eMedicine Specialties > Ophthalmology > Infectious Disease

Trachoma

Author: Anthony W Solomon, MBBS, DTM&H, PhD, MRCP, Specialist Registrar in Infectious Diseases, Lister Unit, Northwick Park Hospital, London; Honorary Lecturer, International Centre for Eye Health, Clinical Research Unit, London School of Hygiene and Tropical Medicine, London
Coauthor(s): Hugh Ringland Taylor AC, MD, MBBS, BmedSc (Melb), DO (Melb), FRACO, FRACS, FAAO, FACS, FAICD, Harold Mitchell Professor of Indigenous Eye Health, School of Population Health, University of Melbourne
Contributor Information and Disclosures

Updated: Sep 5, 2007

Introduction

Background

Trachoma is the leading infectious cause of ocular morbidity. This disease is a chronic keratoconjunctivitis caused by the obligate intracellular bacterium Chlamydia trachomatis.

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).

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.

Pathophysiology

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 chronic follicular conjunctivitis that is clinically indistinguishable from trachoma, including follicular conjunctivitis with pannus and, at times, 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.

Frequency

United States

Trachoma was once endemic in North America and Europe, but it has disappeared in these locations with the improvement of living standards.

International

Trachoma is endemic in parts of Africa, Asia, the Middle East, Latin America, the PacificIslands, and aboriginal communities in Australia. Worldwide, an estimated 84 million people in 55 endemic countries have active trachoma. 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.

Mortality/Morbidity

Blindness from any cause is associated with increased risk of mortality in endemic communities. Approximately 1.3 million people are blind because of trachoma.

Race

  • 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.

Sex

  • 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.

Age

  • 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.

Clinical

History

Two phases of the disease process exist: the active phase and the scarring (cicatricial) phase. As implied above, though, these phases are not stages along a linear pathway of disease pathogenesis; both phases may coexist in the same patient.

  • The active phase resembles many other diseases in which follicular conjunctivitis is a feature. Without laboratory facilities, the diagnosis is solely based on the clinical appearance of active trachoma in someone living in a community where trachoma is endemic or suspected to be endemic.
  • Most patients with active trachoma are relatively asymptomatic.
    • The cicatricial phase has unique clinical features, which lead to definitive diagnosis in most cases.
    • Determine the amount of time that the patient has spent in a trachoma-endemic community and/or near a pool of infection.
    • Conjunctival scarring alone tends to be asymptomatic, though the associated disturbance of the architecture of the tear film (due to scarring and destruction of mucous and serous glands) often leads to dry eye.
    • Trichiasis causes an intensely irritating foreign body sensation, as well as blepharospasm. Ultimately, it leads to corneal scarring.
    • Many patients self-epilate before their presentation.
    • Corneal opacities or scars that cover any part of the pupil impair the patient's vision.

Physical

Active trachoma is characterized by a mucopurulent keratoconjunctivitis. The conjunctival surface of the upper eyelid shows a follicular and inflammatory response. The cornea may have limbal follicles, superior neovascularization (pannus), and punctate keratitis. Infection with C trachomatis concurrently occurs in other extraocular mucous membranes, commonly the nasopharynx, leading to a nasal discharge.

