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10.6 Infectious Uveitis
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CMV lacks; hence, acyclovir is ineffective in
treating CMV-R.The CMV UL-97 protein phosphorylates ganciclovir to its active triphosphate
form, a competitive analogue of the viral DNA
polymerase, and thus blocks the multiplication of
the CMV.The intravenous use of ganciclovir can
lead to resistance. Mutations in the UL97 gene
make the CMV resistant to ganciclovir. Oral valganciclovir, a prodrug of ganciclovir, is equally
effective compared to intravenous ganciclovir in
treating CMV-R [95]. Signicant side effects of
ganciclovir include skin rash, diarrhoea, and haematogenic. Intravitreal ganciclovir inserts have
not been available since 2013. The oral valganciclovir 900 mg is equivalent to 5 mg/kg body
weight of intravenous ganciclovir. Intravitreal
ganciclovir (2 mg/0.1 mL) is effective in nonHIV CMV-R as the disease is most often unilateral. The induction dose is given twice a week
and maintained with a once-a-week intravitreal
injection [96].
10.6.3.4 Prophylaxis forCMV
Retinitis
Valganciclovir prophylaxis is given to all transplant patients as up to 75% of such patients may
develop CMV infection, and up to 30% may
develop a CMV disease. Recently, letermovir, a
CMV terminase inhibitor, has been used effectively as primary prophylaxis in high-risk patients
with allogeneic haematopoietic cell transplantation [97]. The high-risk patients are CMVpositive donors/CMV-negative recipients.
Positive CMV PCR from blood, pp65 antigenemia, and positive serology are some markers for
prophylactic treatment initiation.
10.6.3.5 Alternate Drugs
fortheTreatment ofCMV-R
For patients who develop ganciclovir-resistant
CMV disease and resistant HSV, intravenous foscarnet 90 mg/kg twice daily for 2 weeks, followed by 120mg/kg daily for maintenance, can
be given. It is a highly nephrotoxic drug. The
patient must be hydrated well. Other adverse
reactions include anaemia, nausea, and neurological side effects.
The intravitreal dose of foscarnet is 1.2–
2.4mg once or twice a week for induction and
1.2mg weekly for maintenance. Resistance may
develop if there is a mutation in the viral DNA
polymerase. Unlike ganciclovir, cidofovir does
not need viral kinases for activation and hence
can also be used in ganciclovir-resistant cases of
CMV-R. Cidofovir is given intravenously at
5mg/kg weekly for 3weeks and a maintenance
dose of 5mg/kg every 2weeks. The intravitreal
dose of cidofovir is 20 μg every 6 weeks.
However, its intravitreal use is limited by severe
adverse events like uveitis, cystoid macular
oedema, and irreversible hypotony [98]. Other
therapies include CMV immune globulin therapy
for systemic CMV pneumonia. Progressive cases
of CMV retinitis have been treated with donorderived CMV pp65-specic T cells [99–102].
10.6.3.6 When toStop theAntiviral
Therapy inCMV-R
The guidelines are clear in patients with HIV
infection; once the CD4+ T-cell counts reach
100–150 cells per μL, lesions of CMV-R resolve
spontaneously and do not need any other antiviral
therapy. In patients on immunosuppressive therapy, the dose of IMT is decreased to the level
where the absolute neutrophil count is maintained above 1000 per μL.However, in non-HIV
CMV-R, the guidelines are not clear. It may help
to do PCR for CMV from the blood.
10.6.4 Emerging Viral Infections
andRetinitis
In recent years, arthropod-borne seasonal epidemics of viral fever have increasingly become a
major public health challenge in several regions
of the world, especially South Asia and South
America [103]. Most of these are caused by
single- stranded RNA viruses like dengue, chikungunya, West Nile, Zika, and Ebola that follow
an insect bite from mosquitos of the Aedes species (aegypti or albopictus) that thrive in the tropical and subtropical climate. The severity of
uveitis from the anterior to the posterior segment
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10 Retinal andChoroidal Infections andInammation
may follow days to months following these infections. The diagnosis is based on the detection of
IgM antibodies. Conventional RT-PCR techniques have shown the presence of the chikungunya, Zika, and Ebola virus in the aqueous humour
in patients with uveitis even after the systemic
symptoms have resolved [104–106].
