COMMON EYE INFECTIONS Aging
Dr. Uy
February 12, 2015
Group BagiTwo
Surface Protection of the Eye
The normal conjunctiva & cornea are protected by a
triple-layered tear film.
- Outer oily layer from meibomian glands
- Aqueous layer from lacrimal glands
- Inner layer of mucin, chiefly from conjunctival
goblet cells
Tear Film
- Blinking maintains the integrity of this protective
layer
- Tears produced by lacrimal gland
 High concentration of IgA (0.6g/L)
 Lysozyme (1g/L)
 Lactoferrin (1.2 g/L) –antimicrobial action
Fig 5-47. The 3 primary layers of the tear film covering the
superficial epithelial layer of the cornea. (Vaughan &
Asbury’s Gen Ophthalmology)
Protective Mechanism
- Coating of bacteria by tear IgA, growth inhibition
by lactoferrin iron chelation, and the action of
lysozyme
- Lysozyme (acetylmuramidase) splits bond
between acetylmuramic acid & acetylglucosamine
in peptidoglycan of bacterial cell wall
- Synergy with immunoglobulin & complement is
required for lysis of other bacteria
- IgG (0.05 g/L) & complement found in low
concentration in tears but leak through the
conjunctiva from inflamed vessels
 Causing cell wall lysis by complement
cascade
- From age 40 years, tear volume & concentration
of lacrimal proteins (lysozyme, lactoferrin & IgA)
decrease due to reduced lacrimal gland function.
- But the eye does not become infected more
frequently unless there is concomitant
development of severe dry eye
Normal Tear Flow
- Tear film coming from lacrimal gland, meibomian
gland and goblet cells.
- Tears are squeezed with every blink into the:
 Conjuctival sac → punctum→ canaliculi →
common canaliculus → lacrimal sac →
nasolacrimal duct → nasal cavity
- Beneficial effect of constant tear flow, w/c
removes bacteria & other debris from ocular
surface
- Moderately dry eye develops a compensatory
antibacterial mechanism based on leakage of IgG
& complement.
Tear production
(Lacrimal Duct)
Upper and Lower
Drainage Pipes
Drainage Sac
(Lacrimal Sac)
Drain holes
Main drain
(puncta)
into nose
Corneal Epithelium
- Outermost layer of the eye
- Consists of 5 layers, is transparent & rests on
Bowman’s membrane
- Generated by the limbal stem cells
- Can resurface an epithelial defect w/in 24-48 hrs
- Its surface cells are linked by tight junctions and it
provides an important barrier to invasion of
corneal stroma by microbes
 The epithelium is an efficient barrier to the entrance of
microorganisms into the cornea. If the epithelium is
defective, the avascular stroma and Bowman’s layer
become susceptible to infection with a variety of
organisms, including bacteria, Acanthamoeba, and
fungi.
 Streptococcus pneumoniae (the pneumococcus) is a
true bacterial corneal pathogen
 Other pathogens require a heavy inoculum,
compromised barrier function, or a relative immune
deficiency to produce infection.
 Moraxella liquefaciens, which occurs mainly in
alcoholics (as a result of pyridoxine depletion), is a
classic example of the bacterial opportunist.
Page 1 of 13
Microbial Keratitis
- Increased frequency of microbial keratitis in
certain soft contact lens wearers with a
compromised, hypoxic epithelium, especially
those using extended wear lenses.
- Bacterial keratitis is rare in an eye with a normal
epithelium.
- More common in patients with recurrent
epithelial defects, ex. chronic herpetic disease.
Invasion of the Eye by Pathogens
- To cause infection, the organism has to penetrate
into the eye.
- Facilitated by an epithelial defect or due to a
contaminated contact lens or direct corneal
trauma.
- Penetration of posterior segment by a
contaminated, high velocity fragment or shrapnel,
can cause endophthalmitis.
- Persons wearing contact lenses are of greater risk
 contacts rub on cornea abrasion 
pathogens adhere  infection
Blood-Borne Route
- Considered for endophthalmitis when there is no
history of accidental or surgical trauma
 Possibility of endocarditis, meningococcal
bacteremia, or a previous, possibly
contaminated blood transfusion.
 IV drug users – more likely to develop
endophthalmitis, particularly with Candida
albicans.
Corneal Penetration
- For invasion of the corneal stroma to occur, the
organism must first adhere to the epithelium.
- Pseudomonas aeruginosa is particularly adept in
invading the compromised epithelium from a
superficial source, often from contaminated
contact lenses or eye drops.
Some people mix their own solution and may
have used contaminated water.
- In rabbit experiments, P. aeruginosa has been
shown by us to be able to adhere to damaged
epithelium & to invade corneal stroma within 1
hour, due to release of toxins & proteases.
Contact Lens Wearers
- Initial problem involves bacterial, amoebal or
polymicrobial contamination of the storage case
with adherence of bacteria – or adsorption of
Acanthamoeba – to the lens, which is often
coated with a biofilm protecting the organisms.
Contact Lens
- Acts as a mechanical vector, transferring the
microbes to the corneal epithelium.
- Exacerbated by the sequestration of tear fluid
behind the lens.
- There is dry eyes when wearing contact lens since
there is less corneal sensation
Bacterial Load
- Penetration alone by an organism is not, in most
instances, sufficient to cause infection.
- Organism must proliferate to establish sufficient
numbers of cells to overcome host defenses.
- Very important in eye infection.
- Up to 25% of intraoperative aqueous samples at
cataract surgery contain bacteria.
- Rate of post-operative endophthalmitis following
cataract surgery is low, at 0.1% to 0.7%.
Due to use of pre & intraop antibiotics and the
decreasing virulence of bacteria
- In most cases, the bacterial inoculum is
insufficient to result in multiplication.
- Inactivated by antibacterial substances present in
the anterior chamber (AC) or by antibiotics given
intraoperatively.
- In a few patients, bacterial proliferation does
occur, along with adhesion to intraocular lens, & a
devastating endophthalmitis result.
Virulence of the Organism
- Also dictates the outcome for the patient.
- Usually relates to the production of lethal toxins
by the bacterium, which are quickly effective at
causing tissue necrosis, such as the exotoxins and
proteases liberated by P. aeruginosa
 Streptococcus pyogenes
 Highly virulent for the eye, producing exotoxin A
& needing only a small inoculums.
 As low as 10 cells to cause necrotizing fasciitis of
the lids or a fulminant endophthalmitis within 24
hrs of cataract surgery.
 Pseudomonas aeruginosa
 Cornea’s ability to mount an immediate
immunological reaction to trauma is limited,
hence, P. aeruginosa can establish a fulminant
necrotic infection in the 1st 24 hrs.
 This is unusual in other vascularized sites in the
body.
 While this situation applies to all tissues of the
body, it is different for P. aeruginosa, which is
highly pathogenic for the cornea but not for skin
or other organs of immunocompetent host, except
for the brain.
Page 2 of 13
  Cornea is unique in that it is both avascular and in Discharge
youth at least, lacks professional antigen Watery Acute viral
processing cells except in the peripheral Acute allergic
epithelium. Mucoid Vernal (non-infectious)
 The posterior segment also possess immune- Purulent Severe acute bacterial (like gonorrhea)
privileged compartments & provides an excellent Mucopurulent Mild bacterial or Chlamydial
environment for bacterial multiplication.
Conjunctival epithelium