  • Follicular trachoma (designated TF in the WHO simplified trachoma grading scheme)
    • Follicular trachoma is defined as the presence of 5 or more follicles at least 0.5 mm in diameter in the central part of the upper tarsal conjunctiva.
    • Follicular trachoma indicates active disease.
    • This form is most commonly found in children, with a peak prevalence in those aged 3-5 years. The prevalence rapidly decreases in school-aged children as they leave the pool of re-infection (ie, their family childcare group).
    • Follicles are germinal centers that primarily consist of lymphocytes and monocytes.
    • The presence and involution of follicles at the limbus (corneoscleral border) give rise to the pathognomonic lesion of past active trachoma, Herbert pits.
  • Intense inflammatory trachoma (designated TI in the WHO simplified trachoma grading scheme)
    • Intense inflammatory trachoma is defined as pronounced inflammatory thickening of the upper tarsal conjunctiva that obscures more than one half of the normal deep tarsal vessels.
    • The cause is an intense inflammatory response.
    • The normally thin tarsal conjunctiva develops a velvety thickening.
    • Papillae are visible under slit lamp examination.
    • Intense inflammatory trachoma indicates an increased potential for significant conjunctival scarring and, hence, a higher ultimate risk of blinding disease.
    • Surveying the prevalence of intense inflammatory trachoma in children can help in predicting the risk of future blinding trachoma in that cohort of children.
  • Trachomatous scarring (designated TS in the WHO simplified trachoma grading scheme)
    • Trachomatous scarring is defined as the presence of easily visible scars in the tarsal conjunctiva.
    • Trachomatous scarring indicates past inflammatory disease and a risk of future trichiasis. The more severe the scarring, the higher the risk of subsequent trichiasis.
    • This form may be associated with the development of dry eye syndrome, but chronic, low-grade bacterial conjunctivitis and dacryocystitis may also lead to a weeping eye.
  • Trichiasis (designated TT in the WHO simplified trachoma grading scheme)
    • Trichiasis is defined as at least 1 eyelash rubs on the eyeball or evidence of recent removal of in-turned eyelashes.
    • This is a potentially blinding lesion that can lead to corneal opacification.
    • Trichiasis is due to subconjunctival fibrosis over the tarsal plate that leads to lid distortion.
    • Some vision can be restored with the successful correction of trichiasis.
  • Corneal opacity (designated CO in the WHO simplified trachoma grading scheme)
    • Corneal opacity is defined as easily visible corneal opacity over the pupil that is so dense that it blurs at least part of the pupillary margin when it is viewed through the opacity.
    • Corneal opacity or scarring reflects the prevalence of vision loss and blindness resulting from trachoma.
    • This condition includes pannus, epithelial vascularization, and infiltration only if it involves the central cornea.

Causes

Trachoma is caused by repeated conjunctival infection with C trachomatis. The greatest individual-level risk factor for active trachoma appears to be having a family member with active disease. At the community level, adequate water access for personal hygiene, sanitation, and fly control determine the risk of endemic trachoma.

More on Trachoma

Overview: Trachoma
Differential Diagnoses & Workup: Trachoma
Treatment & Medication: Trachoma
Follow-up: Trachoma
Multimedia: Trachoma
References

References

  1. Bobo LD, Novak N, Munoz B, Hsieh YH, Quinn TC, West S. Severe disease in children with trachoma is associated with persistent Chlamydia trachomatis infection. J Infect Dis. Dec 1997;176(6):1524-30. [Medline].

  2. Dawson CR, Schachter J, Sallam S, Sheta A, Rubinstein RA, Washton H. A comparison of oral azithromycin with topical oxytetracycline/polymyxin for the treatment of trachoma in children. Clin Infect Dis. Mar 1997;24(3):363-8. [Medline].

  3. Grayston JT, Wang SP, Yeh LJ, Kuo CC. Importance of reinfection in the pathogenesis of trachoma. Rev Infect Dis. Nov-Dec 1985;7(6):717-25. [Medline].

  4. Mabey DC, Solomon AW, Foster A. Trachoma. Lancet. Jul 19 2003;362(9379):223-9. [Medline].

  5. Reacher M, Foster A, Huber J. Trichiasis surgery for trachoma: the bilamellar tarsal rotation procedure. WHO/PBL 93.29. Geneva: World Health Organization;. 1993.

  6. Solomon A, Burton M. What's new in azithromyin?. Community Eye Health. Dec 2004;17(52):54-6. [Medline].

  7. Taylor HR, Johnson SL, Schachter J, Caldwell HD, Prendergast RA. Pathogenesis of trachoma: the stimulus for inflammation. J Immunol. May 1 1987;138(9):3023-7. [Medline].

