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Overview of Conjunctivitis

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The conjunctiva is a thin, translucent membrane that lines the anterior surface of the eye. It comprises a bulbar section covering the visible part of the sclera, ending at the limbus, and a palpebral section that lines the inner surface of the eyelids. It provides a protective barrier against invading pathogens and aids in lubrication of the ocular surface by secreting components of the tear film.

Conjunctivitis refers to inflammation of the conjunctiva typically resulting from infection, allergy, or ocular irritation. It may present as dilation of the conjunctival vessels, resulting in hyperaemia and oedema of the conjunctiva, associated discharge, ocular discomfort and itching. Diagnosis is clinical, occasionally cultures are indicated. Treatment depends on aetiology and may include topical antibiotics, antihistamines, mast cell stabilizers, and corticosteroids. Since conjunctivitis and other ocular diseases may present as a “red eye” the differential diagnosis of red eye is important. The focus of this article is on conjunctivitis only.

It is estimated that acute conjunctivitis affects 6 million people annually in the United States (US), with approximately 1% of all primary care office visits in the US being related to conjunctivitis. In 2009, the cost of treating bacterial conjunctivitis alone was estimated to be between 377 to 857 million US dollars per year. No such data exists for South Africa possibly as diagnostic tests are not routinely performed.

The following types of conjunctivitis will be discussed in this article:

A. Bacterial Conjunctivitis
1. Acute:
i. Gonococcal
ii. Chlamydial
iii.Ophthalmia Neonatorum

2. Chronic

B. Viral Conjunctivitis
1. Adenoviral
2. Acute Haemorrhagic
3. Herpes Simplex

C. Allergic Conjunctivitis

1. Allergic Rhinoconjunctivitis
2. Vernal Keratoconjunctivitis
3. Atopic Keratoconjunctivitis
4. Giant Papillary Conjunctivitis

D. Toxic Conjunctivitis

E. Ligneous Conjunctivitis

F. Secondary Conjunctivitis


A. BACTERIAL CONJUNCTIVITIS

Bacterial Conjunctivitis

Bacterial conjunctivitis is infectious, self-limiting, and most frequently seen amongst infants, toddlers, and preschool-aged children. It typically lasts 7 to 10 days without management, and up to three days when treated. It can be subtyped into hyper acute, acute and chronic.

Bacterial conjunctivitis can be contracted directly from infected individuals or can result from an abnormal proliferation of the bacterial flora of the conjunctiva. It is also possible for compromised tear production, disruption of the natural epithelial barrier and suppressed immune system to cause bacterial conjunctivitis.

The most common causes of bacterial conjunctivitis in adults are Staphylococcus aureus, followed by Streptococcus pneumoniae and Haemophilus influenza, while in children it is often caused by Haemophilus influenzae, Streptococcus pneumoniae, and Moraxella catarrhalis.

Clinical presentation:

  • acute conjunctival hyperaemia, most intense in the fornices decreasing towards the limbal region
  • ocular grittiness and burning sensation
  • discharge, usually starts in one eye before affecting the other, and is initially watery then mucopurulent
  • eyelids are frequently crusted and stuck together upon awakening (due to exudate accumulation)
  • preauricular adenopathy

Management thereof in primary care may include use of chloramphenicol or fusidic acid eye drops.

Other topical preparations that can be used for acute bacterial conjunctivitis include fluoroquinolones, and aminoglycosides.

1. Acute Bacterial Conjunctivitis

i. Gonococcal Conjunctivitis

Gonococcal conjunctivitis

This rapid onset, hyper acute conjunctivitis is caused by Neisseria gonorrhoeae, and occurs in infected sexually active patients.

Clinical presentation:

  • conjunctival hyperaemia
  • eyelid oedema
  • severe, continuous, and copious purulent discharge
  • chemosis
  • discomfort or eye pain on palpation
  • decreased vision
  • preauricular adenopathy

The cornea is frequently involved, and if untreated can progress to corneal perforation and endophthalmitis within days. Severe purulent discharge should always be cultured and gonococcal conjunctivitis should be considered. Gonococcal conjunctivitis in adults is uncommon and patients should be referred to an infectious disease practitioner.

