C. trachomatis is an obligate intracellular bacterium with 19 different serovars. Endemic trachoma is caused by serovars A-C,¹⁷ whereas genital chlamydial infection is associated with serovars D-K. During its developmental cycle, C. trachomatis exists as reticulate bodies that are metabolically active in the intracellular stage and as elementary bodies that are the metabolically inactive extracellular form of the organism that can transfer between host cells and organisms.¹⁸ The infectious cycle begins with the attachment of the elementary bodies to the surface of epithelial cells, followed by endocytosis of the bacteria. Inside the host cell, within 6 to 9 hours, the elementary bodies transform into the reticulate form and replicate by binary fission.¹⁸ Chlamydial antigens are believed to induce cell-mediated immune and delayed hypersensitivity responses with the production of proinflammatory cytokines and cellular infiltration forming lymphoid follicles. Some immune cell infiltrates have shown a phenotype suggestive of NK cells.¹⁹ Chronic conjunctival inflammation associated with enriched expression of proinflammatory factors and altered expression of extracellular matrix regulators appear to be important factors in the development of conjunctival scarring.²⁰ Some reticulate bodies transform back into elementary bodies that become extracellular and can transmit the infection to another host.

Individual and environmental risk factors that may facilitate the introduction and transmission of C. trachomatis into vulnerable communities probably include migration of infected individuals who transmit new strains of the bacterium into areas with crowded living conditions.²¹,²² Children with active disease in areas where water is scarce, and face washing less common, often have ocular and nasal secretions that can be a source of bacterial spread.²³ Flies that feed on ocular secretions can also act as vectors for disease transmission.²⁴

Clinically, trachoma is subdivided into early active and late-stage cicatricial disease. Active disease is more commonly found in children and is characterized by chronic, recurrent follicular conjunctivitis, most prominently seen on the upper tarsal conjunctiva. More severe cases may have papillary hypertrophy with engorgement of small vessels, surrounding edema, and inflammatory thickening of the conjunctiva.²⁵ Recurrent or persistent ocular infection leads to conjunctival scarring (Figure 121.1A). During the active phase the superior corneal limbus develops follicles composed of lymphocytes surrounding a reticuloendothelial cell germinal center. When these follicles heal and regress, they result in round, thinned depressions, referred to as Herbert pits, which are a characteristic and pathognomonic finding of trachoma (Figure 121.2).

The late-stage scarring sequelae develop in later life promoted by the inflammatory process but can be seen earlier in cases of more severe disease. Scarring can be relatively mild with only a few linear or stellate scars (Figure 121.1B) or severe with thick fibrotic bands, shortening of the fornix, and symblepharon formation. Contraction of the conjunctiva results in cicatricial entropion that rotates the eyelid margin toward the globe (Figure 121.3). Distortion of the eyelash follicles manifests as secondary trichiasis (Figure 121.4).

In individuals infected with trachoma, progression to conjunctival scarring develops in 23% to 30% over 2 years, and there is a strong relationship between progressive scarring and an increasing number of episodes of clinical inflammation.⁶ Studies have reported progression of conjunctival scarring in 47% of patients followed for 5 years²⁶ and 68.5% followed for 14 years.²⁷ The development of trachomatous trichiasis varies with the presence and degree of conjunctival scarring from less than 10% in patients followed up to 12 years²⁸,²⁹ to more than 38% in cases of severe scarring over 14 years.²⁷