- Herpes simplex virus (HSV), DNA virus, human as natural host.
- Extremely common ocular ionfection & constitute herpetic keratoconjuctivitis
- Major cause os unilateral scarring worldwide
- Most common infectious cause of corneal blindness in developed countries.
Mode of infection:
-HSV-1 :acquired by kissing or coming in close contact w pt suffering from herpes
labialis  cause infection above waist/ upper body
-HSV-II :transmitted to eyes of neonates from infected maternal genitalia / from
genital infection  cause infection below waist (herpes genitalis)
Ocular lesions: -2 forms:i)

Primary Ocular Herpes
Involves non-immunine person
Age: children (6months to 5years old) & teenagers
 Skin lesions (of lids, periorbital region & lid margin a.k.a vesicular
 Acute follicular conjunctivitis
 Keratitis (fine or course epithelial punctate keratitis, dendritic ulcer)

ii) Recurrent Ocular Herpes
-Virus which lies dormant in trigeminal ganglion, reactivaes & cause recurrent
- due to predisposing stress stimuli (eg. Fever due to malaria, flu, UV exposure,
general ill health, mild trauma etc.)
-types:1. Active epithelial keratitis
- punctate epithelial keratitis
- dendritic ulcer
-geographical ulcer
2. Stromal keratitis
3. Trophic keratitis
4. Herpetic iridocyclitis
Epithelial Keratitis
 Symptoms:
 Redness
 Pain

 Photophobia  Tearing / watering  Decreased vision  Signs:  Superficial punctate lesions (fine or course)  Dendritic ulcer of an irregular. Disciform keratitis .branches of dendritic ulcer which enlarge  Treatment: -Antiviral (topical 3% ACICLOVIR eye oitment 5x day) -mechanical debridement  Stromal keratitis  Types: 1. zigzag linear branching  Geographical ulcer.

Frontal nerve more frequently affected than lacrimal & nasociliary nerves. .Rx: steroid eye drops 5x day & antiviral (ACICLOVIR 3%) 2. after reamin dormant for decades.An acute infection of Gasserian ganglion of 5th cranial nerve by varicella-zoster virus (VZV) . Diffuse stromal necrotic keratitis -caused by active viral invasion & tissue destruction .Rx: Antiviral drugs & keratoplasty (but results unsatisfactory) HERPES ZOSTER OPHTHALMICUS (HZO)  Etiology: ..Reactivation. .

later form pustules and crusting ulcers. touching the cornea or conjunctiva). drying. steroids (PREDNISOLONE) &symptomatic relief by antiseptics. with severe neuralgic pain  Ocular lesions:  Conjuctivitis  Zoster keratitis  Epithelial keratitis  Episcleritis  Scleristis  Iridocyclitis  Acute retinal necrosis  Ant. cold compress. entropion(eyelid is rolled inward against the eyeball) and notching.Involvement of external nasal branch of nasociliary nerve which supplies sides of tips & root of nose.- Lesions strictly limited to one side of midline of head.  Hutchinson’s sign . trichiasis(abnormally positioned eyelashes that grow back toward the eye. malaise. Segment necrosis  Secondary glaucoma  Rx: antiviral (ACICLOVIR). oedematous & vesicle formation.  Acute phase lesions: ~ totally resolve within few weeks  General features: sudden onset with fever.  Chronic phase lesions: ~ persist for years  Post herpetic neuralgia – pain which persist even rash has healed  Lid lesions – ptosis. severe neuralgic pain  Cutaneous lesions: red.  Conjuctival lesions – conjuctivitis  Corneal lesions:  Neuroparalytic ulceration  Exposure keratitis  Mucuos plaque keratitis  Scleritis  Uveitis  Lid scarring  Lipid degeneration  Relapsing phase lesions: ~ where acute or chronic lesions reappear few years later  Nummular keratitis  Mucuos palque keratitis  Scleristis .

salt water diving. ACANTHAMOEBA KERATITIS    Etiology: Acanthamoeba castellani (free lying amoeba found in soil. Episcleritis  Secondary glaucoma  Treatment for Herpes Zoster Ophthalmicus (HZO):  Systemic therapy -oral antiviral drugs (ACYCLOVIR) -analgesics -sys. well water. sewage and air) Mode of infection:  Contact lens wearers – using home-made saline from contaminated tap water  Mild trauma – a/w contaminated vegetable matter. hot tube use and exposure to muddy water.steroids -Amitriptyline  Local therapy for skin lesions -antibiotic-corticosteroid skin oitment/lotions  Local therapy for ocular lesions -topical steroids -topical ACYCLOVIR -cycloplegics *ref. bacterial keratitis. Page 102  -FL- B. neuroparalytic keratitis.  Opportunistic infection . Symptoms:  May be asymptomatic  Foreign body sensation  Disproportionate pain . fresh water. AK Khurana 5th ed. sea water. wind blown patients with herpetic keratitis.

