Haemophilus ducreyi (Chancroid)
Authors: Pierre J. Plourde, M.D., FRCPC, , and Allan Ronald, O.C., M.D., FRCPC
Microbiology
Haemophilus ducreyi, a fastidious gram-negative bacillus is a well-known cause of chancroid, a sexually transmitted pathogen which has been associated with the sexual transmission of human immunodeficiency virus (HIV) (32). More recently it has been identified as the etiologic agent in chronic skin ulcers in the South Pacific region (20, 24).
Epidemiology
Chancroid was once commonly seen in sexually transmitted diseases (STD) clinics across Africa, Asia, and Latin America, where its incidence exceeded that of all other genital ulcer diseases combined. However, since 2000 with the widespread use of syndromic approaches to the management of bacterial STDs, chancroid has been rapidly declining as a significant cause of genital ulcers and may have been eliminated in some parts of eastern and southern Africa (9,17,34). The prevalence of chancroid among patients with genital ulcers, in sub-Saharan Africa declined from >60% in the 1970's to <15% between 2001 and 2005 (15, 25, 27, 28, 29), to undetectable in Kenya and Zambia between 2005 and 2010 (9, 17). In North America and Europe, chancroid has been a relatively rare STD with the exception of a short-lived increase in prevalence which occurred from 1975 to1995 related to transmission from female sex workers (5, 8, 21)
Since 2005, H. ducreyi has been newly identified as a cause of chronic skin ulcers in children living in yaws-endemic areas of the South Pacific region (20, 24, 39). First described in 1989 as the cause of a lower extremity chronic ulcer in an adult male (19), until recently there had only been a handful of cases of non-sexually transmitted chronic skin ulcers caused by H. ducreyi reported in the literature (23, 26, 39). The cases reported from surveys of chronic skin ulcers in children conducted in 2013 in Papua New Guinea and the Solomon Islands describe a non-sexually transmitted lower extremity chronic ulcer that is similar in clinical appearance to genital chancroid without marked regional lymphadenopathy or bubo formation. It appears to respond to standard antimicrobial therapy used to treat H. ducreyi (20, 24).
Clinical Manifestations
Chancroid typically presents after a 3 to 10 day incubation with painful, nonindurated, usually purulent genital ulcers, without initial vesicular lesions characteristic of genital herpes. Inguinal adenopathy, often unilateral and tender, occurs in approximately 50% of patients, with about half of these progressing to suppurative adenopathy known as buboes. Untreated, the infection will eventually resolve spontaneously in 1 to 3 months. A successful therapeutic response is usually manifested by decreased ulcer tenderness and pain within 48-72 hours. Complete re-epithelialization of successfully treated ulcers is usually achieved in 7-14 days, but may take up to 28 days in 5-10% of patients. Buboes may continue to suppurate with eventual formation of inguinal ulcers. Bubo rupture may be prevented by timely needle aspiration through adjacent normal skin. HIV seropositivity, may be associated with an increased likelihood of treatment failure (16, 33, 36, 37, 38), but this has not been consistently observed (18).
Much less is known about the presentation and natural history of H. ducreyi as a cutaneous infection described in the South Pacific region presenting as chronic lower extremity ulcers among children living in yaws-endemic areas (20, 24, 39). Individual case reports of H. ducreyi causing lower extremity ulcers have been reported since 1989 in Australia and New Zealand in South Sea Islanders (19, 23, 26, 39). However, only since surveys of chronic skin ulcers in children were conducted in 2013 in Papua New Guinea and the Solomon Islands have lower extremity chronic ulcers similar in clinical appearance to genital chancroid been recognized. H.ducreyi appears to be a significant alternative etiology of chronic ulcers among children who have been assumed to have yaws due to Treponema pallidum subspecies pertenue. The survey in Papua New Guinea found H. ducreyi to be the probable cause of almost 80% of these chronic ulcers in children. Further surveys will be required to determine the epidemiology and clinical significance of this new and emerging manifestation of H. ducreyi infection.
