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OP3.3 | Chronic Conjunctivitis and Trachoma — SDL Guide

Learning Objectives

• Enumerate the causes of chronic conjunctivitis
• Describe the aetiology, pathophysiology, and ocular features of trachoma
• Apply the WHO simplified trachoma grading system (TF, TI, TS, TT, CO)
• Outline the differential diagnosis of chronic follicular conjunctivitis
• Describe the management of trachoma including the WHO SAFE strategy

INSTRUCTIONS

While acute conjunctivitis resolves in days to weeks, chronic conjunctivitis persists beyond four weeks and carries a fundamentally different set of causes, of which trachoma is by far the most important globally. Trachoma — caused by Chlamydia trachomatis serotypes A-C — is the world's leading infectious cause of preventable blindness, affecting hundreds of millions in endemic communities. In India, trachoma was historically endemic across northern and central states and remains a target of the National Programme for Control of Blindness and Visual Impairment (NPCBVI). The WHO five-sign grading system and the SAFE strategy are the pillars of trachoma control and are specifically tested in Indian medical examinations.

References

• AK Khurana — Comprehensive Ophthalmology, 7th ed., Ch. 6: Diseases of Conjunctiva (Trachoma section) (textbook)
• Parsons' Diseases of the Eye, 23rd ed., Ch. 8: Diseases of the Conjunctiva (textbook)

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Version 2.0 | NMC CBUC 2024

The Chronic Red Eye — Causes and Clinical Approach

Chronic conjunctivitis is conventionally defined as conjunctival inflammation persisting for more than four weeks. Unlike acute conjunctivitis where the cause is often immediately obvious (mucopurulent discharge → bacterial; watery + follicular → viral), chronic conjunctivitis requires a more systematic investigation because the causes are diverse and many require systemic treatment rather than just topical antibiotics. The four-week threshold matters clinically because it signals that the body has not mounted a successful self-limiting response, meaning that either the pathogen is persistent (trachoma, Chlamydia, Demodex), the stimulus is ongoing (topical drug toxicity, lid margin disease), or the mechanism is immunological rather than purely infective (phlyctenular conjunctivitis). A clinician who approaches chronic conjunctivitis with the same algorithm as acute conjunctivitis — discharge character plus papillary-vs-follicular reaction — will quickly reach the limits of that framework, because in chronic disease the acute markers have often resolved and been replaced by the stigmata of chronicity: scarring, lid distortion, corneal changes. The four-category framework below provides the structural approach needed.

The causes of chronic conjunctivitis can be organised into four groups:

1. Infective chronic conjunctivitis:
- Trachoma (Chlamydia trachomatis A-C) — the most important; blinding; discussed in detail below.
- Angular blepharoconjunctivitis — caused by Moraxella lacunata, characterised by excoriation and maceration at the medial and lateral canthi, often with a thin mucopurulent discharge; responds to topical zinc sulphate or fluoroquinolones.
- Molluscum contagiosum — a poxvirus that causes pearly nodules on the eyelid margin; these release viral particles that chronically irritate the conjunctiva, causing a follicular conjunctivitis that does not resolve until the lid nodules are removed.
- Demodex blepharitis — Demodex folliculorum mites in the lash follicles; causes chronic anterior blepharitis with cylindrical dandruff at the lash bases and associated conjunctival irritation.

2. Immunological/hypersensitivity conjunctivitis:
- Phlyctenular conjunctivitis — a delayed hypersensitivity reaction, classically to Mycobacterium tuberculosis antigen (or Staphylococcal antigen); presents as a small nodule (phlycten) at the limbus with surrounding hyperaemia; the phlycten migrates across the cornea leaving a leash of vessels.
- Vernal keratoconjunctivitis — included here for completeness, though covered separately as OP3.4.

3. Toxic/drug-induced chronic conjunctivitis:
Long-term use of preserved topical eye drops (particularly those containing benzalkonium chloride as preservative) causes a follicular toxic conjunctivitis; chronic use of eyeliner or mascara can also cause toxic folliculosis.

4. Degenerative causes:
Pterygium and pinguecula cause chronic conjunctival irritation and redness (covered in OP3.5).

The clinical approach to chronic conjunctivitis differs from acute: a careful history of duration, endemic area exposure, travel, lid lesions, systemic disease, and topical medication history is essential before examination.

