Infectious, chlamydial and neonatal conjunctivitis

The conjunctiva is a continuous, vascularised mucous membrane lining the posterior surface of the eyelids (palpebral conjunctiva), reflecting across the superior and inferior fornices, and draping over the anterior sclera up to the corneal limbus (bulbar conjunctiva). The substantia propria contains an extensive mucosa-associated lymphoid tissue (MALT) network with resident lymphocytes, plasma cells, mast cells, and dendritic Langerhans cells. Conjunctival inflammation (conjunctivitis) exhibits distinct biomicroscopic patterns—follicles, papillae, membranes, and cicatrisation—that correlate with underlying infectious, allergic, or autoimmune etiologies.

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1. Acute Infectious Conjunctivitis: Microbial Etiologies

Acute Bacterial Conjunctivitis

Most common in children and elderly patients, classic acute bacterial conjunctivitis presents with acute-onset redness, grittiness, morning eyelid sticking (mattering), and mucopurulent discharge. Common culprits include Streptococcus pneumoniae, Haemophilus influenzae (frequently associated with concurrent otitis media in young children), Staphylococcus aureus, and Moraxella catarrhalis. Biomicroscopy reveals a tarsal papillary reaction (vascular core surrounded by inflammatory cells). While typically self-limiting within 7 to 10 days, broad-spectrum topical antibiotics (chloramphenicol 0.5%, polymyxin B/trimethoprim, or fluoroquinolones) accelerate clinical and microbiological clearance.

Hyperacute Purulent Conjunctivitis (Neisseria gonorrhoeae)

Neisseria gonorrhoeae is a fastidious, sexually transmitted Gram-negative diplococcus capable of penetrating an intact corneal epithelium. It constitutes a medical and ophthalmic emergency.

• Clinical Presentation: Rapid progression within 12 to 24 hours characterised by copious, thick, torrential purulent exudate that overflows the lid margins and re-accumulates within seconds of wiping. Profound chemosis, marked eyelid oedema, and a tender, prominent preauricular lymph node may occur; their absence does not exclude infection.
• Corneal Risk: Rapid stromal invasion and enzymatic degradation by bacterial proteases can lead to stromal liquefaction, descemetocele formation, and corneal perforation within 24 to 48 hours.
• Diagnostics: Immediate conjunctival swab for Gram stain demonstrating intracellular Gram-negative diplococci within polymorphonuclear leukocytes; culture on Thayer-Martin chocolate agar incubated in $5\%\text{ CO}_2$; and nucleic acid amplification testing (NAAT).
• Emergency Treatment: Systemic therapy is mandatory:
  • CDC recommends ceftriaxone 1 g intramuscularly once for adolescent/adult gonococcal conjunctivitis; consider one-time saline lavage and infectious-disease advice.
  • If chlamydia has not been excluded, add the appropriate antichlamydial treatment; the usual non-pregnant adult regimen is doxycycline 100 mg twice daily for seven days. Routine ceftriaxone–azithromycin dual therapy is outdated.
  • Corneal ulceration or disseminated infection needs urgent specialist assessment and a treatment plan for that complication, not automatic extension of a simple-conjunctivitis regimen.

Viral Conjunctivitis: Adenoviral Syndromes

Adenovirus is a non-enveloped double-stranded DNA virus responsible for the vast majority of viral ocular infections. Adenoviral conjunctivitis manifests primarily as two clinical syndromes:

1. Pharyngoconjunctival Fever (PCF): Caused primarily by serotypes 3, 4, and 7; characterized by high fever, pharyngitis, tender preauricular lymphadenopathy, and bilateral follicular conjunctivitis, most commonly in school-aged children.
2. Epidemic Keratoconjunctivitis (EKC): Caused primarily by serotypes 8, 19, 37, 54, and 64; an aggressive, purely ocular infection with high epidemic transmissibility.

Slit-Lamp Biomicroscopy of Adenoviral Conjunctivitis

• Follicular Response: Elevated, translucent, avascular lymphoid germinal centres surrounded by fine peripheral vessels, prominent in the inferior palpebral conjunctiva.
• Petechial Subconjunctival Haemorrhages: Common in severe serotype infections.
• Pseudomembranes vs True Membranes: Coagulated fibrinous exudate adhering to the inflamed conjunctival epithelium. Pseudomembranes can be peeled away leaving an intact epithelium without bleeding. True membranes incorporate the superficial epithelial layers; peeling leaves a raw, actively bleeding bed that predisposes to conjunctival cicatrisation and symblepharon if not removed.
• Nummular Subepithelial Corneal Infiltrates (SEIs): Appear 1 to 3 weeks after the onset of conjunctivitis as round, discrete, grey-white anterior stromal opacities underlying previous focal epithelial lesions. SEIs represent an immune-mediated delayed hypersensitivity reaction to viral capsid antigens retained within the stroma. They induce glare, photophobia, and reduced visual acuity.

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2. Chlamydial Conjunctivitis & Ophthalmia Neonatorum

Adult Inclusion Conjunctivitis (Chlamydia trachomatis Serovars D–K)

An oculogenital infection transmitted by autoinoculation from infected genital secretions in sexually active adolescents and young adults:

• Clinical Manifestations: Subacute or chronic follicular conjunctivitis persisting for weeks or months. Biomicroscopy reveals large, prominent follicles in the inferior fornix, mixed with a fine papillary reaction, superficial micropannus, peripheral subepithelial corneal infiltrates, and non-tender preauricular adenopathy.
• Diagnostics: Conjunctival NAAT swab (gold standard) or Giemsa staining demonstrating basophilic intracytoplasmic Halberstaedter-Prowazek inclusion bodies.
• Therapy: Systemic treatment is essential to eradicate the genital reservoir: Oral Azithromycin 1 g single dose or Oral Doxycycline 100 mg twice daily for 7 to 14 days. Sexual partners must be evaluated and treated concurrently.

Trachoma (Chlamydia trachomatis Serovars A, B, Ba, C)

The leading infectious cause of preventable blindness worldwide. The World Health Organization (WHO) simplified grading system defines:

• TF (Trachomatous inflammation - Follicular): $\ge 5$ follicles ($\ge 0.5\text{ mm}$) on the upper tarsal conjunctiva.
• TI (Trachomatous inflammation - Intense): Pronounced inflammatory thickening of the tarsal conjunctiva obscuring $> 50\%$ of deep normal tarsal vessels.
• TS (Trachomatous conjunctival Scarring): Presence of linear or stellate cicatricial bands (Arlt's line across the superior tarsus).
• TT (Trachomatous Trichiasis): At least one lash rubbing against the eyeball.
• CO (Corneal Opacity): Corneal scarring over the pupil.
• characteristic sign: Herbert's pits—depressed, circular cicatricial depressions at the superior limbus representing resolved limbal follicles. Managed by the WHO SAFE strategy: Surgery for trichiasis, Antibiotics (mass azithromycin distribution), Facial cleanliness, Environmental improvement.

Ophthalmia Neonatorum Chronological Differential

Ophthalmia neonatorum is defined as any conjunctivitis occurring within the first 28 days of neonatal life. The clinical timeline is essential for board examinations:

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Neonatal gonococcal disease needs assessment for disseminated infection and chlamydia. Ceftriaxone requires caution in hyperbilirubinaemic or premature infants and is unsuitable with simultaneous intravenous calcium; CDC provides a cefotaxime alternative in that setting. Chlamydial disease requires systemic treatment and follow-up because topical therapy alone does not address associated respiratory infection. Monitor neonatal macrolide exposure for pyloric stenosis. CDC neonatal gonococcal guidance.