COMMON EYE INFECTIONS

I. Conjunctivitis
II. Blepharitis Blood Neutrophils,
III. Hordeolum/stye/chalazion
Anchoring vessel lymphocytes
septa
and other
IV. Dacryocystitis leukocytes

V. Preseptal/orbital cellulitis
VI. Corneal ulcer
VII. Endophthalmitis

I. CONJUNCTIVITIS Conjunctival Reaction

- Infectious entities FOLLICULAR PAPILLARY
- Acute vs chronic Toxic Allergic (simple, vernal, atopic)
- Bacterial vs viral Chlamydia Bacterial
- Ophthalmic neonatorumn – increase risk in Viral Chronic blepharitis
NSVD neonates Moraxella Contact lens wear
ACUTE CONJUNCTIVITIS Molluscum Superior limbic
- Conjunctival hyperemia keratoconjunctivitis
- Discharge Parinaud oculoglandular Floppy eyelid syndrome
- Eyelid sticking (worse in the morning) syndrome
- Foreign body sensation
- Less than 3 weeks duration of signs and
Papillary Reaction
symptoms.

CHRONIC CONJUNCTIVITIS Type and amount of discharge

- Discharge
- Eyelids sticking (worse in the morning)
- Red eye (conjunctival hyperemia) Severe purulent Scant purulent watery
- Foreign body sensation
- Greater than 3 weeks duration of signs and Gonococcal Bacterial other than Allergic/atopic
symptoms gonococcal

CLINICAL EVALUATION
Symptoms:
- Non-specific sx:
 Tearing
 Irritation
 Stinging
 Burning
 Photophobia
- Pain & foreign body sensation - corneal
involvement
- Itching – allergic conjunctivitis

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Membranes - Tarsal conjunctiva – velvety, beefy red, mild
PSEUDOMEMBRANES TRUE MEMBRANES papillary changes
(no bleeding when (+) bleeding when - Superficial punctuate epithelial erosions
peeled off) peeled - Lymphadenopathy/membranes: not usually
Severe adenoviral Strep pyogenes infection observed
Gonococcal Diphtheria TREATMENT
Ligneous - Spontaneously resolves within 10-14 days even
Stevens-Johnson without medications
- Broad spectrum antibiotic drops: usually gm (+)
Lymphadenopathy coverage
- Viral - Oral antibiotics if with associated URTI
- Chlamydial
- Gonococcal GONOCOCCAL CONJUNCTIVITIS
- Parinaud oculoglandular syndrome - A sexually transmitted disease (STD)
- Causative agent: Neisseria gonorrhea
- Mode of transmission: direct genital-eye
contact, genital-hand-eye contact, maternal-
neonatal
- Symptoms: explosive onset of copious purulent
discharge
- Hyperacute <24 hrs
- Swollen in less than 24 hrs
- Profuse purulent discharge
- Eyelid edematous and tender
- Unless conjunctivitis treated promptly, leads to
Table 5-2 (from Vaughan & Asbury’s Gen Ophthalmology)
corneal ulcer at limbus
- Coalesce to form a ring ulcer
SIMPLE BACTERIAL CONJUNCTIVITIS
- Ulcer may rapidly perforate
- Relatively uncommon
- Source of infection: direct contact or spread of
Image: Profuse purulent discharge
infection from nasal or sinus mucosa
Promiscuous & bad hygiene
- Most common organism
Spurts so don’t get too close
- from nasal passage reflux most especially if you
sneeze a lot
CLINICAL FEATURES
 Moraxella lacunata: 258 (43%)
Signs:
 H. influenzae: 257 (42.8%)
- Eyelid edema and tenderness
 Strep pneumonia: 24 (4%)
- Marked conjunctival hyperemia and chemosis
 Staph epidermidis: 5 (0.8%)
- Preauricular lymphadenopathy
 Staph aureus
- Pseudomembrane formation
CLINICAL FEATURES - Keratitis: 15-40%, superior peripheral ulceration
Symptoms:  perforation – give IV antibiotics
- Acute redness
TREATMENT
- Burning sensation
- Copious, frequent irrigation of conjunctival sac
- Foreign body sensation
with NSS to remove discharge
- Discharge
- Ceftriaxone 1g IM
- Matting of lashes upon waking up
- Admit if with corneal involvement (IV
- Usually bilateral, but 1 eye affected 1-2 days
ceftriaxone)
earlier
- Topical antibiotic drops: broad spectrum with
Signs:
good gm negative coverage
- Eyelid crusting and swelling
- Give antibiotics for Chlamydia infection: 1/3 of
- Usually mucopurulent (+ mucus strands)
patients have concurrent chlamydial
- Injection in the inferior fornix
- Treat sex partner