Trachoma: Pathogen, Epidemiology, and Transmission

Chlamydia trachomatis is an obligate intracellular gram-negative coccobacillus that infects the conjunctival epithelial cells. It has a unique biphasic life cycle: the elementary body (EB) is the extracellular infectious form that attaches to and enters the host epithelial cell; once inside, it converts to the reticulate body (RB), which is the intracellular replicating form; RBs divide by binary fission within an endosome (the inclusion body visible on cytological stain — called a Halberstaedter-Prowazek (HP) inclusion body in conjunctival smears of trachoma), then condense back into EBs, and the cell ruptures to release infectious EBs.

Serotypes causing trachoma: A, B, Ba, C — these infect the conjunctival epithelium but NOT the genital tract (contrast with D-K which infect both). The difference in serotype determines whether the disease is ocular-only (trachoma) or systemic.

Epidemiology:
Trachoma is endemic in 44 countries across Sub-Saharan Africa, the Middle East, Central and South Asia, and parts of Latin America. It is strongly associated with poverty, poor water supply, inadequate sanitation, and overcrowding. In India, the highest burden has historically been in the northern and central states. WHO's target is elimination of trachoma as a public health problem (prevalence of TF in children 1–9 years < 5%) — a target being approached in several previously endemic Indian districts.

Transmission:
Trachoma is transmitted person-to-person through several routes:
- Direct contact with ocular or nasal secretions of an infected person.
- Flies (principally Musca sorbens, the bush fly) that are attracted to ocular discharge and carry viable chlamydiae from one child's eyes to another's.
- Fomites — contaminated cloths, fingers.
- Crowding amplifies all these routes — multiple children sharing a sleeping space, a single water source, and limited face-washing facilities create the conditions for repeated reinfection that drives the cicatricial progression.

Children aged 1–5 years are the main reservoir of active infection in endemic communities. Women are more commonly blinded than men (through repeated exposure while caring for infected children), which is why trachoma is also a gender health issue.

Pathophysiology: From Follicle to Blindness

Understanding the pathological sequence from initial infection to blindness is essential for understanding why trachoma has been so difficult to eliminate — the blinding complications arise not from active infection but from the accumulated scarring of years of repeated reinfections. This distinction is also why antibiotic treatment alone is insufficient once trichiasis has developed.

The pathological progression unfolds in stages:

Stage 1 — Acute follicular inflammation (TF + TI): The initial chlamydial infection in early childhood causes an acute follicular conjunctivitis on the upper tarsal conjunctiva — indistinguishable from viral conjunctivitis on single examination. With repeated reinfection over months to years, the lymphoid follicles coalesce and the inflammation intensifies, recruiting neutrophils, plasma cells, and macrophages. The chlamydial inclusions visible in conjunctival epithelial cells are the histological hallmark of active disease.

Stage 2 — Conjunctival scarring (TS): After repeated episodes of acute inflammation and resolution, the subepithelial connective tissue undergoes progressive fibrosis. The characteristic scar is Arlt's line — a horizontal white fibrous band running parallel to and just below the lid margin on the upper tarsal conjunctiva — which is pathognomonic of trachoma. Generalised conjunctival scarring reduces goblet cell density, contributing to aqueous tear deficiency and dry eye.

Stage 3 — Cicatricial entropion and trichiasis (TT): As the upper tarsal conjunctiva scars and contracts, it progressively distorts the eyelid, turning the lid margin inward (cicatricial entropion). The misdirected eyelashes then rub continuously against the corneal surface (trichiasis). Each blink deposits the lash across the cornea, producing repeated micro-abrasions.

Stage 4 — Corneal opacity (CO): Repeated corneal abrasion from trichiasis triggers corneal vascularisation (pannus — superficial corneal vessels extending from the limbus over the upper cornea) and eventually corneal scarring. The opacity and pannus, if they encroach on the visual axis, produce the irreversible visual loss that defines trachoma blindness. Herbert's pits — pathognomonic limbal scars at the site of resolved limbal follicles — are a marker of prior severe trachoma even in the absence of active disease.

Critical concept: by the time a patient reaches the TT or CO stage, the active chlamydial infection has often spontaneously resolved. The damage is mechanical (lash-on-cornea) and fibrotic, not infectious — which is why surgery to correct trichiasis is the only intervention that can prevent further visual loss at this stage.