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Conjunctivitis
Conjunctivitis
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Conjunctivitis
Other namesPink eye, Madras eye
An eye with viral conjunctivitis
SpecialtyOphthalmology, optometry
SymptomsReddish eye, scratchiness[1]
DurationViral conjunctivitis: up to two weeks[2]
CausesViral, bacterial, allergies[3]
Diagnostic methodBased on symptoms, microbial culture[1]
PreventionHandwashing[1]
TreatmentBased on underlying cause[3]
Frequency3–6 million per year (US)[1][3]

Conjunctivitis, also known as pink eye,[4][5] is inflammation of the conjunctiva, the thin, clear layer that covers the white surface of the eye and the inner eyelid.[6] It makes the eye appear pink or reddish.[1] Pain, burning, scratchiness, or itchiness may occur.[1] The affected eye may have increased tears or be stuck shut in the morning.[1] Swelling of the sclera may also occur.[1] Itching is more common in cases that are due to allergies.[3] Conjunctivitis can affect one or both eyes.[1]

The most common infectious causes in adults are viral, whereas in children bacterial causes predominate.[7][3] The viral infection may occur along with other symptoms of a common cold.[1] Both viral and bacterial cases are easily spread among people.[1] Allergies to pollen or animal hair are also a common cause.[3] Diagnosis is often based on signs and symptoms.[1] Occasionally a sample of the discharge is sent for culture.[1]

Prevention is partly by handwashing.[1] Treatment depends on the underlying cause.[1] In the majority of viral cases there is no specific treatment.[3] Most cases that are due to a bacterial infection also resolve without treatment; however antibiotics can shorten the illness.[1][3] People who wear contact lenses and those whose infection is caused by gonorrhea or chlamydia should be treated.[3] Allergic cases can be treated with antihistamines or mast cell inhibitor drops.[3]

Between three and six million people get acute conjunctivitis each year in the United States.[1][3] Typically they get better in one or two weeks.[1][3] If visual loss, significant pain, sensitivity to light or signs of herpes occur, or if symptoms do not improve after a week, further diagnosis and treatment may be required.[3] Conjunctivitis in a newborn, known as neonatal conjunctivitis, may also require specific treatment.[1]

Signs and symptoms

[edit]
Bloodshot eyes

Red eye, swelling of the conjunctiva, and watering of the eyes are symptoms common to all forms of conjunctivitis. However, the pupils should be normally reactive, and the visual acuity should be normal.[8]

Conjunctivitis is identified by inflammation of the conjunctiva, manifested by irritation and redness. Examination using a slit lamp (biomicroscope) may improve diagnostic accuracy. Examination of the palpebral conjunctiva, which overlies the inner aspects of the eyelids, is usually more diagnostic than examination of the bulbal conjunctiva, which overlies the sclera.[9]

Viral

[edit]
Viral conjunctivitis

Approximately 80% of cases of conjunctivitis in adults and less than 20% in children are due to viruses, with 65% to 90% of these cases being attributed to adenoviruses.[3][7] Viral conjunctivitis is often associated with an infection of the upper respiratory tract, a common cold, or a sore throat. Other associated signs may include pre-auricular lymph node swelling and contact with another person with a red eye.[7] Eye pain may be present if the cornea is also involved.[7] Its symptoms include excessive watering and itching. The discharge in viral conjunctivitis is usually (but not always) watery.[7] The infection usually begins in one eye but may spread easily to the other eye.[citation needed]

Viral conjunctivitis manifests as a fine, diffuse pinkness of the conjunctiva which may be mistaken for iritis, but corroborative signs on microscopy, particularly numerous lymphoid follicles on the tarsal conjunctiva, and sometimes a punctate keratitis are seen.[10]

Allergic

[edit]
An eye with allergic conjunctivitis showing conjunctival edema

Allergic conjunctivitis is inflammation of the conjunctiva due to allergy.[11] The specific allergens may differ among patients. Symptoms result from the release of histamine and other active substances by mast cells, and consist of redness (mainly due to vasodilation of the peripheral small blood vessels), swelling of the conjunctiva, itching, and increased production of tears.[citation needed]

Bacterial

[edit]
An eye with bacterial conjunctivitis

Bacteria are responsible for approximately 70% of conjunctivitis in children and less than 20% of cases in adults.[7] Common bacteria responsible for bacterial conjunctivitis are Staphylococcus including Staph aureus, Streptococcus such as strep pneumoniae,[12] Haemophilus species and Moraxella catarrhalis.[7] Less commonly, Chlamydia spp. and Niesseria species (Neisseria gonorrhoeae and Neisseria meningitidis) may be the cause.[7][13] Infection with Escherichia coli may also cause conjunctivitis, particularly in the neonatal subtype ophthalmia neonatorum.[14] Bacterial conjunctivitis usually causes a rapid onset of conjunctival redness, swelling of the eyelid, and a sticky discharge. Typically, symptoms develop first in one eye, but may spread to the other eye within 2–5 days. Conjunctivitis due to common pus-producing bacteria causes marked grittiness or irritation and a stringy, opaque, greyish or yellowish discharge that may cause the lids to stick together, especially after sleep. Severe crusting of the infected eye and the surrounding skin may also occur. The gritty or scratchy feeling is sometimes localized enough that patients may insist that they have a foreign body in the eye.[citation needed]

Typical membranous conjunctivitis

Bacteria such as Chlamydia trachomatis or Moraxella spp. can cause a nonexudative but persistent conjunctivitis without much redness. Bacterial conjunctivitis may cause the production of membranes or pseudomembranes that cover the conjunctiva. Pseudomembranes consist of a combination of inflammatory cells and exudates and adhere loosely to the conjunctiva, while true membranes are more tightly adherent and cannot be easily peeled away. Cases of bacterial conjunctivitis that involve the production of membranes or pseudomembranes are associated with Neisseria gonorrhoeae, β-hemolytic streptococci, and Corynebacterium diphtheriae. C. diphtheriae causes membrane formation in the conjunctiva of unimmunized children.[15]

Chemical

[edit]

Chemical eye injury may result when an acidic or alkaline substance gets in the eye.[16] Alkali burns are typically worse than acidic burns.[17] Mild burns produce conjunctivitis, while more severe burns may cause the cornea to turn white.[17] Litmus paper may be used to test for chemical causes.[16] When a chemical cause has been confirmed, the eye or eyes should be flushed until the pH is in the range 6–8.[17] Anaesthetic eye drops can be used to decrease the pain.[17]

Irritant or toxic conjunctivitis is primarily marked by redness. If due to a chemical splash, it is often present in only the lower conjunctival sac. With some chemicals, above all with caustic alkalis such as sodium hydroxide, necrosis of the conjunctiva marked by a deceptively white eye due to vascular closure may occur, followed by sloughing off of the dead epithelium. A slit lamp examination is likely to show evidence of anterior uveitis.[18]

Biomarkers

[edit]

Omics technologies have been used to identify biomarkers that inform on the emergence and progression of conjunctivitis. For example, in chronic inflammatory cicatrizing conjunctivitis, active oxylipins, lysophospholipids, fatty acids, and endocannabinoids alterations, from which potential biomarkers linked to inflammatory processes were identified.[19]

Other

[edit]
An eye with chlamydial conjunctivitis

Inclusion conjunctivitis of the newborn is a conjunctivitis that may be caused by the bacterium Chlamydia trachomatis, and may lead to acute, purulent conjunctivitis.[20] However, it is usually self-healing.[20]

Causes

[edit]

Viruses are the most common cause of infectious conjunctivitis.[3] Bacterial infections, allergies, other irritants, and dryness are also common causes. Both bacterial and viral infections are contagious, passing from person to person or spread through contaminated objects or water. Contact with contaminated fingers is a common cause of conjunctivitis. Bacteria may also reach the conjunctiva from the edges of the eyelids and surrounding skin, from the nasopharynx, from infected eye drops or contact lenses, from the genitals, or from the bloodstream.[21] Infection by human adenovirus accounts for 65% to 90% of cases of viral conjunctivitis.[22]

Viral

[edit]

Adenoviruses are the most common cause of viral conjunctivitis (adenoviral keratoconjunctivitis).[23] Herpetic keratoconjunctivitis, caused by herpes simplex viruses, can be serious and requires treatment with aciclovir. Acute hemorrhagic conjunctivitis is a highly contagious disease caused by one of two enteroviruses, enterovirus 70 and coxsackievirus A24. These were first identified in an outbreak in Ghana in 1969 and have spread worldwide since then, causing several epidemics.[24]

Bacterial

[edit]

The most common causes of acute bacterial conjunctivitis are Staphylococcus aureus, Streptococcus pneumoniae, and Haemophilus influenzae.[23][25] Though very rare, hyperacute cases are usually caused by Neisseria gonorrhoeae or Neisseria meningitidis. Chronic cases of bacterial conjunctivitis are those lasting longer than 3 weeks and are typically caused by S. aureus, Moraxella lacunata, or Gram-negative enteric flora.[citation needed]

Allergic

[edit]

Conjunctivitis may also be caused by allergens such as pollen, perfumes, cosmetics, smoke,[26][unreliable medical source?] dust mites, Balsam of Peru,[27] or eye drops.[28] The most frequent cause of conjunctivitis is allergic conjunctivitis, and it affects 15% to 40% of the population.[29] Allergic conjunctivitis accounts for 15% of eye related primary care consultations; most including seasonal exposures in the spring and summer or perpetual conditions.[30]

