eMedicine Specialties > Dermatology > Bacterial Infections

Chancroid

Author: Mark A Crowe, MD, Assistant Clinical Instructor, Department of Medicine, Division of Dermatology, University of Washington School of Medicine
Coauthor(s): Mark A Hall, MD, President/Founder, Central Oregon Dermatology, PC
Contributor Information and Disclosures

Updated: Aug 22, 2008

Introduction

Background

Chancroid is a sexually transmitted genital ulcer disease (GUD) caused by the gram-negative bacillus Haemophilus ducreyi. Chancroid is characterized by the presence of painful ulcers (see image below) and inflammatory inguinal adenopathy.

Chancroid usually starts as a small papule that r...

Chancroid usually starts as a small papule that rapidly becomes pustular and eventually ulcerates. The ulcer enlarges, develops ragged undermined borders, and is surrounded by a rim of erythema. Unlike syphilis, lesions are tender and the border of the ulcer is not indurated. Courtesy of Hon Pak, MD.

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Chancroid usually starts as a small papule that r...

Chancroid usually starts as a small papule that rapidly becomes pustular and eventually ulcerates. The ulcer enlarges, develops ragged undermined borders, and is surrounded by a rim of erythema. Unlike syphilis, lesions are tender and the border of the ulcer is not indurated. Courtesy of Hon Pak, MD.


Chancroid is often referred to as a soft chancre because the lesions are usually not indurated. In contrast, a syphilitic chancre is nontender and indurated. The identification of the causative agent of chancroid was first reported in 1889 by August Ducrey, following experiments in which he autoinoculated patients' forearms with pus from their genital ulcers.1,2,3

Pathophysiology

H ducreyi produces a potent cytolethal distending toxin, which is an important virulence factor in the pathogenesis of chancroid, probably contributing to both the generation and the slow healing of ulcers.4 5

Chancroid, or soft chancre, facilitates human immunodeficiency virus (HIV) transmission. The chemokine receptors CCR5 and CXCR4 belong to the class of 7 transmembrane G-protein–coupled receptors, and their natural ligands are key players in the recruitment of immune cells to sites of inflammation. CCR5 and CXCR4 are the 2 main co-receptors essential for HIV entry. Macrophages in chancroid lesions have significantly increased expression of CCR5 and CXCR4 compared with peripheral blood cells, and CD4 T cells have significant up-regulation of CCR5. The beta-chemokine RANTES (regulated on activation, normal T cell expressed and secreted) are important ligands for CCR5. RANTES is present throughout the papular and pustular stages of chancroid infection but is not present in uninfected control skin.6

Together with the disruption of mucosal and skin barriers, the presence of cells with up-regulated HIV-1 co-receptors in H ducreyi –infected lesions provides an environment that facilitates the acquisition of HIV-1 infection. Effective and early treatment of genital ulceration, and chancroid in particular, is an important part of any strategy to control the spread of HIV infection in tropical countries.7

Frequency

United States

Chancroid is rarely reported in the United States, but regional outbreaks and some endemic transmission occur, principally among migrant farm workers and poor inner-city residents.

International

Because of a lack of readily available, accurate diagnostic tests, the global incidence of chancroid is unknown. An estimated 6 million cases of chancroid occur each year. Chancroid is common in many of the world's poorest regions such as areas of Africa, Asia, and the Caribbean. These regions also have some of the highest rates of HIV infection in the world, and chancroid is common in all 18 countries where adult HIV prevalence surpasses 8%. In addition to regional outbreaks, individual cases are reported sporadically in the developed world, usually in individuals who have recently returned from chancroid-endemic areas or occasionally within the context of localized urban outbreaks, which may be associated with commercial sex work.

Mortality/Morbidity

  • Chancroid produces painful ulcers on the genitals, often (50%) associated with unilateral tender inguinal lymphadenitis (ie, a bubo). Left untreated, the buboes can form fluctuant abscesses that spontaneously rupture, resulting in a nonhealing ulcer.
  • Chancroid has been shown to be a major cofactor in the transmission of HIV-1 infection.8 This relationship has been especially significant in the heterosexual spread of HIV in Africa.7,9

Sex

Males develop chancroid most often, with a male-to-female ratio of 3-25:1.10

  • Uncircumcised men develop chancroid more often than circumcised men.11 Patients who are uncircumcised do not respond to treatment as well as those who are circumcised.12,13
  • Chancroid is more common in heterosexual men.14
  • Female prostitutes, either with active disease in the form of genital ulcers or as asymptomatic carriers, are an important reservoir for chancroid infection.

Age

Chancroid is most prevalent in sexually active and promiscuous males, with a mean patient age of 30 years.

Clinical

History

  • After an incubation period of 3-7 days, the patient develops painful, erythematous papules at the site of contact. The chancroid papules become pustular and then rupture, usually forming 1-3 painful ulcers.
  • Men usually have chancroid symptoms directly related to the painful genital lesions or inguinal tenderness. Most females are asymptomatic but may present with less obvious symptoms, such as dysuria, dyspareunia, vaginal discharge, pain on defecation, or rectal bleeding. Constitutional symptoms of chancroid, such as malaise and low-grade fevers, may be present.
  • Most commonly, males with chancroid report a history of recent contact with a prostitute. In addition, men who are infected are less likely to have used condoms and more likely to report a history of more than 2 sexual partners in the preceding 3 months.
  • Oral sex has also been documented in the transmission of chancroid.