Page 4 of 13
ADULT CHLAMYDIAL CONJUCTIVITIS  Children <12yo (25mg/kg 2wks)
- Also an STD - Topical drops
- Chlamydia trachomatis serotypes D to K  Erythromycin/Tetracycline
- Generally in young patients  Broad spectrum: 4t gen
- With concomitant genitourinary infection: fluoroquinolones
 Females: cervicitis - Treat sex partner
 Males: urethritis
- Mode of transmission: direct (touching) or TRACHOMA
indirect (splashes and ejaculations) contact - Chlamydia trachomatis serotypes A, B, C
with genital secretion. - Disease of underprivileged, poor hygienic
conditions
CLINICAL FEATURES - Common fly – major vector in infection-
Symptoms: reinfection cycle
- Subacute onset – 1 wk incubation (to 2 - Leading cause of preventable blindness in the
weeks), persist for months world
- Maybe unilateral or bilateral - Early: mixed papillary/follicular reaction
- Scant mucopurulent discharge - Late: conj scarring (Arlt lines)
- Mild redness and discomfort - Limbal follicles leading to uneven surface
- Symptoms may persist for months (Herbert pits)
Signs:
- Large follicles most prominent in the inferior
palpebral conjunctiva and fornix
- Follicles in the bulbar conjunctiva and
semilunar fold (specific sign); not present in
neonates (only papillary reaction) Scar tissue Hebert pits
- (-) membrane formation
- Corneal involvement: peripheral corneal VIRAL (ADENOVIRAL) CONJUNCTIVITIS
infiltrates (usually superior), micropannus, - Epidemics common in schools, workplaces and
ulcers, neovascularization doctors’ offices
- Tender lymphadenopathy - Wide spectrum of signs and symptoms
- Mode of transmission: direct or indirect
contamination of respiratory or ocular
secretions
- Incubation period: 4-10 days
- Infectious period: 7-12 days
“Sago-like” appearance. Follicular reaction TWO SYNDROMES
1. Epidemic keratoconjunctivitis (EKC)
TREATMENT - 11 virus serotypes – serotypes 8, 11 and 19
- Resolves spontaneously in 6-18 mo if left most common
untreated - Infection transmitted by hand-eye contact, or
- Cannot be killed by common conjunctivitis meds through instruments and solutions
- Systemic therapy - (-) systemic symptoms
 Azithromycin 1 g single dose - Keratitis: 80% reason for check-up
 Doxycycline 100 mg BID x 2-3 wks 2. Pharyngoconjunctival fever (PCF)
 Erythromycin 500 mg QID x 2-3 wks - Serotypes 3, 4, and 7
- Topical therapy - Transmitted by respiratory droplets
 Tetracycline ointment QID x 6 wks - (+) URTI and fever
Chlamydial Conjunctivitis treatment - Keratitis: 30%
- Oral antibiotics
 Azithromycin 1g single dose CLINICAL FEATURES
 Doxycycline 100mg BID for 1-2 wks Symptoms:
 Erythromycin 500mg QID for 1 wk - Acute onset
 Allergy to doxy/tetra - Watery discharge

Page 5 of 13
 - Redness  Angular blepharitis
- Photophobia - When associated with conjunctival
- Mild foreign body sensation inflammation: blepharoconjunctivitis
- Usually bilateral but 1 eye more severe
Signs: INFECTIOUS BLEPHARITIS
- Eyelid swelling - Staphylococcus aureus – most common cause
- Follicular reaction - Usually in younger individuals
- Conjunctival chemosis - Burning, itiching, foreign body sensation
- Small subconjunctival hemorrhages/petechiae - Papillary reaction
- Pseudomembranes - Minimal mucopurulent discharge
- Tender lymphadenopathy - Fibrinous scales, matted crusting around lashes
- Occasional ulceration
TREATMENT - Associated with poliosis, madarosis, trichiasis
- Self-limiting for 2 weeks  Poliosis – decrease or absence of melanin
- Supportive  Madarosis – absence or loss of lashes
 Ice compresses  Trichiasis – abnormally positioned lashes
 Chilled artificial tears
- Patient education
 Frequent handwashing
 Avoid sharing personal items
- For MDs
 Don’t forget to clean equipment and crusting and denting ulceration in the border
instruments
May be iatrogenic if medical hygiene not STAPHYLOCOCCAL BLEPHARITIS
observed - outside going in
 Image: a - Infection of lid margin, lash bases, follicles
pseudomembrane. True - Recurrent hordeola or conjunctivitis
membranes bleed  Hordeola = timus-timus
profusely. - Chronic: thickened and scarred lids
Removed so that meds Gram (+) cocci in clusters
could penetrate the eye
Conjunctiva
What about topical steroids?  Mild hyperemia and a chronic, papillary
- Conjunctival pseudomembranes conjunctivitis
- Severe foreign body sensation and chemosis Corneal
- Decreased visual acuity due to keratitis  Toxic punctuate epithelial kerattis
 Steroids do not shorten natural course.  Catarrhal corneal infiltrates and phlyctenulosis
 May even cause chronic adverse  Peripheral corneal neovascularization
conjunctivitis by prolonging viral  Peripheral subepithelial opacities
shedding Toxins
 Corneal lesions may recur if steroids  Greater activity of bacterial lipases and sterol and
discontinued prematurely fatty wax esters
- Topical NSAIDs (ketorolac or diclofenac) in lieu  Cell-mediated immunity
of steroids  Burning, itching, and irritation that is typically
- No commercially available topical antivirals worse in the morning
 Topical cidofovir 1% shows promise TREATMENT
 Issues with local toxicity - Warm compresses
to decrease swelling and
II. BLEPHARITIS faster recovery
- Infectious or inflammatory  Washed with dilute
- 3 types baby shampoo for
 Staphylococcal approximately 1 minute (clean the lashes)
 Seborrheic o Rub at lashes
Page 6 of 13
 - Antibiotic ointment (2-8 weeks) III. HORDEOLUM/ STYE/ CHALAZION
 Bacitracin and erythromycin, neomycin HORDEOLUM CHALAZION
and aminoglycosides - Inspissation and secondary timus-timus
 Systemic tetracycline infection of sebaceous - Evolve from
 Topical corticosteroids – used only in cases glands hordeola
of corneal hypersensitivity infiltrates or - Internal or external (stye) - Chronic
neovascularization - Painful, red, tender nodular granulomatous
masses in upper/lower nodules
ANGULAR BLEPHARITIS eyelid - Painless lid masses
- inside going out - Self-limiting
- Primarily from a spill-over chronic
conjunctivitis HORDEOLUM OR STYE
- Etiology: Moraxella (warm countries),
Staphylococcus (cold) - External – anterior eyelid margin,
- Ulceration and maceration of lateral canthal often gland of Zeis, Mol, hair follicle
region due to proteolytic enzymes - Internal – meibomian gland
- Minimal discharge
- Chronic papillary and follicular conjunctivitis CHALAZION