Other

[edit]

Diagnosis

[edit]
The procedure of conjunctival swabs

Cultures are not often taken or needed, as most cases resolve either with time or typical antibiotics. If bacterial conjunctivitis is suspected, but no response to topical antibiotics is seen, swabs for bacterial culture should be taken and tested. Viral culture may be appropriate in epidemic case clusters.[33]

A patch test is used to identify the causative allergen in allergic conjunctivitis.[34]

Although conjunctival scrapes for cytology can be useful in detecting chlamydial and fungal infections, allergies, and dysplasia, they are rarely done because of the cost and the general dearth of laboratory staff experienced in handling ocular specimens. Conjunctival incisional biopsy is occasionally done when granulomatous diseases (e.g., sarcoidosis)[35] or dysplasia are suspected.[36]

Classification

[edit]

Conjunctivitis may be classified either by cause or by extent of the inflamed area.[citation needed]

Causes

[edit]
  • Allergy
  • Bacteria
  • Viruses
  • Chemicals
  • Autoimmune

Neonatal conjunctivitis is often grouped separately from bacterial conjunctivitis because it is caused by different bacteria than the more common cases of bacterial conjunctivitis.[37]

By extent of involvement

[edit]

Blepharoconjunctivitis is the dual combination of conjunctivitis with blepharitis (inflammation of the eyelids).[38]

Keratoconjunctivitis is the combination of conjunctivitis and keratitis (corneal inflammation).[39]

Blepharokeratoconjunctivitis is the combination of conjunctivitis with blepharitis and keratitis. It is clinically defined by changes of the lid margin, meibomian gland dysfunction, redness of the eye, conjunctival chemosis, and corneal inflammation.[40]

Differential diagnosis

[edit]

Some more serious conditions can present with a red eye, such as infectious keratitis, angle-closure glaucoma, or iritis. These conditions require the urgent attention of an ophthalmologist. Signs of such conditions include decreased vision, significantly increased sensitivity to light, inability to keep the eye open, a pupil that does not respond to light, or a severe headache with nausea.[41] Fluctuating blurring is common, due to tearing and mucoid discharge. Mild photophobia is common. However, if any of these symptoms is prominent, considering other diseases such as glaucoma, uveitis, keratitis, and even meningitis or carotico-cavernous fistula is important.[citation needed]

A more comprehensive differential diagnosis for the red or painful eye includes:[41]

Prevention

[edit]

The most effective prevention is good hygiene, especially avoiding rubbing the eyes with infected hands. Vaccination against some of the causative pathogens, such as Haemophilus influenzae, pneumococcus, and Neisseria meningitidis is also effective.[42]

Povidone-iodine eye solution has been found to prevent neonatal conjunctivitis.[43] It is becoming more commonly used globally because of its low cost.[43]

Management

[edit]

Conjunctivitis resolves in 65% of cases without treatment, within 2–5 days. The prescription of antibiotics is not necessary in most cases.[44]

Viral

[edit]

Viral conjunctivitis usually resolves on its own and does not require any specific treatment.[3] Antihistamines (e.g., diphenhydramine) or mast cell stabilizers (e.g., cromolyn) may be used to help with the symptoms.[3] Povidone-iodine has been suggested as a treatment, but as of 2008, evidence to support it was poor.[45]

Allergic

[edit]

For allergic conjunctivitis, cool water poured over the face with the head inclined downward constricts capillaries, and artificial tears sometimes relieve discomfort in mild cases. In more severe cases, nonsteroidal anti-inflammatory medications and antihistamines may be prescribed. Persistent allergic conjunctivitis may also require topical steroid drops.[46]

Bacterial

[edit]

Bacterial conjunctivitis usually resolves without treatment.[3] Topical antibiotics may be needed only if no improvement is observed after 3 days.[47] No serious effects were noted either with or without treatment.[48] Because antibiotics speed healing in bacterial conjunctivitis, their use may be considered.[48] Antibiotics are also recommended for those who wear contact lenses, are immunocompromised, have disease which is thought to be due to chlamydia or gonorrhea, have a fair bit of pain, or have copious discharge.[3] Gonorrheal or chlamydial infections require both oral and topical antibiotics.[3]

The choice of antibiotic varies based on the strain or suspected strain of bacteria causing the infection. Fluoroquinolones, sodium sulfacetamide, or trimethoprim/polymyxin may be used, typically for 7–10 days.[23] Cases of meningococcal conjunctivitis can also be treated with systemic penicillin, as long as the strain is sensitive to penicillin.[citation needed]

When investigated as a treatment, povidone-iodine ophthalmic solution has also been observed to have some effectiveness against bacterial and chlamydial conjunctivitis, with a possible role suggested in locations where topical antibiotics are unavailable or costly.[49]

Chemical

[edit]

Conjunctivitis due to chemicals is treated via irrigation with Ringer's lactate or saline solution. Chemical injuries, particularly alkali burns, are medical emergencies, as they can lead to severe scarring and intraocular damage. People with chemically induced conjunctivitis should not touch their eyes to avoid spreading the chemical.[50]

Epidemiology

[edit]

Conjunctivitis is the most common eye disease.[51] Rates of disease are related to the underlying cause, which varies by age as well as the time of year. Acute conjunctivitis is most frequently found in infants, school-age children, and the elderly.[21] The most common cause of infectious conjunctivitis is viral conjunctivitis.[29]

It is estimated that acute conjunctivitis affects 6 million people annually in the United States.[3]

Some seasonal trends have been observed for the occurrence of different forms of conjunctivitis. In the Northern Hemisphere, the occurrence of bacterial conjunctivitis peaks from December to April, viral conjunctivitis peaks in the summer months, and allergic conjunctivitis is more prevalent throughout the spring and summer.[21]

History

[edit]

An adenovirus was first isolated by Rowe et al. in 1953. Two years later, Jawetz et al. published on epidemic keratoconjunctivitis.[52]: 437  "Madras eye" is a colloquial term that has been used in India for the disease.

Outbreak in Pakistan

[edit]

In September 2023, a significant outbreak of conjunctivitis occurred in Pakistan. The outbreak began in Karachi and quickly spread to Lahore, Rawalpindi, and Islamabad. By the end of the month, over 86,133 cases had been reported in Punjab alone. The rapid spread of the disease led to the temporary closure of schools in the region. This event marked one of the largest outbreaks of Pink Eye in the country's recent history.[53][54][55][56]

Society and culture

[edit]

Conjunctivitis imposes economic and social burdens. The cost of treating bacterial conjunctivitis in the United States was estimated to be $377 million to $857 million per year.[3] Approximately 1% of all primary care office visits in the United States are related to conjunctivitis. Approximately 70% of all people with acute conjunctivitis present to primary care and urgent care.[3]

See also

[edit]

References

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[edit]
Revisions and contributorsEdit on WikipediaRead on Wikipedia
from Grokipedia
Conjunctivitis, commonly known as pink eye, is an of the , the thin, transparent membrane that lines the inner surface of the and covers the part of the eyeball, often resulting in redness due to dilated blood vessels. This condition is one of the most common and treatable eye disorders, affecting people of all ages, with bimodal incidence peaks in children under 7 years (highest in ages 0-4) and young adults aged 22-28. The primary causes of conjunctivitis are divided into infectious and noninfectious categories, with viral infections—particularly adenovirus (which accounts for 65-90% of viral cases)—being the most common cause, responsible for up to 80% of acute cases overall, followed by bacterial pathogens like Staphylococcus aureus and Haemophilus influenzae, and allergic reactions affecting 15-40% of the population. Viral and bacterial forms are highly contagious, spreading through direct contact with infected eye secretions, contaminated surfaces, or respiratory droplets, while allergic conjunctivitis is triggered by environmental allergens such as pollen and is seasonal, peaking in spring and summer. Other less common etiologies include chemical irritants, contact lens overuse, foreign bodies, fungi, parasites, or blocked tear ducts in newborns. Symptoms typically include redness or pink discoloration of the eye, swollen eyelids, itching, burning, a gritty sensation, increased tearing, and discharge that may crust over the lashes overnight, varying by type—purulent for bacterial, watery for viral or allergic. is primarily clinical based on history and , including discharge characteristics and associated , though cultures or rapid antigen tests may be used for severe or recurrent cases. Treatment depends on the cause: supportive care with and cold compresses for viral cases, which often resolve in 1-2 weeks; topical antibiotics like fluoroquinolones for bacterial infections; and antihistamines or avoidance for allergic types, with complications such as corneal involvement rare but potentially vision-threatening if untreated. Prevention emphasizes practices, including frequent handwashing, avoiding eye touching, and not sharing personal items, particularly in contagious forms.

Overview

Definition

Conjunctivitis, commonly known as pink eye, is an of the , the thin, transparent mucous membrane that lines the inner surface of the eyelids and covers the anterior portion of the , or white part of the eye. This condition arises from various triggers leading to vascular congestion and tissue swelling in the affected area. The term "pink eye" stems from the characteristic redness of the ocular surface, caused by dilation and engorgement of the conjunctival blood vessels. Conjunctivitis affects individuals across all age groups and is generally self-limiting, often resolving spontaneously within one to two weeks, though its potential for contagion depends on the specific . In the United States, the condition accounts for an estimated 6 million cases annually.

