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Conjunctivitis: Justine S. Villanueva
Conjunctivitis: Justine S. Villanueva
Justine S. Villanueva
Anatomy
The conjunctiva is the thin,
transparent mucous membrane that
covers the posterior surface of
the lids and the anterior surface
of the sclera.
Palpebral Conjunctiva
Lines the posterior surface of the lids
and is firmly adherent to the tarsus.
Bulbar Conjunctiva
Loosely attached to the orbital
septum in the fornices and is folded
many times.
This allows the eye to move and
enlarges the secretory conjunctival
surface.
Conjunctival Fornix
Forms the junction between the
bulbar and palpebral
conjunctivas.
It is loose and flexible, allowing the
free movement of the lids and
eyeball.
Key features
Conjunctivitis
The most common eye disease
worldwide.
It varies in severity from a mild
hyperemia with tearing to a severe
conjunctivitis with copious purulent
discharge.
Causes of Conjunctivitis
Bacterial
Chlamydial
Viral
Rickettsial
Fungal
Parasitic
Immunologic
Chemical or irritative
Idiopathic
Associated with Systemic Disease
Secondary to Dacrocystitis or canaliculitis
Signs of Conjunctivitis
Hyperemia
Tearing
Exudation
Pseudoptosis
Papillary Hypertrophy
Chemosis
Follicles
Pseudomembranes and membranes
Symptoms of
Conjunctivitis
Infectious Conjunctivitis
I. Bacterial Infections
Characterized by a rapid onset of
unilateral conjunctival
hyperemia, lid edema, and
mucopurulent discharge.
The second eye typically becomes
involved 12 days later.
Pathogenesis
involves a disruption of the host
defense mechanisms
Bacterial conjunctivitis can be
classified into three clinical types:
acute, hyperacute, and chronic.
A. Hyperacute (Purulent)
Bacterial Conjunctivitis
May be caused by N. gonorrhoeae,
Neisseria kochii and N.
meningitidis.
The most common cause is N.
gonorrhoeae.
Marked by a profuse purulent
exudate
This oculogenital disease is seen
primarily in neonates and sexually
active young adults.
Transmission
Contact with infected urine or genital
secretions.
B. Acute Mucopurulent
(catarrhal) Conjunctivitis
usually begins unilaterally with
hyperemia, irritation, tearing,
mucopurulent discharge, and
mattering of the lids.
Often occurs in epidemic form and is
called pinkeye.
H. influenzae, S. pneumoniae,
and Moraxella catarrhalis- occur
more commonly in young children
and may occur in institutional
epidemics.
H. influenzae- associated with
systemic infection, including
upper respiratory infections, and
acute otitis media.
Treatment
Topical antibiotic drops or ointments
Usually self- limited, lasting 7-10
days.
Antibiotic therapy usually speeds the
resolution and lessens the severity of
the disease.
C. Subacute
Conjunctivitis
Often caused by H. Influenzae and
occasionally by E. coli and proteus
species.
H. influenzae infectioncharacterized by a thin, watery or
flocculent exudate.
D. Chronic Bacterial
Conjunctivitis
lasting longer than 3 weeks
occurs in patients with nasolacrimal
duct obstruction and chronic
dacryocystitis.
may result from a number of
organisms and is often associated with
blepharitis.
The most common organisms are S.
aureus and Moraxella lacunata;
Treatment
Proper antimicrobial therapy
Good lid hygiene, which includes
warm compresses and eyelid
scrubs.
Azithromycin drops and
erythromycin or bacitracin
ointments are effective adjunct
topical antibiotics.
Treatment
For severe inflammationantibiotic and corticosteroid
combination drops or ointments
can be rubbed into the lid margins
after the lid scrubs.
Oral therapy with tetracycline 250
mg four times a day, doxycycline 100
mg 12 times a day, or minocycline
50 mg 12 times a day may be
needed for more severe infections.
Laboratory Findings
Organism identified by microscopic
examination of conjunctival
scrapings stained with Grams stain
or Giemsas stain.
Complications and
Sequelae
Chronic Marginal Blepharitis
Conjunctival scarring
Corneal ulceration
Prognosis
Acute bacterial conjunctivitis is
almost always self-limited.
It may last up to 10-14 days, if
properly treated at least 1-3 days.