Recommendations by the US Centers for Disease Control and Prevention for management of gonococcal conjunctivitis is intramuscular ceftriaxone and frequent saline lavage of the eye. Sexual partners of the patient should be referred for evaluation.

ii. Chlamydial Conjunctivitis

Chlamydial Conjunctivitis

This type of acute bacterial conjunctivitis is caused by Chlamydial trachomatis (serotypes D to K). Also known as Adult Inclusion Conjunctivitis, it is a sexually transmitted condition often occurring in sexually active patients with concomitant genital infection, having an incubation period of 2 to 19 days. Rarely, it may be acquired from contaminated, incompletely chlorinated swimming pool water.

Clinical presentation:

  • unilateral mucopurulent discharge
  • tarsal conjunctiva may be more hyperaemic than the bulbar conjunctiva
  • tarsal follicular response occasionally with superior corneal opacities
  • swollen preauricular lymph nodes on the side of the affected eye

If symptoms of bacterial conjunctivitis are experienced along with a marked tarsal follicular response for longer than 3 weeks, and there is failure to respond to topical antibiotics, then conjunctival smears, bacterial cultures, and tests for chlamydia, with referral to a genitourinary clinic is indicated. Management of chlamydial conjunctivitis involves use of systemic antibiotics, typically azithromycin, doxycycline or erythromycin.

iii. Ophthalmia Neonatorum

Ophthalmia Neonatorum or Neonatal conjunctivitis occurs in the first 4 weeks after birth, and may be the result of a bacterial, chlamydial or viral infection acquired from an infected mother during vaginal delivery. Common agents are Neisseria gonorrhoeae and Chlamydia trachomatis.

a. Gonococcal Neonatal Conjunctivitis

This is a hyperacute bacterial infection with an incubation period of 2 to 5 days and time of onset about 24 to 48 hours postpartum. It is more severe than chlamydial neonatal conjunctivitis as it can progress to corneal perforation, endophthalmitis and blindness if untreated.

Clinical presentation:

  • severe hyperacute purulent discharge
  • severe eyelid oedema
  • marked chemosis
  • marked bulbar conjunctival injection
  • preauricular lymphadenopathy

Management consists of prophylaxis in the form of erythromycin or tetracycline ophthalmic ointment. If symptoms are present, then intravenously or intramuscular Ceftriaxone is indicated.

b. Chlamydial Neonatal Conjunctivitis

This is an acute bacterial infection with an incubation period and time of onset approximately 5 to 14 days postpartum.

Clinical presentation:

  • eyelid oedema
  • bulbar conjunctival injection
  • initial watery discharge, later becomes mucopurulent
  • no follicles
  • pseudomembrane formation
  • severe cases may result in conjunctival scarring and peripheral pannus with corneal scarring

Untreated cases may persist for 3 to 12 months, and unlike with adult chlamydial infection, neonatal C. trachomatis infection does not present with palpebral follicles as neonates do not have lymphoid tissue. Management is prophylaxis with erythromycin ophthalmic ointment immediately after birth, and if indicated, intravenous azithromycin or erythromycin may be adopted.

2. Chronic Bacterial Conjunctivitis

This refers to any conjunctivitis lasting more than 4 weeks, with Staphylococcus aureus, Moraxella lacunata, and enteric bacteria being the most common causes. Most forms of chronic conjunctivitis are bilateral, although often asymmetric. Staphylococcus aureus and Moraxella lacunata may also cause chronic conjunctivitis in patients with associated blepharitis, and the latter may also cause angular conjunctivitis resulting in a white discharge at the outer canthus. Chronic bacterial conjunctivitis may also occur in patients with chronic dacryocystitis or nasolacrimal duct obstruction and is unilateral in these cases (on the affected side).

Clinical presentation:

  • conjunctival hyperaemia
  • purulent or mucopurulent discharge
  • bilateral eyelid adherence due to sticky discharge, especially upon awakening
  • burning sensation
  • frequent styes
  • foreign body sensation
  • loss of eyelashes

Management consists of identifying and treating the underlying cause. In general, all broad-spectrum antibiotic eye drops seem to be effective in treating bacterial conjunctivitis. The choice of antibiotic to use would depend on certain factors, like availability of antibiotics, patient allergies and resistance, and cost.

Bacterial conjunctivitis is a self-limiting condition and may either resolve spontaneously or take about 2 weeks for recovery without treatment. Benefits of antibiotic treatment include rapid recovery, decrease in transmissibility and the patient can return sooner to school or work. Antibiotic treatment should be implemented if there is a purulent or mucopurulent discharge, if patient uses contact lenses, patient is immunocompromised or if gonococcal or chlamydial conjunctivitis is suspected. Topical steroids should be avoided because of the risk of potentially prolonging the course of the disease and potentiating the infection.