     Watering Photophobia Blurred vision Blepharospasm (involuntary tight closure of eyelids) Signs: Initial lesions: Limbitis (94% of cases)  Radial keratoneuritis  Epitheliopathy in any forms (a) Punctate epitheliopathy (b) Epithelial ridges (c) Pseudo or true dendrites (d) Irregular epitheliopathy Advance cases: Patchy stromal infiltrates  Satellite infiltrates  Central of paracentral ring infiltrates* with overlying epithelial defects  Hypopyon *Ring infiltrates Severe cases: Ring abscess*  Hypopyon & stromal necrosis* .

PCR.*Ring abscess *Stromal necrosis  Clinical diagnosis: -difficult -made by exclusion. direct visualization of cysts  Potassium hydroxide (KOH) mount  Calcoflour white stain  Lactophenol cotton blue stain  Culture on non-nutrient agar (E. bacterial or fungal keratitis.  Complications:  Scleritis  Stromal melting  Perforation  Investigations: (corneal scraping)  Confocal microscopy – diagnostic. .coli enriched) may shows trophozoites & cysts.  Other mothods: immunohistochemistry. out of non-responsive patients being treated for herpetic.

Neomycin & Paromycin (d) Imidazoles – eg. Polyhexamethylene biguanide(PHMB) & Chlorhexidine (c) Aminoglycosides – eg.k. keratitis lagophthalmos) Causes:  Extreme proptosis (due to any cause will allow inadequate closure of lids)  Bell’s palsy or any other cause of facial palsy  Simblepharon*  Deep coma (with inadequate closure of lids)  Physiological lagophthalmos (during sleep)  Mustle tone reduction in Parkinsonism  Mechanical lid scarring due to burns. Treatment:  Debridement  Topical amoebicide (a) Diamidines – eg. after full course of max.medical therapy & quiescent phase of at least 6 months. Clotrimazole & Miconazole  Long term prophylactic therapy with PHMB  Penetrating keratoplasty (in non-responsive case. *Symblepharon. *ref. is a partial or complete adhesion of the palpebral conjunctiva of the eyelid to the bulbar conjunctiva of the eyeball . trauma etc. AK Khurana 5th ed. (a. EXPOSURE KERATITIS   When eyes are covered insufficiently by lids and there is loss of protective mechanism by blinking.a. Propamidine isethionate & Hexamidine (b) Biguanides – eg. Page 107  -FL- C.

 Symptoms:  Ocular irritation  Burning sensation  Foreign body sensation  Redness  Signs:  Drying of cornea  Punctate epithelial defects  Corneal ulceration. Page 109 -FL- D.  Disturbance in corneal sensation  metabolic activity of corneal epithelium is disturbed. Causes:  Congenital: i) Riley-Day Syndrome ii)Congenital insensitivity to pain . AK Khurana 5th ed. lead to accunulation of metabolites  edema in cells & exfoliation  ulceration & corneal changes. NEUROTROPHIC KERATOPATHY    Loss of corneal sensation owing to damage of sensory nerve supplying the cornea Pathogenesis: unclear. followed by bacterial superinfection  Treatment: Prophylaxis: Artificial tears  Instillation of ointment  Closure of lids during sleep (bandage/tape)  Bandage contact lenses  Temporary tarsorrhaphy  Treat the cause of exposure Permanent treatment:    Tarsorrhaphy Gold plate for upper lid Conjuctival flap Proptosis management *ref.

cycloplegics. located in lower one half of cornea & hv grey heaped-up epithelial border) Treatment:  Conventional treatment: antioboitics. Page109 -FL- . Herpes Zoster Ophthalmicus) iv) Syphilitic (leutic) neuropathy v) Injury to ganglion vi) Systemic causes: diabetic. lubricating drops & patching  Special treatment: Topical nerve growth factor drops & autologois serum drops  Amniotic membrane transplantation (in case of large non healing ulcers)  Lateral tarsorrhaphy to promote healing & prevent relapse.iii)Anhydrotic ectodermal dysplasia  Acquired: i) Trigeminal nerve damage (following alcohol block or electrocoagulationof Gasserian ganglion or section of the sensory root of 5th nerve) ii) Neoplasm iii) Infection (by HSV.  *ref: AK Khurana 5th ed. leprosy  Symptoms:  red eye  swollen eyelids  defective vision  Signs:  Ciliary congestion  Corneal signs i) Sensation decreased ii) Sheen is lost iii) Punctate epithelial erosions involve interpalpabral area iv) Franks epithelial defects v) Corneal ulcer formation (horizontally oval.