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Chlamydial Genitourinary Infections

  • Author: Shahab Qureshi, MD; Chief Editor: Michael Stuart Bronze, MD  more...
 
Updated: Feb 22, 2016
 

Background

Chlamydial infection can cause disease in many organ systems, including the genitourinary tract. Chlamydiae are small gram-negative obligate intracellular microorganisms that preferentially infect squamocolumnar epithelial cells. They include the genera Chlamydia (of which the type species is Chlamydia trachomatis) and Chlamydophila (eg, Chlamydophila pneumoniae and Chlamydophila psittaci).

C trachomatis can be differentiated into 18 serovars (serologically variant strains) on the basis of monoclonal antibody–based typing assays. These serovars are associated with different medical conditions, as follows:

  • Serovars A, B, Ba, and C – Trachoma, a serious eye disease endemic in Africa and Asia that is characterized by chronic conjunctivitis and can lead to blindness
  • Serovars D-K – Genital tract infections
  • Serovars L1-L3 – Lymphogranuloma venereum (LGV), which is associated with genital ulcer disease in tropical countries

C trachomatis infection affects the cervix, urethra, salpinges, uterus, nasopharynx, and epididymis[1, 2, 3] ; it is the most commonly reported bacterial sexually transmitted disease (STD) in the United States and a leading cause of infertility in women. C trachomatis infection causes other diseases as well, including conjunctivitis, pneumonia or pneumonitis, afebrile pneumonia syndrome (in infants born vaginally to infected mothers), Fitz-Hugh-Curtis syndrome, and trachoma (the world’s leading cause of acquired blindness).[4]

C pneumoniae infection is spread via respiratory droplets and causes pharyngitis, bronchitis, and pneumonia. C psittaci infection is spread by bird droppings and aerosols and causes psittacosis. These infections are not discussed in this article.

At present, fewer than 50% of sexually active young females in the United States are screened for the presence of chlamydiae. Nationally, the annual screening rate increased from 25.3% in 2000 to 43.6% in 2006, then decreased slightly to 41.6% in 2007.[5]

The US Preventive Services Task Force Screening has released a recommendation statement for chlamydial infections, in which routine Chlamydia screening of sexually active young women is recommended to prevent consequences of untreated chlamydial infection (eg, pelvic inflammatory disease (PID), infertility, ectopic pregnancy, and chronic pelvic pain).[6, 7] A guideline synthesis is also available from the National Guideline Clearinghouse.[8]

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Pathophysiology

The pathophysiologic mechanisms of chlamydial infection are poorly understood at best. Chlamydia infects columnar epithelial cells, which places the adolescent female at particular risk because of the presence of the squamocolumnar junction on the ectocervix until early adulthood. The initial response of epithelial cells to infection 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. A 40-kd major outer membrane protein (MOMP) and 10- and 60-kd chlamydial heat-shock proteins (cHSPs) have been implicated in the immunopathologic response, but further studies are needed to provide a better understanding of these cell-mediated immune responses.[9]

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.

The bacterium is usually spread through sexual activity. An infected male has a 25% chance per sexual encounter of transmitting the infection to an uninfected female. Chlamydiae can be vertically spread as well. The transmission rate from infected mother to newborn is 50-60%, causing conjunctivitis (in most cases) or pneumonia (in 10-20% of cases; see Afebrile Pneumonia Syndrome).

Infection of the genital tract is the most common clinical presentation. The incubation period is 1-3 weeks. Approximately 50% of infected males and 80% of infected females are asymptomatic, but infection may cause a mucopurulent cervicitis in females and urethritis in males. Ascending infection can result in PID in women and is the most common cause of epididymitis in men younger than 35 years. Of women with PID, 5-10% develop perihepatitis (ie, Fitz-Hugh-Curtis syndrome).

Although patients with any STD are at increased risk of coinfection with another STD, coinfection of chlamydia and gonorrhea is most common. Forty percent of women and 20% of men with chlamydial infection are co-infected with gonorrhea. Patients with chlamydia also have a higher frequency of Reiter syndrome (ie, urethritis, conjunctivitis, reactive arthritis) than the general population.

