Presentations describing Occular manifestations in HIV AIDS. Important topic in Ophthalmology

1. OCULAR
MANIFESTATIONS OF HIV
Dr Prabhjot Singh
Armed Forces Medical College, Pune

2. REFERENCES
✓Uveitis- Robert B. Nussenblatt
✓Ryan’s Retina
✓Ophthalmology- Myron Yanoff and Jay S. Duker
✓Kanski’s Clinical Ophthalmology
✓Namrata Sharma- Corneal ulcers, Diagnosis and Management
✓Parsons’ Diseases of the Eye
✓AAO
✓Jakobiecs Principles and Practice of Ophthalmology

3. QUESTIONS ASKED PREVIOUSLY IN MUHS EXAM
✓ Ocular Manifestations Of AIDS/ARN- (LAQ)
✓ Ocular manifestations of AIDS. Summer 2009,2010,2012,2016,2017, Winter 2016
✓ Ocular manifestations of various STDs. Summer 2014,2015, Winter 2013,2015
✓ Toxoplasma retinochoroiditis. Summer 2016
✓ Etiology, C/f and Rx of Ocular toxoplasmosis
✓ CMV retinitis. Summer 2018
✓ Herpes Zoster Ophthalmicus
✓ Ocular manifestations of AIDS and impact of HAART
✓ Ocular manifestations of AIDS and Acute Retinal Necrosis

4. ✓Ocular manifestations of HIV infection occur in every tissue of the eye, from the
eyelids to the optic nerve
✓The most common findings include dry eye, a retinal microvasculopathy, and CMV
retinitis.

5. INTRODUCTION
✓ (HIV/AIDS) is a ds immune system caused by infection with human
immunodeficiency virus
✓ leads to gradual decrease in CD4+ T lymphocytes causing subsequent opportunistic
infections and neoplasia
✓ 70-75% of patients infected with HIV will develop some form of ocular involvement

7. OCULAR MANIFESTATIONS OF HIV/AIDS
✓ Direct infection by HIV
✓ Opportunistic infections
✓ Neoplasia and
✓ Drug related

8. OCULAR MANIFESTATIONS OF HIV ACCORDING TO SITE
A) ADNEXAL MANIFESTATIONS
B) ANTERIOR SEGMENT MANIFESTATION
C) POSTERIOR SEGMENT MANIFESTATIONS
D) NEURO-OPHTHALMIC MANIFESTATIONS
E) ORBITAL MANIFESTATIONS

9. A) EYELID AND ADNEXAL MANIFESTATIONS
1. Preseptal Cellulitis
2. Bacillary angiomatosis
3. Herpes zoster ophthalmicus
4. Molluscum contagiosum
5. Kaposi’s sarcoma
6. Herpes simplex virus cutaneous vesicles
7. Kaposi’s sarcoma
8. Stevens–Johnson syndrome

10. PRESEPTAL CELLULITIS
Pathogenesis:
infection of subcutaneous tissue anterior to the orbital septum.
Causes:
skin trauma (S. aureus, S. pyogenes), spread from local or
remote infection (e.g. stye, dacryocystitis, sinusitis).
Diagnosis:
Presentation: unilateral tender, red and swollen lid
Signs: proptosis and chemosis are absent. Optic nerve function
and ocular motility are unimpaired.
CT: opacification anterior to the orbital septum

11. HERPES ZOSTER OPHTHALMICUS
➢ 5-15% of HIV patients.
➢ Reactivation of a latent infection by VZV in
the dorsal root of trigeminal nerve .
Presentation:-
➢ 3- to 5-day prodromal phase of tiredness,
fever, malaise and headache precedes the
appearance of the rash.
➢ Pain in the affected dermatome.

12. Signs:
✓erythematous maculopapular rash on the
forehead respecting the midline
✓appearance of groups of vesicles within
24hours
✓confluent vesicles
✓periorbital oedema
✓Hutchinson’s sign refers to the rash of HZO
affecting the skin on the tip and side of the
nose and correlates strongly with involvement
of the eye.
✓Dendritic and stromal keratitis, conjunctivitis,
blepharitis, uveitis , hemorrhagic hypopyon,
scleritis, retinitis, and encephalitis.