Dengue is the most common mosquito-borne
viral infection that has become endemic in more
than 100 countries and is characterized by fever,
headache, myalgia, and arthralgia. Haemorrhagic
dengue infection may be fatal. Ocular manifestations result from ischaemic, inammatory, or
thrombocytopenic mechanisms that manifest as
maculopathy, optic neuropathy, vasculitis, retinal
haemorrhages, and multifocal retinitis,
Intensive basic science research is currently
focused on elaborating on the pathogenic mechanism of these viral infections. Zika virus infection may be asymptomatic or mild, but it gained
widespread recognition upon realizing that in
utero infection was associated with microcephaly
in the newborn. Zika virus-associated anterior
uveitis was described only recently [107].
Furthermore, nearly half of the patients who
develop redness of the eyes during fever may
develop hypertensive anterior uveitis [108].
RT-PCR can demonstrate the Zika virus
RNA.The Zika virus possibly enters the eye riding in myeloid cells. In a human cell line model
of iris pigment epithelium, the Zika virus was
shown to mount an active type 1 interferon recognition and molecular defence response to limit
the ocular inammatory response in most individuals [106].
West Nile fever is caused by a positive singlestranded neurotropic RNA virus that remains
asymptomatic in most people. However, ~20% of
cases may develop a self-limiting u-like illness.
Less than 1% may develop meningitis, encephalitis, or a polio-like illness, of which 80% develop
self-limiting bilateral multifocal chorioretinitis
lesions [109].
10.6.4.1 Treatment ofPost-Fever
Retinitis
Most of these infections are self-limiting; currently, no antiviral treatment is available. Many
of these patients may require supportive treatment during their systemic illness. While systemic corticosteroids are widely used for
controlling the immune-mediated inammatory
reaction, controlled studies to prove their efcacy
are lacking.
Preventive strategies remain the mainstay,
including public health measures to control mosquito breeding and wearing long-sleeved protective clothing. Several vaccines, including those
for Ebola, Zika, chikungunya, and dengue, have
shown promise in animal models and are either
approved or in the process of approval for use in
humans. Waxing and waning epidemics of these
infections and uncertainty of cost-efcacy of
human trials and uptake remain a public health
challenge [110].
10.6.5 Bacterial Infectious Uveitis-
Spirochetal Infections
Treponema, Borrelia, and leptospira are three of
the most common gram-negative spirochetal
infections that cause uveitis. Treponema palli-
dum and Borrelia burgdorferi are among the
most invasive bacteria. These bacteria can easily
move through the skin and other body surfaces
freely in and out of the blood vessels. Treponema
pallidum can cross the blood-brain barrier and
even the placenta to cause congenital syphilis.
Leptospira is also highly mobile in water but
needs a skin abrasion or a cut to enter the body.
Although it causes a multiorgan disease, it is
mainly localized in the kidneys and excreted in
the urine of infected mammals [111]. All three
infections can be prevented with appropriate
measures.
10.6.5.1 Syphilis
In the last two decades, there has been a steady
rise in the incidence of primary and secondary
syphilis from 2.1/100,000 to 9.5/100,000 population in the USA, mainly because of men having
sex with men. HIV commonly accompanies
syphilis, and all patients with syphilis must be
tested for HIV infection. In our clinic studies,
there was no syphilitic uveitis in our 2004 study
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[36], but in the 2017 study, 8 of the 507 infec-
tious uveitis cases were due to syphilis [35]. For
a long time, syphilis has been known as a great
mimic and may manifest as anterior uveitis,
intermediate uveitis, retinal vasculitis (Fig.10.9),
neuro- retinitis, optic neuritis, or placoid chorioretinopathy. Posterior uveitis accounts for nearly
50% of the cases. In recent years, multimodal
imaging studies have provided clues to a possible syphilis aetiology. Fundus autouorescence
studies show a speckled or well- demarcated
hyperautouorescence. Structural OCT changes
are characterized by loss of the external lining
membrane and patchy disturbances of the ellipsoid zone, which are reversible. The RPE layer
shows granular/nodular hyperreective projections into the outer retina. Preretinal dots seen on
OCT as hyperreective dots suggest a syphilitic
infection.