Classification

Conjunctivitis is primarily classified by its into infectious and non-infectious categories, with infectious forms further subdivided into viral and bacterial subtypes, while non-infectious includes allergic, chemical or irritant-induced, and other causes such as autoimmune or neoplastic conditions. Viral conjunctivitis, often caused by adenoviruses, represents the most common infectious type, followed by bacterial infections from pathogens like or . Non-infectious types encompass allergic reactions mediated by IgE and release, as well as irritant exposures from chemicals or foreign bodies. Other forms, such as those linked to systemic autoimmune diseases like ocular pemphigoid, fall into miscellaneous categories due to their distinct underlying mechanisms. A secondary classification considers the extent of involvement, distinguishing between unilateral (affecting one eye) and bilateral (affecting both eyes) presentations, as well as localized versus diffuse conjunctival inflammation, which aids in differentiating etiologies during clinical assessment. For instance, bacterial conjunctivitis may initially present unilaterally before becoming bilateral, whereas allergic forms typically involve both eyes symmetrically with diffuse involvement. This spatial categorization is crucial for guiding diagnostic approaches, as unilateral cases often prompt evaluation for foreign bodies or focal infections. Conjunctivitis is also categorized by duration and pattern, with acute forms lasting less than 4 weeks, chronic persisting beyond 4 weeks, and recurrent or hyperacute variants indicating severe or repeated episodes. specifically includes seasonal (triggered by pollen or environmental allergens) and perennial (year-round, often due to indoor irritants) subtypes, reflecting exposure patterns. These temporal distinctions help predict and strategies, such as monitoring chronic cases for underlying systemic issues. Neonatal conjunctivitis, also known as ophthalmia neonatorum, forms a distinct subgroup occurring within the first month of life, primarily due to perinatal exposure to bacteria like or during passage through the birth canal, necessitating prompt evaluation to prevent complications like corneal scarring. This category is separated owing to its unique risks and higher potential for severe outcomes compared to adult-onset forms.

Pathophysiology

General Mechanisms

Conjunctivitis is fundamentally an inflammatory condition of the , where the initial response to , , or involves of the conjunctival blood vessels. This dilation increases blood flow to the area, resulting in the characteristic redness or hyperemia observed clinically. Concurrently, increased allows the leakage of plasma proteins and fluid into the surrounding tissues, leading to conjunctival edema () and the production of , which manifests as tearing, discharge, or crusting depending on the severity. These vascular changes are mediated by local release of vasoactive mediators and represent a universal hallmark across all forms of conjunctivitis. The inflammatory cascade in conjunctivitis is driven by a complex interplay of signaling molecules, including pro-inflammatory cytokines such as interleukin-6 (IL-6) and tumor factor-alpha (TNF-α). These cytokines are secreted by activated epithelial cells, resident immune cells, and infiltrating leukocytes, promoting further amplification of through recruitment of neutrophils, , and macrophages to the conjunctival tissues. , primarily released from degranulated mast cells upon stimulation, exacerbates this process by binding to H1 receptors on endothelial cells, enhancing and permeability while contributing to symptoms like itching and irritation. This cascade establishes a self-perpetuating cycle of tissue damage and repair unless resolved. Conjunctival goblet cells, specialized epithelial cells within the conjunctival mucosa, are integral to the ocular surface defense by secreting gel-forming , primarily MUC5AC, which form a protective layer in the tear film. In the context of , these cells respond to stimuli by increasing mucin production, which can lead to excessive secretion and contribute to the viscous seen in many cases; conversely, chronic induced by cytokines like TNF-α can reduce goblet cell density and function, disrupting tear film stability and exacerbating dryness and epithelial damage. This dual role underscores goblet cells' contribution to both protective barriers and pathological responses in conjunctival . The underlying conjunctivitis exhibits variations between innate and adaptive arms, tailored to the underlying trigger. Innate immunity provides rapid, non-specific protection through components in the tear film, such as and immunoglobulins, which limit spread and initiate the inflammatory cascade via receptors on epithelial cells. In contrast, adaptive immunity, predominant in allergic forms, involves antigen-specific T-cell activation and production, leading to sustained lymphocytic infiltration and chronic . These distinctions highlight how general mechanisms adapt to specific contexts without altering the core vascular and cellular responses.

Etiology-Specific Pathways

Infectious pathways in conjunctivitis involve pathogen invasion of the conjunctival epithelium, leading to cellular damage and inflammation. For viral causes, such as adenoviruses, which cause up to 90% of viral conjunctivitis cases, the pathogen adheres to epithelial cell receptors via projecting fibers like pentons, facilitating entry and intracellular replication. This replication culminates in epithelial cell lysis, releasing viral particles and inducing superficial punctate keratopathy along with subepithelial infiltrates, particularly in epidemic keratoconjunctivitis caused by serotypes 8, 19, or 37. Bacterial pathogens, including Haemophilus influenzae, Streptococcus pneumoniae, and Staphylococcus aureus, colonize the ocular surface through direct contact or compromised epithelial barriers, particularly in children, contact lens wearers, and immunocompromised individuals. These bacteria produce toxins and enzymes that exacerbate epithelial disruption, promoting purulent discharge and potential keratitis. Secondary bacterial superinfection frequently complicates viral conjunctivitis, as epithelial lysis weakens local defenses, allowing opportunistic bacterial overgrowth and intensified inflammatory responses. Allergic pathways are characterized by an IgE-mediated reaction, where exposure triggers rapid in the . Upon re-exposure, allergens cross-link IgE antibodies bound to high-affinity FcεRI receptors on sensitized s, prompting the release of preformed mediators such as , , and leukotrienes, alongside newly synthesized cytokines and prostaglandins. This induces immediate , itching, and of and , amplifying ocular surface . Dominance of Th2 immune responses further sustains the process, with cytokines like IL-4 promoting B-cell class switching to IgE production and IL-13 enhancing mucus secretion and epithelial barrier dysfunction. These Th2-skewed signals, including IL-5 for recruitment, create a chronic inflammatory milieu in forms like vernal or atopic keratoconjunctivitis. Chemical pathways initiate direct toxic injury to the conjunctival upon exposure to irritants, acids, or alkalis, bypassing immune mediation. Alkalis, such as or , penetrate deeply by saponifying cell membrane , causing and widespread epithelial denudation that extends to stromal layers. Acids, like , provoke protein coagulation on the surface, limiting deeper invasion but still resulting in ischemic and sloughing of the epithelium. Irritants, including alcohols or environmental pollutants, induce through generation, leading to , protein modification, and in conjunctival cells. This oxidative damage disrupts tear film stability and triggers secondary inflammatory cascades via release, such as TNF-α, exacerbating surface . Chronic forms of arise from persistent exposure, driving progressive and tissue remodeling in the . In conditions like vernal or atopic keratoconjunctivitis, ongoing allergen or autoantigen stimulation activates conjunctival and myofibroblasts, marked by α-smooth muscle actin expression, leading to excessive deposition and subepithelial collagen accumulation. This results in forniceal shortening, , and ankyloblepharon, impairing ocular motility and lubrication. Th2-derived cytokines, particularly IL-13 and TGF-β from CD11b+ dendritic cells and T-helper cells, form a feedback loop that sustains proliferation and inhibits matrix degradation, culminating in irreversible scarring. In autoimmune variants like ocular , chronic progresses through phases of injury, proliferation, and , with persistent autoantigen-driven responses amplifying remodeling.

Types of Conjunctivitis

Viral Conjunctivitis

Viral conjunctivitis, the most prevalent form of infectious conjunctivitis in adults, is primarily caused by adenoviruses, which account for approximately 80% of cases, followed by and enteroviruses. Adenoviral serotypes such as 3, 4, 7, 8, 19, and 37 are most commonly implicated, often leading to epidemic keratoconjunctivitis (EKC) in outbreaks. Emerging strains, including A24 variant (CVA24v), have been associated with outbreaks since 2023, notably in regions like , Bhutan, and the islands, with continued outbreaks reported in 2024-2025 in (e.g., , ) and the (e.g., , ). The involves viral entry and replication within conjunctival and corneal epithelial cells, resulting in cytopathic effects such as cell swelling, lysis, and . This replication triggers an inflammatory response, including recruitment of immune cells and release of cytokines, which contributes to conjunctival hyperemia and . In adenoviral cases, late-phase subepithelial infiltrates in the arise from a reaction to viral antigens, potentially persisting beyond the acute infection. Characteristic signs and symptoms include unilateral or bilateral ocular redness, watery discharge, foreign body sensation, burning, itching, and , often with preauricular indicating viral etiology. Symptoms typically emerge after a 5- to 12-day and peak within 3 to 5 days, resolving over 1 to 2 weeks in most cases, though discomfort may linger. Severe adenoviral infections may present with follicular conjunctivitis or, in EKC, corneal involvement manifesting as subepithelial opacities. Diagnosis relies on clinical pattern recognition, including the presence of watery discharge and , to differentiate from other forms. In outbreak settings or atypical cases, confirmatory (PCR) testing of conjunctival swabs identifies the specific virus, serving as the gold standard for etiologic confirmation. Rapid antigen tests may aid initial assessment but have lower sensitivity compared to PCR. Treatment is predominantly supportive, emphasizing cold compresses, , and ointment to alleviate symptoms and prevent secondary bacterial . For herpetic cases, topical or oral antivirals such as acyclovir are indicated to reduce duration and complications. No specific antiviral therapy is approved for adenoviral conjunctivitis, though Phase 2 trials evaluating IVIEW-1201 were completed in 2024, with Phase 3 studies planned or initiated as of 2025 to explore targeted interventions to shorten and symptom resolution. Strict measures, including handwashing and isolation, are essential to curb transmission. Complications are uncommon but may include pseudomembrane formation on the tarsal in severe adenoviral infections, potentially leading to scarring if not managed promptly. , manifesting as punctate or geographic epithelial defects, occurs rarely and can impair vision temporarily due to corneal . Persistent subepithelial infiltrates may require topical corticosteroids in refractory cases, under specialist supervision to avoid exacerbating infection.