  8. Thylefors B, Dawson CR, Jones BR, West SK, Taylor HR. A simple system for the assessment of trachoma and its complications. Bull World Health Organ. 1987;65(4):477-83. [Medline].

  9. West S, Munoz B, Lynch M, Kayongoya A, Chilangwa Z, Mmbaga BB, et al. Impact of face-washing on trachoma in Kongwa, Tanzania. Lancet. Jan 21 1995;345(8943):155-8. [Medline].

Further Reading

Keywords

Chlamydia trachomatis, C trachomatis, chronic keratoconjunctivitis, SAFE strategy for trachoma, trichiasis, simplified trachoma grading scheme, trachomatous scarring, corneal opacity

Contributor Information and Disclosures

Author

Anthony W Solomon, MBBS, DTM&H, PhD, MRCP, Specialist Registrar in Infectious Diseases, Lister Unit, Northwick Park Hospital, London; Honorary Lecturer, International Centre for Eye Health, Clinical Research Unit, London School of Hygiene and Tropical Medicine, London
Anthony W Solomon, MBBS, DTM&H, PhD, MRCP is a member of the following medical societies: Royal College of Physicians of the United Kingdom
Disclosure: Pfizer Inc Grant/research funds Researcher; International Trachoma Initiative Grant/research funds Researcher; Pfizer Inc Support to attend the Trachoma Scientific Exchange in Phoenix, 2006 Review panel membership

Coauthor(s)

Hugh Ringland Taylor AC, MD, MBBS, BmedSc (Melb), DO (Melb), FRACO, FRACS, FAAO, FACS, FAICD, Harold Mitchell Professor of Indigenous Eye Health, School of Population Health, University of Melbourne
Hugh Ringland Taylor AC, MD, MBBS, BmedSc (Melb), DO (Melb), FRACO, FRACS, FAAO, FACS, FAICD is a member of the following medical societies: American Academy of Ophthalmology, American Ophthalmological Society, and Association for Research in Vision and Ophthalmology
Disclosure: Nothing to disclose.

Medical Editor

Anastasios J Kanellopoulos, MD, Assistant Program Director, Clinical Associate Professor, Department of Ophthalmology, Manhattan Eye, Ear, and Throat Hospital, New York University
Anastasios J Kanellopoulos, MD is a member of the following medical societies: American Academy of Ophthalmology, Association for Research in Vision and Ophthalmology, Eye Bank Association of America, and International Society of Refractive Surgery
Disclosure: Nothing to disclose.

Pharmacy Editor

Simon K Law, MD, PharmD, Assistant Professor of Ophthalmology, Jules Stein Eye Institute; Chief of Section of Ophthalmology Surgical Services, Department of Veterans Affairs Healthcare Center, West Los Angeles
Simon K Law, MD, PharmD is a member of the following medical societies: American Academy of Ophthalmology, American Glaucoma Society, and Association for Research in Vision and Ophthalmology
Disclosure: Nothing to disclose.

Managing Editor

Christopher J Rapuano, MD, Professor, Department of Ophthalmology, Jefferson Medical College; Co-Chairman of the Cornea Service, Co-Chairman of Refractive Surgery Department, Wills Eye Hospital
Christopher J Rapuano, MD is a member of the following medical societies: American Academy of Ophthalmology, American Society of Cataract and Refractive Surgery, Eye Bank Association of America, Pennsylvania Medical Society, and Philadelphia County Medical Society
Disclosure: Allergan Honoraria Speaking and teaching; Allergan Consulting fee Consulting; Alcon Honoraria Speaking and teaching; Inspire Honoraria Speaking and teaching; RPS Ownership interest Other

CME Editor

Lance L Brown, OD, MD, Ophthalmologist, Affiliated With Freeman Hospital and St John's Hospital, Regional Eye Center, Joplin, Missouri
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Chief Editor

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Hampton Roy Sr, MD is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, and Pan-American Association of Ophthalmology
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