II. Chlamydial
Conjunctivitis
1. Trachoma
2. Inclusion Conjunctivitis
Trachoma
Ancient Greek rough eye
results from C. trachomatis
serotypes AC
Endemic in many parts of the world
including Africa, the Middle East,
Latin America, Central Asia, and
South-East Asia.
Trachoma
Trachoma is usually bilateral.
Manifests as a mild, mucopurulent
conjunctivitis that is typically
self-limiting and heals without
permanent sequelae.
It is spread by direct contact or
fomites, usually from other family
members.
Clinical Findings
Initially a chronic follicular conjunctivitis of
childhood that progresses to conjunctival
scarring.
The constant abrasion of inturned lashes
and a defective tear film lead to corneal
scarring, usually after the age of 30 years.
Resembles bacterial conjunctivitis at onset.
Herberts pits- pathognomonic cicatrical
remains of follicles in established
trachoma.
Complications
Conjunctival scarring
Corneal ulceration
Bacterial corneal infections
Corneal scarring
Treatment
3- to 4-week course of oral
tetracycline (tetracycline 1 g/day or
doxycycline 100 mg/day) or oral
erythromycin.
Prognosis
Characteristically, a chronic disease
of long duration.
Under good hygienic conditions, the
disease resolves or becomes milder
so that severe sequelae are avoided.
Adult Inclusion
Conjunctivitis
results from C. trachomatis
serotypes DK.
Usually occurs in sexually active
young people
The chlamydial agent infects the
urethra of the male and the cervix of
the female.
Transmission
Transmission to the eyes of adults is
usually by oral-genital sexual
practices or hand to eye
transmission
The incubation period is 412 days.
Clinical Findings
Unilateral red eye with mucopurulent
discharge, marked hyperemia,
papillary hypertrophy, and a
predominant follicular conjunctivitis.
Laboratory Findings
Diagnosis is based upon the clinical
appearance plus laboratory tests.
Basophilic intracytoplasmic epithelial
inclusions are seen with Giemsa
staining of conjunctival scrapings
Immunofluorescent staining of the
conjunctival scrapings is also useful.
Serum immunoglobulin G (IgG) titers to
chlamydia may be obtained
Treatment
It is important to treat all sexual partners
simultaneously to prevent re-infection and
to rule out other venereal diseases, such as
gonorrhea and syphilis.
A single 1 g dose of azithromycin or
doxycycline 100 mg twice a day for 7 days
are the recommended treatments.
Tetracyclines should be avoided in children
younger than 7 years of age and in
pregnant or lactating women.
Neonatal conjunctivitis
(ophthalmia neonatorum)
defined as any conjunctivitis that occurs
within the first month of life
It may be a bacterial, viral, or
chlamydial infection or a toxic response
to topically applied chemicals.
precise identification of the cause is
essential.
the duration of the exposure is an
important factor in the development of
disease.
Source:
Duker, Jay S. and Yanoff, Myron
(2014). Ophthalmology (4th ed).
Elsevier Saunders. Philadelphia, USA
Chlamydial Infections
The most frequent cause of neonatal
conjunctivitis in the United States is C.
trachomatis.
Symptoms typically develop 514 days after
delivery and may be unilateral or bilateral.
Initially, infants have a watery discharge that
may progressively turn mucopurulent.
Signs include lid edema, a papillary
conjunctival response, and
pseudomembrane formation
Treatment
Topical therapy alone is not sufficient
to treat chlamydial conjunctivitis.
Recommended treatment is oral
erythromycin syrup 50 mg/kg/day in
four divided doses for 14 days.
Mother and sexual partners should be
treated with oral azithromycin 1 gram in a
single dose or oral amoxicillin 500 mg
three times daily for 7 days
Source:
Duker, Jay S. and Yanoff, Myron
(2014). Ophthalmology (4th ed).
Elsevier Saunders. Philadelphia, USA
Neisserial Infections
Neonatal conjunctivitis caused by N.
gonorrhoeae, a Gram-negative
diplococcus that can penetrate an
intact epithelium, has decreased
significantly since the advent of
prophylaxis.
Clinical Manifestations
Development of a hyperacute
conjunctivitis 2448 hours after
birth characterized by marked eyelid
edema, profound chemosis, and
excessive purulent discharge.