Diagnosis is based on treponema tests such as
uorescent treponema antibody or the syphilis
IgG, treponema haemagglutination, and nontreponemal tests such as VDRL or RPR.Since
nearly half of the patients with ocular syphilis
may have CNS involvement, it is recommended
that CSF be tested, and all ocular syphilis be
treated as neuro-syphilis. The treatment includes
three to four million units of penicillin G administered intravenously every 4 h for 2 weeks.
Alternately, IV or IM ceftriaxone, oral doxycycline (not advised in pregnant women), and
amoxicillin or erythromycin may be used.
Interestingly, following primary chancre, there is
a latent phase during which there is only serological evidence of infection. Most of the ocular
involvement is seen in the primary or secondary
stage of the infection. Once fully treated, the
organism Treponema pallidum is eliminated from
the body. This infectious cause of uveitis is curable, so it must be ruled out in all patients with
uveitis. The subject has been recently reviewed
[112].
Fig. 10.9 (A) A 24-year-old man (a) presented with reti-
nal vasculitis (frosted branch angiitis, black arrows). He
revealed a history of high-risk behaviour and tested positive for syphilis. Syphilitic retinitis (blue arrows) was seen
in a 31-year-old man (b). (B) A 38-year-old man with
metamorphopsia left eye. Visual acuity was 6/6. Twomonth history of penile painless sore. Translucent welldemarcated outer placoid chorioretinitis placoid lesion (a,
black arrows). Subretinal precipitate-like lesions (a, blue
arrow) and focal perivascular lesions (a, red arrow).
Fundus autouorescence shows punctate hyperautouorescent lesions (b). Fundus uorescein angiography in the
late frame shows mild staining of the optic disc and posterior pole with hypouorescent punctate lesions that correspond to the hyperautouorescent lesions seen in b (c).
Treponema pallidum haemagglutination and venereal disease research laboratory tests were positive. The placoid
lesion resolved one month following intravenous ceftriaxone 1g twice daily for 14days (d). OCT at presentation
shows highly characteristic nodular lesions of the RPE
(e), which disappear following treatment (f). (Images
courtesy of Dr. Alok Sen, Sadguru Chikitsa Nethralya,
Chitrakoot, MP, India)
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a
d e
Fig. 10.9 (continued)
b
c
f
10.6.5.2 Lyme borreliosis
While the vector (black-legged tick)-borne Lyme
borreliosis caused by Borrelia Burgdorferi is
showing an upward trend in the endemic areas of
several countries of Europe and North America,
the ocular Lyme borreliosis is uncommon or perhaps underdiagnosed because of the nonavailability of serological tests in many parts of
the world. Ocular Lyme borreliosis manifests in
the late stages of infection as intermediate uveitis
or retinal vasculitis and should be considered in
the differential diagnosis, especially in people
with a history of erythema migrans (red skin rash
spreading in a ring fashion), following a tick bite
and those who come from Lyme-endemic areas.
Unlike syphilis, routine screening for Lyme borreliosis is not recommended in patients with uveitis [113].
gans resides in the kidneys of many animals and
rodents. The soil gets contaminated from the
urine of infected animals, where the organisms
can survive for months. Epidemics follow heavy
rainfall and ooding of agricultural elds. The
organisms enter humans through broken skin or
mucosa. Unlike other spirochetal infections that
produce skin lesions at the portal of entry, this
infection does not leave any trace of entry. People
engaged in agricultural activities or water sports
are more prone to contract this infection. While
most infected patients present with mild disease,
nearly 10% develop severe disease and show evidence of cytokine storm, including acute fever,
headache, and severe haemorrhagic multiorgan
involvement. Like all spirochetal infections,
Leptospira is susceptible to penicillin, ampicillin,
ceftriaxone, and doxycycline and needs aggressive supportive therapy during acute infection.