Viral Conjunctivitis

B. VIRAL CONJUNCTIVITIS

Approximately 80% of acute conjunctivitis is attributed to viruses, with adenoviruses being the primary cause in 65% to 90% of viral conjunctivitis. Other viruses such as herpes simplex virus (HSV) may also be implicated. Viral conjunctivitis is of an infectious nature, is highly contagious, spreading through direct contact via contaminated fingers, medical instruments, swimming pool water, or fomites. Adenoviral conjunctivitis is self-limiting typically lasting 2 to 3 weeks. The incubation period can be 5 to 12 days and risk of transmission may be up to 10 to 14 days after onset of infection. Chronic conjunctivitis with significant corneal involvement is termed keratoconjunctivitis.

1. Adenoviral Conjunctivitis

Adenoviral conjunctivitis

Adenovirus serotypes 3, 4 and 7 cause pharyngoconjunctival fever which is characterised by sudden onset of high fever, pharyngitis (sore throat), enlarged preauricular lymph nodes and bilateral conjunctivitis. Adenovirus serotypes 8, 19, 37 and 54 may cause epidemic keratoconjunctivitis (EKC) while enterovirus type 70 has been responsible for outbreaks of acute haemorrhagic conjunctivitis in Africa and Asia.

Clinical presentation:

  • conjunctival hyperaemia
  • watery discharge
  • ocular irritation, usually begins in one eye and spreads rapidly to the other
  • follicles may be present on the palpebral conjunctiva
  • preauricular lymph node is often enlarged and painful

A differentiating feature between viral and bacterial conjunctivitis is that lymphadenopathy is present in up to 50% of viral conjunctivitis. In severe adenoviral conjunctivitis, and EKC, patients may experience:

  • severe symptoms of conjunctival hyperaemia
  • chemosis
  • acute watery discharge
  • ipsilateral lymphadenopathy
  • follicular conjunctivitis
  • subconjunctival haemorrhages
  • eyelid oedema
  • photophobia
  • foreign body sensation due to corneal involvement
  • pseudomembranes of fibrin and inflammatory cells on the tarsal conjunctiva
  • blurry vision

It is possible for residual corneal subepithelial opacities to be visible microscopically for up to 2 years after a bout of severe viral conjunctivitis has resolved.

Viral conjunctivitis is highly contagious and tends to spread quickly in closed communities, like schools, workplace environments and hospitals. It is transmitted via respiratory and ocular secretions and the virus can be transmissible up to 12 days from of onset of conjunctivitis.

Management of viral conjunctivitis typically involves providing symptomatic relief with use of cold compresses, artificial tears and topical antihistamines, as it usually resolves spontaneously in about 2 weeks. Antiviral medications and topical antibiotics are not indicated. Topical steroids are only used when there is severe inflammation or keratitis affecting visual acuity. Herpes simplex keratitis must be ruled out before topical corticosteroid use is contemplated. Steroids do not shorten the natural course of the disease. Patients should be referred to an ophthalmologist if symptoms do not resolve after 7 to 10 days.

2. Acute Haemorrhagic Conjunctivitis

Acute Haemorrhagic Conjunctivitis

Acute Haemorrhagic Conjunctivitis (AHC) is uncommon and often associated with widespread epidemics, especially in tropical and subtropical regions. The viruses associated with picornavirus, Coxsackievirus A24 or enterovirus 70 are responsible for this. While highly contagious, AHC is self-limiting and there are rare complications. It has a rapid onset, and resolves within 1 to 2 weeks.

Clinical presentation:

  • acutely painful eye
  • watery discharge
  • photophobia
  • foreign body sensation
  • eyelid oedema
  • subconjunctival haemorrhages begin as petechiae which then coalesce, can involve the entire subconjunctiva
  • transient superficial punctate keratitis

3. Herpes Simplex Virus

Herpes Simplex Virus

The herpes simplex virus (HSV) may result in an acute conjunctivitis which is usually unilateral. This virus can lead to herpetic keratitis and possibly loss of vision. Type 1 HSV is the most common causative organism and Type 2 is the usual cause in neonates, though it can rarely be seen in adults as well. The Herpes zoster virus, responsible for shingles, can also affect the conjunctiva.