The discharge is often so copious that
it re-accumulates immediately after
the eye has been wiped clean.
Laboratory
Diagnosis is made by identification
of Gram-negative intracellular
diplococci on conjunctival
smears.
Prompt diagnosis by examination of
an immediate Gram stain is essential
to timely and effective therapy.
Treatment
Local treatment consists of aqueous
penicillin G drops 10 000 20 000
units.
Drops are given every hour with a
loading dose of one drop every 5
minutes for 30 minutes.
Systemic therapy should also be instituted
with intravenous or intramuscular
ceftriaxone 2550 mg/kg in a single dose
Adenoviral
Conjunctivitis
Viral conjunctivitis is extremely
common.
The diagnosis can usually be made
clinically.
Adenoviruses produce the most
common viral conjunctivitides
with varying degrees of severity.
Spectrum of Adenoviral
Conjunctivitis
Follicular conjunctivitis
Pharyngoconjunctival fever
Epidemic keratoconjunctivitis.
A. Follicular
Conjunctivitis
is the mildest form and is
associated with adenovirus
serotypes 1 through 11 and 19.
It has an acute onset and is initially
unilateral with possible
involvement of the second eye
within 1 week.
Clinical Manifestation:
watery discharge
conjunctival hyperemia
usually accompanied by follicular and
papillary conjunctival changes with
preauricular lymphadenopathy on the
affected side.
Pharyngoconjunctival Fever
is the most common ocular adenoviral
infection
Produced by adenovirus serotypes 3, 4,
and 7.
Clinical Manifestations:
combination of pharyngitis, fever, and
conjunctivitis
The conjunctivitis is predominantly
follicular with a scant watery discharge,
hyperemia, and mild chemosis.
The cornea may be involved with a fine
punctate epitheliopathy.
Epidemic
Keratoconjunctivitis
produced by adenovirus serotypes 8, 19, and
37.
It is a more severe type of conjunctivitis and
typically lasts for 721 days.
EKC produces a mixed papillary and follicular
response of the conjunctival stroma with a
watery discharge, hyperemia, chemosis, and
ipsilateral preauricular lymphadenopathy.
Subconjunctival hemorrhages, conjunctival
membrane formation, and lid edema are
common.
Treatment
Amelioration of symptoms and
minimization of transmission of this highly
contagious disease.
During the stage of acute conjunctivitis,
treatment is usually supportive and includes
cold compresses and decongestant eye
drops.
When patients have decreased visual acuity
or disabling photophobia from
subepithelial opacities, topical
corticosteroid therapy may be beneficial.
Transmission
Usually occurs from eye to fingers to
eye, but tonometers, contact lenses,
and eye drops are other routes of
transmission.
Patients may be infectious for up to
14 days after onset and outbreaks
are especially common in
ophthalmology offices and clinics.
Preventive Measures
Frequent hand washing
Relative isolation of infected
individuals in an office setting.
Disinfection of ophthalmic
instruments.
Acute Hemorrhagic
Conjunctivitis
Clinical Manifestations:
Rapid onset of severe, painful follicular
conjunctivitis with chemosis, tearing, lid edema,
and tiny subconjunctival hemorrhages.
The hemorrhages are petechial at first and then
coalesce, appearing post-traumatic.
The cornea may demonstrate a fine punctate
keratopathy and, rarely, subepithelial opacities.
The conjunctivitis resolves within 46 days, but
the hemorrhages clear more slowly. The disease
occurs in epidemics, especially in developing
countries.
Clinical Manifestations:
Ocular irritation
Watery discharge
Mixed papillary and follicular conjunctivitis
Hemorrhagic conjunctivitis
Preauricular lymphadenopathy
Most cases are unilateral but may become bilateral.
Epidermal vesicular eruptions of the eyelids and lid
margins may accompany the conjunctivitis and the
cornea may be involved.
Corneal involvement may include a coarse,
punctate epithelial keratitis, marginal infiltrates, or
a dendritic ulcer
Treatment
The conjunctivitis usually resolves
spontaneously in 714 days without
treatment.