13. Stromal Keratitis Sectoral Iris Atrophy

14. MANAGEMENT
○ Intravenous acyclovir 10 mg/kg 3 times per day for 7 days in severe cases
○ Oral acyclovir 800mg 5t/d for 7-10 days ideally commenced within 72hours of
onset
○ This treatment reduces the frequency of recurrences.

15. MOLLUSCUM CONTAGIOSUM
• 20% of HIV patients
• by DNA poxvirus
• Signs- pale, waxy, umbilicated nodules with
cheesy material
• ipsilateral chronic follicular conjunctivitis
• Spontaneous resolution in the immunocompetent
• Rx- Lid margin lesions with secondary
conjunctivitis may be treated with: (a) shave
excision, (b) cauterization, (c) cryotherapy, (d)
curettage, or (e) laser.

16. KAPOSI SARCOMA
• slowly growing vascular tumour
• almost exclusively in AIDS.
• flat bright-red lesion that may mimic a
subconjunctival haemorrhage.
• Complications include trichiasis and entropion
formation.
• Rx-
Radiation therapy ,
Intralesional chemotherapy with Vinblastine, a
interferon, and liposomal Daunorubicin. ,
Surgical excision of the tumor.

17. STEVENS–JOHNSON SYNDROME -TEN
✓Cell-mediated hypersensitivity immune reaction
✓Presentation: flu-like symptoms for up to 14 days.
✓Acute signs:
haemorrhagic crusting of
the lid margins
papillary conjunctivitis
punctate corneal epithelial
erosions progressing to
larger epithelial defects
excoriated skin on hand

18. Treatment
✓Topical
(a) lubricating drops
(b) steroids
(c) topical cyclosporin 0.5%
✓Systemic steroids
✓Bandage and scleral lenses
✓PROSE :
Prosthetic replacement of the ocular surface
ecosystem
constant lubrication provided by a reservoir of
sterile saline incorporated in a highly gas-
permeable plastic prosthesis.

19. CONJUNCTIVAL / SCLERAL MANIFESTATIONS
✓Dry eye
✓Kaposi’s sarcoma
✓Microvasculopathy
✓Microsporidial conjunctivitis
✓Herpesvirus conjunctivitis
✓Scleritis

20. CONJUNCTIVAL MICROVASCULOPATHY
Conjunctival microvasculopathy, seen in about 75% of patients, is characterized by
telangiectasia, segmental dilatation, comma- shaped fragments and sludging in the
smaller blood vessels.

21. CORNEA
✓Ulcerative keratitis
✓Dry eye
✓Herpes simplex keratitis
✓Herpes zoster ophthalmicus
✓Microsporidiosis
✓Syphilitic keratitis
✓Tuberculosis
✓Gonorrhea

22. ANTERIOR SEGMENT MANIFESTATIONS
✓More than 50% of HIV-positive patients
✓Common symptoms include irritation, pain, photophobia, redness and decreased
vision
✓ 1)Keratoconjunctivitis sicca
✓ 2)Keratitis
✓ 3)Iridocyclitis

23. KERATOCONJUNCTIVITIS SICCA
✓ 10-20% of patients who are HIV positive.
✓ The etiology is related to HIV-mediated
inflammation and damage of the accessory and
major lacrimal glands.
✓ Patients complain of burning uncomfortable red
eyes
✓ Artificial tears and lubricating ointment.

24. UVEA
✓ Anterior uveitis (may be secondary to systemic drug toxicity with rifabutin or
cidofovir).
✓ Immune recovery uveitis
✓ CMV uveitis

25. IRIDOCYCLITIS
✓ The etiology of iridocyclitis in HIV-positive patients
includes sequelae of retinitis, retinochoroiditis, and drug
toxicity ( rifabutin, cidofovir), secondary to direct toxic effect
upon the non-pigmented epithelium of the ciliary body.
✓Mild iridocyclitis associated with viral retinitis due to
CMV,HSV, VZV.
✓Severe, seen in association with ocular toxoplasmosis,
tuberculosis, syphilis, or bacterial or fungal retinitis.