Clinical presentation:

  • initially almost always unilateral and progresses to the fellow eye over following few days
  • possible severe ocular pain
  • thin, watery discharge
  • follicular conjunctivitis may present
  • herpetic vesicles on the eyelids or lid margin
  • lid oedema and ecchymosis
  • punctate epitheliopathy
  • in severe cases, there can be an irregular corneal reflex due to corneal epithelial defect (dendritic epithelial keratitis)

Management includes topical and oral antivirals to shorten the course of the disease. Topical corticosteroids should be avoided because they potentiate the virus. If a patient with conjunctivitis is not responding to antibiotic therapy, herpetic conjunctivitis should be considered, and these patients should be referred to an ophthalmologist.

C. ALLERGIC CONJUNCTIVITIS

Allergic Conjunctivitis

Allergic conjunctivitis is a non-infectious inflammation of the conjunctiva caused by a hypersensitivity reaction due to the presence of a specific allergen. Diagnosis is usually clinical and it can be broadly classified into allergic rhinoconjunctivitis, vernal keratoconjunctivitis, atopic keratoconjunctivitis and giant papillary conjunctivitis.

Clinical presentation:

  • bilateral mild to intense ocular itching (uncommon in non-allergic eye conditions)
  • conjunctival hyperaemia
  • photosensitivity (photophobia in severe cases)
  • eyelid oedema
  • chemosis
  • watery or stringy discharge
  • concomitant rhinitis is common, or other atopic diseases, such as eczema or asthma
  • chronic itching can lead to chronic eyelid rubbing, periocular hyperpigmentation, and dermatoblepharitis

Allergic conjunctivitis has an extended course, with variable severity of symptoms throughout the allergy season. This is a differentiating feature of allergic conjunctivitis as recurrences within a short period of time are unlikely in bacterial or viral conjunctivitis.

1. Allergic Rhinoconjunctivitis

Acute allergic conjunctivitis is a common condition often caused by pollen. Typically occurring in spring or summer, it is characterised by acute itching and watery discharge with the hallmark of chemosis. Allergic rhinitis and conjunctivitis are systemic inflammatory conditions and often coexist. Allergic conjunctivitis is a comorbidity of asthma and rhinitis. Allergic rhinoconjunctivitis (ARC) can be classified into seasonal or perennial allergic conjunctivitis.

Seasonal allergic conjunctivitis (SAC), associated with the hay fever season, is caused by airborne mould spores or pollen, commonly occurring during spring, and summer, and is a Type 1 (immediate) hypersensitivity response, while perennial allergic conjunctivitis (PAC) occurs throughout the year worsening in autumn when exposure to dust mites and fungal allergens is greatest. Patients present with a transient mild, itchy, watery, nonspecific papillary conjunctivitis, often with chemosis and lid oedema, which may be associated with sneezing and nasal discharge.

Management includes avoidance of the offending allergen, and use of saline solution or artificial tears to dilute and remove the allergens. Topical decongestants, antihistamines, mast cell stabilizers, combination antihistamine with mast cell stabiliser, nonsteroidal anti-inflammatory drugs and corticosteroids may be indicated. Studies reveal that antihistamines were superior to mast cell stabilizers in providing short-term benefits.

2. Vernal Keratoconjunctivitis

Vernal keratoconjunctivitis

Vernal keratoconjunctivitis (VKC), also known as ‘spring catarrh’, is a self-limiting condition primarily affecting males between the age of 5 to 25 years living in warm, dry climates. This Type 1 and Type 4 (delayed) immune reaction is commonly seen in patients who suffer from atopic disease (eczema and asthma) or seasonal allergies. It typically recurs during spring and subsides in the autumn and winter. Many children may outgrow the condition by early adulthood. Patients with VKC, however, have a higher incidence of corneal ectasia conditions like keratoconus and pellucid marginal degeneration.

Clinical presentation:

  • extreme, persistent ocular itching
  • rope-like mucus discharge
  • ‘Cobblestone’ papillary conjunctivitis of the upper tarsal conjunctiva (hallmark of severe vernal disease)
  • Horner-Trantas dots (mucoid nodules with discrete white superficial dots, at the limbus)
  • pseudogerontoxon (arc of corneal scarring occurring with longstanding inflammation of the limbus)
  • other corneal signs include diffuse epithelial keratitis, and a superficial shield-like ulcer

Management of VKC is similar to ARC. Topical steroids, such as fluorometholone or prednisolone, are used if there is severe discomfort caused by keratopathy.