LGV is rare in the United States but is responsible for 10% of cases of genital ulcer disease in tropical countries. Localized inguinal adenopathy and ulceration develop 2-12 weeks after exposure. Proctitis, rectal strictures, and lymphatic obstruction with secondary elephantiasis can occur in untreated disease.

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Etiology

Chlamydial transmission usually is caused by sexual contact through oral, anal, or vaginal intercourse. Neonatal infection (eg, conjunctivitis or pneumonia) may occur secondary to passage through the birth canal of an infected mother. Specific risk factors for chlamydial infection include the following:

  • Nonwhite race
  • Multiple sexual partners or a new sexual partner
  • Age 15-24 years (especially < 19 years)
  • Poor socioeconomic conditions (eg, homelessness)
  • Exchange of sex for drugs or money
  • Single marital status
  • Intercourse without a barrier contraceptive
  • History of a previous STD or current coinfection with another STD
  • Certain cytokine polymorphisms – These have been associated with severe disease and risk of tubal factor infertility [10]
  • Certain variants in Toll-like receptor 1 and 4 genes – These predispose to infection [11]
  • Having been a foster child (males only) [12]
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Epidemiology

United States statistics

Chlamydial infection is the most frequently reported infectious disease in the United States, and its prevalence is highest in persons aged 24 years or younger.[13] The annual incidence of C trachomatis genital infections was estimated to be 2.86 million cases in the United States in 2008.[14]

Sexually active female populations average chlamydial carriage rates of about 20%. Many patients are asymptomatic. The incidence is 2-3 times that of Neisseria gonorrhoeae.

The prevalence of chlamydia has been reported to be as high as 14% among African American females aged 18-26 years and 17% among females with a history of gonorrhea or chlamydia in the previous 12 months. In addition, approximately 100,000 neonates are exposed to chlamydiae annually. The 2007-2012 National Health and Nutrition Examination Survey (NHANES) indicates that an estimated 1.8 million persons aged 14-39 years in the United States have a genital chlamydial infection.[15]

International statistics

More than one million sexually transmitted infections (STIs) are acquired every day worldwide.[16] C trachomatis genital tract infections are common, with an estimated 105.7 million new worldwide cases in 2008.[17] Serosurveys have documented similar incidence figures in Australia,[18] New Zealand,[19] France,[20] Germany,[21] and the Netherlands.[22] A report from the World Health Organization (WHO) Initiative for Vaccine Research (IVR) estimated that there were more than 140 million cases of C trachomatis infection worldwide.[23]

Age-, sex-, and race-related demographics

Age factors in chlamydial genitourinary infection relate to the age of first sexual exposure and the frequency of exposure. Chlamydia is most prevalent in persons aged 15-24 years. Acquisition rates are comparable for the 2 sexes. Women are more likely to be asymptomatic than men (80% vs 50%); however, they are also more likely to develop long-term complications (eg, PID and infertility).

Data from 2011 demonstrate that the disease is most common in adolescents and young adults aged 15-24 years, with higher rates in women and African Americans than in Hispanics and non-Hispanic whites.[24]

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Prognosis

Antibiotic treatment is 95% effective for first-time therapy. The prognosis is excellent if treatment is initiated early and the entire course of antibiotics is completed. Although treatment failures with primary therapies are quite rare, relapse may occur with alternative therapies. Reinfection is very common and is related to nontreatment of infected sexual partners or acquisition from a new partner; thus all sexual partners should be treated.

Deaths are rare and are caused by progression to salpingitis and tuboovarian abscess with rupture and peritonitis. The most significant morbidity occurs when repeated episodes of chlamydia lead to obstruction and scarring of the fallopian tubes, resulting in partial or total sterility. Chlamydia is an indirect cause of mortality from ectopic pregnancies.[25] Mortality due to ectopic pregnancy is probably more common than is death due to tuboovarian abscess.

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Patient Education

Appropriate counseling of infected individuals must be performed. Inform patients of the possible long-term risks and complications of their infection, including the possibility of infertility. Educate them regarding the risk of other STDs. Counsel patients to take steps to prevent reinfection. They should avoid sexual contact until their treatment is completed and all partners also have been evaluated and treated. They should also consider using latex condoms to minimize the chances of reinfection.

