2. Introduction
Virus is a small infectious agent , unicellular , that replicates only
inside the living cells of other organisms
The free independent particle form is known virion.
It consist of three parts: a) Genetic material i.e. DNA or RNA b)
protein coat called capsid c) lipid envelope
Classification
- dsDNA viruses: Adenoviruses , Herpesviruses, Poxvirus
- ssDNA viruses: Parvoviruses
- dsRNA viruses: Reoviruses
- ssRNA viruses(+): Picornaviruses , Togaviruses
- ssRNA viruses(-): Orthomyxoviruses , Rhabdoviruses
- ssRNA RT viruses: Retroviruses(HIV)
- dsDNA RT viruses:Hepadenaviruses
4. Moluscum contagiosm
- Skin infection caused by human specific
ds-DNA pox virus
- typically affects otherwise healthy
individuals
- Peak incidence between 2 to 4 yrs of age
- transmitted by contact or subsequently
by auto-innoculation
5. - Histopathology shows central pit &
lobulated hyperplastic lobulated
epidermis with intracytoplasmic inclusion
bodies- HENDERSON PETTERSON
BODIES that displaces nucleus to the
edge of the cell
- Bodies are small & eosinophilic near
surface & large & basophilic deep down.
6. Diagnosis:
- Clinically single or multiple pale waxy
umbelicated nodules develops with white
cheesy material consisting of infected
degenerated cells.
- Lesions on lid margins may shed virus
into the tear film giving rise to secondary
ipsilateral chronic follicular conjunctivitis.
7. Treatment
- Spontaneous resolution will usually
occurs in few months , so treatment may
not be necessary particularly in children.
- Can be treated by shave excision
cauterisation , chemical ablation ,
cryotherapy & pulse dye therapy.
8. Adenovirus
Adenovirus (non enveloped ds DNA )being
most frequent 90%
May be sporadic or occurs in epidemics in
environments such as workplaces,
hospitals , schools.
Highly contagious infection is facilitated by
ability of the virus to survive on the dry
surface for weeks and by the fact that viral
shedding may occur for days before the
symptoms appear.
Transmits by contact with respiratory or
ocular secretions via fomites.
9. Clinical features:
- Varies from mild subclinical to severe
inflammation
- h/o contact with acute conjunctivitis is
present.
* Non specific acute follicular conjunctivitis.
- mc clinical form of viral conjunctivitis.
- Patient presents with watering , redness,
irritation & mild photophobia.
-Contralateral eye affected 1-2 days later.
-systemic features like common cold , sore
throat may be present.
10. * Pharyngo conjunctival fever.
- Caused mainly by adenovirus serovars 3
,4 & 7
- Spreads by droplets within families with
URTI
- Keratitis develops in about 30% cases
- Photophobia is a prominent feature.
* Epidemic keratoconjunctivitis
- Caused mainly by adenovirus serovar 8 , 19 &
37
- Most severe adenovirus infection.
- Keratitis which may be marked may develops in
11. * Acute hemorrhagic conjunctivitis.
- Occurs in tropical areas.
- Caused by enterovirus & coxackievirus.
- Has rapid onset & resolves within 2-3 weeks
- Conjunctival haemorrhage is marked.
*Chronic relapsing adenoviral conjunctivitis
- Chonic non specific conjunctival follicles or
papillae persists over uyears.
- It is rare & eventually self limiting
12.
13. Signs:
- Lid edema
- Lymphadenopathy – tender preauricular
- Conjunctival hyperaemia with upper tarsal
conjunctival follicles & papillae some times.
- In severe inflammation there occurs
Haemorrhage , chemosis , membrane or
pseudomembrane formation & scarring.
- Adenoviral Keratitis shows epithelial microcysts
common in early stage .
- PEK ocuring with in 7 to 10 days & resolving
over 2 wks.
- Focal subepithelial or stromal infiltrates
- Anterior uveitis some times present.
14. Investigations:
- Usually not necessary but considered when diagnosis is
in doubt or failure to resolve.
* Gimsa stain
- Shows predominantly mononuclear cells in adenovirus
infection & multinuclear giant cells in herpatic infection
* Nucleic acid amplification
- PCR is sensitive & specific for viral DNA.