3. Atopic Keratoconjunctivitis

Atopic Keratoconjunctivitis

Atopic keratoconjunctivitis (AKC) is a rare, chronic bilateral disease of eye typically developing in adulthood. The pathophysiology is incompletely understood, but likely represents a combination of Type 1 and Type 4 hypersensitivity reactions. It is associated with genetic and environmental risk factors including asthma, allergic rhinitis, environmental allergens, food allergies and sensitivities. Typically, patients have atopic dermatitis (eczema) or asthma in childhood, with AKC symptoms developing later in life. Although AKC is a perennial disease, symptoms may worsen in the winter. AKC is usually diagnosed clinically along with patient medical and family history.

Clinical presentation:

  • intense, bilateral itching of the conjunctiva, eyelids and periorbital skin
  • conjunctival hyperaemia
  • chemosis during active inflammatory phase
  • burning sensation
  • profuse watery discharge
  • photophobia
  • blurry vision
  • eyelids and periorbital skin may become erythematous (thickened dry skin, tylosis)
  • papillary conjunctivitis
  • meibomian gland disease may be present
  • possibly ectropion, trichiasis and madarosis
  • severe conjunctival disease can result in scarring and symblepharon
  • Horner-Trantas dots may or may not be present
  • corneal involvement can vary from punctate epithelial erosions to ulcers and even perforation, while peripheral vascularization and pannus may also occur.

With AKC, the lower tarsal conjunctiva is usually hyperaemic and oedematous whereas in VKC the upper eyelid is most often affected. If left untreated, AKC may progress to any of the following, ulceration, scarring, cataract, keratoconus (secondary to chronic eye rubbing), and corneal vascularization.

Clinically, AKC is very similar to VKC, and there is controversy regarding classification of the two diseases. It has been proposed that VKC is a childhood form of AKC that evolves into AKC in adulthood. However, VKC can be present without signs of atopic disease. VKC is generally regarded to end at puberty, with severity of symptoms fluctuating during the seasons. Atopic disease is a perennial condition and peaks in adulthood. AKC persists for many years in contrast to VKC, and is associated with high rates of significant visual morbidity.

Management depends on the severity of the symptoms with mild disease being treated similarly to other allergic eye disease, i.e. avoid the allergen, cold compresses and topical mast cells stabilizers and antihistamines. Systemic antihistamines may be used in atopic disease, with oral steroids and cyclosporine generally reserved for severe disease or for treatment of dermatologic disease. Only in severe cases should topical steroid therapy be considered, with therapy being tapered as quickly as possible while avoiding rebound inflammation. Prolonged treatment with oral steroids must be avoided due to long term side effects of raised intraocular pressure and cataract formation.

4. Giant Papillary Conjunctivitis

Giant Papillary Conjunctivitis

The mechanisms for giant papillary conjunctivitis (GPC) are poorly understood however it is thought to occur secondary to mechanical stimulation of the tarsal conjunctiva by a contact lens, ocular prosthesis, exposed sutures, scleral buckles, corneal surface irregularity or filtering blebs. Another possible cause is a Type 1 or Type 4 hypersensitivity reaction due to build-up of proteinaceous deposits and cellular debris on the surface of the contact lens.

Clinical presentation:

  • ocular discomfort
  • itchy eyes
  • mucous discharge
  • foreign body sensation
  • excessive contact lens movement or lens decentration
  • blurry vision due to excessive lens movement or lens deposits
  • hyperaemia of upper palpebral region
  • enlarged papillae on upper tarsal conjunctiva

Management may include any of the following, change in contact lens modality to frequent replacement schedule, change of lens material, and/or lens care solutions, halt contact lens wear or decrease lens wear schedule. If patient wears an ocular prosthesis, then regular polishing and cleaning of prosthesis is indicated.

D. TOXIC CONJUNCTIVITIS

Toxic Conjunctivitis

This is an acute or subacute Type 4 hypersensitivity reaction which may occur with prolonged use of topical drops or contact lens solutions that contain preservatives, such as benzalkonium chloride or thiomersal. This may also occur in certain topical medication that may or may not contain preservatives such as miotics, as well as topical preparations that contain vasoconstrictors. It may also be caused by the use of certain cosmetics (in particular, eye liners and mascara), or skin moisturisers near the eye.

