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Ocular System

Trachoma

Chronic mucopurulent keratoconjunctivitis caused by Chlamydia trachomatis leading to scarring of the inner surface of the eyelids and erosion of the corneal surface, which eventually leads to blindness.

Introduction

Chronic mucopurulent keratoconjunctivitis caused by Chlamydia trachomatis leading to scarring of the inner surface of the eyelids and erosion of the corneal surface, which eventually leads to blindness.

  • M/C cause of preventable blindness worldwide
  • #3 M/C cause of blindness overall (after cataract & glaucoma)
  • Trachoma is a Disease of poverty

History:

The history of this disease began as early as 8000 B.C. Taborisky and MacCallan believe Central Asia to be the origin. Old documents refer to Chinese therapies (2600 B.C.) and Hippocratic Corpus, as well as works of several physicians; including Celsus (1st century A.D.), Discorides (40–91 A.D.), and Galen (129–216 A.D.). Trachoma was prevalent in Europe between 1200 A.D. and 1700 A.D. Military activities helped the expansion of trachoma. In 1798, “Egyptian military ophthalmia” infected three thousand of Napoleon’s troops in the Egyptian war, blinding many. Napoleonic Wars accelerated the spread of trachoma across Europe. In 1810, British scientists proposed cleanliness, isolation, and improvement in the living conditions of soldiers as a measure to prevent the spread of trachoma. A new source of infection emerged as immigrants moved to the new land, America, at the end of the 19th century. In 1897, trachoma was the first disease classified as a dangerous contagious disease by the U.S. government. Infected immigrants were sent back to Europe by the United States Public Health Service physicians.

The causative agent of trachoma was not visualized until 1907, when Halberstaedter and von Prowazek described the presence of inclusion bodies (Halberstaedter-Prowazek bodies) inside infected cells. They believed the organism to be a protozoon. The transmissibility of trachoma was by then already firmly established in the minds of the public. Hundreds of Russian and Austro-Hungarian First World War conscripts, for example, evaded military service by infecting their own eyes with discharges wiped from the eyes of trachoma patients. Meanwhile, unconvinced by the findings of Halberstaedter and von Prowazek, researchers nominated a variety of bacteria, fungi, and viruses as the underlying pathogen. It was not until 1957 in Peking that T’ang and his colleagues completed the first successful isolation, using chicken embryos whose yolk sacs had been inoculated with material from infected human eyes. They were able to serially passage the organism in eggs and to use this material to infect the eyes of rhesus monkeys, producing characteristic clinical signs of trachoma and, on one occasion, inclusion bodies. Based on filtration experiments, they believed the trachoma agent to be a virus. T’ang et al.’s methods were successfully replicated by Collier and Sowa in the Gambia in 1958. The isolates obtained were noted both to have the same antigen as and to physically resemble the agents of psittacosis and lymphogranuloma venereum and the agent of some cases of cervicitis and mucopurulent conjunctivitis of the newborn.


Epidemiology

Map of trachoma endemic countries in 2009.
Map of trachoma endemic countries in 2009. | Silvio P. Mariotti, WHO/NMH/PBD.

Transmission:

  • Direct eye to eye spread during close contact
  • Hand-eye contact
  • Indirect spread on fomites
  • Transmission by eye-seeking flies

Pathophysiology

Chlamydia trachomatis (serotypes A, B, Ba, and C)

Ocular surface chlamydia infection causes a chronic inflammatory reaction, which is characterized by the presence of lymphocytic, monocytic, plasma cells and macrophages infiltrates. Prolonged inflammation induces conjunctival scarring as a result of recurrent and chronic conjunctival follicular reinfection. During a chlamydial infection the normal architecture of the conjunctival epithelium is disrupted, the goblet cells are lost and the normal, loose, vascular subepithelial stroma is replaced with compact bands of type IV and type V collagen.

Blindness from trachoma occurs from conjunctival scarring which is attributed to recurrent infection. Subtarsal conjunctival scarring leave fibrotic bands in which scar contraction leads to entropion, trichiasis, and eventually corneal opacification. Scar-tissue formation can result in loss of meibomian glands and degeneration of the tarsal plate. Dry eye can further compromise host immune responses at the ocular surface.

Recurrent inflammation of the eyelids leads to a cascade of conjunctival scarring, entropion, and inturned eyelashes (trichiasis) scratch the cornea further putting those affected at risk for secondary ulcers and eventually blindness.

Active ‘inflammatory’ stage: Common in pre-school children

Mild and may only result in trachomatous conjunctivitis (follicular/papillary). Intense cases are characterized by the presence of papillary hypertrophy.

Chronic ‘cicatricial’ stage: Commonly occurs in middle age

Recurrent infection elicits a chronic immune reaction of cell-mediated delayed hypersensitivity (Type 4) response. This repeated insult leads to scarring and other forms of permanent damage. Most of the scarring in this stage is prominent on the upper tarsal plate. This scar tissue contracts leading to in-turning of the lid, causing entropion, and this entropion eventually leads to trichiasis. Entropion is the most common cause of trichiasis in trachoma patients. Trichiasis, however, may also result from aberrant lashes or metaplastic lashes in rare cases. Ultimately, blinding corneal opacification can develop.

Presentation

McCallan’s classification (1908):

  • Stage I (Incipient trachoma or stage of infiltration)
  • Stage II (Established trachoma or stage of florid infiltration)
  • Stage III (Cicatrising trachoma or stage of scarring)
  • Stage IV (Healed trachoma or stage of sequelae)

WHO “FISTO” staging:

  1. TF | Trachomatous inflammation – follicular: Presence of five or more follicles (>0.5 mm) in the upper tarsal conjunctiva
  2. TI | Trachomatous inflammation – intense: Pronounced inflammatory thickening of the tarsal conjunctiva that obscures more than half of the deep normal vessels
  3. TS | Trachomatous scarring: Presence of scarring in the tarsal conjunctiva
  4. TT | Trachomatous trichiasis: At least one lash rubs on the eyeball
  5. CO | Corneal opacity: Easily visible corneal opacity over the pupil
WHO simplified system for trachoma
WHO simplified system for trachoma: (a) Normal conjunctiva, showing area to be examined. (b) Follicular trachomatous inflammation (TF). (c) Intense trachomatous inflammation (TI) (and follicular trachomatous inflammation). (d) Conjunctival scarring (TS). (e) Trichiasis (TT). (f) Corneal opacity (CO). | World Health Organization

Diagnosis

Diagnosis of trachoma is made on clinical grounds. Laboratory testing is typically unavailable or unaffordable for clinical care in areas where trachoma is endemic, antibiotics used against active disease can usually be provided at low or no cost to the patient, and those antibiotics are well tolerated by both children and adults, making presumptive treatment for suspected chlamydial infection a logical therapeutic approach

Differential diagnosis:

  • Allergic conjunctivitis (M/C cause of a red itchy eye)
  • Viral conjunctivitis: Red eye and foreign body sensation
  • Bacterial conjunctivitis: Purulent discharge
  • Inclusion conjunctivitis

Management

WHO “SAFE” strategy:

Public health strategy with a combination of the three elements of primary, secondary and tertiary prevention.
  • S: Surgery (relieving entropion and trichiasis and maintaining complete lid closure)
  • A: Antibiotic use (DOC: Azithromycin 1g single oral dose 20mg/kg)
  • F: Facial hygiene
  • E: Environmental changes

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