26. POSTERIOR SEGMENT MANIFESTATIONS
• HIV retinopathy- Microvasculopathy
(cotton-wool spots, retinal hemorrhages)
• HIV-related retinochoroiditis
1. CMV retinitis
2. Acute retinal necrosis
3. Progressive outer retinal necrosis
4. Syphilis
5. Toxoplasmosis
6. Pneumocystis choroidopathy
7. Choroidal cryptococcosis
8. Choroidal pneumocystosis
9. Candidiasis
10.Histoplasmosis
11.Mycobacterial infection

27. HIV RETINOPATHY
✓ 50-70% of HIV-infected patients
✓Arteriolar occlusion l/t interruption of the axoplasmic flow and the subsequent
accumulations of axoplasmic debris, which manifests as cotton-wool spots.
✓Increased plasma viscosity, immune-complex deposition, and a direct cytopathic
effect of the virus on the retinal vascular endothelium are believed to be involved.

28. ✓asymptomatic and transient, but it may contribute to the optic nerve atrophy
seen in many of the patients. Common findings may include the following:
Cotton-wool spots
Intraretinal hemorrhages
Roth spots (white-centered hemorrhages)
Retinal microaneurysms
✓ No treatment is indicated for HIV retinopathy.
✓ These patients require observation only

29. HIV-RELATED RETINOCHOROIDITIS
✓Viral - CMV , VZV and less commonly HSV .
✓Bacterial - Mycobacterium tuberculosis and Treponema pallidum .
✓Parasitic- Toxoplasma gondii and Pneumocystis jiroveci
✓Fungal- Candida, Cryptococcus neoformans, and Histoplasma capsulatum,
as well as, Sporothrix, and Aspergillus species.

30. CYTOMEGALOVIRUS RETINITIS
✓ Neurotropic virus with tendency to infect neural tissues and retina.
✓ Seen in 15-40% patients of AIDS . rate declining with arrival of HAART.
✓ more frequent after renal transplantation than after bone marrow transplantation
✓ Usually in CD4<50/microlitre

31. CLINICAL PRESENTATION
• Asymptomatic or give rise to a wide range of visual
symptoms
• Depending on its anatomic location and
complicating factors
small peripheral lesions -asymptomatic
posterior lesions involving macula/ optic
nerve or a/c vitirits can gradually
reduce visual acuity, cause floaters,
photophobia, or visual feld defects
Wide-angle fundus photography and FFA may be of
benefit if the diagnosis is uncertain.

32. ✓ AC and vitreous reaction- minimal
✓ Cataract is later-stage fnding
✓ some vitritis is virtually always present
✓ significant vitritis can occur
in patient with relatively high CD4 counts
or if the patient is immune competent or
if the area of retinitis is large.
In immunocompetent individual

33. ✓ CMV uveitis
- presents with small granulomatous
kp’s in a linear distribution
- Endothelial ‘coin lesions’ are
typical
- Iris atrophy and flattening
- Corneal edema
✓ Corneal endotheliitis
may occur manifests with areas of
progressive sectoral stromal and/or
bullous edema which may be
reversible with antiviral treatment

34. FUNDUS EXAMINATION
✓ reveals necrotizing retinitis
✓ early stages- lesion is as small as a cotton-wool
spot ( unlike cotton-wool spot it will enlarge in size
and can occur in any retinal area)
✓ The disease progresses along the retinal blood
vessels, causing confluent areas of retinal
whitening, associated with intraretinal
hemorrhages and hard exudates
✓ The lesions progress in a ‘brushfire’ manner, led
by
- an active border - typically advances by
250–350 µm/wk
- satellite lesions

35. Morphological variants of CMVR
1. Granular morphology - present without
much retinal whitening or haemorrhage
2. frosted branch angiitis- diffuse vascular
venous sheathing resembling frosted
branches of tree
frosted branch angiitis also found in
- toxoplasmosis
- post-viral retinal vasculitis
- steroid-responsive retinal vasculitis.