Bacterial Conjunctivitis

Bacterial conjunctivitis, a common form of infectious conjunctivitis, is particularly prevalent in children and results from bacterial colonization of the conjunctival surface. The primary causative agents include Staphylococcus aureus, Streptococcus pneumoniae, and Haemophilus influenzae, which account for most cases in both children and adults. In neonates, Neisseria gonorrhoeae is a significant pathogen, often acquired through vertical transmission during birth. This condition is more frequent in pediatric populations due to higher exposure in school settings and immature immune responses. The involves bacterial adherence to the compromised conjunctival , where normal such as staphylococci and streptococci overgrow following disruptions in host defenses, such as minor trauma or viral coinfection. Certain produce toxins that exacerbate inflammation and tissue damage, while formation by pathogens like S. aureus promotes persistent infection and resistance to clearance, ultimately leading to the accumulation of purulent . This inflammatory response causes conjunctival hyperemia and , distinguishing it from noninfectious forms. Characteristic include sticky yellow-green purulent or that often mats the eyelids upon waking, conjunctival injection, and mild ocular discomfort or foreign body sensation. Unlike viral or allergic variants, itching is typically absent, and the condition is unilateral at onset but may become bilateral. Most uncomplicated cases resolve spontaneously within 7 to 10 days without intervention, though symptoms can persist longer in the absence of treatment. Diagnosis is primarily clinical, relying on the history of purulent discharge and eyelid crusting in the absence of severe pain or vision changes that might suggest deeper involvement. In mild cases, no further testing is needed, but for severe presentations, neonates, or treatment failures, conjunctival swabs for Gram staining or bacterial culture are recommended to identify the pathogen and guide therapy. Treatment focuses on topical antibiotics to accelerate resolution and reduce contagiousness, with options including erythromycin ointment or fluoroquinolone drops applied four times daily for 5 to 7 days. For gonococcal cases, systemic antibiotics such as ceftriaxone are essential alongside topical agents. Emerging therapies, such as the antibiotic-NSAID combination NTC014 (a quinolone with bromfenac), completed Phase II trials in late 2024 (MIRAKLE study), demonstrating non-inferiority to antibiotic monotherapy with faster symptom relief and microbiological eradication. Complications are uncommon in routine cases but can be severe in untreated gonococcal infections, including corneal ulceration, , and potential blindness due to rapid progression.

Allergic Conjunctivitis

Allergic conjunctivitis is an immune-mediated inflammatory condition of the triggered by environmental allergens, distinguishing it as a non-infectious form of ocular . It affects approximately 15-40% of the global population and is characterized by a reaction. Primary causes include exposure to airborne allergens such as , dust mites, animal dander, and mold spores, often exacerbated by , , and environmental factors like . The condition manifests in several types, with seasonal allergic conjunctivitis (SAC) being the most common, occurring during high-pollen seasons like spring and summer due to tree and grass pollens. Perennial allergic conjunctivitis (PAC) presents year-round with milder symptoms, primarily triggered by indoor allergens such as house dust mites and pet dander, often worsening in autumn. A more severe variant, (VKC), typically affects young males aged 5-20 in warm, dry climates and involves recurrent episodes linked to allergens and climatic factors. Pathophysiologically, allergic conjunctivitis involves where allergens cross-link IgE antibodies on sensitized mast cells and basophils, leading to rapid and release of mediators like , , and leukotrienes. This initiates an immediate phase of , characterized by and increased . A late-phase response follows, involving of , T cells, and additional inflammatory cells, which perpetuate conjunctival and hyperemia through release. Clinically, patients experience intense typically bilateral ocular itching as the hallmark symptom, though rarely unilateral if allergen exposure is asymmetric, often accompanied by excessive tearing, conjunctival (swelling), and injection (redness) from dilated blood vessels, which can be localized in such cases. Symptoms typically persist or recur with ongoing exposure and may include watery or mucoid discharge; in VKC, additional features like , thick , and giant papillae on the tarsal are common. These manifestations are usually self-limiting but can significantly impair quality of life during peak exposure periods. Diagnosis relies primarily on a detailed history of exposure and atopic conditions, supplemented by clinical examination revealing characteristic signs like conjunctival hyperemia and . Conjunctival scrapings or impression cytology can confirm the presence of , supporting the allergic etiology, while allergy testing such as skin prick or serum IgE levels may identify specific triggers. excludes infectious causes through absence of purulent discharge or . Treatment focuses on symptom relief and inflammation control, beginning with allergen avoidance strategies. Topical antihistamines (e.g., emedastine) and dual-action antihistamine-mast cell stabilizers (e.g., ) are first-line therapies, providing rapid relief from itching and redness by blocking and preventing mediator release. For severe or refractory cases, particularly VKC, short-term topical corticosteroids (e.g., ) are used to suppress , though with caution due to risks like . Emerging therapies include reproxalap, a reactive species modulator under FDA review as of 2025 for potential use in to reduce and symptoms. Immunomodulators like cyclosporine may be employed in chronic forms. Complications are rare in mild SAC and PAC but more frequent in VKC, where chronic inflammation can lead to corneal involvement, including superficial punctate keratitis or shield ulcers—raised epithelial defects that occur in 3-20% of cases and risk permanent scarring or vision loss if untreated. Prompt management is essential to prevent these sequelae.

Chemical and Irritant Conjunctivitis

Chemical and irritant conjunctivitis arises from direct exposure to external agents that damage the conjunctival surface without involving infectious or allergic pathways. Primary causes include environmental irritants such as in swimming pools, tobacco smoke, and airborne pollutants, as well as chemical exposures like acids (e.g., from battery leaks) and alkalis (e.g., from cleaning products or lime from construction materials). Overuse or improper care of contact lenses, including exposure to contaminated solutions, also commonly triggers this form by causing mechanical irritation and toxic buildup on the ocular surface. The involves direct to the conjunctival , where irritants disrupt the balance, leading to protein denaturation and tissue . Acids typically cause by precipitating proteins, forming a barrier that limits deeper penetration, whereas alkalis induce through of cell membranes and free radical generation, resulting in more severe and penetrating damage. This acute injury provokes an inflammatory response with , , and release of inflammatory mediators, exacerbating conjunctival hyperemia without the immune-mediated features seen in allergic cases; exposure to irritants like dust, smoke, chlorine, or chemicals can cause localized redness by affecting specific areas of the eye, leading to dilated blood vessels in those regions, and uneven dry eye can contribute to localized irritation. Symptoms manifest immediately upon exposure, characterized by intense burning pain, conjunctival redness, and a sensation, often accompanied by tearing and mild mucous discharge. Severity varies by agent; for instance, alkali exposures produce more profound symptoms and tissue destruction than acids due to their deeper penetration. In cases involving chlorine gas or smoke, patients may experience and from epithelial sloughing, while contact lens-related irritation can lead to discomfort that worsens with prolonged wear. Diagnosis relies primarily on a detailed of recent exposure to confirm the irritant source, supplemented by clinical examination revealing conjunctival injection and . Testing the tear film with paper is essential for chemical exposures, aiming to neutralize it to 7.0–7.2 to assess the need for further intervention; slit-lamp biomicroscopy may reveal epithelial defects or corneal involvement. Unlike infectious forms, routine cultures are unnecessary unless secondary is suspected. Treatment prioritizes immediate removal of the irritant through copious with normal saline or , ideally for at least 30 minutes or until normalizes, to minimize ongoing damage. Symptomatic relief includes cycloplegic agents like to reduce ciliary spasm and pain, along with topical lubricants; antibiotics are reserved for cases with secondary bacterial infection and are not routinely indicated. For milder irritants like smoke or , and avoidance of the trigger often suffice for resolution within hours to days. Complications are more likely with severe chemical burns, particularly from alkalis, and can include conjunctival scarring, (adhesions between and eyelid), and ischemic damage leading to limbal deficiency. Untreated exposures may progress to corneal opacification or perforation, necessitating surgical interventions like amniotic membrane transplantation in refractory cases.