10.6.5.3 Leptospiral Uveitis
Leptospirosis is another spirochetal disease seen
in subtropics and tropics, the regions with a
humid climate. The organism Leptospira interro-
The microscopic agglutination test is the gold
standard but requires dealing with live organisms
and is thus not commonly available. The other
tests are ELISA, macroscopic agglutination, and
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PCR.The circulating spirochetes disappear with
the development of antibodies, but the bacteria
may survive in the immune-privileged sites,
including the eyes. Uveitis is a late complication
seen in the convalescent phase of the disease, and
nearly half develop hypopyon, panuveitis, and
rapidly developing white cataracts. PCR from the
aqueous humour is positive for leptospira DNA
in nearly 80% of the patients with uveitis [114].
The treatment at this stage requires aggressive
corticosteroid therapy. It is still unclear if systemic antibiotic therapy in the acute phase will
prevent the occurrence of uveitis [115].
10.6.6 Other Bacterial Uveitis:
Mycobacterium tuberculosis
The pathology of uveitis caused by
Mycobacterium Tuberculosis (MTB) from the
enucleated globes was known long before the
discovery of the MTB in 1882 by Robert Koch
[116]. However, the diagnosis of tubercular uveitis (TBU) in the clinic remains a major challenge
even today. The cornerstone of the diagnosis of
the MTB infection (Koch’s postulates), namely
the demonstration of the presence of the acid-fast
bacilli (AFB) either on smear examination or a
positive culture from the TB-affected tissues, can
hardly be ever possible from the uids or tissues
of a seeing eye. Thus, the diagnosis of TB uveitis
(TBU) to date is based on corroborative evidence
rather than fullling Koch’s postulates.
10.6.6.1 Lessons fromthePast-TB or
No TB
More than 100 years ago, when tuberculosis
infection of the lungs was rampant across the
world, most patients with uveitis were attributed
to tuberculosis more as a reection of faith rather
than evidence. Before the advent of chemotherapy for treating TB, Woods, in many of his publications on the aetiology of uveitis, reported a
steady decline in uveitis attributed to TB from
80% in 1941 to 20% in 1960 [117, 118]. Because
of the wide variation in the clinical phenotypes of
TBU, some of the cases due to sarcoidosis, brucellosis, toxoplasma, and histoplasmosis, aetiolo-
gies that were yet to be discovered, may have
been earlier labelled as TBU.In one such telling
example, Verhoeff diagnosed a case of TB necrotizing retinitis on histopathology but 25 years
later admitted that the reported case had the pathological features of toxoplasmosis retinitis [119]
and not TB [120].
10.6.6.2 Endemicity ofTB
andTubercular Uveitis
Before Dr. Woods, several authors who sought
denitive evidence of TB reported its prevalence
from 2 to 11%, while those who applied less stringent criteria estimated the prevalence of TBU in
their clinic to vary from 40 to 48% [117, 118].
Undoubtedly, with an incidence of TB at 250–
300/100,000 population in that era, the true prevalence may have been between 10 and 40%. As seen
in the discussion below, high-burden countries
show a high prevalence of TBU in their clinics.
Several measures taken 100years ago, including the declaration of TB as a notiable disease,
identication of crowded dwellings, poor
hygiene, and poor nutrition as possible risk factors, and the availability of anti-TB drugs in the
1950s, have dramatically reduced the incidence
of TB from 250–300/100,000 population to
2–10/100,000in the Western countries. However,
it continues to be a hyperendemic and a major
public health problem in several regions of the
world, including India, China, Indonesia,
Philippines, Pakistan, Nigeria, Bangladesh, and
S. Africa, where the incidence continues to be
higher than 200/per 100,000 population.