36. Spectrum of fundus appearance
1. Indolent form
- faint granular opacification or brush fire -
location -not overlying vessel
- less aggressive
- no or minimal retinal hemorrhagen or
inflammatory vascular sheathing

37. Spectrum of fundus appearance
1. Fulminant form
• dense confluent area of retinal
opacification
• location along vesseles
• retinal hemorrhage
• Inflammatory perivascular sheathing
2. Frosted branch angiitis form
• usually neglected case
• indicate insufficient control of disease
• seen in patients who lost to follow up after
treatment

38. When retinal inflammation subsides,
it leaves an atrophic-appearing retina,
sometimes with associated
pigmentation
Fluffy retinal infiltrates and necrosis
are associated with scattered
hemorrhages, this creates what has
been called the "scrambled eggs and
ketchup“or ‘pizza pie appearance of
severe CMVR

39. The area of retinal involvement in CMVR has been divided into 3 concentric
zones
Zone 1- the posterior pole, defined as the area within 3000 µm of the foveal
center or 1500 µm around the optic nerve head.
Zone 1 disease threatens the macula, PMB, or optic nerve. So it is immediately
vision threatening
Zone 2- extends from the borders of
zone 1 to the ampullae of the vortex veins
Zone 3- the retina peripheral to zone 2

40. PROGRESSION
✓New lesions physically away from old lesion may be formed by hematogenous
spread.
✓An old lesion spreads at its borders to involve new, previously uninfected retina.
✓Once retinal cell death occurrs & only glial scar remains, the atrophic retina is again
transparent with underlying RPE stippling.
✓It is most important to pay attention to the edge of the lesions to look for
advancement.

41. ✓ Patients with CMV retinitis may not complain of symptoms because the lesions
begin in the periphery, or because the patient often does not notice an increase in
floaters or a new scotoma.
✓ Therefore, it may make clinical sense to screen patients who are at risk with CD4+
counts <50–100 cells/µL.
✓ A reasonable screening frequency is every 3 or 4 months for this population

42. IMMUNE RECOVERY UVEITIS
rejuvenated immune response against residual viral antigen following HAART
✓This is a cause of limited visual outcome in CMV retinitis
✓Manifestations include
• vitritis
• cystoid macular edema
• epiretinal membranes
• variable anterior uveitis
• severe enough progressing to phthisis in
some cases.

43. THE AIDS CLINICAL TRIAL GROUP DEFINED
IRU
decrease in vision accompanied by at least 2 of the following signs in the
absence of active CMV retinitis:
✓presence of >2+ inflammatory cells in the vitreous
✓cystoid macular edema (CME)
✓or epiretinal membrane (ERM) formation in patients receiving antiretroviral
therapy with evidence of immune reconstitution
Immune reconstitution, in turn, was defined as a CD4+ count of 100 cells/μL
or more.

44. REACTIVATION OF CMV RETINITIS
✓ characterized by reopacification of the border of the lesion followed by advancement.
✓ Smoldering cytomegalovirus (CMV) retinitis is a low grade of retinitis border activity
that is associated with slow progression of retinitis. It may be difficult to diagnose
without fundus photographs.
✓wide-angle fundus photographs are a more sensitive indicator of retinitis progression
than clinical examination by indirect ophthalmoscopy

45. DIAGNOSIS
✓usually made clinically
✓In atypically clinical presentation, the diagnosis should be confirmed by laboratory
tests.
✓Serological evidence of past infection with CMV (igG) is common in AIDS patients
and thus has limited diagnostic value
✓Blood viral cultures- positive in 45%
✓urine viral cultures - 71% of new CMVR cases
✓Vitreous PCR - 95% sensitive and highly specific in untreated cases of CMVR
✓Chorioretinal biopsy can be examined histopathologically in difficult cases

46. TREATMENT
✓ Oral Valganciclovir.
✓ Oral ,Intravenous, and Intravitreal ganciclovir.
✓ Intravenous and Intravitreal Foscarnet or combined intravenous Ganciclovir and
Foscarnet
✓ Intravenous Cidofovir
All Inhibit CMV DNA polymerase.