Other Forms

Other forms of conjunctivitis encompass specialized variants such as neonatal infections, chronic infectious conditions like , drug-induced reactions, and autoimmune-associated cases, which differ from the primary viral, bacterial, allergic, or irritant categories due to their unique etiologies and presentations. Neonatal conjunctivitis, also known as ophthalmia neonatorum, arises from perinatal transmission of pathogens during delivery, with chlamydial and gonococcal infections being prominent causes. Chlamydial neonatal conjunctivitis is caused by serovars D-K acquired from maternal genital tract infection, while gonococcal cases stem from . In pathophysiology, chlamydial involves intracellular replication of the bacterium in conjunctival epithelial cells, leading to an inflammatory response with , whereas gonococcal triggers a hyperacute purulent reaction due to bacterial endotoxin release. of gonococcal neonatal conjunctivitis typically manifest within 24-48 hours of birth, featuring severe eyelid , copious purulent discharge, and , potentially progressing to corneal ulceration if untreated. Chlamydial cases present later, around 5-14 days, with milder mucopurulent discharge, conjunctival injection, and pseudomembrane formation. Diagnosis relies on Gram staining and culture for gonorrhea, revealing gram-negative diplococci, and Giemsa staining or nucleic acid amplification tests (NAATs) for chlamydia to detect intracytoplasmic inclusions. Treatment for gonococcal conjunctivitis requires systemic (25-50 mg/kg IV single dose) or , alongside saline irrigation to remove discharge, while chlamydial is managed with oral erythromycin (50 mg/kg/day for 14 days) or (20 mg/kg single dose), evaluating the mother and partner for concurrent infections. Trachoma represents a chronic form of infectious conjunctivitis endemic in certain regions, caused by repeated ocular exposure to Chlamydia trachomatis serovars A-C, often through direct contact or fly vectors in areas with poor sanitation. The pathophysiology involves persistent follicular hyperplasia in the tarsal conjunctiva from repeated infections, progressing through inflammatory stages to cicatricial scarring, entropion, and trichiasis. Early signs include conjunctival follicles and lymphoid aggregates, evolving to chronic dryness, corneal opacity, and scarring; symptoms encompass irritation, tearing, and photophobia, with late-stage vision loss from corneal abrasion by inturned lashes. Diagnosis is primarily clinical using the WHO simplified grading system, supplemented by PCR detection of C. trachomatis DNA in conjunctival swabs, and Giemsa staining for elementary bodies in resource-limited settings. Treatment follows the SAFE strategy: systemic azithromycin (20 mg/kg single oral dose for children, 1 g for adults) for active infection, surgical correction of trichiasis, facial cleanliness, and environmental improvements to reduce transmission. Complications include irreversible blindness from corneal scarring, making trachoma the leading infectious cause of blindness worldwide, affecting an estimated 1.9 million people. Drug-induced conjunctivitis can emerge as a reaction to medications, including recent reports of ocular adverse events from immune checkpoint inhibitors (ICIs) used in , such as and nivolumab. These agents provoke immune-related adverse events through T-cell activation against self-antigens, leading to conjunctival inflammation in approximately 1% of cases, often manifesting as part of . involves immune-mediated epithelial damage and vascular changes, with symptoms including red eyes, irritation, foreign body sensation, and mild discharge, typically appearing weeks to months after initiation. is clinical, supported by exclusion of other causes via slit-lamp examination and discontinuation trials, with the aiding causality assessment. Management entails prompt discontinuation of the offending drug, for mild cases, and topical corticosteroids for persistent inflammation, rarely requiring ICI cessation. Autoimmune conjunctivitis, exemplified by keratoconjunctivitis sicca in Sjögren's syndrome, results from systemic autoimmune attack on lacrimal glands, primarily affecting women over 40. The underlying pathophysiology features lymphocytic infiltration and autoimmune epithelitis of exocrine glands, reducing tear production and causing evaporative dry eye with secondary conjunctival inflammation. Signs and symptoms include chronic ocular dryness, grittiness, burning, redness, and filamentary keratitis, often accompanied by xerostomia. Diagnosis involves Schirmer's test for tear quantity (<5 mm/5 min), fluorescein staining for ocular surface damage, and confirmatory salivary gland biopsy showing focal lymphocytic sialadenitis, alongside serologic tests for anti-SSA/Ro and anti-SSB/La antibodies. Treatment focuses on supportive measures like preservative-free artificial tears and punctal occlusion, with anti-inflammatory options such as topical cyclosporine or lifitegrast, and systemic immunosuppressants (e.g., hydroxychloroquine) for severe cases.

Diagnosis

Clinical Evaluation

The clinical evaluation of suspected conjunctivitis begins with a detailed patient history to identify key features that guide and . Clinicians assess the onset of symptoms, distinguishing acute presentations (typically within days) from chronic ones (lasting weeks to months), as well as whether involvement is unilateral or bilateral, which may suggest infectious versus systemic etiologies. The character of ocular discharge is critical: purulent or often points to bacterial causes, while watery discharge is more common in viral or allergic forms. Symptom differentiation includes evaluating for prominent itching, which strongly suggests , versus pain or foreign body sensation, which may indicate infectious or irritant processes; or discomfort in bright light further refines the assessment. Exposures and contacts are probed, including recent upper respiratory infections, close contact with individuals having red eyes, environmental allergens like or animal dander, use, or chemical irritants, as these can pinpoint transmission routes or triggers. Physical examination follows, starting with measurement of to detect any impairment, which is uncommon in uncomplicated conjunctivitis but warrants further investigation if present. External inspection reveals eyelid swelling, crusting, or matting, while slit-lamp biomicroscopy allows detailed evaluation of conjunctival injection—diffuse redness of the bulbar and tarsal —and assessment for corneal involvement such as infiltrates or ulcers. Eversion of the eyelids exposes the superior tarsal to identify follicles (small, avascular elevations typical of viral processes) or papillae (vascularized projections seen in allergic or bacterial cases), aiding in etiological clues. Preauricular or submandibular may also be palpated, particularly in viral infections. Type-specific signs, such as preauricular nodes in adenoviral cases, provide additional context but require correlation with . Red flags during evaluation necessitate urgent ophthalmologic referral to rule out sight-threatening conditions. These include significant vision loss, severe ocular pain disproportionate to findings, (pus in the anterior chamber), or profound , which may signal corneal ulceration, , or acute angle-closure rather than isolated conjunctivitis. In resource-limited settings, basic tools like a penlight can suffice for initial injection assessment, but slit-lamp use is standard for precision. For chronic or recurrent conjunctivitis, emerging includes of tear biomarkers to differentiate inflammatory subtypes. Tear cytokines, such as interleukin-6 or tumor necrosis factor-alpha, are elevated in inflammatory dry eye-associated conjunctivitis and can help distinguish it from noninflammatory causes. Similarly, oxylipins—lipid-derived inflammatory mediators like hydroxyeicosatetraenoic acids—serve as diagnostic biomarkers in ocular cicatrizing conjunctivitis, a chronic scarring form, with specific profiles aiding in targeted . These non-invasive tear sampling techniques enhance clinical differentiation when standard and exam are inconclusive.

Laboratory and Imaging Tests

Laboratory tests for conjunctivitis are typically reserved for cases where clinical evaluation is inconclusive, such as severe, recurrent, or atypical presentations, to identify infectious agents or underlying immune responses. Bacterial conjunctivitis diagnosis may involve conjunctival swabs for Gram staining and culture to isolate pathogens like Staphylococcus aureus or Haemophilus influenzae, particularly in neonates or immunocompromised patients where empirical treatment fails. Viral etiologies, especially adenovirus, are confirmed via polymerase chain reaction (PCR) on conjunctival swabs, which offers high sensitivity and specificity compared to traditional viral culture; for instance, real-time PCR detects adenoviral DNA in over 90% of epidemic keratoconjunctivitis cases. Point-of-care immunochromatographic assays, such as the AdenoPlus or QuickVue test, provide rapid detection of adenovirus in ocular swabs within 10 minutes; these CLIA-waived tests have a sensitivity of 85-96% and specificity of 96-100% relative to PCR or culture, enabling quick identification of contagious cases in outpatient or emergency settings. Allergy testing is indicated when allergic conjunctivitis is suspected based on history of atopy or bilateral symptoms. Skin prick testing (SPT) identifies IgE-mediated sensitization to common aeroallergens like pollen or dust mites by wheal-and-flare response within 15-20 minutes, correlating well with clinical symptoms in seasonal allergic conjunctivitis. Alternatively, serum-specific IgE assays quantify allergen-specific antibodies, providing a non-invasive option for patients on antihistamines that could interfere with SPT, though tear IgE measurement is emerging for direct ocular assessment. Imaging modalities are infrequently required but aid in evaluating corneal complications. Fluorescein staining, applied topically and viewed under cobalt blue light, reveals epithelial defects or ulcers associated with corneal involvement in infectious or chemical conjunctivitis, guiding to prevent progression. (OCT) of the anterior segment visualizes subepithelial infiltrates in adenoviral cases, measuring corneal thickness and monitoring resolution non-invasively, which is particularly useful in persistent . Conjunctival biopsy is performed in chronic or suspected autoimmune conjunctivitis to confirm diagnoses like ocular cicatricial pemphigoid. and direct on biopsy specimens detect linear IgG or C3 deposits at the basement membrane, essential for distinguishing cicatrizing conditions from infections. These tests' interpretations align with specific etiologies, such as PCR positivity supporting viral pathways detailed elsewhere.