IV. Rickettsial
Conjunctivitis
All rickettsiae recognized as
pathogenic for humans may attack
the conjunctiva, and the conjunctiva
may be their portal of entry
V. Fungal Conjunctivitis
Candidal Conjunctivitis
caused by candida species (usually
Candida albicans) is a rare infection
that usually appears as a white
plaque.
This may occur in diabetics or
immunocompromised patients as an
ulcerative or granulomatous
conjunctivitis.
Treatment
Responds to amphotericin B (38mg/ml) in aqueous solution
Applications of nystatin
dermatologic cream (100,000 U/g)
four to six times daily.
VI. Parasitic
Conjunctivitis
Loa Loa
is a filarial nematode that is transmitted from human
to human by the bite of an infected female deer fly
(genus Chrysops) that is indigenous to West and
Central Africa.
Lives in the connective tissue of humans and
monkeys.
Monkeys may be its reservoir.
The parasite is transmitted by the bite of the horse or
mango fly.
The mature worm may then migrate to the lid, the
conjunctiva, or the orbit.
Diagnosis
Infection with Loa loa is accompanied
by a 60-80% eosinophilia.
Diagnosis is made by identifying the
worm on removal or by finding
microfilariae in blood examined at
midday.
Treatment
Diethylcarbamazine is currently the
drug of choice
Non Infectious
Conjunctivitis
Toxic Follicular
Conjunctivitis
follows chronic exposure of the
conjunctiva to a variety of foreign
substances.
Including:
molluscum contagiosum of the lid
margin
infection of the lashes by Phthirus pubis
use of eye cosmetics, and prolonged use
of eye medications.
Molluscum contagiosum
Infections
caused by a poxvirus and are common in
patients with HIV.
They are characterized by elevated, round,
pearly white, waxy, noninflammatory
lesions with umbilicated centers.
The virus itself does not grow in the
conjunctiva rather the conjunctivitis is a toxic
reaction to its proteins.
Treatment:
Removal of the lesion or curettage until it bleeds
internally eliminates this condition.
Clinical Manifestation
Pain
Discharges
Photophobia
Scarring may seriously reduce vision
Toxic epidermal
necrolysis
is a severe variant of erythema
multiforme major that is
characterized by massive denudation
of the epidermis and is more
commonly seen in children and in
patients with AIDS.
Treatment
Treatment often varies with the
severity of the condition.
In the acute phase, local treatment
involves lubrication of the ocular
surface.
Systemic corticosteroids (prednisone
6080 mg/day for 34 weeks) may
help control the acute disease
Epidermolysis bullosa
comprises a group of skin and mucous
membrane diseases that are characterized by
the tendency to form blisters after minor
trauma.
Symptoms occur shortly after birth or in early
childhood and have a tendency to recur
throughout the patients life.
Lesions occur chiefly on the extensor surface of
the joints and other areas exposed to trauma.
The severe dystrophic type that leads to
scarring may also produce conjunctival scars.
Treatment
Treatment is based on the severity of
disease.
A majority of patients can be treated
conservatively with ocular lubricants.
Various corneal surgeries including
keratoplasty may be indicated if significant
scarring and visual loss occurs.
Tarsorrhaphy and ectropion/entropion
surgery may be considered for patients with
more severe disease.
Graft-versus-host
disease (GVHD)
is a common complication of
allogeneic bone marrow transplant
and is due to donor grafted cells
attacking host tissue antigens.
Involved tissues include skin, GI
tract, lungs, liver, and eyes.
Clinical Manifestation
Treatment
Aggressive lubrication, autologous
serum tears, punctal plugs, and
decreasing ocular inflammation with
topical steroids and/or topical
cyclosporine or tacrolimus.
Xeroderma Pigmentosa
is an autosomal recessive disease
characterized by impaired ability to
repair UV damage to DNA.
Ocular manifestations include:
keratoconjunctivitis sicca, photophobia,
tearing, blepharospasm, and burning.
Conjunctival inflammation, telangiectasia,
and hyperpigmentation are common
findings and patients often develop
pingueculae or pterygia.
Sources
Duker, Jay S. and Yanoff, Myron
(2014). Ophthalmology (4th ed).
Elsevier Saunders. Philadelphia, USA
Riordan-Eva, Paul and Whitcher, John
P (2008). Vaughan & Asburys
General Ophthalmology (17th ed).
Lange Medical Publications.
END