Trachoma is the world’s leading cause of preventable blindness of infectious origin. This disease is a chronic keratoconjunctivitis caused by the obligate intracellular bacterium Chlamydia trachomatis. 
C trachomatis can be spread by either direct contact with an infected person's eyes or nose or indirect contact, such as through contact with clothing or flies that have come into contact with an infected person's eyes or nose. Poor sanitation, crowded living conditions, and insufficient clean water and toilets can also increase the spread of trachoma. Disease transmission occurs primarily between children and the women who care for them. Some have characterized this transmission cycle by describing trachoma as a disease of the crèche (day nursery). Flies that transmit trachoma preferentially lay their eggs on human feces lying exposed on soil.
Repeated episodes of reinfection within the family cause chronic follicular or intense conjunctival inflammation (active trachoma), which leads to tarsal conjunctival scarring. The scarring distorts the upper tarsal plate and, in some individuals, leads to entropion and trichiasis (cicatricial trachoma). The end result includes corneal abrasions; corneal scarring and opacification; and, ultimately, blindness.
Prevention of trachoma-related blindness requires a number of interventions. The World Health Organization (WHO) and their partners endorse the surgery, antibiotics, facial cleanliness, and environmental improvement (SAFE) strategy for trachoma control.  The interventions are discussed in greater detail in Treatment.
Trachoma is caused by serovars A, B, Ba, and C of C trachomatis. Different serovars predominate in different families and in different communities.
Chlamydiae are gram-negative, obligate intracellular bacteria. The species C trachomatis causes trachoma and also genital infections (serovars D-K) and lymphogranuloma venereum (serovars L1-L3). Serovars D-K occasionally cause a subacute follicular conjunctivitis that may be clinically indistinguishable from trachoma, including follicular conjunctivitis with pannus, but rarely conjunctival scarring. However, these genital serovars do not typically enter stable transmission cycles within communities. Therefore, they are not involved in the genesis of trachoma blindness. Regardless of the serovar (which is determined by polymorphisms in a surface-exposed protein), isolates of C trachomatis obtained from the eye have mutations that inactivate the genes coding for tryptophan synthase, whereas genital isolates have a functional enzyme. 
Infection causes inflammation, that is, a predominantly lymphocytic and monocytic infiltrate with plasma cells and macrophages in follicles. The follicles are typical germinal centers with islands of intense B-cell proliferation surrounded by seas of T cells. Recurrent conjunctival reinfection causes the prolonged inflammation that leads to conjunctival scarring. Scarring is associated with atrophy of the conjunctival epithelium, loss of goblet cells, and replacement of the normal, loose, vascular subepithelial stroma with thick compact bands of type IV and type V collagen.
The clinical changes are a delayed-type hypersensitivity reaction to the chlamydial antigens (thought to be HSP-60). This induces an immune response with germinal centers (seen as follicles) and intense inflammatory infiltrate and the formation of papillae. Over time, this intense inflammation leads to scar formation, which, in turn, causes contraction and buckling of the tarsal plate of the upper lid, producing entropion and trichiasis.
Trachoma was once endemic in North America and Europe, but it disappeared in these locations during the 20th century as living standards in those locations improved.
Trachoma is endemic in parts of Africa, Asia, the Middle East, Latin America, the Pacific Islands, and aboriginal communities in Australia. [4, 5, 6, 7, 8] Worldwide, an estimated 229 million people in 53 countries live in trachoma-endemic areas. In hyperendemic areas, most members of nearly all families may have active disease. When the overall community prevalence decreases to around 20%, active disease is clearly seen to cluster in families. In 1 of 5 families, most children have active trachoma (as opposed to 1 in 5 children in most families). This clustering becomes more apparent in communities as the prevalence decreases.
Blindness from any cause is associated with increased risk of mortality in endemic communities. Approximately 1.2 million people are blind because of trachoma.
A disease of poverty and poor hygiene, trachoma has no racial preponderance.
Trachoma persists in areas with poor personal and community hygiene, for example, communities with inadequate access to water and sanitation in hot, dry, dusty climates.
Trachoma typically affects the most marginalized, deprived members of a community.
Active disease most commonly occurs in preschool children of both sexes and their (usually female) care providers.
Trichiasis and blindness may be 2-4 times more common in women than men.
Active disease most commonly occurs in preschool children, with the highest prevalence in children aged 3-5 years.
Cicatricial disease is most common in middle-aged adults. The age group in which cicatricial disease begins to appear depends on the intensity of transmission in the community. In areas of extremely high endemicity, rare cases of trichiasis occur in children younger than 10 years.
Because of repeat infection, aging may be accompanied by sequential worsening of disease. Young children have follicular trachoma with intense conjunctival inflammation; young adults, especially mothers, have trachomatous scarring; and middle-aged patients or grandparents have trichiasis and corneal opacity. However, these signs are not mutually exclusive. Individuals may have episodes of follicular trachoma with intense conjunctival inflammation even after cicatricial complications develop; therefore, follicles, scarring, and trichiasis may all be present in the same patient.