Laboratory Diagnosis
The diagnosis of H. ducreyi infection is complicated by difficulties encountered in isolating the organism in culture as well as its clinical presentation which can be confused with syphilis, genital herpes viral infection, and more recently with yaws in children (20, 24). Specific selective enriched culture media which are available only in specialized reference laboratories have sensitivities ranging from less than 50% to over 80%. Non-culture diagnostic antigen detection tests including nucleic acid amplification technologies such as PCR are sensitive and specific diagnostic modalities (14), but continue to be mostly used as research and survey tools. Hence, in most clinical settings the diagnosis of H. ducreyi infection remains a clinical diagnosis with exclusion of other pathogens.
Susceptibility In Vitro and In Vivo
Due to the relative rarity since 2000 of H. ducreyi infection as a cause of chancroid, H. ducreyi minimal inhibitory concentrations (MICs) have not been reported since the 1990's. The MICs to cephalosporins, macrolides, and quinolones have historically been 0.25 mg/ml or less (see Table 1). Repeated observations have revealed that a successful therapeutic response requires antibiotic regimens which produce blood or tissue levels of the drug above its MIC for H. ducreyi for at least 36-48 hours. This can be achieved by administering short half-life antibiotics for 5 to 7 days or by giving a single dose of an agent with a long half-life. When treating chancroid, single dose regimens are preferred over multidose as adherence to therapy is a major contributor to successful STD control. However, there may be a higher failure rate with single dose regimens in immune compromised HIV patients (16, 33, 36, 37, 38)
Virtually all strains of H. ducreyi causing chancroid have carried a plasmid-mediated tetracycline-resistance determinant and a beta-lactamase. Therefore H. ducreyi is inherently resistant to both tetracyclines and penicillins. Although trimethoprim in combination with sulphonamides was formerly a highly efficacious single dose or short course (3 to 5 day) therapy worldwide (31), it can no longer be recommended as resistance to both trimethoprim and sulphonamides exceeded 50% in many areas of Asia and sub-Saharan Africa (4, 30, 35). This resistance may be chromosomally-mediated as a trimethoprim/sulphonamide-associated plasmid has not been identified.
The absence of any MIC data on H. ducreyi strains causing the more recently described chronic lower extremity ulcers in children in the South Pacific region precludes any conclusive commentary. However, it appears that this presentation of H. ducreyi infection may respond well to single-oral-dose azithromycin (24, 26).
Antimicrobial Therapy
The recommended first line therapy for chancroid according to Centers for Disease Control and Prevention (CDC) STD treatment guidelines is one of four regimens: azithromycin 1 g orally in a single dose, ceftriaxone 250 mg intramuscularly in a single dose, ciprofloxacin 500 mg orally 2 times a day for 3 days, or erythromycin base 500 mg orally 3 times a day for 7 days (6). Treatment regimens for chronic ulcers in children caused by H. ducreyi have not been studied, hence recommended antimicrobial treatment options at this time cannot be recommended. Nevertheless, it appears that single-oral-dose azithromycin 30 mg/kg may be effective in children (24, 26).
When cost is a factor, erythromycin and ciprofloxacin may have more favorable profiles, although the advantage of single-oral-dose administration makes azithromycin an attractive option as well. Ceftriaxone costs will be higher due to additional costs of injection administration time and supplies.
Of the cephalosporins, ceftriaxone has received the most study for the treatment of chancroid, and for the most part has consistently demonstrated high clinical and microbiologic efficacy (near 100%) at a single dose of 250 mg intramuscularly (22, 33). However, ceftriaxone clinical and microbiologic failures have been associated with HIV seropositivity and the presence of a foreskin, despite MICs of less than 0.008 mg/ml (36). However, other studies have not demonstrated any adverse effect of HIV infection on the efficacy of single-dose treatments of chancroid (18, 33). There are no major contraindications to the administration of ceftriaxone, although intramuscular administration may not always be practical. Although minimal cross-reactivity exists between the penicillins and third generation cephalosporins, caution should be exercised in patients with a history of anaphylactic reactions to penicillins.