DIAGNOSIS - Chronic lipogranuloma of Zeis or

- Clinical appearance meibomian gland
- Swab - Forms as a discrete mass (you do
 Gram(+) cocci in clusters: S. aureus internal aspiration to prevent
 Gram(-) rods with boxcar appearance: scarring of the face)
Moraxella
Remember: TREATMENT
All COCCI are gram POSITIVE, except, Neisseria, HORDEOLUM CHALAZION
Veilonella, Moraxella (cocci to short rods). - Warm - Incision and curettage
moist - Occasionally responsive to steroid:
compresses topical/intralesional
- Antibiotics: - Recurrent lesions: biopsy
topical, oral consider cancer
edges are in Doc’s practice, he
macerated. prescribes 2-3 gtts per eye IV. DACROCYSTITIS
daw naga”HABAS” so as to treat the ACUTE DACROCYSTITIS
macerated area. - Various etiologies
- Complete nasolacrimal duct obstruction
TREATMENT (prevalent drainage of tears from lacrimal sac to
- Lid hygiene (remove the crust because it may nose) – common factor
harbor the organism) - Chronic tear stasis and retention – secondary
 Lid scrub 2-3x/day bacterial infection without emotional crying
 Warm compresses - Edema and erythema below medial canthal
- Broad spectrum with high gm (+) coverage: tendon with lacrimal sac
topical bacitracin and erythromycin, oral distention
tetracycline, doxycycline, or erythromycin can - patient usually presents with
be used in resistant cases history of heavy tearing.
- Corticosteroids
 Not all cases, only with strong inflammation Complications
- Mucocoele formation
- Chronic conjunctivitis
- Orbital cellulitis

Page 7 of 13
TREATMENT - Eyelid edema, erythema and inflammation may
- Avoid irrigation or probing until infection be severe.
subsides - Globe uninvolved.
- Warm compresses - Pupil reaction, visual acuity, ocular motility
- Topical antibiotics unaffected.
- Oral antibiotic - Pain on eye movement and chemosis absent
 Gm (+): most common
 Gm (-): diabetic, immunocompromised In children: sinusitis
- IV antibiotics if with - Haemophilus influenza
cellulitis - Gm (+) cocci
- Incision and drainage (if - CT of PNS if no focus
with abscess) identified
- Dacryocystorhinostomy - Oral or IV antibiotics
(DCR) In teenagers and adults
 done if it is not - Superficial source: trauma, hordeolum
swollen anymore - S. aureus from trauma
 to make new - Oral or IV antibiotics
drainage - Surgical drainage if abscess formation