Clinical presentation:

  • erythema of eyelid skin
  • foreign body or burning sensation
  • ocular irritation
  • excessive watering
  • conjunctival hyperaemia
  • follicular conjunctivitis

Management involves discontinuing the medication causing the reaction. Use of a cold compress, preservative free artificial tears, or if indicated, a mild topical steroid may help shorten the recovery time. If eye makeup is used, advise patient to discard current makeup and to replace eye makeup every 3 months. Hand hygiene when applying makeup should be emphasized.

E. LIGNEOUS CONJUNCTIVITIS

Ligneous conjunctivitis is a chronic, recurrent conjunctivitis presenting with fibrinous pseudomembranes on the palpebral conjunctiva. Approximately 50% of cases are bilateral. It may be inherited in an autosomal recessive pattern due to mutations in the plasminogen gene, and in other genes associated with type I plasminogen deficiency, resulting in impaired healing of injured conjunctival mucosa. An accumulation of a serofibrinous material forms the fibrin-rich pseudomembranes, which harden giving it a characteristic “woody” appearance. Surgical excision of ligneous pseudomembranes can intensify the inflammation and formation of pseudomembranes.

Clinical presentation:

  • mucoid discharge
  • tearing
  • conjunctival hyperaemia
  • in latter stages there is palpebral conjunctival pseudomembrane formation, (the mucosa thereof thickens to a wood-like consistency)

This may be preceded by or coincide with systemic signs, such as fever, upper respiratory tract infection, ear infections, or urogenital tract infection in females. No risk factors are associated as it has genetic inheritance.

There is no definite protocol on management, as surgical removal alone results in a rapid recurrence of pseudomembranes. Pre- and post-treatment with the topical plasminogen, topical or systemic fresh frozen plasma, topical steroids, topical cyclosporine, or topical heparin is suggested as conjunctive therapy. Withdrawal of these topical agents, however, may result in rapid recurrence of pseudomembranes with possible long term effects of corneal scarring, neovascularisation and visual impairment.

F. SECONDARY CONJUNCTIVITIS

Conjunctivitis may occur secondary to certain systemic conditions, mechanical irritation or chronic disorders, including amongst others, keratoconjunctivitis sicca, Lyme disease, and blepharitis.  

  1. Systemic viral conditions, like varicella, measles and mumps, can result in an associated follicular conjunctivitis while varicella-zoster virus secondary infection commonly causes conjunctivitis as part of ophthalmic shingles. Conjunctivitis may also occur due to the human immunodeficiency virus.
  2. Meibomitis is a chronic inflammation of the lid margins, associated with dry eye and chronic dacryocystitis, presenting with chronic epiphora, may be associated with a chronic or recurrent unilateral conjunctivitis.
  3. Conjunctivitis may occur secondary to anterior blepharitis. This type of blepharitis may be caused by the staphylococcus species.

Clinical presentation:

  • Hard scales and crusting mainly located around the bases of the lashes
  • Mild papillary conjunctivitis and chronic conjunctival hyperaemia
  • Long-standing cases may develop scarring and tylosis, madarosis, trichiasis and poliosis
  • Associated tear film instability and dry eye syndrome
  • AKC may be present in patients with atopic dermatitis

Management includes warm compresses, lid scrubs, antibiotic treatment and artificial tears.

  1. Molluscum contagiosum is a skin infection caused by a poxvirus that affects typically healthy children between the ages of 2 and 4 years. Transmission is by contact, with subsequent autoinoculation. Lesions on the lid margin may shed the virus into the tear film and give rise to a secondary ipsilateral chronic follicular conjunctivitis.

Clinical presentation:

  • multiple, dome shaped, umbilicated nodule on eyelid or lid margin
  • chronic follicular conjunctivitis
  • chronic unilateral ocular irritation
  • mild watery or mucoid discharge

Spontaneous resolution usually occurs within a few months so treatment may not be necessary unless complications such as a significant secondary conjunctivitis is present. Options include shave excision, cauterization, chemical ablation, and cryotherapy of lesions.

  1. Trachoma is the leading cause of preventable irreversible blindness in the world. It is associated with overcrowding and poor hygiene. Trachoma is commonly linked with serotypes A, B, Ba and C of Chlamydia trachomatis. It is transmitted through contact with infected persons, fomites or by flies.