* Viral culture
- 100 % specific but is expensive , slow & requires
specific transport medium.
* Serology
- detection of IgG & IgM.
15. Treatment
- Spontaneous resolution of adenovirus infection occurs in
2-3 weeks so no specific treatment is required.
- Reduction of transmission risk:
-by meticulous hand hygiene , avoiding eye rubbing ,
towel sharing . Adequate disinfection of instruments &
clinical surfaces after examining patients with povidone
iodine.
Which is highly effective against adenovirus.
- Topical steroids
-prednisolone eye drops 0.5% may be required in
membranous or pseudomembranous conjunctivitis
& in keratitis . These should be used cautiously because
it may enhance viral replication & period of infectivity.
16. - Symptomatic treatment
- Discontinuation of contact lenses if using
- Artificial tears mostly preservative free , gives
symptomatic relief . Its better if supplied in
single dose unit which may reduce transmission
risk.
- Warm compresses
- Topical NSAIDs in steroid weaning period
- Removal of symptomatic membrane or
pseudomembrane.
- topical antibiotics cover to prevent secondary
bacterial infection.
17. Herpes simplex virus
Herpetic eye disease is the most common
infectious cause of corneal blindness in
developed countries
60% of corneal ulcers in developing countries
DS -DNA virus with ecosahedral capsid
surrounded by envelope of carbohydrates , lipids
& glycoproteins.
Herpes simplex virus (HSV)
◦ Two subtypes are HSV-1 and HSV-2
HSV-1 causes infection above the waist (principally the face,
lips and eyes)
HSV-2 causes acquired infection (genital herpes). Rarely
HSV-2 transmitted to the eye
◦ HSV transmission is facilitated in conditions of
18. Immune defence mechanism for
HSV.
Both humoral and cell mediated response
HSV can exists as whole virion in stroma and
cause inflammatory response
residual viral Ag in corneal transplant can leads
to graft rejection.
ENDOTHELITIS When endothelium gets
infected elicits cellular response cell lysis
shedding of virus into aqueous IRITIS
Immune defence mechanism leads to tissue
destruction scarring & corneal opacity.
19. MECHANISM OF LATENCY AND
REACTIVATION
After peripheral entry during primary infection
HSV travels in a retrograde fashion to various
ganglion .
Here it resides – TG, cervical,sympathetic,
brain stem . Process begins with in 1 to 2 days
of primary infection andmay take several weeks
to complete .
The ICPO ( infectedcell protein no 0) or
junctional region of viral genome is retained in
the host cell nucleus during latent viral state.
During reactivation large amount of virion is
released from host cell. Ophthalmic division of
V CN is most common source.
21. Congenital & neonatal infection
85% acquired during post partum period
5% intrauterine infection i.e. 1 in 300000 births
with features of microphthalmos , retinal
dysplasia, optic atrophy & chorioretinitis.
Also with marked skin , vital organs &
neurological lesions
Ocular features: conjunctivitis,epithelial keratitis,
stromal immune reaction, cataract , necrotizing
chrioretinitis.
22. Primary Infection.
Occurs after 6 months because up to 6
months maternal antibodies are present.
Presents with acute conjunctivitis ,
keratoconjunctivitis with non suppurative
lymphadenopathy or diffuse punctate keratitis
As a rule it is confined to epithelium clinically
due to lack of previous immunologic
stimulation.
23. Reccurent infaction.
Disease may present as
1.Blepharoconjuctivitis
2.Episcleritis, scleritis
3. Infectious epithelial keratitis
a.corneal vesicles
b.dendritic ulcer
c .geographic ulcer(amoeboid)
d.limbal ulcer (marginal)
4. Neurotrophic keratopathy
5. Stromal keratitis
a. Necrotizing stromal keratitis
b. Immune (interstitial)keratitis
c.Immune rings
d.Limbal vasculitis
e.Disciform keratitis
6. Endothelitis-Disciform-Diffuse-Linear
7. Iridocyclitis
8. Trabeculitis
24. 1.Blepharoconjuctivitis & 2.Episcleritis,
scleritis
Represents more localised infection
Vesicles develops which may break & form scab
which heals without scarring.