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Contributor Information and Disclosures
Author

Shahab Qureshi, MD Attending Physician in General Internal Medicine, St Catharine's General Hospital; Associate Clinical Professor (Adjunct), McMaster University School of Medicine, Canada

Shahab Qureshi, MD is a member of the following medical societies: College of Physicians and Surgeons of Ontario, Ontario Medical Association

Disclosure: Nothing to disclose.

Specialty Editor Board

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

Disclosure: Received salary from Medscape for employment. for: Medscape.

Chief Editor

Michael Stuart Bronze, MD David Ross Boyd Professor and Chairman, Department of Medicine, Stewart G Wolf Endowed Chair in Internal Medicine, Department of Medicine, University of Oklahoma Health Science Center; Master of the American College of Physicians; Fellow, Infectious Diseases Society of America

Michael Stuart Bronze, MD is a member of the following medical societies: Alpha Omega Alpha, American Medical Association, Oklahoma State Medical Association, Southern Society for Clinical Investigation, Association of Professors of Medicine, American College of Physicians, Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Acknowledgements

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.

Marc James Grella, MD Clinical Instructor, Department of Pediatrics, Massachusetts General Hospital

Marc James Grella, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Pediatrics, American Medical Association, and Massachusetts Medical Society

Disclosure: Nothing to disclose.

Jonathan A Handler, MD HSG Chief Deployment Architect, Microsoft Corporation, Adjunct Associate Professor, Department of Emergency Medicine, Northwestern University, Feinberg School of Medine

Jonathan A Handler, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine

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.

Debra E Houry, MD, MPH Director, Center for Injury Control, Associate Professor of Emergency Medicine, Department of Emergency Medicine, Emory University

Debra E Houry, MD, MPH is a member of the following medical societies: American College of Emergency Physicians, American Medical Association, American Public Health Association, and Society for Academic Emergency Medicine

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.

Ashir Kumar, MD, MBBS, FAAP Professor Emeritus, Department of Pediatrics and Human Development, Michigan State University College of Human Medicine

Ashir Kumar, MD, MBBS, FAAP is a member of the following medical societies: American Association of Physicians of Indian Origin and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Richard Lavely, MD, JD, MS, MPH Lecturer in Health Policy and Administration, Department of Public Health, Yale University School of Medicine

Richard Lavely, MD, JD, MS, MPH is a member of the following medical societies: American College of Emergency Physicians, American College of Legal Medicine, and American Medical Association

Disclosure: Nothing to disclose.

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.

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.

Mark R Schleiss, MD American Legion Chair of Pediatrics, Professor of Pediatrics, Division Director, Division of Infectious Diseases and Immunology, Department of Pediatrics, University of Minnesota Medical School

Mark R Schleiss, MD is a member of the following medical societies: American Pediatric Society, Infectious Diseases Society of America, Pediatric Infectious Diseases Society, and Society for Pediatric Research

Disclosure: Nothing to disclose.

Russell W Steele, MD Head, Division of Pediatric Infectious Diseases, Ochsner Children's Health Center; Clinical Professor, Department of Pediatrics, Tulane University School of Medicine

Russell W Steele, MD is a member of the following medical societies: American Academy of Pediatrics, American Association of Immunologists, American Pediatric Society, American Society for Microbiology, Infectious Diseases Society of America, Louisiana State Medical Society, Pediatric Infectious Diseases Society, Society for Pediatric Research, and Southern Medical Association

Disclosure: Nothing to disclose.

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

Kelley Struble, DO is a member of the following medical societies: American College of Physicians and Infectious Diseases Society of America

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

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

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Pap smear showing chlamydia in the vacuoles. Magnification, 500x. Image courtesy of the National Institutes of Health, National Cancer Institute.
This photomicrograph reveals McCoy cell monolayers with Chlamydia trachomatis inclusion bodies; magnified 200X. Image courtesy of the Centers for Disease Control and Prevention.
CT scan of adolescent with chlamydial Fitz-Hugh-Curtis syndrome demonstrating perihepatic fluid collection anterior to liver.
CT scan of adolescent with chlamydial Fitz-Hugh-Curtis syndrome demonstrating free peritoneal fluid.
 
 
 
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