Although TBU data from the uveitis clinics are
not available from all such places, where available, it shows a signicant prevalence of TBU in
India (19.85–22.8%), Myanmar (32.37%),
Vietnam (8.95%), Thailand (8.5%), Singapore
(6.7%), and Sri Lanka (6.2%). However, some of
the developed countries, Australia (4.2%), New
Zealand (3.1%), and S.Korea (1.66%), show a
low prevalence of TBU.In the last 30years, TBU
prevalence has consistently been 0.2–0.6% of all
cases of uveitis in the USA [121]. It is to be noted
that the incidence of TB in the US population is
one of the lowest in the world at 2/100,000 population, most of it in foreign-born persons.
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10.6.6.3 Clinical Phenotypes
ofTubercular Uveitis
The TBU manifests in various phenotypes, most
commonly as multifocal serpiginous-like choroiditis, retinal periphlebitis, choroidal granuloma,
panuveitis, anterior uveitis, and even intermediate uveitis [122–125]. The diagnosis is often
made by recognizing the clinical phenotype in
vulnerable populations (high-burden TB countries) who show immunological or radiological
evidence of tuberculosis. Recently, a systematic
review and meta-analysis on the global prevalence of TBU found a 7% prevalence in TB highburden countries and 3% in low-burden countries,
peaking at 11% in sub-Saharan Africa [126].
However, the authors found a high degree of heterogeneity among the studies because of the need
a
b
for standard diagnostic criteria that pose a major
question of the validity of any gures given for
TBU.
Serpiginous-like Choroiditis
Tubercular serpiginous-like choroiditis
(TB-SLC) is the most common phenotype of
TBU, rst reported in 2003 [127] from India, a
TB-endemic country. It is characterized by multifocal lesions (>90%) that show actively advancing greyish-white lesions (Fig. 10.10). Focal
lesions appear in crops. As some of these are
healing, new ones may appear elsewhere in the
retina. Uncommonly, the TB-SLC may be a single placoid lesion. The lesions heal centrally and
expand centrifugally and become conuent.
TB-SLC is predominantly seen in young men
c
d
e
Fig. 10.10 (A) A 36-year-old man presented with exten-
sive scarring of the right eye (a) and a healed choroiditis
scar just above the fovea in the left eye (b). Within 8weeks
of presentation, he had blurring of vision in the left eye
and showed plaque-like multifocal lesions in the left eye
(c). The lesions showed a central healing and centrifugal
spread at the margins (d). At 10months following anti-TB
treatment with oral corticosteroids, the lesions healed and
did not recur (e). (B) The active choroiditis lesions (f) on
FFA were hypouorescent in the dye transit. Note speckled transmission hyperuorescence in healed lesions (g).
The hypolesions become hyperuorescent in the late
frames (h). (C) Left eye fundus photograph (a) and fundus
autouorescence (b) of a 45-year-old woman with a large
placoid lesion in the macula and multifocal active lesions
of serpiginous-like choroiditis. The active margins of the
lesion are hypouorescent in early (c) and hyperuorescent in late phases (d). The centre of the lesion shows
transmission hyperuorescence, both in the early (c) and
late phases (d). (Reproduced with the permission of the
publishers from Bansal, R., Sharma, A., & Gupta, A.