CHRONIC DACRYOCYSTITIS ORBITAL CELLULITIS

- Distension of lacrimal sac - Active infection posterior
- Massage of lacrimal sac to orbital septum
 Reflux of mucoid material through - >90% from acute/chronic
canalicular system bacterial sinusitis
- Diagnostic probing and irrigation should be - Fever, proptosis, chemosis
confined in upper system - Restriction in ocular
 Probing of NLD ineffective in achieving motility
permanent patency in adults - Pain on eye movement
- DCR - Decrease in visual acuity
 You have to flush in order to assess Extension from periorbital structure
patency; if there is flow to the nose, you - PNS, face and lids, dacryocystitis, dental
do not need to do DCR. infection
Exogenous
V. PRESEPTAL/ORBITAL CELLULITIS - Trauma (rule out foreign body), post-surgical
CELLULITIS (orbital, periorbital)
- Bacterial infections of the orbit or periorbital Endogenous
soft tissues from 3 sources: - Septic embolism
 Direct spread from adjacent sinusitis or Intraorbital
teeth infection - Hx of surgery
 Direct inoculation from trauma or skin - Endolphthalmitis, dacryoadenitis
infection Involvement of orbital apex
 Bacteremia from distant focus (otitis media, - cranial nerve involvement
pneumonia) - Decreased vision & Papillary abnormalities
High percentage proceed to abscess formation
PRESEPTAL CELLULITIS - Subperiosteal space, adjacent to infected sinus,
Patient complains of pain upon movement of orbital soft tissues
eyeballs - Leads to progressive proptosis and clinical
- Inflammation/infection confined to eyelid and deterioration even with appropriate antibiotics
periorbital structures anterior to orbital Delay in treatment
septum. - Orbital apex syndrome
- Orbital structures posterior to orbital septum - Cavernous sinus thrombosis
not infected. - Blindness, cranial nerve palsies, brain abscess
- Death

Page 8 of 13
Do CT of PNS and ENT referral.
In children: often single organism
- Surgical drainage if no response in 24-48 hrs
In adults: multiple organisms
- Gm (+) cocci, H. influenza, anaerobes
CORNEAL ULCER (KERATITIS)
- Infectious
 Bacterial
caused by bacteria capable of penetrating intact
epithelium including N. Gonorrhoeae and H.
Influenzae. Other bacteria are capable of producing
keratitis only after compromisation of the integral
integrity with the ff factors:
a. contact lens wear – most common
predisposing factor in patents with previously
normal eyes
b. pre-existing corneal disease – trauma,
bulluous keratopathy, exposure, and diminished
corneal sensation
c. other factors – chronic blepharoconjunctivitis,
chronic dacryocystitis, tear film deficiency, topical
steroid therapy and hypovitaminosis A.
CLINICAL FEATURES:
1. Presentation – foreign body sensation which
progress to photophobia, blurring of vision, pain,
eyelid edema and discharge.
2. Signs (in chronological order)
-conjunctival and circumcorneal injection
-epithelial defect associated with an infiltrate
around the margin and base
-enlargement of the infiltrate associated with
stromal edema
-secondary sterile anterior uveitis with hypopyon
-progressive ulceration may lead to corneal
perforation and bacterial endophthalmitis
 Fungal
a.k.a keratomycosis
most common pathogens are filamentous fungi
(Aspergillus and Fusarium spp.) and C. albicans
rare but can cause severe stromal necrosis and
enter the anterior chamber by penetrating the intact
Descement membrane. Once in the anterior chamber,
the infection is very difficult to control.
CLINICAL FEATURES:
1. Presentation – gradual onset of foreign body
sensation which progress to photophobia,