Differential Diagnosis

Conjunctivitis, characterized by diffuse conjunctival injection and often accompanied by discharge, must be differentiated from other causes of red eye to avoid missing vision-threatening conditions. Key mimics include , which involves corneal and typically presents with severe pain, , decreased , and fluorescein staining revealing epithelial defects or infiltrates, unlike the usually preserved vision and lack of corneal involvement in conjunctivitis. , an intraocular , is distinguished by ciliary flush (perilimbal injection), , , and anterior chamber cells or flare on slit-lamp examination, contrasting with the diffuse redness and absence of pupillary changes or intraocular findings in uncomplicated conjunctivitis. Acute angle-closure glaucoma manifests as a painful red eye with marked vision reduction, halos around lights, mid-dilated fixed pupils, and a firm globe due to elevated intraocular pressure, features not seen in conjunctivitis where pain is mild or absent and intraocular pressure remains normal. Dry eye syndrome often mimics mild conjunctivitis with bilateral redness, foreign body sensation, and reflex tearing but lacks significant discharge and shows punctate epithelial erosions on staining rather than overt conjunctival inflammation. Episcleritis presents with sectoral redness, mild tenderness, and dilated episcleral vessels that blanch with topical phenylephrine, differing from the diffuse injection and potential discharge of conjunctivitis, with normal vision preserved in both but episcleritis lacking systemic associations common in some conjunctivitis forms. In neonates, conjunctivitis differentials include , a congenital causing unilateral epiphora, lid swelling, and purulent reflux from the punctum upon medial canthal pressure, unlike the more diffuse bilateral involvement and lack of a palpable mass in infectious neonatal conjunctivitis. Gonococcal conjunctivitis, a severe form, is distinguished by its hyperacute onset with profuse purulent discharge, lid edema, and risk of corneal perforation, often bilateral and requiring urgent Gram staining to identify gram-negative diplococci, contrasting with milder bacterial causes. Drug-related conjunctivitis, such as from topical medications or preservatives, typically arises shortly after exposure with watery discharge and unilaterality if unilateral instillation occurred, while infectious forms like viral (watery, preauricular ) or bacterial (purulent) develop more gradually and may spread bilaterally, aiding distinction based on timing and exposure history.
ConditionKey Distinguishing FeaturesCitation
Severe pain, , corneal defects on fluorescein staining, decreased vision
Ciliary flush, anterior chamber inflammation, blurred vision
Halos, firm globe, elevated IOP, severe pain
Bilateral itching, no discharge, punctate erosions
Sectoral redness, blanches with , mild discomfort
Neonatal DacryocystitisUnilateral mass, reflux on pressure, minimal redness
Gonococcal ConjunctivitisHyperacute purulent discharge, lid , gram-negative diplococci

Management and Treatment

Supportive Care

Supportive care for conjunctivitis focuses on alleviating symptoms and promoting comfort through non-pharmacological interventions that are applicable across all types of the condition. Cold compresses, applied several times daily to the closed eyelids, help reduce swelling and soothe by constricting blood vessels and providing a cooling effect. Artificial tears, particularly preservative-free formulations refrigerated prior to use, offer lubrication to combat dryness and flush out irritants, improving ocular surface comfort without introducing additional chemicals. Over-the-counter redness-relief eye drops, such as those containing vasoconstrictors (e.g., tetrahydrozoline), should be avoided, as they can cause rebound vasodilation and exacerbate long-term irritation. These measures are recommended as initial steps to manage discomfort while the underlying cause resolves. Patients should refrain from rubbing their eyes to prevent worsening irritation and potential spread of infection. Lid hygiene plays a crucial role in maintaining cleanliness and preventing secondary complications, especially when crusting or discharge is present. Warm soaks using a clean, lint-free cloth wrung out in warm water can soften and remove crusts from the eyelids, typically applied for 5-10 minutes multiple times a day to facilitate gentle cleaning. Individuals with conjunctivitis should avoid wearing contact lenses or applying eye makeup entirely until symptoms fully resolve and an approves resumption, as these can exacerbate irritation, harbor pathogens, and prolong recovery. Proper cleaning of eyeglasses or other eyewear is also advised to minimize recontamination. To prevent transmission, particularly for infectious forms, strict isolation practices are essential. Frequent handwashing with and after touching the eyes or face, combined with avoiding close contact with others, significantly reduces spread. Personal items such as towels, pillowcases, bedding, and eye makeup should not be shared, and separate linens are recommended during the active period to limit indirect transmission. With appropriate supportive care alone, most cases of conjunctivitis resolve spontaneously within 1 to 2 weeks, depending on the , as the body's clears the or irritant without additional intervention.

Pharmacological Interventions

Pharmacological interventions for conjunctivitis target the underlying , with treatments tailored to bacterial, allergic, viral, or other forms to alleviate symptoms and prevent complications. Standard therapies emphasize topical agents for localized effects, while systemic options are reserved for severe or specific cases like herpetic infections. Selection of medications must consider the conjunctivitis type to avoid ineffective or harmful use, such as antibiotics in viral cases. In resource-limited settings, such as in Nigeria, Africa, and many developing countries, pharmacological management follows WHO-aligned guidelines and national standard treatment protocols, emphasizing cost-effective, available medications. For bacterial conjunctivitis (most common treatable form), topical antibiotics are the primary intervention, applied as ointments or drops to eradicate pathogens and reduce symptom duration. In resource-limited settings, first-line treatment is topical chloramphenicol 0.5% eye drops (every 2–4 hours) or 1% eye ointment (3–4 times daily) for 5–7 days, due to its availability, low cost, and broad-spectrum activity, despite rare concerns about aplastic anemia with topical use. Alternatives include tetracycline 1% eye ointment (especially in children and for trachoma-endemic areas), erythromycin 0.5% ointment, or fluoroquinolones (ciprofloxacin/ofloxacin drops) when available and resistance patterns allow. In other settings, common agents include tobramycin (0.3% solution, 1-2 drops every 4 hours for 5-7 days), polymyxin B/trimethoprim, or fluoroquinolones like for contact lens-associated infections. These are effective in mild to moderate cases, though many resolve spontaneously within 7-10 days without treatment. Antibiotics should be avoided in viral or , as they provide no benefit and may contribute to resistance. For hyperacute bacterial forms, such as gonococcal, with (1 g intramuscularly single dose) plus is required. In trachoma (hyperendemic in parts of Africa), the WHO SAFE strategy is employed, including mass distribution of single-dose oral azithromycin for active disease in endemic communities. Systemic antibiotics are rarely needed except in severe cases or neonatal gonococcal/chlamydial conjunctivitis. For viral conjunctivitis (often adenovirus), treatment is supportive only: saline irrigation, cold compresses, lubricating drops. Antibiotics are not indicated unless secondary bacterial infection occurs. For allergic conjunctivitis, and vasoconstrictors offer symptomatic relief by blocking release and reducing ocular hyperemia. Topical dual-action agents like (0.025% solution, 1 drop twice daily) combine and stabilization effects, improving itching and redness within hours. Other topical options include olopatadine and sodium cromoglicate. Oral , such as loratadine, may supplement for moderate cases. Intracanalicular dexamethasone inserts (DEXTENZA), approved by the FDA in 2021 for adults and expanded to pediatric patients aged 2 years and older in 2025, provide sustained release over 30 days to control intense itching and inflammation in severe cases, as evidenced by Phase 3 trials demonstrating superior relief compared to topical agents. These are contraindicated in infectious forms due to potential masking of symptoms. Corticosteroids, such as topical or , are used cautiously for severe inflammatory conjunctivitis, including allergic or post-viral cases, to suppress and discomfort. They are typically prescribed short-term (e.g., 1 week taper) under ophthalmologic due to risks like elevated , formation, or exacerbation of underlying infections. Steroids are avoided in active bacterial or herpetic infections without concurrent antimicrobials, as they can prolong viral replication or corneal perforation. Antiviral therapy is indicated for herpetic conjunctivitis caused by or zoster viruses. Oral acyclovir (400 mg five times daily for 7-10 days) is the standard for epithelial with conjunctival involvement, reducing duration and severity. Topical options like trifluridine (1% drops, 9 times daily) or gel may be used adjunctively. Routine antivirals are not recommended for common adenoviral conjunctivitis, which is self-limited. For neonatal conjunctivitis, prophylaxis with tetracycline 1% or erythromycin 0.5% eye ointment at birth is standard. Treatment depends on etiology, with systemic plus topical antibiotics for gonococcal/chlamydial causes.