Physical

  • With chancroid, a small papule is the initial lesion at the site of infection. The papule rapidly becomes pustular and eventually ulcerates. The ulcer enlarges, develops ragged undermined borders, and is surrounded by a rim of erythema. The border of the chancroid ulcer is not indurated as in syphilis. A grayish fibrinous membrane covers the base of the ulcer. Autoinoculation results in multiple sites of infection in various stages of evolution.
  • In men, the most common site of the chancroid infection is the foreskin, but it may also occur less commonly on the shaft, the glans, or the meatus of the penis. In women, chancroid ulcers most commonly occur on the labia majora, but they may also occur on the labia minora, the thighs, the perineum, or the cervix.
  • As many as 50% of chancroid patients have tender, fixed, inguinal lymphadenopathy, usually unilaterally, that when fluctuant is called a bubo and is highly specific for chancroid, as seen in the images below.

  • This patient shows the characteristic lesions of ...

    This patient shows the characteristic lesions of chancroid. The bubo on the right side drained spontaneously. The bubo in the left inguinal canal required needle aspiration.

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    This patient shows the characteristic lesions of ...

    This patient shows the characteristic lesions of chancroid. The bubo on the right side drained spontaneously. The bubo in the left inguinal canal required needle aspiration.


  • Close-up view of chancroid ulcers.

    Close-up view of chancroid ulcers.

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    Close-up view of chancroid ulcers.

    Close-up view of chancroid ulcers.

  • A probable chancroid diagnosis can be made if all the following criteria are met15,16,17 :
    • The patient has one or more painful genital ulcers.
    • The patient has no evidence of Treponema pallidum infection by darkfield examination of ulcer exudate or by serologic testing for syphilis performed at least 7 days after the onset of ulcers.
    • The clinical presentation, the appearance of genital ulcers, and, if present, the presence of regional lymphadenopathy are typical for chancroid.
    • Test results for herpes simplex virus (HSV) performed on the ulcer exudate are negative.18
  • The combination of a painful ulcer and tender inguinal adenopathy, symptoms occurring in one third of patients, suggests a diagnosis of chancroid; when accompanied by suppurative inguinal adenopathy, these signs are almost pathognomonic.

Causes

  • H ducreyi (a short gram-negative bacillus) causes chancroid.
  • See Pathophysiology.
  • Chancroid is closely associated with prostitution. H ducreyi can survive only in subgroups of the population with a sufficient turnover of sex partners. Chancroid is not a sustainable infection in sexual networks with low rates of partner change.

More on Chancroid

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

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Further Reading

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Keywords

chancroid, HIV transmission, soft chancre, genital ulcers, STD, genital ulcer disease, GUD, Haemophilus ducreyi, H ducreyi, sexually transmitted disease, genital ulcer, bubo

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Contributor Information and Disclosures

Author

Mark A Crowe, MD, Assistant Clinical Instructor, Department of Medicine, Division of Dermatology, University of Washington School of Medicine
Mark A Crowe, MD is a member of the following medical societies: American Academy of Dermatology and North American Clinical Dermatologic Society
Disclosure: Nothing to disclose.

Coauthor(s)

Mark A Hall, MD, President/Founder, Central Oregon Dermatology, PC
Mark A Hall, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.

Medical Editor

Janet Fairley, MD, Professor and Head, Department of Dermatology, University of Iowa
Janet Fairley, MD is a member of the following medical societies: American Academy of Dermatology, American Dermatological Association, American Federation for Medical Research, and Society for Investigative Dermatology
Disclosure: Nothing to disclose.

Pharmacy Editor

Richard P Vinson, MD, Assistant Clinical Professor, Department of Dermatology, Texas Tech University School of Medicine; Consulting Staff, Mountain View Dermatology, PA
Richard P Vinson, MD is a member of the following medical societies: American Academy of Dermatology, Association of Military Dermatologists, Texas Dermatological Society, and Texas Medical Association
Disclosure: Nothing to disclose.

Managing Editor

Paul Krusinski, MD, Director of Dermatology, Professor, Department of Internal Medicine, Fletcher Allen Health Care, University of Vermont
Paul Krusinski, MD is a member of the following medical societies: American Academy of Dermatology, American College of Physicians, and Society for Investigative Dermatology
Disclosure: Nothing to disclose.

CME Editor

Joel M Gelfand, MD, MSCE, Medical Director, Clinical Studies Unit, Assistant Professor, Department of Dermatology, Associate Scholar, Center for Clinical Epidemiology and Biostatistics, University of Pennsylvania
Joel M Gelfand, MD, MSCE is a member of the following medical societies: Society for Investigative Dermatology
Disclosure: AMGEN Consulting fee Consulting; AMGEN Grant/research funds Investigator; Genentech Grant/research funds investigator; Centocor Consulting fee Consulting; Abbott Grant/research funds investigator; Abbott Consulting fee Consulting; Novartis  investigator; Pfizer Grant/research funds investigator; Celgene Consulting fee DMC Chair; NIAMS and NHLBI Grant/research funds investigator

Chief Editor

Dirk M Elston, MD, Director, Department of Dermatology, Geisinger Medical Center
Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.

 
 
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