Chlamydial Genitourinary Infections 

  • Author: Kelley Struble, DO; Chief Editor: Burke A Cunha, MD   more...
 
Updated: Jan 17, 2012
 

Background

Chlamydiae are small gram-negative obligate intracellular microorganisms that preferentially infect squamocolumnar epithelial cells.

Chlamydia trachomatis is one of the 4 species (also including Chlamydia puerorum, Chlamydia psittaci, and Chlamydia pneumoniae) in the genus Chlamydia. C trachomatis can be differentiated into 18 serovars (serologically variant strains) based on monoclonal antibody–based typing assays. Serovars A, B, Ba, and C are associated with trachoma (a serious eye disease that can lead to blindness), serovars D-K are associated with genital tract infections, and L1-L3 are associated with lymphogranuloma venereum (LGV).

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Pathophysiology

The pathophysiologic mechanisms of chlamydiae are poorly understood at best. The initial response to infected epithelial cells is a neutrophilic infiltration followed by lymphocytes, macrophages, plasma cells, and eosinophilic invasion. The release of cytokines and interferons by the infected epithelial cell initializes this inflammatory cascade.

Infection with chlamydial organisms invokes a humoral cell response, resulting in secretory immunoglobulin A (IgA) and circulatory immunoglobulin M (IgM) and immunoglobulin G (IgG) antibodies and a cellular immune response. Recent studies have implicated a 40-kd major outer membrane protein (MOMP), as well as 10- and 60-kd chlamydial heat-shock proteins (cHSP), in the immunopathologic response, but further studies are needed to better understand these cell-mediated immune responses.[1]

Chlamydiae have a unique biphasic life cycle that is adaptable to both intracellular and extracellular environments. In the extracellular milieu, the so-called elementary body (EB) is found. EBs are metabolically inactive infectious particles; functionally, they are spore-type structures. Once inside a susceptible host cell, the EB prevents phagosome-lysozyme fusion and then undergoes reorganization to form a reticulate body (RB).

The RB synthesizes its own DNA, RNA, and proteins but requires energy in the form of adenosine triphosphate (ATP) from the host cell. After a sufficient amount of RBs have formed, some transform back into EBs, exiting the cell to infect others.

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Epidemiology

Frequency

United States

Chlamydia is the most commonly reported infectious disease in the United States; 1.1 million infections were reported in 2007, with the highest prevalence among sexually active females aged 15-24 years.[2]

International

In recent reports, the World Health Organization (WHO) estimated 140 million cases of C trachomatis infection worldwide.[3]

Mortality/Morbidity

Although urogenital carriage of chlamydiae often is asymptomatic, the most common manifestation of disease is local mucosal inflammation associated with a discharge, urethritis in the male, and urethritis/vaginitis/cervicitis in the female.

  • Chlamydia is one of the leading causes of pelvic inflammatory disease (PID) and infertility in women. The risk of ectopic pregnancy in women who have had PID is 7-10 times greater than that for women without a history of PID. In 15% of women who have contracted PID, chronic abdominal pain is a long-term manifestation that most likely is related to pelvic adhesions in the ovaries and fallopian tubes.
  • Chlamydial infections increase the risk for acquiring HIV infection by increasing genital mucosal inflammation.
  • Pregnant women infected with chlamydia can pass the infection on to their infants during delivery, which may develop into chlamydial pneumonia or chlamydial conjunctivitis.

Race

The incidence of chlamydial infection is not related to race per se but rather to the sexual histories of the individuals and, particularly, to the frequency and use (or nonuse) of barrier protection.

Sex

Although the presence of asymptomatic infection with genitourinary chlamydiae can differ, acquisition is similar for both sexes.

Age

Age factors in chlamydial genitourinary infection relate to the age of first sexual exposure and the frequency of exposure.

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Contributor Information and Disclosures
Author

Kelley Struble, DO  Fellow, Department of Infectious Diseases, University of Oklahoma College of Medicine

Disclosure: Nothing to disclose.

Coauthor(s)

Larry I Lutwick, MD  Professor of Medicine, State University of New York Downstate Medical School; Director, Infectious Diseases, Veterans Affairs New York Harbor Health Care System, Brooklyn Campus

Larry I Lutwick, MD is a member of the following medical societies: American College of Physicians and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Rhett L Jackson, MD  Associate Professor and Vice Chair for Education, Department of Medicine, Director, Internal Medicine Residency Program, University of Oklahoma College of Medicine; Assistant Chief, Medicine Service, Oklahoma City Veterans Affairs Hospital

Rhett L Jackson, MD is a member of the following medical societies: American College of Physicians-American Society of Internal Medicine and American Medical Association

Disclosure: Nothing to disclose.

Renuka Heddurshetti, MD  Fellow in Infectious Diseases, Department of Internal Medicine, State University of New York at Brooklyn

Renuka Heddurshetti, MD is a member of the following medical societies: American College of Physicians and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Jeffrey Blitstein, MD  Staff Physician, Department of Internal Medicine, Division of Infectious Disease, VA New York Harbor Health Care System at Brooklyn

Disclosure: Nothing to disclose.

Specialty Editor Board

John M Leedom, MD  Professor Emeritus of Medicine, Keck School of Medicine of the University of Southern California

John M Leedom, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, American Society for Microbiology, Infectious Diseases Society of America, International AIDS Society, and Phi Beta Kappa

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Eleftherios Mylonakis, MD  Clinical and Research Fellow, Department of Internal Medicine, Division of Infectious Diseases, Massachusetts General Hospital

Eleftherios Mylonakis, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians, American Society for Microbiology, and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Chief Editor

Burke A Cunha, MD  Professor of Medicine, State University of New York School of Medicine at Stony Brook; Chief, Infectious Disease Division, Winthrop-University Hospital

Burke A Cunha, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

References

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  13. [Guideline] Centers for Disease Control and Prevention. Update to CDC's sexually transmitted diseases treatment guidelines, 2006: fluoroquinolones no longer recommended for treatment of gonococcal infections. MMWR Morb Mortal Wkly Rep. Apr 13 2007;56(14):332-6. [Medline]. [Full Text].

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  23. Martin DH, Mroczkowski TF, Dalu ZA. A controlled trial of a single dose of azithromycin for the treatment of chlamydial urethritis and cervicitis. The Azithromycin for Chlamydial Infections Study Group. N Engl J Med. Sep 24 1992;327(13):921-5. [Medline].

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