of fungus is
Candida albicans, the incidence rate of which has
increased over the past few decades and has been reported
to vary between 2% and 45% among patients with
systemic fungal infection.
Clinical features
Fungal endophthalmitis (FE) is characterized by creamy
white, well-circumscribed chorioretinal lesions, often in
the posterior pole with associated yellow or white fluffy
vitreous opacities. These lesions originate from the choroid
and spread through full-thickness retina to eventually
break through into the vitreous cavity (Fig. 5). Vitreous
fungus balls sometimes coalesce to form the classic string
of pearls configuration. With treatment, chorioretinal
scars develop in areas of previously active chorioretinitis.
Other cicatricial changes may also occur including epir-
etinal membrane, tractional retinal detachment, and
hypotony from cyclitic membranes.
35
Infectious causes of posterior uveitisMandelcorn
Fig. 5 This is a case of an active fungus choroidal infiltrate spreading from the choroidal space into the retina. Note on the
fluorescein angiogram how the lesion is spreading inward and displacing the retinal tissue and vessels aside as it invades into
the inner retinal layers (and vitreous). After treatment, the lesion heals, leaving a pigmented ring.
Treatment
Treatment of FE may include amphotericin B, although
systemic toxicity, namely, renal dysfunction, remains a
concern. There is also poor ocular penetration because
nonfenestrated capillaries in the eye do not permit
penetration of large and poorly lipid-soluble molecules.
Intravitreal amphotericin at doses of 5 to 10 mg/0.1 ml has
been shown to be safe.19 More recent reports suggest that
intravitreal voriconazole may be a safe alternative.2022
There is evidence that there is a significant therapeutic role
to vitrectomy in FE. One published series reported good
outcomes using only vitrectomy and systemic antifungal
agents alone with no intravitreal antifungal agents.23
VIRAL (sstteeVe)
Background
Viral retinopathies are a spectrum of disease predomi-
nantly of the herpes family of viruses (VZV, HSV, CMV,
EBV). The clinical picture often depends on the hosts
immune status; acute retinal necrosis (ARN) is most often
found in an immunocompetent host, whereas progressive
outer retinal necrosis (PORN) and CMV are seen in an
immunocompromised host. Herpes viruses as the cause of
ARN has been confirmed by culture and PCR in many
studies since the early 1980s.2426 More recent studies have
demonstrated the clinical utility of PCR in diagnosing
ARN using anterior chamber fluid27 with a positive
predictive value approaching 99% in some studies.28
36 CAN J OPHTHALMOL VOL. 48, NO. 1, FEBRUARY 2013
Clinical features
In all cases of suspected viral panuveitis, it is very useful
to complete a careful anterior segment examination to
look for diagnostic clues that may suggest a herpetic
cause. Corneal sensation is a useful test along with careful
inspection of the iris for subtle transillumination defects
that suggest underlying herpetic disease.
ARN
The clinical criteria set by the American Uveitis Society
for a diagnosis of ARN include 1 or more foci of retinal
necrosis with discrete borders, peripheral retina location,
rapid progression of disease in the absence of therapy,
evidence of occlusive vasculopathy and arteriolar involve-
ment, and prominent inflammatory reaction in the
vitreous and anterior chamber. The evolution of ARN
starts with moderate-to-severe vitritis that progresses to
involve peripheral, well-delimited patches of retinal necro-
sis. Without treatment, the lesions tend to rapidly progress
in a circumferential pattern in 5 to 10 days. As the active
phase resolves, the retinitis recedes and begins to pigment
and scar with associated retinal atrophy. A sharp demarca-
tion line forms between affected and normal retina,
which has a high risk for retinal breaks and detachment
(50-75%). Bilateral disease (known as BARN) occurs in up
to 35% of cases usually within 6 weeks.
