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Trachoma

  • Author: Hugh Ringland Taylor, AC, MD, MBBS, BMedSc(Melb), DO(Melb), FRANZCO, FRACS, FAAO, FACS, FAICD; Chief Editor: Hampton Roy, Sr, MD  more...
 
Updated: Aug 10, 2015
 

Background

Trachoma is the leading infectious cause of ocular morbidity. This disease is a chronic keratoconjunctivitis caused by the obligate intracellular bacterium Chlamydia trachomatis.[1]

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.[2] The interventions are discussed in greater detail in Treatment.

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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 lymphogranulomavenereum (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.[3]

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 subepithelialstroma 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.

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Epidemiology

Frequency

United States

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.

International

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.

Mortality/Morbidity

Blindness from any cause is associated with increased risk of mortality in endemic communities. Approximately 1.2 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.

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Contributor Information and Disclosures
Author

Hugh Ringland Taylor, AC, MD, MBBS, BMedSc(Melb), DO(Melb), FRANZCO, FRACS, FAAO, FACS, FAICD Harold Mitchell Professor of Indigenous Eye Health, Melbourne School of Population and Global Health, University of Melbourne

Hugh Ringland Taylor, AC, MD, MBBS, BMedSc(Melb), DO(Melb), FRANZCO, FRACS, FAAO, FACS, FAICD is a member of the following medical societies: American Academy of Ophthalmology, American Ophthalmological Society, Association for Research in Vision and Ophthalmology

Disclosure: Nothing to disclose.

Coauthor(s)

Anthony W Solomon, MBBS, DTM&H, PhD, MRCP Wellcome Trust Intermediate Clinical Fellow, Senior Lecturer, Department of Clinical Research, London School of Hygiene and Tropical Medicine; Honorary Consultant Physician, The Hospital for Tropical Diseases, UK

Anthony W Solomon, MBBS, DTM&H, PhD, MRCP is a member of the following medical societies: American Society of Tropical Medicine and Hygiene, Royal College of Physicians, Royal Society of Tropical Medicine and Hygiene

Disclosure: Received grant/research funds from International Trachoma Initiative for researcher; Received member of trachoma expert committee from International Trachoma Initiative for review panel membership; Received member of scientific advisory board from Queen Elizabeth Diamond Jubilee Trust for review panel membership.

Specialty Editor Board

Simon K Law, MD, PharmD Clinical Professor of Health Sciences, Department of Ophthalmology, Jules Stein Eye Institute, University of California, Los Angeles, David Geffen School of Medicine

Simon K Law, MD, PharmD is a member of the following medical societies: American Academy of Ophthalmology, Association for Research in Vision and Ophthalmology, American Glaucoma Society

Disclosure: Nothing to disclose.

Christopher J Rapuano, MD Professor, Department of Ophthalmology, Jefferson Medical College of Thomas Jefferson University; Director of the Cornea Service, Co-Director of Refractive Surgery Department, Wills Eye Hospital

Christopher J Rapuano, MD is a member of the following medical societies: American Academy of Ophthalmology, American Ophthalmological Society, American Society of Cataract and Refractive Surgery, Contact Lens Association of Ophthalmologists, International Society of Refractive Surgery, Cornea Society, Eye Bank Association of America

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Cornea Society, Allergan, Bausch & Lomb, Bio-Tissue, Shire, TearScience, TearLab<br/>Serve(d) as a speaker or a member of a speakers bureau for: Allergan, Bausch & Lomb, Bio-Tissue, TearScience.

Chief Editor

Hampton Roy, Sr, MD Associate Clinical Professor, Department of Ophthalmology, University of Arkansas for Medical Sciences

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

Disclosure: Nothing to disclose.

Acknowledgements

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.

Denise Mabey, FRCOphth, MBBS Consulting Staff, Department of Ophthalmology, St Thomas Hospital of London

Disclosure: Nothing to disclose.

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. 1997 Dec. 176(6):1524-30. [Medline].

  2. 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]. [Full Text].

  3. West SK, Munoz BE, Mkocha H, Gaydos C, Quinn T. Risk of Infection with Chlamydia trachomatis from Migrants to Communities Undergoing Mass Drug Administration for Trachoma Control. Ophthalmic Epidemiol. 2015 Jun. 22 (3):170-5. [Medline].

  4. Kalua K, Chirwa T, Kalilani L, Abbenyi S, Mukaka M, Bailey R. Prevalence and risk factors for trachoma in central and southern Malawi. PLoS One. 2010 Feb 5. 5(2):e9067. [Medline]. [Full Text].

  5. Baker MC, Mathieu E, Fleming FM, et al. Mapping, monitoring, and surveillance of neglected tropical diseases: towards a policy framework. Lancet. 2010 Jan 16. 375(9710):231-8. [Medline].

  6. Solomon AW, Pavluck AL, Courtright P, Aboe A, et al. The Global Trachoma Mapping Project: Methodology of a 34-Country Population-Based Study. Ophthalmic Epidemiol. 2015 Jun. 22 (3):214-25. [Medline].

  7. Katibeh M, Hosseini S, Yaseri M, Aminifar MN, Mahdavi A, Jafarinasab MR, et al. Prevalence and Risk Factors for Trachoma in Rural Areas of Sistan-va-Baluchestan Province, Iran: A Population-Based Study. Ophthalmic Epidemiol. 2015 Jun. 22 (3):208-13. [Medline].

  8. Ramyil A, Wade P, Ogoshi C, Goyol M, Adenuga O, Dami N, et al. Prevalence of Trachoma in Jigawa State, Northwestern Nigeria. Ophthalmic Epidemiol. 2015 Jun. 22 (3):184-9. [Medline].

  9. Evans JR, Solomon AW. Antibiotics for trachoma. Cochrane Database Syst Rev. 2011 Mar 16. CD001860. [Medline].

  10. West S, Munoz B, Lynch M, et al. Impact of face-washing on trachoma in Kongwa, Tanzania. Lancet. 1995 Jan 21. 345(8943):155-8. [Medline].

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

  12. 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. 1997 Mar. 24(3):363-8. [Medline].

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

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

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

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

 
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Trachomatous inflammation, follicular (TF), is the presence of 5 or more follicles (each at least 0.5 mm in diameter) on the central part of the upper tarsal conjunctiva. Images from the Slides/Text Teaching Series, No. 7, Trachoma, published by The International Centre for Eye Health, Institute of Ophthalmology, 11-43 Bath St, London EC1V 9EL, United Kingdom. Photograph courtesy of John D. C. Anderson, MD.
Trachomatous inflammation, intense (TI) is pronounced inflammatory thickening of the upper tarsal conjunctiva that obscures more than one half the normal deep tarsal vessels. Photograph courtesy of Allen Foster, MD.
Trachomatous conjunctival scarring (TS) is the presence of easily visible scars in the tarsal conjunctiva.
Trachomatous trichiasis (TT) is defined as the presence of at least 1 eyelash rubbing on the eyeball or evidence of recent removal of in-turned lashes. Photograph courtesy of John D. C. Anderson, MD.
Easily visible corneal opacity over the pupil; it is so dense that at least part of the pupil margin is blurred when viewed through the opacity. Photograph courtesy of John D. C. Anderson, MD.
The image on the left shows intense inflammatory trachoma, and the image on the right shows allergic conjunctivitis with the typical cobblestone papillae. Courtesy of John D. C. Anderson, MD, and Murray McGavin, MD.
 
 
 
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