Emerging Therapies

In the realm of viral conjunctivitis, particularly adenoviral forms, no FDA-approved specific antiviral treatments exist, leaving management reliant on supportive measures and off-label options. Urcosimod (formerly OK-101), a lipid-conjugated chemerin peptide agonist of the ChemR23 receptor, completed Phase 2 trials in 2025 with positive results for neuropathic corneal pain, which shares inflammatory pathways with viral conjunctivitis, positioning it for potential FDA discussions as of September 2025. For allergic conjunctivitis, reproxalap, a reactive aldehyde species (RASP) modulator, is under FDA review as of 2025 for addressing and driven by reactive s in the ocular surface. The resubmitted , accepted in July 2025 following a Complete Response Letter earlier that year, targets both dry eye disease and , with a PDUFA target action date of December 16, 2025, and prior Phase 3 data showing reductions in ocular redness and itching. In bacterial conjunctivitis, NTC014, a fixed-dose combination of a and an NSAID, showed promising full results in the Phase 2 MIRAKLE trial announced in December 2024, achieving non-inferior microbiological eradication to monotherapy while enhancing symptom resolution through effects. The multicenter, randomized study reported faster clinical improvement in adults, positioning NTC014 as a potential first-in-class option to address both infection and associated discomfort. Drug-induced conjunctivitis linked to , such as checkpoint inhibitors (e.g., PD-1/ and CTLA-4 inhibitors), has seen rising incidence reports in 2024, often manifesting as immune-related adverse events with conjunctival hyperemia and . Emerging management strategies include topical , which resolved symptoms in a reported case of nivolumab-associated conjunctivitis without interrupting cancer therapy, highlighting its role in for these irAEs. Consensus guidelines emphasize early multidisciplinary intervention to balance ocular recovery with ongoing immunotherapy.

Prevention

Hygiene and Lifestyle Measures

Maintaining strict personal hygiene is essential to prevent the transmission of infectious conjunctivitis and reduce recurrence risks. Frequent handwashing with soap and water for at least 20 seconds, particularly before and after touching the eyes or handling potentially contaminated items, significantly lowers the spread of bacteria and viruses. Avoiding rubbing or touching the eyes prevents the introduction of pathogens from hands or surfaces, while cleaning any eye discharge multiple times daily using a fresh, clean wet washcloth or cotton ball—followed by discarding the cotton and washing the cloth in hot water and detergent—helps remove infectious material. Additionally, disinfecting shared surfaces like doorknobs, counters, and personal items such as bedding and towels by washing them in hot water with detergent disrupts pathogen survival and transmission. For allergic conjunctivitis, lifestyle adjustments to minimize exposure to triggers are key to preventing flare-ups. Using high-efficiency particulate air () filters in home systems captures airborne allergens like and , reducing their concentration indoors. Wearing wraparound outdoors creates a barrier against entry, especially during high- seasons or windy conditions, thereby limiting irritant contact with the ocular surface. Staying indoors on dry, windy days and showering after outdoor activities to wash away adhered allergens further aids in avoidance. Contact lens wearers must adhere to rigorous hygiene protocols to avoid conjunctivitis, particularly microbial keratitis associated with poor care. Proper cleaning and storage of lenses according to manufacturer instructions, using fresh solution each time, prevents bacterial buildup, while opting for daily disposable lenses minimizes contamination risks compared to reusable ones. During active infection, contact lenses should be discarded, and wear discontinued until cleared by an eye care professional to prevent prolonged exposure and recurrence. In communal settings, policies promoting exclusion during contagious phases help curb outbreaks. Individuals with bacterial or viral conjunctivitis should stay home from school or work until symptoms improve and they receive clinician approval, typically after 24-48 hours of effective treatment or when no longer shedding the pathogen, to avoid close contact transmission. Allergic conjunctivitis does not require exclusion, as it is non-infectious.

Vaccination and Prophylaxis

Vaccination plays a limited but important role in preventing certain bacterial forms of conjunctivitis, particularly those caused by type b (Hib) and . The Hib conjugate vaccine, administered as part of routine childhood schedules, protects against invasive Hib and has been shown to reduce the incidence of Hib-associated conjunctivitis by preventing and subsequent . Similarly, pneumococcal conjugate vaccines (PCV15 or PCV20), recommended for all children younger than 5 years and high-risk groups, decrease nasopharyngeal carriage of vaccine-type , thereby lowering the risk of bacterial conjunctivitis caused by this pathogen. These vaccines do not cover all bacterial causes, such as nontypeable H. influenzae or other species, but their widespread use has contributed to overall reductions in bacterial conjunctivitis rates among vaccinated populations. For neonatal conjunctivitis, particularly ophthalmia neonatorum, prophylactic application of 0.5% erythromycin ophthalmic ointment to both eyes within the first hour of birth is recommended to prevent gonococcal and chlamydial infections acquired during delivery. This intervention is highly effective against , reducing the risk of gonococcal ophthalmia by over 90% when applied promptly, and is endorsed by the U.S. Preventive Services Task Force for all newborns regardless of maternal infection status. However, its efficacy against is limited, with studies showing it prevents only about 20-50% of cases, necessitating additional systemic treatment if chlamydial infection is suspected; despite this, it remains a standard practice due to its safety profile and broad applicability. In regions endemic for , a chronic form of conjunctivitis caused by , the World Health Organization-endorsed strategy serves as the cornerstone of prophylaxis and control. Adopted in 1993, integrates surgery to correct trichiasis (the inturned eyelashes that damage the ), mass antibiotic administration (typically ) to clear ocular , promotion of facial cleanliness to reduce bacterial transmission via hands and flies, and environmental improvements such as enhanced access to and sanitation to interrupt the cycle of reinfection. of has led to significant progress, with over 44 million people receiving antibiotics in 2024 alone, advancing toward global elimination targets by 2030. No currently exist to prevent viral conjunctivitis, which accounts for the majority of cases and is often caused by adenoviruses. into adenovirus vaccines has focused primarily on respiratory infections, with live oral vaccines against serotypes 4 and 7 used in settings since , but these do not confer protection against ocular due to limited cross-immunity. Ongoing studies explore recombinant and vector-based platforms targeting ocular serotypes like 8 and 19, which cause keratoconjunctivitis, but no licensed for conjunctivitis prevention has emerged as of 2025, highlighting the need for further clinical trials.

Complications and Prognosis

Short-Term Complications

In viral conjunctivitis, which accounts for the majority of cases and is often caused by adenovirus, secondary bacterial infections can develop due to disrupted ocular defenses and bacterial , leading to purulent discharge and prolonged symptoms. This complication is more common in children and immunocompromised individuals, where initial viral facilitates colonization by bacteria such as or . Prompt can resolve these secondary infections, preventing escalation to more severe local involvement. Lid cellulitis, or preseptal cellulitis, represents another acute risk, particularly in bacterial conjunctivitis cases where infection spreads from the to the surrounding tissues anterior to the . This manifests as swelling, erythema, and tenderness, often stemming from pathogens like or species, and requires systemic antibiotics to avert progression. In viral cases, it may arise secondarily if untreated, emphasizing the need for vigilant monitoring during acute episodes. Allergic conjunctivitis exacerbations can lead to pronounced , characterized by conjunctival edema that may balloon outward, especially in acute forms affecting younger patients. Severe itching and rubbing can further contribute to transient ptosis, or drooping of the , due to mechanical irritation and inflammation of the tarsal plate. These features typically resolve with topical antihistamines or stabilizers within hours to days, but recurrent episodes heighten the risk of corneal involvement such as punctate in viral or allergic types. Chemical conjunctivitis, triggered by exposure to irritants like or industrial agents, poses an immediate threat of if is inadequate or delayed, as the chemical penetrates the causing sloughing and ulceration. burns, in particular, exacerbate this by saponifying in the corneal surface, leading to deeper tissue damage that manifests as pain, , and hazy vision shortly after exposure. Immediate and thorough flushing with saline is critical to mitigate these short-term effects and restore ocular surface integrity. In neonates, untreated gonococcal conjunctivitis caused by can rapidly progress to systemic , with the bacterium disseminating via the bloodstream to cause , , or multi-organ failure. This hyperacute form presents with copious purulent discharge and marked within days of birth, underscoring the urgency of prophylactic ocular antibiotics at delivery to interrupt transmission from infected mothers. Early diagnosis via and culture allows for intravenous administration, which effectively halts septic progression in most cases.

Long-Term Outcomes

The majority of conjunctivitis cases, particularly those caused by bacterial or viral agents, resolve completely without long-term sequelae, with excellent prognosis for full recovery as long as the remains uninvolved. Most acute infections are self-limited, clearing within 1 to 3 weeks and rarely leading to chronic issues in otherwise healthy individuals. However, certain subtypes carry a higher risk of enduring complications that can impair vision over time. Trachoma, a chronic form of bacterial conjunctivitis caused by , remains the leading infectious cause of blindness worldwide, affecting millions in endemic areas and resulting in (inward turning of the eyelid) and due to repeated scarring from untreated infections. These sequelae develop progressively over years of reinfection, leading to irreversible in severe cases if the disease advances unchecked. Vernal keratoconjunctivitis (VKC), an allergic variant, often recurs seasonally and can cause long-term corneal scarring, shield ulcers, and potential vision loss from chronic inflammation if not managed aggressively. In advanced instances, this leads to or persistent opacities that compromise . Permanent damage is rare overall but occurs in untreated herpetic conjunctivitis, where can induce recurrent corneal scarring, neovascularization, and ulceration, culminating in significant vision loss or blindness. Similarly, chemical conjunctivitis from burns penetrates deeply, causing , conjunctival cicatrization, and corneal opacification that may require surgical intervention and result in lifelong visual deficits.