PORN
In PORN, VZV is the more likely herpes virus, as has
been demonstrated in histopathologic studies where VZV

Fig. 6 Progressive outer retinal necrosis with confluent retinitis and necrosis. After treatment, there is diffuse pigmentary
change and retinal atrophy (B).
is more heavily detected in the RPE and outer retinal
layers.29 The evolution of PORN involves multifocal
lesions throughout the peripheral retina with opacification
of the deep retinal layers, with or without areas of
confluence (Fig. 6). Perivenular clearing of retinal opaci-
fication is also described. In contrast with ARN, cases of
PORN have macular lesions in up to 32% of cases. Given
that patients are immunocompromised and that there is
more outer retinal involvement, there is often minimal or
no intravitreal inflammation. There is also more rapid
progression of lesions in PORN than in ARN.30 Bilateral
disease is reported in more than 70% of patients.
CMV
CMV retinitis can be categorized as fulminant with
large areas of hemorrhage and a white, edematous or
necrotic retina (also known as pizza pie) or granular, in
Fig. 7 Granular cytomegalovirus retinitis with an active
border.
Infectious causes of posterior uveitisMandelcorn
which a more indolent progression occurs with lesions
that are more peripheral with minimal edema, exudate, or
hemorrhage (Fig. 7). Another subtype is known as frosted
branch angiitis with significant perivascular sheathing
(Fig. 8). CMV is also classified by its area of involvement:
zone 1 is within 1500 mm of the optic nerve or 3000 mm
of the fovea; zone 2 extends from zone 1 to the equator;
and zone 3 is the remaining anterior retina, terminating at
the ora serrata.31
Treatment
CMV retinitis is treated by intravenous induction using
5 mg/kg twice daily ganciclovir for 2 to 3 weeks followed by
5 mg/kg/day as maintenance. Intravenous foscarnet is an
alternative option. Local treatment with intravitreal ganci-
clovir may also be considered. Oral valganciclovir may also
be considered as an effective alternative to intravenous
ganciclovir.32
Treatment of ARN includes intravenous acyclovir for
7 to 14 days33 or oral valacyclovir.34 There is a growing
trend to replace intravenous acyclovir with oral valacy-
clovir. The use of intravitreal foscarnet and/or ganciclovir
is also a useful adjunct in obtaining disease control. These
injections can be given 1 to 2 times per week for the first
2 weeks and then on an as needed basis. Oral antiviral
medications should be continued for at least 3 months to
decrease the immediate risk for recurrence. Systemic
corticosteroids may also be initiated shortly after antiviral
treatment to control the inflammatory response.
Given the greater risk for VZV encephalitis in bilateral
PORN, systemic foscarnet and ganciclovir are more
commonly used for 7 to 14 days. In addition, intravitreal
foscarnet and/or ganciclovir can be used 1 to 2 times per
week for 2 weeks, then as needed. Oral antiviral medica-
tion should be continued for 3 months. Steroids are
usually not needed given the limited inflammatory reac-
tion. HIV medication highly active antiretroviral therapy
(HAART) should be initiated in consultation with an
CAN J OPHTHALMOL VOL. 48, NO. 1, FEBRUARY 2013 37
Infectious causes of posterior uveitisMandelcorn
Fig. 8 Severe frosted branch angiitis secondary to cytomegalovirus in a patient with newly diagnosed untreated HIV and a
high viral load.
infectious disease specialist if the patient tests positive
for HIV.
Given the high risk for rhegmatogenous retinal detach-
ment in up to 50% to 75% of patients, there are
advocates for prophylactic laser photocoagulation that
may reduce the risk for retinal detachment to less than
17%.35 Prophylactic laser demarcation should be applied
in 3 to 4 rows at the posterior border of the advancing
retinitis. A high percentage of patients will experience
retinal detachment despite laser prophylaxis.
CONCLUSION
The differential diagnosis of posterior uveitis is exten-
sive and includes infection, inflammation, and neoplastic
causes. It is useful in clinical practice to rule out infectious
causes first and to consider the most common infectious
etiologies at the onset. These include syphilis, toxoplas-
mosis, TB, endogenous endophthalmitis, and viral causes
(HSV, VZV, CMV). A careful history, physical examina-
tion, and use of ancillary diagnostic testing are required to
come to the correct diagnosis and treatment. In the case
of infectious causes of posterior uveitis, prompt correct
treatment is often curative.
Disclosure: The authors have no proprietary or commercial
interest in any materials discussed in this article.
Acknowledgements: The author acknowledges Drs. Thomas
A. Albini and Ruwan Silva for their contribution of Figure 8.
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