blurring of vision and discharge. Topical steroids
enhance fungal replication and corneal invasion.
Progression is much slower and less painful than
in bacterial infection
2. Signs vary with infectious agent
a. Filamentous keratitis
-greyish, stromal infiltrate with a dry
texture and indistinct margins
- surrounding satellite, feathery, finger-like
lesions and immune ring infiltrates
- underlying endothelial plaque and
hypopyon may be present
b. Candida Keratitis
-yellow-white ulcer associated with dense
suppuration similar to a bacterial keratitis
 Acanthamoeba
protozoa
may co -exist with opportunistic organism especially
with herpetic keratitis
CLINICAL FEATURES:
1. Presentation – presents with blurred vision and
severe pain characteristically disproportionate
to clinical signs
2. Signs (in chronological order)
-limbitis, small patchy anterior stromal and
perineural infiltrates (radial keratoneuritis) are
seen during the first 1-4 weeks
-overlying epithelium may be intact/manifest
punctuate or pseudo-dendritic keratitis
-gradual enlargement and coalescence of the
infiltrates may form a central or paracentral ring
abscess
-small white satellite lesion may develop
peripheral to the ring
-slowly progressive stromal opacification.
Scleritis and descemetocele formation
TREATMENT:
- Antiamoebic
 Propamide isothionate
 Polyhexamethylene biguanide
 Chlorhexidine
- Steroids
 Controversial, delays healing
- NSAIDS
 Better alternative, topical and oral
- Surgery
 Corneal transplant
 Viral
Page 9 of 13
 - Inflammatory Wessely ring
Causative agents - Fungal (11.5%)
- Pneumococcus (Strep) - Pneumococcus (4.2%)
- Pseudomonas - Pseudomonas (3.3%)
- Moraxella - Moraxella (2.2%)
- Fungal Hypopyon
Gram (+) Gram (-) - Fungal (60%)
Staph Pseudomonas - Pseudomonas (51%)
- distinct borders, - scalloped borders, - Pneumococcus (38%)
- rapidly - rapidly - Moraxella (36%)
progressive progressive - By gravity pus descends
(collagenases) Scleritis
Strep Moraxella - Pseudomonas (9.9%)
- advancing border, - mild progression, - Fungal (3.7%)
- deep penetration, - with or without lid
- intense AC findings Corneal perforation
reaction - Early perforation, 1st
Mycobacterium Neisseria week – Pseudomonas
- solitary or - peripheral - Medium-size, 2nd week
multifocal, (superior), perforation –
- delayed onset - rapidly Pneumococcus
progressive - Medium-size, 2nd week
no perforation – fungal
Corneal ulcer TREATMENT
- Clinical features Pseudomonas
- Size of ulcer infiltrate - Polymyxin B
- Border of ulcer infiltrate - Fluoroquinolones:
Advancing border  Ciprofloxacin
- Moraxella (23.3%)  Levofloxacin
- Pneumococcus (22%)  Gatifloxacin
- Fungal (2.8%)  Moxifloxacin
- Pseudomonas (2.5%) - Aminoglycosides:
Fern-like infiltrate  Tobramycin
- Fungal (20%)  Gentamycin
- Pseudomonas (5.8%) Pneumococcus
- Moraxella (0.7%) - Sulfacetamide (Alcon, Sensomed, Allergan,
- Pneumococcus (0.8%) Vistapharm)
- Chloramphenicol + sulfacetamide (Novartis)
Brush-like border
- Oral penicillins
- Pseudomonas (24%)
- Fluoroquinolones: levofloxacin,
- Fungal (20%)
gatifloxacin, moxifloxacin
- Moraxella (8%)
Moraxella
- Pneumococcus (4%)
- Nearly anything! 
Pseudoepithelial plaque
Empiric treatment
- Fungal (38.4%)
- Broad spectrum antibiotics
- Should be scraped off
 Fluoroquinolones: ofloxacin, ciprofloxacin,
lightly
levofloxacin, gatifloxacin, moxifloxacin
Give Amphotericin B
 Fortified topical antibiotics
Needs corneal transplant
- Cycloplegics (to dilate the pupil) for pain and
synechia prevention
 Stat dose of atropine at least