Macrolides
Macrolide antibiotics have also enjoyed success in treating chancroid for several years without any significant evidence of the emergence of resistance. The World Health Organization recommends both azithromycin 1 g orally as a single dose and erythromycin 500 mg orally 4 times a day for 7 days as first line therapy for chancroid. Some countries recommend erythromycin doses as low as 250 mg 3 times a day for 7 days to lower costs of therapy without unnecessarily reducing efficacy (12). Although lower dose regimens of erythromycin may be more economically feasible in the developing world, they should be recommended with caution as clinical efficacy of lower dose regimens are unfavorable (1, 3, 7, 12). Azithromycin, with lower MICs to H. ducreyi than erythromycin and a favourable pharmacokinetic profile results in good clinical and microbiologic cures rates when administered as a single oral dose (22). However, caution with single-oral-dose azithromycin should be taken with HIV positive uncircumcised men where efficacy may be reduced (38). Azithromycin should not be taken with food or antacids containing magnesium or aluminum, as interference with absorption may result leading to potential decreased efficacy.
Quinolones
Since quinolones have consistently demonstrated very low MICs against H. ducreyi in vitro, they have also received considerable attention with respect to the treatment of chancroid. The World Health Organization also recommends ciprofloxacin 500 mg orally twice daily for 3 days as a first line therapy for chancroid. Studies using ciprofloxacin performed prior to 1990 consistently revealed high clinical and microbiologic cure rates with regimens ranging from 500 mg twice a day for 3 days (recommended by CDC) to 500 mg in a single oral dose (1, 33). Attempts at administering a long acting quinolone in a single dose have produced mixed results (30, 37). Treatment failures after a single dose of ciprofloxacin may be related to a higher prevalence of mixed-etiology chancroid ulcers coinfected with syphilis and/or herpes simplex virus in HIV infected individuals, rather than HIV infection alone (18). The safety of quinolones has not been established in pregnancy or in persons less than 18 years of age, and hence use of quinolones for these individuals should proceed with caution only if the potential benefits outweigh the potential risks and no alternative treatments are available.
Syndromic Approach to Genital Ulcers
A syndromic approach to the management of genital ulcers has been adopted by many developing countries since the 1980's (40). Syndromic management essentially consists of treating all genital ulcers at the point of first contact with a health care provider, with antibiotics which are effective against both syphilis and chancroid, once considered the two most common treatable bacterial causes of genital ulcers. Therefore, first line treatment recommended for genital ulcers is usually erythromycin or ciprofloxacin (to treat chancroid) combined with penicillin (to treat syphilis). In the absence of adequate laboratory facilities, it was anticipated that this syndromic approach would improve the control of genital ulcer diseases. In fact, this syndromic approach to the treatment of bacterial genital ulcers has been credited with both the virtual elimination of chancroid and syphilis from sub-Saharan African countries as well as the emergence of herpes simplex as the current dominant cause of genital ulcers in most countries (15, 17, 25, 27, 29). This successful reduction and possible elimination of chancroid using syndromic approaches to genital ulcer disease control is now resulting in requests for the adoption of the WHO recommendation to include antiherpetic treatment in syndromic genital ulcer management algorithms (15, 17, 25, 27, 28, 29). Some have even suggested that where reliable consistent genital ulcer survey data reveal the absence of chancroid from certain regions, it might be possible to remove chancroid treatment from genital ulcer treatment algorithms (15, 17)
The treatment and control of yaws in children relies on the mass administration of single-oral-dose azithromycin to children with lower extremity ulcers (20, 24), not unlike the syndromic approach to the management of chancroid in the absence of laboratory confirmation of the diagnosis. It remains to be determined if such mass administration of azithromycin will also result in the control of chronic lower extremity ulcers caused by H. ducreyi in children in the South Pacific.
Endpoints of Monitoring Therapy
Successful therapy of chancroid should reveal markedly reduced tenderness, absence of purulence, and partial re-epithelialization of ulcers at a follow-up evaluation 7 days after the initiation of therapy. The natural history of successful response to therapy in chronic non-venereal ulcers caused by H. ducreyi is unknown.
Vaccines
Currently, there are no H. ducreyi vaccines available.