3. Infectious epithelial keratitis
Punctate epithelial keratitis- develops within 2 hrs &
coalesce to form dendratic ulcer.
Dendratic ulcer- mc presentation
- Branching linear lesions with terminal bulbs & swollen
epithelial borders that contain live virus.
- Dendratic pattern is due to function of viral linear
spread by contagious cell to cell movement .
- it gives double staining pattern:
# along length of lesion stains with fluorescein
# terminal bulbs stains with Rose Bengal
- corneal sensations reduced in 70% cases.
25.
26.
27. geographic ulcer(amoeboid):
-it is due to enlargement of dendratic ulcer.
- extends through Bowmens membrane & has
scalloped margins.
limbal ulcer (marginal):
- It lies proximal to limbus due to intense
inflammation
-Typically presents with epithelial defect with
underlaying stromal infiltrates & limbal injection.
- Resistant to antiviral therapy & corneal
sensations are retained compared to central
corneal ulcer.
30. 4. Neurotrophic keratopathy
d/t damage to gasserian ganglion
Leads to impaired corneal sensations &
decreased tear secretion.
Signs: irregular cornea with decreased corneal
lustre characterised by persistent oval epithelial
defect with grey thickened borders formed by
heaped up epithelium .
Complicates as stromal scarring,
neovascularisation , necrosis , secondary
bacterial infection, perforation.
31. 5. Stromal keratitis
Necrotising stromal keratitis – d/t stromal
invasion & may leads to thinning or
perforation.
Interstitial keratitis
-d/t Retained viral antigen within the
stroma triggers an intrastromal
inflammation. Epithelium is intact.
- C/F – stromal infiltration, stromal
edema, immune ring ,stromal
neovascularization & lipid keratopathy.
32. Disciform keratitis-
- d/t delayed hypersensitivity reaction to HSV.
-Primarily, endothelitis occurs, leading to
disciform corneal edema due to imbibition of
aqueous humour
- examination revels stromal edema either
central or paracentral ,microcystic epithelial
edema , Folds in DM , iritis , KP’s
-Raised IOP if associated with trabeculitis.
- Corneal sensation decreased.
Posterior segment complications of HSV:
- Cystoid macular edema, Epiretinal membrane,
papillitis ,retinal fibrosis and retinal detachment
( 8% HSV, 25 % VZV)
33. 6 Endothelitis:
- Inflammatory reaction of the endothelium
leading to stromal and epithelial edema
- Presence of KPs
- Pathogenesis – immunological –presence of
HSV-1 antigen in endothelial cells.
- Types:
- Disciform
- Diffuse Endothelitis – entire cornea is
involved
- Linear Endothelitis – line of KPs on the
endothelium that progresses from periphery
to centre
35. - Supported by antibiotics and cycloplegics
- Gentle debridement before application of
topical drugs
- Primary corneal disease responds slowly but
well to therapy, usually heals without
scarring because of the absence of immune
reaction.
- If no healing occurs think about Neurotropic
ulcer.
36. Neurotropic keratitis :
- Stop all unnecessary medications
- Gentle debridement of boggy epithelium
- Artificial tears
- Mild steroids – If active stromal keratitis
+nt
- Therapeutic soft contact lenses
- Cycloplegics: if iritis is +nt
- Cyanoacrylate glue – if perforation
occurs.
37. Necrtotising stromal keratitis:
- Topical AV +AB +Cycloplegics + Patch graft + conjuctival
flapping / glue application.
CI for steroids
≈ HSV Conjunctivitis
≈ Mild diffuseEndothelitis
≈ Mild immunostromal keratitis without prior steroids
≈ IEK
≈ Noninflammed neurotrophic keratopathy
INDICATIONS FOR TOPICALSTEROIDS
≈ Marginal keratitis
≈ Mod disciform diffuse Endothelitis
≈ Mod immunostromal keratitis
≈ Mod trabeculitis
≈ Inflamed neurotrophic keratopathy
38. Indications for oral
≈ Severe disciform & diffuse Endothelitis
≈ Severe immune stromal keratitis
≈ All cases of linear Endothelitis
≈ Severe trabeculitis
Prophylaxis against recurrence
≈ Tab acyclovir 400 mg bd * 12- 18 days
≈ Valacyclovir 500mg bd months * 12 - 18 months
≈ Tab famcyclovir 250 mg bd * 12 -18 months
Surgical treatment
≈ Conjuctival flap
≈ Tarsorrhapy:
≈ Lamellar keratoplasty
≈ PKP
39. VARICELLA ZOSTER VIRUS
Spread by saliva droplets, or direct contact with
infected rash.
