Updated: Sep 1, 2009
Chancroid is a sexually transmitted infectious disease characterized by painful ulcers, bubo formation, and painful inguinal lymphadenopathy. The causative organism, Haemophilus ducreyi, was found by Ducrey in 1889. It is a gram-negative coccoid-bacillary rod, which is usually located in the extracellular spaces.
H ducreyi enters the skin through an epithelial break, usually following some minor trauma such as sexual intercourse. Once the bacteria have breached the integument, it recruits keratinocytes, fibroblasts, endothelial cells, and melanocytes to secrete interleukin 6 (IL-6) and interleukin 8 (IL-8). IL-8 induces polymorphonuclear neutrophils (PMNs) and macrophages to form intradermal pustules. IL-6 stimulates T-cell interleukin 2 (IL-2) receptor expression, which, in turn, stimulates CD4 cells in the region. H ducreyi secretes a cyto-lethal distending toxin (HdCDT) that causes apoptosis and necrosis of human cells such as myeloid cells, epithelial cells, keratinocytes, and primary fibroblasts.1 This toxin inhibits cell proliferation and induces cell death causing the characteristic ulcer formation seen in chancroid.
H ducreyi is also able to evade phagocytosis leading to slow healing of ulcers. For an unknown reason, macrophages in ulcers have greater CCR5 and CXCR4 chemokine receptors, which are receptors for human immunodeficiency virus (HIV) entry, than normal cells.
Chancroid is rare in the United States. Localized endemic outbreaks may occur within isolated STD and prostitution populations where it may coexist with other STDs.
Annual global incidence is about 6 million cases per year.2 Chancroid is more common in areas of low socioeconomic status such as Africa, Asia, and the Caribbean. It has also been found to be more common in areas where the prevalence of HIV is high (>8%). Other risk factors are low education level, risky sexual behavior, other sexually transmitted diseases, noncircumcision, and older male homosexuals.3 Note that the frequency of chancroid as well as other bacterial STDs has recently shifted away from bacterial infections and toward viral etiologies such as herpes simplex virus (HSV) and HIV.
If chancroid is diagnosed and treated early, it can be cured easily and quickly. H ducreyi produces painful ulcers and painful inguinal lymphadenopathy known as buboes. These may rupture after becoming an abscess. Scarring in this region may be permanent. Open sores secondary to H ducreyi infection also facilitate the transmission of HIV. Immunocompromised patients have lower cure rates and more complications.
The male-to-female ratio is between 3 and 25:12 , depending on the geographic region being studied. Although males are affected more often, female sex workers appear to be the reservoir of the disease.
Mean patient age is 30 years.
The patient complains of painful papules, pustules, or ulcers. They may also have dyspareunia, vaginal discharge, fever, or weakness. Patients may report a history of unprotected contact with a prostitute. HIV-positive and other immune compromised patients may have an atypical presentation.
The organisms enter through breaks in the skin on the genitals, which is where an erythematous papule will form, becoming a pustule in 2-3 days. The pustule ulcerates in a matter of weeks, and lymphadenopathy also usually is seen. The ulcer is characterized by a soft chancre with irregular borders and possibly a ring of erythema. Painful inguinal lymphadenopathy or bubo formation is present in 50% of patients.4 Lymphadenopathy is usually unilateral, and lymph nodes may rupture.
H ducreyi, a gram-negative bacillus, is the causative organism.
Herpes Simplex
Lymphogranuloma Venereum
Syphilis
Traumatic ulceration
Squamous cell carcinoma
Granuloma inguinale
Behçet disease
Extracutaneous Crohn disease
Drug eruption
Allergic reaction
Chlamydia trachomatis
The goal of therapy is to eradicate the microorganism. Since treatment of chancroid may accompany treatment of gonorrhea, it is important to be aware of the updated CDC guidelines for treating STDs. In April 2007, the Centers for Disease Control and Prevention (CDC) updated treatment guidelines for gonococcal infection and associated conditions. Fluoroquinolone antibiotics are no longer recommended to treat gonorrhea in the United States. The recommendation was based on analysis of new data from the CDC's Gonococcal Isolate Surveillance Project (GISP). The data from GISP showed the proportion of gonorrhea cases in heterosexual men that were fluoroquinolone-resistant (QRNG) reached 6.7%, an 11-fold increase from 0.6% in 2001. The data were published in the April 13, 2007, issue of the Morbidity and Mortality Weekly Report.7 This limits treatment of gonorrhea to drugs in the cephalosporin class (eg, ceftriaxone 125 mg IM once as a single dose). Fluoroquinolones may be an alternative treatment option for disseminated gonococcal infection if antimicrobial susceptibility can be documented. For more information see, the CDC's Antibiotic-Resistant Gonorrhea Web site; CDC Updated Gonococcal treatment recommendations (April 2007); or Medscape Medical News on CDC Issues - New Treatment Recommendations for Gonorrhea.
These agents are always indicated in chancroid. Therapy must be aimed at covering all likely pathogens according to the clinical setting.
Used to treat mild to moderately severe infections caused by susceptible strains of microorganisms. Indicated for chlamydial and gonorrheal infections of genital tract.