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Shotgun treatment HERPES SIMPLEX KERATITIS
- Fortified vancomycin/cefazolin (Gm +) - HSV 1
- Fortified gentamycin/tobramycin (Gm -)  DNA virus
- Topical anti-fungals  Common: 90% human population serpositive
- Amikacin  Primary infection
- Anti-amoebics (especially for contact lens o In children, thru droplet, subclinical
wearers) o Recurrence: immune-compromised
Then what? 2 Forms:
- Refer? EPITHELIAL KERATITIS DISCIFORM
- Manage? KERATITIS
st
1 follow up: 1 day – 4 days - Decreased corneal - Decreased
- If it’s not getting worse in 24 hours, let it be! sensation corneal sensation
- Check if right drug is given (resistance?) - Epithelial ulceration - Epithelial edema
- Check compliance - Anterior stromal infiltrates overlying stromal
- Rare organisms: mycobacteria, amoeba, etc. - Dendrites with terminal infiltrates
- Culture again? bulbs, centrifugal spread to - DM folds
- Corneal biopsy? form geographic lesions - Anterior uveitis
 Histopath Treatment Treatment
 Cultures - Topical antivirals - Topical antivirals
- AC tap (ganciclovir, - Topical steroids
- Prepare for PKP, LKP, patch graft trifuorothymidine) given together
- Debridement with antivirals
Bacterial keratitis treatment - Never use steroids
- Antibiotic drops - Systemic antivirals
 Based on history, clinical appearance, corneal  >=2 attacks/yr
scrapings  Effect disappears once
- Atropine drops oral administration is
- Steroid drops – controversial stopped.
- IV antibiotics (impending corneal perforation)
- Surgery
 Penetrating keratoplasty