The maculopapular rash appears in successive
crops
IP: 12- 17 days after lesion or until the
cutaneous sores crust over
Contagious period approx 1 day before & 1 wk
after appearance of rash.
40. Clinical disease :
Congenital varicella syndrome:
- If mother contracts varicella during first or
second trimester of pregnancy.
- Ocular findings chorioretinits, optic
nerveatrophy or hypoplasia, congenital
cataract and Horner Syndrome
- Systemic findings hemiparesis, bulbar
palsies, cicatricial skin lesions in a
dermatomal distribution, developmetal
delay, & learning difficulties.
- No specific treatment .
- Vericella vaccination should be given all
women with no history of previous varicella.
41. Classical varicella ocular findings
- Lesions on the lids or on conjunctiva +nt in form
of small vesicular or papular eruptions that
resolve without difficulty but may rarely turn to
very red , painful, punched out ulcers with sec
reaction in the eye.
- Cornea may develop superficial punctate
keratitis or branching dendritic without terminal
knobs
- Less frequently - Iritis, lid necrosis, intersticial
keratitis with neovascularisation, ulceration with
corneal melting ,extraocular muscle palsies,
internal ophthalmolplegia , cataract ,
chorioretinitis, and optic neuritis.
42. DIAGNOSIS AND TREATMENT
- Diagnosis based on acute or recent history of
systemic with ocular or periocular involvement
with vesicles.
- Tab Acyclovir 20mg/kg 4t/d * 5 days or 800mg
4t/d * 5days if pt weight is > 40 kg
- Local antibiotics
- Steroids not used during acute infection as this
may ameliorate the viral process.
- IV acyclovir may be used in severe cases.
43. HERPES ZOSTER OPHTHALMICUS
first described by Hutchinson in 1865
MC involves nasocilliary br of ophthalmic division of
trigeminal nerve. HZO lies dormant in Trigeminal
ganglion.
Hutchinson’s sign – vesicles at tip of nose .
Clinical features:
- Prodrom : 2 to 3 days of malaise associated with fever,
headache& hypoaesthesia with pain & burning in
affected dermatome
44. - Release of virus from sensory nerve endings
Macular rash papular vesicular within
24 hrs
- New vesicles continue to develop x 4 days
- Vesicles become filled with turbid yellow fluid
or hemorrhage
-Rash evolves to dry crusts over 2 to 3 wks
46. Reactivation
Virus travel along enters into eye via cillary
nerve
Sensory axon to skin
Causes demyelination Direct spread immune
response
of neuron
Epithelial keratitis stromal
keratitis
perineuritis & perivaculitis
around long & short cilliary nerves
and vessels
47. ZOSTER SINE HERPETE (ZSH):
- Reactivated VZV that causes only neurological symptoms
such as dermatological neuralgia or neuropathy and there is,
by definition,no rash.