47. CYTOMEGALOVIRUS RETINITIS
✓Valganciclovir is the drug of choice for the treatment of CMV retinitis.
Induction is 900 mg BD
then 900 mg OD for maintenance.
✓ For Ganciclovir
start induction with 5 mg/kg IV every 12 hours for 14 days,
then change to a maintenance IV dose of 5 mg/kg/day for 7 days.
✓ Both l/t myelosuppression

48. CYTOMEGALOVIRUS RETINITIS
Foscarnet
✓ Induction with 60 mg/kg IV every 8 hours for 14 days.
✓ Maintenance IV dose of 90-120 mg/kg/day.
✓ Hydration with 1000 mL of isotonic sodium chloride solution is recommended
because of renal toxicity associated with foscarnet

49. CYTOMEGALOVIRUS RETINITIS
Cidofovir
✓ Induction dose - 5 mg/kg IV over 1 hour once weekly for 2 weeks.
✓ Maintenance dose - 5 mg/kg over 1 hour once every other week.
✓ Renal toxicity, Iritis and Ocular hypotony.

50. TREATMENT

51. Intra-ocular Therapy of Viral Retinitis :
• Ganciclovir : 2mg/0.05mL biweekly injections
• Foscarnet : 2.4mg/0.05mL biweekly injections
• Cidofovir : 20 µg 6 weekly injections

52. INTRAVITREAL GANCICLOVIR IMPLANT
✓Sustained release Intravitreal implant.
✓1microgram/hour for 8 months.
✓Surgically implanted through pars plana.
✓Doesn’t treat systemic disease or contralateral eye

53. `
✓ ARN
✓ CMV retinitis
✓ Progressive outer retinal necrosis .
53

54. ACUTE RETINAL NECROSIS
✓ devastating fulminant retinal vaso-occlusive necrotizing retinitis
✓ characterized by the acute onset of a fulminant panuveitis
✓ with confluent, well-demarcated areas of retinitis,
✓ plus prominent anterior uveitis, occlusive retinal and choroidal vasculitis, vitritis,
and papillitis.
Etiology
✓ months or years after primary infection
✓ or following cutaneous or systemic herpetic infection
✓ history of recurrent cutaneous herpetic outbreaks.
✓ VZV , HSV , CMV, EBV

55. ACUTE RETINAL NECROSIS
Pathology
✓ Direct lytic viral infection of retina
✓ Immune complex disease, T-cell mediated inflammation
✓ Full-thickness retinal necrosis
✓ Choroiditis (granulomatous)
✓ Combined TRD and RRD
✓ Optic nerve: Infiltrated with plasma cells or infarcted
✓ Vitreous cavity: Sloughed retinal cells with macrophages and PMNs
Electron microscopy: Viral particles in all layers of retina and RPE

56. ACUTE RETINAL NECROSIS
✓ Patient population -
- Otherwise healthy
- Either sex
- Bimodal age group – 20 years and 50 years
- More likely in subclinical immune dysfunction
✓ HLA Haplotypes
HLA-DQw7
HLA-DR4 in US population
HLA-Aw33, B44, DRw6 in Japanese

57. C/F:-
Initial presentation
✓ acute unilateral loss of vision, photophobia, floaters, and pain.
✓ Periorbital pain, Scleritis, episcleritis
✓ Fellow eye involves 36% pts within 6 wks of disease onset
✓ but sometimes months or years later.
then pt develops - Panuveitis
✓beginning with granumatous anterior uveitis
✓posterior synechiae
✓elevated IOP
✓Vitiritis
Within 2 weeks
classic
triad
occlusive retinal arteriolitis
vitritis multifocal yellow- white
peripheral retintis

58. Early - peripheral retinal
lesions.
Within days- confluent 360°
creamy retinitis
Acute retinal necrosis
with dense white retinal
infiltrate in retinal
periphery.
Confluent peripheral
retinitis.

59. ✓ progresses in posterior direction,
leaving full-thickness retinal necrosis,
arteriolitis, phlebitis, and occasional
retinal hemorrhage
✓ Widespread necrosis of the
peripheral and midzonal retina,
multiple posterior retinal breaks, and
proliferative vitreoretinopathy
✓ l/t combined tractional RD in 75% of
patients
✓ Optic nerve swelling and a RAPD
may develop
RD with
multiple,
posterior
retinal
breaks
vitritis,
multifocal and
confluent areas
of retinitis,
retinal
vasculitis,
retinal h.age,
ONH edema,
and RD

60. AMERICAN UVEITIS SOCIETY CRITERIA
FOR DX OF ARN
✓ Solely dependent on
clinical findings
✓ Independent of etiologic
agent/immune status of
patient