(2012). Intraocular tuberculosis. Expert Review of
Ophthalmology, 7(4), 341–349. https://doi.org/10.1586/
eop.12.42)
B
C
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f
g
h
a
b
c
Fig. 10.10 (continued)
d
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10 Retinal andChoroidal Infections andInammation
(M:F: 3:1). When rst seen, >60% of the patients
may have bilateral involvement, often one eye
showing healed lesions that have gone unnoticed
by the patient. In most patients, the lesions are
non-contiguous to the optic disc. There is a variable amount of vitreous inammation. Most
lesions are located in the posterior pole, but in
half of the patients, these lesions are also seen
nasally to the optic disc. The lesions heal with
retinal atrophy and a variable amount of pigmentation. Patients at presentation may have >6/12
visual acuity in the affected eye [128]. Notably,
the foveal centre remains unaffected until late in
the disease. The central healed lesion on FFA
shows transmission mixed uorescence, whereas
the active advancing edge shows initial hypouorescence with late staining. On ICG angiography,
the lesions are hypouorescent and remain hypouorescent even in the late stages. The disease
course is best followed on fundus autouorescence, as the lesions become hypoautouorescent from initial hyperuorescence [129]. The
TB-SLC lesions may progress after initiating
anti-TB therapy [130]. If ultra-wide eld fundus
imaging is used to monitor the course of the
disease, the paradoxical worsening may be seen
in nearly 36% of the eyes [131]. On OCT angiography, the multifocal TB-SLC lesions show a
ow decit in the choriocapillaris layer corresponding to the hypouorescent lesion on ICG
angiography. As the lesions heal, the ow decit
areas are completely reversed, unlike in the placoid type of SLC, which shows the persistence of
ow decit consistent with atrophy of the choriocapillaris [132–134].
Anecdotal pathological reports indicate the
presence of AFB in the RPE or choroid of the
patients with TB-SLC.The AFB was rst demonstrated from the homogenate of the choroid
from an endo biopsy of a lesion initially diagnosed as a non-responsive viral retinitis but
looked suspiciously like TB-SLC, an entity then
unknown. Following anti-TB therapy, the lesion
was completely healed [135]. In an enucleated
eye, AFB was demonstrated from the necrotic
RPE [136]. In a patient of SLC who showed paradoxical worsening following anti-TB therapy, a
biopsy of the inner choroid revealed a caseous
granuloma, with Langhans giant cells, and PCR
for MTB DNA was positive from the subretinal
uid [137]. Using at least three different types of
molecular techniques (rpo gene sequencing,
GeneXpert and MTBDR plus assay), the MTB
genome was detected from the undiluted vitreous
samples obtained at pars plana vitreous surgery
in patients with multifocal serpiginoid choroiditis
(SLC) including drug-resistant MTB in three
eyes [138].
The TB-SLC needs to be differentiated from
the classic serpiginous choroiditis (CSC) seen in
the TB-non-endemic regions of the world. It is a
rare bilateral organ-specic recurrent autoimmune disorder seen in middle-aged persons that
may show a relentless progression. Some patients
respond to immunosuppressive therapy. The
monofocal lesion typically starts in the peripapillary choroid, involves the overlying RPE and the
outer retina, and shows a nger-like, serpentine,
or jigsaw-like progression. There is no or minimal inammatory reaction in the vitreous cavity.
The advancing tip is greyish-white and hyperautouorescent. The lesions heal with minimal pigmentation but leave a profound atrophy of the
affected retina and choroid. The macula affects
nearly 90% of patients with permanent vision
loss [139].
Choroidal Granuloma
Choroidal granuloma is the most familiar phenotype of TBU to physicians as often these patients
have systemic disseminated TB.The choroidal
granuloma(s) are usually seen in the posterior
pole near the arcades but could be present in the
nasal retina. These are uncommon in the fundus
periphery. Most patients will have a solitary large
yellowish granuloma with or without exudative
retinal detachment (Fig. 10.11). However, they
are usually small if there is more than one granuloma. The most common cause of exudative retinal detachment in TBU is choroidal granuloma
[140]. TB granulomas are usually associated with
other signs of inammation, including cells in the
AC or the vitreous cavity, keratic precipitates,
posterior synechiae, and retinal periphlebitis.
Presenting visual acuity is usually less than 6/60
due to exudative retinal detachment involving the
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macula. One of the most characteristic features of
the TB choroidal granuloma is the presence of
small intraretinal haemorrhage(s) suggestive of
increased vascularization of the granulomas. On
FFA, the highly vascular nature of the TB choroidal granuloma is apparent and shows early hyperuorescence with extensive staining and leakage
of the dye in the late frames. On optical coherence tomography (OCT), the TB choroidal granulomas often show a dome-like elevation of the
RPE and inltration of the outer retina
(Fig.10.11c, d).