Epidemiology

Prevalence and Incidence

Conjunctivitis is a common ocular condition worldwide, accounting for 1-2% of primary care visits globally. In the United States, it affects approximately 6 million individuals annually, representing about 1% of all primary care consultations. The disease is particularly prevalent among children, where bacterial forms constitute 50-75% of cases, often peaking in winter months due to school-related transmission. Viral conjunctivitis predominates in adults, comprising up to 80% of cases and typically peaking during summer. Bacterial conjunctivitis has an estimated incidence of 135 cases per 10,000 population per year in the United States, based on 2024 data. Allergic conjunctivitis exhibits a lifetime prevalence of 15-40%, with rates rising in urbanized areas due to increased exposure to pollutants and allergens. Recent epidemiological studies highlight ongoing challenges with specific subtypes, such as (AHC) in . A 2025 analysis of data from 2004-2023 in Zhejiang Province, , reported 52,119 total cases with an average annual incidence of 5.37 per 100,000 population, showing highest rates among individuals aged 10-19 years (18.33% of cases) and 30-39 years (16.78%), alongside seasonal peaks from August to October. Risk factors for infectious conjunctivitis include overcrowding or close living quarters, which facilitate transmission of viral and bacterial pathogens through direct contact or fomites. For , —characterized by a genetic predisposition to IgE-mediated hypersensitivity—significantly increases susceptibility, often co-occurring with conditions like or . wear elevates the risk of bacterial conjunctivitis by approximately fourfold, primarily due to microbial contamination from poor or extended wear practices that compromise ocular surface defenses. Demographically, —a chronic form of infectious conjunctivitis caused by —is more prevalent in tropical and subtropical regions, particularly in rural, low-income communities in , , and parts of the where is limited. Bacterial conjunctivitis disproportionately affects children, accounting for 23% of bacterial conjunctivitis cases in those under 2 years old, compared to lower rates in adults, due to immature immune responses and higher exposure in group settings like daycare. Recent trends indicate a rise in allergic conjunctivitis cases linked to and ; for instance, increased particulate matter and elevated temperatures have been associated with higher outpatient visits for ocular allergies, exacerbating symptoms through prolonged seasons and irritant exposure. In viral conjunctivitis, post-2023 shifts include the emergence of A24 variant (CVA24v), with a detection rate of 33.3% (63/189 cases) in acute conjunctivitis surveillance in Shenzhen, , from 2018 to 2024, marking its first local identification in 2023. In low-resource areas, conjunctivitis complications—such as corneal scarring, vision impairment, or progression to -related blindness—are more frequent due to delayed access to treatment, inadequate infrastructure, and recurrent infections in impoverished settings. As of 2025, the reports that 18 countries have eliminated as a problem, with an additional six countries achieving elimination targets in 2025, reducing the global population at risk from over 250 million in 2010 to 113.8 million.

History

Early Recognition and Etymology

The term "conjunctivitis" derives from the Latin "," referring to the that joins or connects the eyelids to the eyeball, combined with the "-itis," denoting . This nomenclature emerged in the early , with the earliest recorded use appearing around 1821 in to describe of this specific ocular . The word "" itself originated in the 1540s from medical Latin "membrana conjunctiva," emphasizing its connective role in ocular . Early descriptions of what is now recognized as conjunctivitis date back to , where the condition was broadly termed "," encompassing various forms of eye inflammation, redness, and discharge. (c. 460–370 BCE), in the , documented symptoms such as redness of the eye, swelling of the eyelids resembling a cut ripe fig, and associated discharges, often linking them to humoral imbalances like excess or . These accounts, found in treatises like "On Sight," provided some of the first systematic observations of ocular irritation and secretion, though without distinguishing specific etiologies. In the 2nd century CE, of (129–216 CE) advanced these observations by defining more precisely as an of the , noting purulent discharges and vascular engorgement as key features. 's descriptions, based on dissections and clinical cases, emphasized the role of local in producing symptoms like tearing and crusting, influencing medical understanding for centuries. Nineteenth-century microbiological advances marked a pivotal shift toward identifying infectious causes of conjunctivitis. In 1879, Albert Neisser isolated (the gonococcus), linking it to purulent forms of the disease, particularly in neonatal cases transmitted during birth. This discovery, built on emerging bacteriological techniques, enabled differentiation of bacterial conjunctivitis from viral or allergic variants, laying foundational work for modern classification.

Notable Outbreaks and Advances

In 1953, Wallace P. Rowe and colleagues isolated human adenoviruses from degenerating human tissue in culture, marking the first identification of these viruses and establishing their role as causative agents in respiratory and ocular infections, including epidemic keratoconjunctivitis (EKC). This discovery linked adenoviruses, particularly types 8 and 19, to outbreaks of severe, highly contagious keratoconjunctivitis, which had previously been enigmatic and often misattributed to bacterial causes. The mid-20th century saw pivotal advances in bacterial conjunctivitis management with the introduction of topical in the 1940s, including penicillin ointments that effectively treated staphylococcal infections responsible for many cases. By the 1990s, (PCR) diagnostics revolutionized pathogen identification in conjunctivitis, enabling rapid detection of viral agents like adenovirus and enteroviruses from ocular swabs, which improved outbreak control and reduced unnecessary use. For , a chronic chlamydial form of conjunctivitis, the World Health Organization's SAFE strategy—encompassing surgery, , facial cleanliness, and environmental improvements—was adopted in 1997, leading to a 92% reduction in the global population at risk since 2002 through mass distribution and hygiene interventions. Notable outbreaks in the 21st century include the 2023 epidemic in Pakistan's Punjab province, where over 86,000 cases of viral conjunctivitis were reported in September alone, primarily due to coxsackievirus A24 variant, prompting school closures and heightened public health measures. Globally, acute hemorrhagic conjunctivitis (AHC) waves caused by coxsackievirus A24 have recurred, with significant episodes in (2023), (2023), and the islands of and (2024), characterized by sudden, self-limiting but highly transmissible subconjunctival hemorrhages. Recent therapeutic advances include evaluations in phase II studies of povidone-iodine-dexamethasone combinations for adenoviral conjunctivitis and the initiation of phase II trials in April 2025 for SHG-112, a ophthalmic nanoformulation by targeting the condition.

Society and Culture

Economic and Public Health Impact

Conjunctivitis imposes a substantial economic burden in the United States, with estimates of total direct and indirect costs for pediatric conjunctivitis ranging from $2.0 billion to $2.7 billion annually as of , primarily driven by lost productivity from work absences and expenses related to medical visits and treatments. Globally, the conjunctivitis treatment market is estimated at approximately USD 5.08 billion in , reflecting the widespread demand for diagnostics, pharmaceuticals, and supportive care across various forms of the condition. From a perspective, conjunctivitis accounts for about 1% of all visits in the United States, straining healthcare resources and necessitating efficient and protocols. Contagious cases, particularly bacterial and viral types, often lead to absences lasting 5-7 days to prevent transmission, contributing to educational disruptions and increased parental caregiving burdens. The chronic variant known as , a severe form of infectious conjunctivitis, remains the leading infectious cause of blindness worldwide, affecting an estimated 1.2 million people as of 2025, predominantly in regions of and where challenges exacerbate its impact; as of November 2025, 18 countries worldwide, including as the latest in the region, have eliminated trachoma as a problem. Rising costs associated with are notable due to the need for ongoing management, including antihistamines, corticosteroids, and , as the of severe cases continues to increase amid environmental allergens. These factors underscore the condition's broader societal toll, with occasional large-scale outbreaks amplifying and healthcare demands in affected communities.

Misconceptions and Stigma

One prevalent misconception about conjunctivitis, often referred to as pink eye, is that all cases are bacterial and thus require antibiotic treatment. In reality, the majority of conjunctivitis cases are viral or allergic, which are self-limiting and do not respond to antibiotics; viral cases typically resolve within 7-14 days without intervention, while allergic conjunctivitis is managed with antihistamines or avoidance of allergens. This belief drives overprescription, with studies showing that up to 60% of antibiotic eye drops for acute conjunctivitis are unnecessary, contributing to antimicrobial resistance and potential side effects like corneal irritation. The fear of contagion surrounding infectious forms of conjunctivitis often leads to , resulting in unnecessary isolation of affected individuals, particularly in educational and settings. policies frequently mandate exclusion until 24-48 hours after starting treatment for bacterial cases, even though suggests that mild viral or bacterial conjunctivitis does not warrant routine isolation to prevent outbreaks. This overcaution can exacerbate feelings of exclusion and disrupt daily life, as the condition's visible redness amplifies perceptions of high transmissibility despite varying contagion risks across subtypes. In certain cultural contexts, reliance on herbal remedies for neonatal conjunctivitis can delay access to prompt medical care, increasing risks of complications like vision impairment from untreated ophthalmia neonatorum. For instance, in parts of , traditional birth attendants commonly apply concoctions or home remedies to newborns' eyes before seeking help, which may introduce contaminants or postpone prophylaxis. Similar practices in regions like and involve natural substances such as or surma (kohl), rooted in longstanding beliefs, but these can hinder early and treatment. Educational gaps further perpetuate self-treatment errors, as many individuals fail to distinguish allergic conjunctivitis from infectious types, leading to inappropriate use of over-the-counter remedies or avoidance of care. , characterized by bilateral itching and seasonal triggers, is non-contagious and responds to measures, yet it is often mistaken for bacterial infection, prompting unnecessary . Surveys indicate that approximately 19% of people incorrectly believe allergic forms can spread person-to-person in a 2025 study of residents, fostering stigma and delaying targeted interventions like allergen avoidance or mast cell stabilizers.

References

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