61. APPROACH FOR DIAGNOSIS
✓Clinical picture pathognomonic in many cases
✓ Atypical/difficult diagnostic cases may need tests to support the diagnosis
✓ Immunocompetence
✓ Check for Syphilis
✓ Diagnostic Vitrectomy: may be justified for uncertain diagnosis
✓ PCR: Most sensitive and specific for Herpes detection
✓ PCR in multiplex for VZV, HSV, CMV and Toxoplasmosis
✓ Endoretinal biopsy: - High clinical suspicion, negative PCR, Taken from transition zone,
Acute stages Better yield
✓ Witmer Quotient: diagnostic value, even in early stages of ARN syndrome

62. DIFFERENTIAL DIAGNOSIS
✓ PORN
✓ CMV Retinopathy
✓ Syphilitic Retinitis
✓ Toxoplasmosis
✓ Large cell lymphoma
✓ Acute multifocal hemorrhagic retinal vasculitis

63. Atypical
Toxoplasmosis
CMV ARN
Immunocompromised
hosts – mimics ARN
Only in
immunosuppressed
Immune competent or
compromised both
intense vitritis severe vitritis
More hemorrhages
fulminant presentation more rapid course
Periphery is less involved mainly post pole involved initialy- perephery

64. TREATMENT OF ARN
I/v Aciclovir (10mg/kg) 8 hourly
After 24–48 hr
if significant inflammation - systemic corticosteroids (prednisone 1 mg/kg/day)
Anticoagulants for hyper-coagulable state
Following I/v Aciclovir-
treat with T. acyclovir 800 mg 5t/d or
T Valacyclovir 1 g orally TDS, or
T Famciclovir 500 mg TDS for 3 months.

65. TREATMENT OF ARN
Extended antiviral therapy - reduce c/l ds or b/l ARN by 80% over 1 year.
Oral valacyclovir - 2 g TDS is an alternative to I/v acyclovir as induction
therapy.
Intravitreal Ganciclovir (2.0 mg/0.1 mL) and Foscarnet (1.2–2.4 mg/0.1 mL) -
achieve a rapid induction in combination with both I/v and oral antivirals
vitrectomy / laser photocoagulation to prevent retinal detachment

66. PROGNOSIS
✓Untreated – Poor prognosis –
RD in 75% cases
Optic nerve dysfunction
Macular involvement
✓ Involvement of second eye:
Untreated – 36% of patients
Appropriate Antiviral treatment – 3% of p

67. PROGRESSIVE OUTER RETINAL NECROSIS
(VZV RETINITIS)
✓ morphologic variant of ARN
✓ profoundly immunosuppressed
✓ in advanced AIDS (CD4+ ≤50 cells/µL).
✓ caused by VZV
✓ In contrast to ARN,
the posterior pole may be involved early significant vitritis typically absent

68. PROGRESSIVE OUTER RETINAL NECROSIS
(VZV RETINITIS)
✓ retinal vasculature is minimally involved
✓ The visual prognosis is poor
✓ often resistant to treatment with intravenous acyclovir alone,
✓ successful management has been reported with combination systemic and
intraocular therapy using foscarnet and ganciclovir

69. PORN
Perivascular clearing of retinal opacification -Mud-crack appearance

70. multifocal areas of white retinitis in
PORN
5 days later, showing rapid
progression and confluence of the
areas of the viral retinitis

71. PORN
Initial
presenta
tion
Day 3
Day 6

72. PORN ARN
Multifocal lesions
deep retinal opacification
without distinct granular borders
one or more foci
full thickness retinal necrosis
discrete borders
extremely rapid progression
no consistent direction of disease spread
Rapid progression
circumferential spread
no vascular inflammation Oclusive vasculopathy
Perivascular
clearing of
opacification
Prominant
Vitirtis

74. TUBERCULOSIS
✓ The most common ocular manifestation is
anterior uveitis and disseminated
choroiditis.
✓ Manifests as areas of necrosis
surrounded by mononuclear and giant
cells.
✓ Unifocal or multifocal yellowish, grayish,
or whitish choroiditis, mostly in the
posterior pole.