HZO : OCULAR FINDINGS
Lid & adnexa
≈ Blepharitis secondary to staph aurius,
≈ Vessicular lid erruption
≈ Cicastrical entropion with or without trichiasis
≈ Cicastrical ectropion
≈ Canaliculitis
≈ Ptosis
≈ Dacroadenitis
Conjunctiva
≈ Follicular conjuctivitis
≈ Papillary conjunctivitis
≈ Vesicular conjunctivitis
≈ Conjunctival scarring
50. Corneal changes:
PEK – 2 days
- Associated with conjunctivitis
- Characterized by blotchy swollen epithelial cells
- Coarse PEKs are peripheral, multiple, raised small
&focal in appearance & stain with rose bengal
Pseudodentrites – 4-6 days
- PEK coalesce to form multiple dendritic / stellate
lesionsof swollen raised epithelium
- Broader, more plaque like and without central
ulceration– diff from HSV
51. Anterior stromal infiltrates – 10days
- Represents reaction to soluble viral antigen /
directinvasion
- Hazy granular dry infiltrate just under
Bowman’smembrane
Keratouveitis/Endothelitis – 7- 15 days
- Represents direct viral invasion of endothelium
- Sudden onset DM folds + stromal +epithelial edema
- Uveitis ranges from few KPs to severe granulomatous
reaction centered around the DM
52. Serpiginous ulceration – 1months
- Corneal thinning due to limbal vasculitis by immune
mechanism
- Characteristic crescentric shape & peripheral location
- Vascularization & perforation
Sclerokeratitis – 1 month
- Scleralization, vascularization & stromal thinning or
peripheral faceting of cornea
Corneal mucous plaques – 2-3month
- Coarse grey branching lesions on the surface of swollen
epithelial cells
- Can be wiped off the surface leaving abnormal but
intact epithelium
- Neurotropic or immune mechanism
53. IRIDOCYCLITIS :
- Ant uveal tract is involved in HZO second only
to cornea in frequency
- HZ irits differ from HS irits in that the former is a
lymphocytic/plasma cell vascultits, where as the
latter is a diffuse lymphocytic infiltrate of the iris
stroma( there may be asso ischemic limbal
vasculitis)
- FFA reveals occlusion of iris vessels at sites of
atrophy.
- As a result of vasculits and ischemia, zoster
iritis, may also cause hypopyon, hyphema,
heterochromia iridis,sympathetic ophthamia,
hypotony, and phthisis
54. GLAUCOMA
- Potential reduction in IOP due to HZ necrosis of ciliary
body and pars plicata may be counterbalanced by
impairment of outflow by pigment and cellular debris
clogging the TM, acute trabecultits, and sec angle
closure caused by ant synechae formation
- Depending upon the resulting imbalance the IOP may
range from abnormally low to marked sec glaucoma.
- Most common sec complication of VZV
Post herpetic neuralgia :
- Pain that persists after the acute rash of HZ has abated.
- Resolves within 1yr
- M/A – preferential loss of large inhibitory fibres in the
nerve with subsequent increase in nociceptive
transmission
55. Ramsay Hunt syndrome
- 7th nerve palsy + loss of taste over ant 2/3rd
tongue + ear pain + vesicles in external auditory
canal or pinna .
In immunosuppressed patient – Skin lesions –
Large (10 to 20 mm), multiple, punched out
ulceration with black eschar and a peripheral
rim of vesiculation & positive VZV culture.
56. DIAGNOSIS
Tzanck technique: Slide is prepared from
the fluid of the fresh bullae shows -
Multinucleated giant epithelial cells.
Immune detection – Elisa & PCR
57. Treatment
ACTIVE DISEASE
oral Antivirals for 7 days , starting within 72 hrs
TCA’s( eg nortryptyline, desipramine) Pain control - 25-
75 mg PO * 3months
Nonnarcotic or short term narcotic analgesic.
Immunocompromised patients with any zoster –iv
Acyclovir 15-20 mg/kg/day
58. Dermal eruptions:
- cool compresses, and mechanical
cleansing of the involved skin are
helpful.
- Topical antibiotic ointment may inhibit
scarring and decrease the possibility of
bacterial super infection.
- Topical corticosteroid ointment should be
avoided ,at least during the initial few
days after the acute dermatologic crisis,
during which active replicating virus is
present in the epidermis and dermis
59. Exposure keratopathy:
- Topical antibiotic ophthalmic ointment TDS
Dendritiform keratopathy: therapy 2-3 wk
• 3% vidarabine ointment,or
• 1% trifluridine 5t/d
• Oral antivirals ( as in active ds)
Immune keratopathy, episcleritis, scleritis, or iritis:
• Topical steroids: slow taper
• Oral NSIAD’S
• Cycloplegics for iritis.
Glaucoma:
• Topical beta blockers
• No miotics
• Topical steroids if glaucoma is due to inflammatory
trabeculitis.