Recurrent trachomatous conjunctivitis results in Type 4 hypersensitivity reaction potentially resulting in a loss of vision. There is an ‘active’ inflammatory stage and a ‘cicatricial’ chronic stage, with some overlap.

i. Active trachoma is most common in pre-school children and has the following clinical presentation:

  • mixed follicular/papillary conjunctivitis
  • mucopurulent discharge
  • superior epithelial keratitis
  • pannus formation

ii. Cicatricial trachoma is prevalent in middle age patients and clinical presentation is as follows:

  • Linear or stellate conjunctival scars in mild cases, or broad confluent scars (Arlt line) in severe disease.
  • Superior limbal follicles may form a row of shallow depressions upon resolution (Herbert pits)
  • Trichiasis, distichiasis, corneal vascularization and cicatricial entropion
  • Severe corneal opacification
  • Dry eye caused by destruction of goblet cells

Management includes antibiotic treatment for the patient and all family members (azithromycin or Erythromycin). Topical tetracycline ointment is less effective than oral treatment.  Facial cleanliness is an important preventative measure, as is improved access to clean water and sanitation, and control of flies.

 INFECTION CONTROL PROCESS FOR INFECTIOUS CONJUNCTIVITIS

It is imperative that the health care provider has an active infection control protocol in place. If there is an occurrence of infectious conjunctivitis, it is important that both patient and health care provider follow this protocol.    

  1. The patient should be advised of the following to reduce risk of transmission:
  • stay isolated during the infective phase
  • wash hands thoroughly and frequently
  • avoid touching their eyes, or shaking hands with others
  • avoid swimming
  • do not share items, such as towels, pillowcases, eye drops or cosmetics
  • wipe work surfaces and often used areas, as the virus can remain on inanimate surfaces for weeks
  • adhere to follow up appointments
  1. The health care provider should ensure the following:
  • re-educate staff on the importance of personal hygiene, especially handwashing before and after patient contact (20 second scrub)
  • Surfaces within the examination room and waiting area should be cleaned and disinfected as a means of reducing transmission of virus to other patients
  • if possible, avoid using procedures/equipment that require ocular surface contact, for example contact tonometry, during infective phase
  • institute high-level disinfection of shared or reusable equipment that come into contact with patient eyes – by immersing equipment in 3% hydrogen peroxide for a minimum of 10 minutes
  • use of disposable tonometer tips and single-dose eye drops
  • having a separate examination room for triaging patients with suspected adenoviral ocular infections
Type of Conjunctivitis Bacterial Viral Allergic Chlamydial Ligneous
Onset

 

Infectious

Acute/Chronic

Infectious

Acute

Non-Infectious

Seasonal/Acute/Chronic

Infectious

Acute/Chronic

Non-Infectious

(Genetic Inheritance)

Chronic

Laterality Bilateral Unilateral Bilateral Unilateral Bilateral in 50%
Discharge Purulent/

Mucopurulent

Watery Watery Mucopurulent Mucoid
Itching None To Mild None To Mild Severe None To Mild None To Mild
Palpebral Conjunctiva Reaction Papillary Follicular Papillary with Chemosis Follicular Pseudomembranes
Lymph Node Involvement Uncommon Often Present None Often present in AIC Uncommon,

Only if Systemic Involvement

Associated Sore Throat & Fever Yes Yes No No Uncommon,

Only if Systemic Involvement

Table 1.  Overview of Conjunctivitis 

REFERENCES

  1. American Optometric Association. Care of the Patient with Conjunctivitis. 2002
  2. Azari, AA, Barney, NP. Conjunctivitis: A Systematic Review of Diagnosis and Treatment. JAMA. 2013; 310(16): 1721-1729
  3. Bowling, B. Kanski’s Clinical Ophthalmology: A Systematic Approach 8th Ed. 2016. Elsevier Limited.
  4. Chigbu, DI, Labib, BA. Pathogenesis and management of adenoviral keratoconjunctivitis. Inf Drug Resist 2018:11 981-993
  5. Richards, A, Guzman-Cottrill, JA. Conjunctivitis. Ped Rev 2010; 31(5): 196-208
  6. Rosarioa, N, Bielory, L. Epidemiology of allergic conjunctivitis. Curr Opin Allergy Clin Immunol. 11:471-476
  7. Tarabishy, AB, Jeng, BH. Bacterial conjunctivitis: A review for internists. Cleveland Clinic J Med. 2008; 75(7): 507-512

 

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