75. TOXOPLASMA RETINOCHOROIDITIS
✓ focal necrotizing retinitis, with white infiltration and surrounding retinal
edema..
✓ Clinical manifestations- Ocular and Systemic

76. Symptoms
✓ Unilateral acute or subacute onset of floaters
✓ Blurring and photophobia.
✓ ‘Spill-over’ anterior uveitis is common- it
may be granulomatous or resemble Fuchs
uveitis syndrome
✓ Satellite lesion- A single inflammatory focus
of fluffy white retinitis or retinochoroiditis
associated with a pigmented scar is typical.
✓ involve the posterior pole Typical ‘satellite’ lesion adjacent
to an old scar

77. • De novo foci not associated with an old
scar
• Vitritis impairs fundus visualization.
• ‘Headlight in the fog’ - classic description
of a white retinal inflammatory nidus
viewed through vitritis
• Retinal vessels in the vicinity of an active
lesion may show perivasculitis with diffuse
venous sheathing and segmental arterial
plaques ( )

78. ✓ Optic disc oedema is common
✓ Causes of permanently reduced vision (around 25% of eyes) include
• macular inflammatory lesions and oedema,
• optic nerve involvement,
• vascular occlusion
• serous, RRD, TRD
• late secondary choroidal neovascularization
✓ On an average, the inflammation lasts for ~4 months.
✓ About one-third of the patients have recurrent attacks.

79. ✓ Punctate outer retinal toxoplasmosis is an atypical manifestation featuring
clusters of small (25–75 µm diameter) grey–white lesions.

81. ✓Atypical presentations of ocular toxoplasmosis
• neuroretinitis,
• papillitis, and
• intraocular inflammation
without retinochoroiditis
✓ Healing
• in immunocompetent - within 6–8 weeks
• vitreous opacities take longer to clear.
• The inflammatory focus is replaced by a sharply demarcated atrophic scar that develops
a pigmented border
✓Recurrence:
• average number of recurrent attacks per patient is 2.7;
• within five years more than half of patients may experience a further episode

82. COMPLICATIONS OF TOXOPLASMOSIS
RETINOCHOROIDITIS
✓ Posterior synechiae
✓ Macular edema,
✓ Dragging of the macula secondary to a peripheral lesion,
✓ RD
✓ Chorioretinal vascular anastomosis
✓ Choroidal neovascularization
✓ BRAO, BRVO
✓ OA
✓ Cataract, and Glaucoma
✓ Unilateral pigmentary retinopathy simulating retinitis pigmentosa (as a late sequela of
recurrent ocular toxoplasmosis )

83. Macular involvement Juxta papillary lesion involving ONH

84. Periarteritis
resulting in BRAO
FA shows extensive non-
perfusion at the
posterior pole

85. serous macular detachment FA shows hyperfluorescence
d/t pooling of dye

86. Choroidal neovascularization
adjacent to an old scar
FA shows corresponding
hyperfluorescence

87. INVESTIGATIONS
✓Clinical examination findings
✓Serology
• IgG abs
• IgM abs- in newborns -congenital infection.
in adults- acquired ds
• IgA abs - congenital toxoplasmosis
✓Ocular fluid antibody assessment- Goldmann–Witmer coefficient >3
• Ratio of specific IgG in aqueous humour to that in serum
• Intraocular production of specific anti-Toxoplasma antibodies
• PCR testing of intraocular fluid

88. IMAGING
✓ Macular OCT- macular oedema
✓ B-scan ultrasonic - RD in the presence of
severe vitritis.
✓ FAF may facilitate monitoring of inflammatory
activity
✓ CT brain is done immunocompromised pt-
concomitant CNS involvement
Wide-field autofluorescence image of the eye with
toxoplasmosis

89. TREATMENT
✓ Can’t be eradicated
✓ Parasite activity and multiplication may be reduced, with a decrease in size of the
eventual retinochoroidal scar.
✓ Spontaneous resolution generally occurs, treatment is not administered in every
case.
Clear indications-
✓ sight-threatening lesion involving the macula, PMB, ONH or a major blood vessel
✓ severe vitritis
✓ immunocompromised.