VIRAL KERATITIS
- Herpes simplex virus
 Epithelial keratitis
HERPEX ZOSTER OPHTHALMICUS
 Disciform keratitis
- Caused by varicelle zoster virus (VZV)
- Varicella zoster virus
- Vesicular eruption follow distribution of
ophthalmic division of CN V, respects midline
VIRAL EYELID INFECTION
- Most commonly after the sixth decade
- HSV
- Reactivation of VZV in trigeminal ganglion
 Primary HSV type 1 infection usually
- Supraorbital and supratrochlear branches of the
occurs in childhood
frontal nerve are most commonly involved
 Multiple vesicles on a raised,
edematous, erythematous base After an attack of chickenpox, virus remains
 Usually self-limited disease lasting dormant in the sensory root ganglia by retrograde
3-12 days spread along sensory nerves from skin lesions.
 Topical trifluridine or antiviral Later, it reactivates and migrates back down the
ointment sensory nerves to the skin and eye and cause
characteristic lesion
- Varicella Zoster Virus - Hutchinson’s sign:
 Primary VZV - Childhood - Lesions at
tip of nose
 Pseudodendrites;

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 KP’s uveitis, increased intraocular pressure - Etiology: S. epidermidis, S. aureus, Strep,
 Treatment: prednisolone 1% acetate QID Pseudomonas, Proteus
then taper - Sources: external bacterial flora, contaminated
- Keratitis can be epithelial, nummular, or instruments and solutions
disciform - Severity reflects the virulence of offending
- Other findings: blepharoconjunctivitis, organism
episcleritis/scleritis, anterior uveitis with
sectoral iris atrophy PREVENTION
- Pre-op treatment of pre-existing infection
CLINICAL PHASES - Pre-op povidone-iodine
a. acute – may totally resolve - Meticulous draping
- systemic features: influenza like illness (fever, - Prophylactic antibiotics
malaise, depression and headache which lasts
up to a week before appearance of rash), TREATMENT
preherpetic neuralgia (develops over - Identify causative organisms
distribution of the ophthalmic nerve), skin rash - Antibiotic
(starts with macules which rapidly progress to  Intravitreal injections
papules and vesicles to pustules which begin to o Gm (+) – Vancomycin 1 mg/0.1 Ml
crust and scar after a few days) o Gm (-) – Amikacin 0.4 mg/0.1 mL or
b. chronic – may persist for years Ceftazidime 2 mg/0.1 mL
- Keratitits: nummular, disciform, neutrophic,  Periocular
mucous plaque  Topical
c. relapsing – acute and chronic lesions reappear (even  Systemic
10 years after), may be precipitated by sudden - Vitrectomy
steroid withdrawal or reduction of topical if heavy loads of bacteria are present
steroids. Most common lesions include - Intravitreal injections
episcleritis, scleritis, iritis, glaucoma and
nummular, disciform and mucous plaque PICTURES (Different Keratitis)
keratitis. 1. Pneumococci

TREATMENT OF VZV/HZO
- Oral acyclovir 20 mg/kg QID or 800 mg 5x/day
for 1 wk
- Famcyclovir 500 mg TID x 1 wk
- Valcyclovir 1 g TID x 1 wk
- Oral antibiotic for secondary bacterial infection
- Post-herpetic neuralgia (felt even if lesions are 2. Pseudomonas
already healed)
 Capsaicin – drug that depletes substance P
 Amitriptyline hydrochloride 25 mg to 150
mg OD PO

VI. ENDOPHTHALMITIS
- Exogenous
 Trauma
 Post-op
- Endogenous
 Bacteremia (UTI, pneumonia)

ACUTE POST-OP ENDOPHTHALMITIS

- Devastating complication
- Patient will surely go blind

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3. Pneumococci Usually the injection is done at the temporal sides.

---END---
Sources:
Red- audio
Italized - upper class notes
Book: Vaughan & Asbury’s Gen Ophthalmology
Kanski’s Clinical Ophthalmology Fifth Edition

4. Fungal Note takers:

D Delos Reyes, JM Dizor, JRA Futolan

Editor:
R Gabor

VIDEO SNAPSHOTS
1. Chalazion Removal

2. Intravitreal Injection

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