1 g PO once
<12 years: Not established
>12 years: 10 mg/kg PO on day 1 followed by 5 mg/kg days 2-5 suggested
May increase toxicity of theophylline, warfarin, and digoxin; aluminum and/or magnesium antacids may decrease effects; cyclosporine may increase risk of nephrotoxicity and neurotoxicity
Documented hypersensitivity; hepatic impairment; concurrent pimozide use (sudden death may occur)
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Site reactions can occur with IV route; bacterial or fungal overgrowth may result with prolonged use; may increase hepatic enzymes and cholestatic jaundice; caution in impaired hepatic function, prolonged QT intervals, or pneumonia; caution in hospitalized, geriatric, or debilitated patients
Third-generation cephalosporin with broad-spectrum, gram-negative activity; lower efficacy against gram-positive organisms and higher efficacy against resistant organisms than earlier generation cephalosporins. Arrests bacterial growth by binding to 1 or more penicillin-binding proteins.
250 mg IM once
Not established
50-75 mg/kg/d IV divided q12h suggested; not to exceed 2 g/d
Probenecid may increase levels; ethacrynic acid, furosemide, and aminoglycosides may increase nephrotoxicity
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Adjust dose in renal impairment; caution in breastfeeding women and allergy to penicillin
Blocks peptide bond formation by blocking peptidyl tRNA translocation from the A- to the P- site. Inhibits bacterial growth.
250 mg erythromycin stearate/base (or 400 mg ethylsuccinate) PO q6h 1 h ac, or 500 mg q12h
Alternatively, use 333 mg PO q8h; increase up to 4 g/d depending on severity of infection
Not established
30-50 mg/kg/d (15-25 mg/lb/d) PO in divided doses suggested
May increase toxicity of theophylline, digoxin, carbamazepine, and cyclosporine; may potentiate anticoagulant effects of warfarin; lovastatin or simvastatin increases risk of rhabdomyolysis
Documented hypersensitivity; hepatic impairment
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Caution in liver disease; estolate formulation may cause cholestatic jaundice; adverse GI effects are common (give doses pc); discontinue if nausea, vomiting, malaise, abdominal colic, or fever occur
Bactericidal antibiotic that inhibits bacterial DNA synthesis, and consequently growth, by inhibiting DNA-gyrase in susceptible organisms. Indicated for pseudomonal infections and those due to multidrug-resistant gram-negative organisms. If co-infection with gonorrhea suspected, do not use fluoroquinolones. CDC no longer recommends fluoroquinolones for gonorrhea or related conditions because of resistance.
500 mg PO bid for 3 d
Not established
Antacids, iron salts, and zinc salts may reduce serum levels; administer antacids 2-4 h before or after taking fluoroquinolones; cimetidine may interfere with metabolism of fluoroquinolones; reduces therapeutic effects of phenytoin; probenecid may increase serum concentrations; may increase toxicity of theophylline, caffeine, cyclosporine, and digoxin (monitor digoxin levels); may increase effects of anticoagulants (monitor PT)
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
In prolonged therapy, perform periodic evaluations of organ system functions (eg, renal, hepatic, hematopoietic); adjust dose in renal function impairment; superinfections may occur with prolonged or repeated therapy
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chancroid, genital ulcer, chancre, STD, sexually transmitted disease, painful ulcers, bubo formation, painful inguinal lymphadenopathy, Haemophilus ducreyi, sexually transmitted infectious disease
Ninfa Mehta, MD, Staff Physician, Department of Emergency Medicine, State University of New York Downstate Medical Center, Kings County Hospital
Ninfa Mehta, MD is a member of the following medical societies: American Association of Physicians of Indian Origin, American Medical Association, and American Medical Student Association/Foundation
Disclosure: Nothing to disclose.
Mark A Silverberg, MD, FACEP, MMB, Assistant Professor, Assistant Residency Director, Department of Emergency Medicine, State University of New York Downstate College of Medicine; Consulting Staff, Department of Emergency Medicine, Staten Island University Hospital, Kings County Hospital, University Hospital, State University of New York Downstate at Brooklyn
Mark A Silverberg, MD, FACEP, MMB is a member of the following medical societies: American College of Emergency Physicians, American Medical Association, Council of Emergency Medicine Residency Directors, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
David FM Brown, MD, Assistant Professor, Division of Emergency Medicine, Harvard Medical School; Vice Chair, Department of Emergency Medicine, Massachusetts General Hospital
David FM Brown, MD is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine
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Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
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Barry J Sheridan, DO, Chief, Department of Emergency Medical Services, Brooke Army Medical Center
Barry J Sheridan, DO is a member of the following medical societies: American Academy of Emergency Medicine
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John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
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Barry E Brenner, MD, PhD, FACEP, Professor of Emergency Medicine, Professor of Internal Medicine, Program Director, Emergency Medicine, University Hospitals, Case Medical Center
Barry E Brenner, MD, PhD, FACEP is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Chest Physicians, American College of Emergency Physicians, American College of Physicians, American Heart Association, American Thoracic Society, Arkansas Medical Society, New York Academy of Medicine, New York Academy of Sciences, and Society for Academic Emergency Medicine
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