TB choroidal granulomas are amenable to
4-drug anti-TB therapy, with nearly 80% of the
eyes responding to the treatment with the restoration of useful vision. Surgical interventions may
be disastrous in such eyes [125]. A new paradigm
of host-directed therapies is emerging in the
treatment of tuberculosis. The TB granulomas
are hypoxic and lead to overexpression of vascu-
lar endothelial growth factor (VEGF), resulting
in increased granuloma vascularization. By
restoring the endothelial barrier, anti-VEGF
agents facilitate exchanges of small molecules,
such as anti-TB drugs, to reach the core of the
granuloma [141–143]. The rst successful application of this strategy in clinical practice was
achieved using anti-VEGF therapy as an adjunct
in tubercular choroidal granulomas that showed
paradoxical worsening on initiation of anti-TB
therapy [144]. The granuloma vasculature may
start exudation months or years later; hence, the
patient needs to be kept under follow-up for any
new symptoms [145]. Very high levels of VEGF
have been found in the aqueous humour in these
patients, and weekly anti-VEGF intravitreal
injections combined with the conventional anti TB therapy, corticosteroids, and intravitreal
moxioxacin led to prompt regression of these
granulomas. Previously, the regressing TB granu-
c
d
Fig. 10.11 (A) Tubercular choroidal granuloma seen as a
solitary large yellowish granuloma in the posterior pole
(a). Three weeks later, following initiation of systemic
steroids and anti-tubercular therapy, the granuloma healed
with scarring (b). OCT shows exudative retinal detachment (c) during active granuloma, and resolution of uid
(d) at 3weeks during healing of granuloma. (B) Right eye
fundus photograph of a 32-year-old man with choroidal
granuloma and retinal vasculitis. The visual acuity was
counting ngers and the QuantiFERON-TB Gold test was
positive. After 9 months of anti-tubercular therapy and
oral corticosteroids, the eye was quiescent with visual
acuity 6/9. (Reproduced with permission from Bansal, R.,
Sharma, A., & Gupta, A. (2012). Intraocular tuberculosis.
Expert Review of Ophthalmology, 7(4), 341–349. https://
doi.org/10.1586/eop.12.42). (C) A case of TB choroidal
granuloma with intraretinal haemorrhage (a). Fluorescein
angiography shows the classical retinal angiomatous proliferation feeding the granuloma. (Images reproduced
with permission of the publishers from Gupta, A., Gupta,
V. (2016). Tuberculosis. In: Zierhut, M., Pavesio, C.,
Ohno, S., Orece, F., Rao, N. (eds) Intraocular
Inammation. Springer, Berlin, Heidelberg. https://doi.
org/10.1007/978- 3- 540- 75387- 2_105)
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10 Retinal andChoroidal Infections andInammation
1a
1b
Fig. 10.11 (continued)
lomas showed a corresponding decrease in the
aqueous humour VEGF levels [146]. Nonresponding TB choroidal granuloma may harbour drug-resistant MTB, which can be detected
using various PCR techniques, including semiautomated GeneXpert quantitative PCR, requiring multidrug-resistant treatment [147–149].
covered ‘thread-like retinal vessels’ on the resolution of vitreous haemorrhage and who had
sudden onset of glaucoma (most likely neovascular glaucoma), the other three had resolution of
vitreous haemorrhage without leaving a trace
(https://wellcomecollection.org/works/
haupyuh9). Since then, idiopathic vitreous haem-
orrhage in young people has been labelled as
Retinal Periphlebitis
Henry Eales (1880) reported in Birmingham
medical review four cases of recurrent vitreous
haemorrhage and epistaxis in young, otherwise
normal men who were habitually constipated. He
noted dilated retinal veins and arteries in these
patients. Except for one patient in whom he dis-
Eales’ disease. Except for his case # 1, none of
the other patients he observed had any apparent
cause of vitreous haemorrhage. A review of his
description of the cases reveals that, except for
case #1, none of them possibly resulted from retinal periphlebitis. Others likely represented examples of Valsalva retinopathy. For over 140years,
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