90. ✓ Prednisolone (1 mg/kg)
✓ Pyrimethamine
• LD 75–100 mg for 1–2 days
• MD 25–50 mg OD for 4 weeks
✓ Sulfadiazine
• 1 g QID for 3–4 weeks is usually given in combination with pyrimethamine.
✓ Intravitreal therapy with clindamycin (1 mg) & dexamethasone (400 µg)
• in reactivated infection. 2 to 3 injections (2-weekly intervals)
✓ Azithromycin, Co-trimoxazole, Clindamycin, Atovaquone
✓ Topical steroid and mydriatic may be given for anterior uveitis.

91. For active retinochoroiditis
within 2-3 mm of the disc or fovea
which threatens vision
or peripheral lesion associated with severe vitritis
start first-line therapy for 3-6 weeks, as follows:-
(1) pyrimethamine 75 mg PO load, 25 mg PO twice daily, plus,
(2) folinic acid 3-5 mg PO twice weekly (to reduce the adverse effect of bone
marrow toxicity of pyrimethamine), and
(3) sulfadiazine 2 g PO load, then 1 g PO 4 times daily.

92. PNEUMOCYSTIS JIROVECII CHOROIDITIS
✓Choroidal infiltrates that contain the microorganisms.
✓elevated, plaquelike, yellow white lesions
located in the choroid, with minimal vitritis
✓FFA- Hypofluorescent early phase
and Hyperfluorescent later phases.
✓Treatment - 3- week regimen of i/v trimethoprim (20 mg/kg/day) + sulfamethoxazole
(100 mg/kg/day) or pentamidine (4 mg/kg/day).

93. Vitreous
opacity
Present Absent
Peripheral
retinal
Infiltrate
Central
Retinal
Infilterate
Exuda
tive
RD
Central
Retinal
Infilterate
Peripheral
retinal
Infiltrate
ARN Behcet Ds VKH CMVR
Toxopla
smosis
Toxoplas
mosis PORN
Toxoplas
mosis
SO

94. NEURO-OPHTHALMOLOGIC MANIFESTATIONS
✓ 10-15% of patients who are infected with HIV
✓Causes
• Meningitis,
• Meningeal and Parenchymal Lymphoma,
• Neurosyphilis, and
• Toxoplasmosis
• Papilledema
• Optic neuritis
• Cranial nerve palsies
• Ocular motility disorders
• Visual field defects

95. ORBITAL MANIFESTATIONS
✓ Orbital lymphoma,
✓ Orbital cellulitis due to Aspergillus infection
✓ Orbital Kaposi's sarcoma

96. OCULAR MANIFESTATION OF HIV INFECTION IN
CHILDREN
✓ Fewer ocular manifestations
✓ low incidence of CMV retinitis.
✓ reason -altered immune response to HIV or
✓ lower prevalence of CMV seropositivity in children.
✓ HIV-infected children are at increased risk for neurodevelopmental delay

97. OCULAR TOXICITY OF ANTIRETROVIRAL DRUGS
Rifabutin
intraocular inflammation uveitis- 33%
Cidofovir
uveitis and intraocular hypotony - 25- 30%
Gancyclovir & Acyclovir
corneal epithelial inclusion termed corneal lipidosis.
Atovaquone
long-term can corneal subepithelial deposits.
Rifabutin toxicity

98. OCULAR TOXICITY OF ANTIRETROVIRAL DRUGS
Didanosine-
RPE mottling and hypertrophy
overall decreased retinal function
.

99. TIPS IN THE MANAGEMENT OF A PATIENT WITH
SUSPECTED OCULAR HIV
Do’s (when to suspect and test for HIV)
Younger patients (<45 years) with HZO or typical ocular manifestations
Corneal perforation in a patient with HZO infection
Molluscum lesions in a young adult
Atypical presentations of ocular disease
Overlook patient’s CD4+ counts and HIV treatment regime

100. Don’t’s (pertaining to careful systemic and treatment history)
Dont Overlook early HIV microangiopathy
Dont treat IRU with aggressive steroid therapy without monitoring for signs of
CMV retinopathy (CMVR) reactivation
Consider all CMVR to be HIV-related.
Rule out other causes of immunosuppression, organ transplantation, diabetes
mellitus, local steroid therapy (intra/ periocular)

101. THANK YOU