60. Tennuous, hazy epithelium in anaesthetic cornea
• Early lateral tarsorraphy and lubrication with artificial tear
and tear ointment.
• Allow vascularisation to progress to aid in healing any
ulcer.
• Topical steroids with caution and only at low doses to
minimize any inflammation
Exposure keratopathy or corneal ulceration or thinning
• Lateral tarsorrhapy
• Therapeutic soft contact lens
• Tissue adhesive for progressive thinning
• Conjuctival flap, transplant, or keratoprosthesis
61. Postherpetic neuralgia:
• TCAs ( eg nortryptyline, desipramine) : 25mg titrated up
to 75mg. Caution if pt has cardiac ds.
• Gabapentin: 300mg bd.
• Slow release opoids added if TCAs +/- gabapentin not
sufficiently effective
• Capsaicin cream TDS
• Lidocaine skin patches or cream, 12 h on, 12hr off
painful skin area
• Frontal or nasal nerve block
• Trigeminal ganglion ablation contraindiacted
62. HIV Infection of eye.
- Sexually transmitted diseases caused by human
immuno deficiency virus.
- HIV depletes CD4+ T cells which are vital to the
initiation of immune response to pathogens.
- Systemic features:
1) Flu like illness within 2-4 weeks of infection.
2) Clinical latency – asymptomatic period of
several years .
3) AIDS – develops in half of HIV patients with in
10 yrs of infection when CD4+ count starts
falling <200 or any of AIDS defining condition.
63. AIDS defining conditions include opportunistic infections
such as respiratory or oesophagial candidiasis ,
Pneumocystis jurovecii pneumonia , cryptosporidiosis ,
CMV retinitis specific tumours including kaposi sarcoma
, lymphoma,etc
Ocular features:
- Eyelid- Blepheritis , Kaposi sarcoma,
molluscum contagiosm , HZO
- Orbit- cellulitis , B cell lymphoma
- Conjunctiva – kaposi sarcoma , squamous cell
carcinoma , microvasculopathy
- Cornea – keratoconjunctivitis sicca , keratitis
- Anterior uveitis- associated with ocular infection or drug
toxicity e.g. Rifabutin , cidofovir .
64. HIV related retinal microangiopathy
- develops in about 70 % of cases .
- Associated with increased plasma HIV – RNA levels &
declining CD 4+ count , its is a marker for increased risk
for CMV retinitis.
- Postulated cause include immune complex deposition ,
HIV infection of retinal vascular endothelium .
- Manifested as cotton wool spots , retinal haemorrhages,
microaneurysms ,.
- Mostly asymptomatic mostly resolves spontaneously.
• Viral retinitis:CMV retinitis , acute retinal necrosis ,
progressive retinal necrosis.
• Secondary infections– toxoplasmal chorioretinitis ,
pneumocystis choroiditis , Histoplasma chorioretinitis
Cryptococcal choroiditis, candidiasis, syphilis ,
tuberculosis
• Neoplastic : b-cell intraocular lymphoma
65.
66. Cytomegalovirus retinitis
- CMV is a herpes virus causing no or minimal
constitutional symptoms in healthy individuals & CMV
retinitis in inmmunocompromised patients like AIDS
where it is a reactivation of latent infection.
- Strong association witha low CD4+ count .
- Without treatment , severe visual loss is inevitable. But
with advent of HAART , incidence & severity has
decreased.
CLINICAL FEATURES:
- Reduced visual acuity (macular involvement ), floaters
(vitritis) , some times asymptomatic as indolent retinitis
often starts in periphery .
- Anterior Uveitis. – mild with little or on cilliary injection.
67. - Cataract :- common in later stage.
- Vitritis :- is typically mild , except in immune recovery.
- Retinitis:- one or two areas of dense white retinal
infiltration associated with flame shaped haemorrhages
. (pizza pie or margherita pizza ) beginning peripherally
extending along large vascular arcade. Indolent retinitis
is more peripheral & less aggressive.
- Optic neuritis:- from direct spread or primary
involvement
- Retinal necrosis:- occur when active inflammation has
settled down , leaving an irregular pigmentation ,
atrophy & holes frequently leading to RD. Major cause
of visual morbidity.