Prevention or Infection Control
Successful control of chancroid is achievable and affordable using a multifaceted approach including prompt identification and treatment of cases with simple syndromic management algorithms, accompanied by treatment of all recent sexual contacts within the previous 14 days, combined with sensitive and appropriate counseling and prevention education messages (34). Eradication of infection in persons who are sources of multiple infections, such as sex trade workers, can be effective in controlling chancroid outbreaks (34). As with any STD, identification and treatment of recent sexual partners is crucial. Properly used condoms can also reduce the transmission of chancroid. Dramatic reductions in the number of cases in not only the United States but also in sub-Saharan Africa in the last 5-15 years have demonstrated that the complete eradication of H. ducreyi as a cause of genital ulcer disease is possible (34). It is unknown if similar syndromic management approaches will successfully control or eliminate H. ducreyi as a cause of chronic lower extremity ulcers in children in the South Pacific.
Controversies, Caveats, or Comments
Although several studies primarily from Kenya in the 1990s suggested that concomitant HIV infection may reduce chancroid cure rates, no study systematically measured immunologic function in participants (16, 36, 37, 38). A publication from Rwanda actually disputed the adverse impact of HIV on the therapy of chancroid, demonstrating equivalent clinical cure rates of 75% to 80% in HIV negative and positive men, respectively, treated with a single 500 mg dose of ciprofloxacin (4). These investigators also did not find any correlation between CD4+ lymphocyte counts and clinical efficacy. Another subsequent study from Kenya did not demonstrate any adverse effect of HIV infection on the response to treatment in individuals infected with chancroid (18).
Nevertheless, the CDC recommends that if no clinical improvement is noted 7 days after initiation of a first line antibiotic for the treatment of chancroid, consideration should be given to the possibility of i) coinfection with HIV, ii) another diagnosis (especially herpes genitalis), iii) non-adherence to or malabsorption of the antibiotic, or iv) resistance to the prescribed antimicrobial (6).
The emergence of cutaneous manifestations in children with no history of genital infections or sexual abuse in Papua New Guinea and the South Sea Islands was unexpected and raises many questions. Earlier studies in volunteers have characterized many of the virulence factors that enable H. ducreyi to cause cutaneous infections and demonstrated the natural history and pathological features of genital infection (2, 11). The epidemiology and risk factors of these recently described cutaneous ulcers in children remain to be determined. Is genital chancroid present among sexually active adults in these populations? Occasional finger lesions have been reported in individuals with genital chancroid presumably from autoinoculation. The occurrence of yaws and 'chancroid' with similar skin manifestations in children creates significant challenges for the elimination of H. ducreyi (34). The epidemiologic association of HIV acquisition with H. ducreyi creates an additional dilemma. Are these chronic inflamed ulcers a potential entry site for HIV (10)? Are they responsible for any systemic illnesses? Will mass treatment (with azithromycin) eliminate H. ducreyi and cure chronic ulcers in populations? Are there any risks of this recently described syndrome spreading globally? Only careful well planned field investigation will determine if chronic cutaneous ulcers due to H. ducreyi infection is a harbinger of more serious persistence and spread of H. ducreyi in the populations at risk.
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Table
Table 1. In vitro Sensitivities of Haemophilus ducreyi (13,18,30,33)
| Antimicrobial Agent | MIC50 (mg/mL) | MIC90 (mg/mL) | MIC Range (mg/mL) |
|---|---|---|---|
| Penicillin G | 64.0 | 64.0 | 0.25~64.0 |
| Amoxicillin clavulanate | 2.0 | 8.0 | 0.03~16.0 |
| Trimethoprim-Sulfamethoxazole | 1.0 | 32.0 | 0.15~64.0 |
| Tetracycline | 16.0 | 32.0 | 2.0~64.0 |
| Ceftriaxone | 0.004 | 0.004 | 0.001~0.25 |
| Cefixime | 0.06 | 0.25 | 0.015~0.5 |
| Erythromycin | 0.008 | 0.25 | 0.002~4.0 |
| Azithromycin | 0.004 | 0.03 | 0.002~0.125 |
| Ciprofloxacin | 0.004 | 0.04 | 0.002~2.0 |
| Ofloxacin | 0.008 | 0.03 | 0.004~0.125 |
| Fleroxacin | 0.008 | 0.125 | 0.004~0.125 |
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