68.
69.
70. - Frosted branch angitis:- marked vascular sheathing ,
also seen in other conditions also ,but the term is used
for a distinct idiopathic disorder.
- Immune recovery uveitis(IRU):- cause of limited visual
outcomes in CMV retinitis , thought to be due to a
rejuvenated immune response to residual viral antigen
following immune reconstruction with HAART.
TREATMENT:
- HAART : mainstay of t/t to restore innate ability of host
to suppress CMV activity.
- Valgancyclovir: pro drug of gancyclovir given orally for
induction 900 mg bd for 3 weeks & maintenence 900
mg daily. Neutropenia is a common side effect due to
bon marrow suppression but treated with filgrastin.
- Gancyclovir slow release intravitreal implants: - less
commonly used when intolerance of systemic t/t .
71. - Intravitreal antiviral drugs: in patients with
immediately sight threatening lesions (lesions
close to the macula or optic nerve head ) ,
intravitreal inj of gancyclovir (2mg/inj) or
foscarnet (2.4 mg) or fomivirsen 330
micrograms or cidofovir 20 micrograms with
current systemic treatment.
- IV Gancyclovir , cidofovir & foscarnet – less
commonly used d/t systemic side effects.
- Vitrectomy with endolaser demarcation & silicon
oil temponade for RD is successful in 75%
cases
- Steroids : for Immune recovery uveitis but
should be used cautiously
- Screening : pts with HIV should be screened
72. Progressive Retinal necrosis:
- Also known as PORN – posterior outer retinal necrosis.
- Rare but devastating necrotising retinitis usually caused
by VZV other herpes virus.
- Occurs predominantly in AIDS may be associated with
other immuno-compromised states particularly drug
introduced,
CLINICAL FEATURES:
Presents with rapidly progressive U/L or B/L visual loss.
Anterior Uveitis & vitritis are minimal in contrast to CMV
retinitis & ARN.
Retinitis:
a) Early : Multifocal yellow white homogenous
deep retinal infiltrates . Macular involvement giving
cherry red spot.
73. b) Established / moderate retinitis: sings spread very
rapidly with extensive full thickness retinal necrosis.
signs of vasculitis are absent.
c) Late: scarring is plaque like characterised as ‘ cracked
mud ’ like rhegmatogenous RD is common.
INVESTIGATION:
- Vitreous and or aqueous PCR assay for viral DNA &
antibody assay
TREATMENT:
- Immune rescue with HAART together with aggressive
antiviral therapy. Vitreoretinal surgery for RD
74.
75.
76. Acute retinal necrosis:
- Rare but devastating necrotising retinitis.
- Typically affects otherwise healthy individuals.
- tends to caused by Herpes simplex virus in young &
VZV in older patients.
- Prognosis is poor due to retinal or optic nerve ischemia
or RRD.
- Systemic features:- simultaneously associated with
HSV encephalitis and hepatic skin infection.
- Ocular features:- presents with uniocular blurred vision
& floaters & pain.
- American uveitis society : defined criteria for diagnosis.
77. 1) Prominent anterior uveitis & vetritis
2) One or more foci of peripheral retinal necrosis .
deep yellow white infiltrates with well defined
borders. Retinal haemorrhage but less
prominent than CMV retinitis. When acute
lesions resolve after 6-12 weeks , leaving
behind necrotic retina with hyperpigmneted
borders .Secondary RRD.
3) Circumferential spread of retinal involvement .
Posterior pole involvement in late. Optic
neuritis sometimes.
4) Occlusive retinal vasculitis including artritis .
5) Rapid progression of disease in absence of
treatment.
78. TREATMENT:
- Acyclovir iv 10 mg/kg every 8 hrly for 10-14
days followed by orally 800 mg five tid for 6-12
weeks.
- Oral valacyclovir , famciclovir good substitute
with better tolerability.
- iv gancyclovir & foscarnet may enhance
prognosis.
- Systemic steroids started 24 hrs after initiation
of antiviral therapy
- Laser retinopexy around necrotic area may be
used to try to prevent RRD.
- Vitrectomy with silicon oil tamponade for
RRD.
