Aetiology

Chancroid is caused by Haemophilus ducreyi, a fastidious, gram-negative coccobacillus. It is a strictly human pathogen transmitted primarily via unprotected sex, or by auto-inoculation. H ducreyi can infect skin, mucosal surfaces, and lymph nodes. Survival outside the human host is brief.[17]

Most of the data on risk factors for chancroid pertains to genital infection which has been more extensively studied. For genital disease, risk factors include unprotected sex, a high number of sex partners (>15 per year), contact with a sex worker, cocaine use, poor hygiene, and lack of circumcision.[23][24]​​[25]​ The rate of transmission per sexual act has been approximated at 0.35.[15] Non-genital disease is most commonly seen in children living in remote and rural settings; a major risk factor for transmission is physical proximity to a confirmed ulcer case.​[3][4][5][6]​​[20]

H ducreyi has developed resistance to multiple antimicrobials, but most isolates largely remain susceptible to macrolides and quinolones.[26]​ Genital chancroid is an important co-factor in HIV transmission.[27]​​

Pathophysiology

Haemophilus ducreyi is highly infectious. In an experimental model, inoculation of only 1 colony-forming unit induced papule formation in 50% of volunteers.[28] Another study found that 70% of women who had contact with an infected man developed the disease.[29][30]​

The incubation period is 3-7 days.[31]​ H ducreyi has a brief period of infectivity and requires a frequent turnover of sexual partners to be maintained within a population.[11][29][32]​ For this reason, sex workers have been an important reservoir in most epidemics.

The sequence of pathogenesis is as follows:

  • The skin, which provides an excellent barrier to infection, is breached, usually by a tear or abrasion. H ducreyi enters the breach and preferentially attacks the mucosal epithelium.[33][34]

  • At the site of entry, epithelial cells are infiltrated by polymorphonuclear leukocytes and macrophages. This leads to the secretion of interleukin (IL)-2 and IL-6, recruiting mononuclear cells to the dermis, including CD4 cells.[17][33]

  • The inflammatory reaction manifests as 1 or more painless papules on an erythematous base, which over the next few days either resolve spontaneously or become pustular and ulcerate. Women are more likely to have spontaneous resolution of the papule, whereas men are more likely to progress to the pustular stage.[35][36]

  • If left untreated, the ulcers are slowly destructive and may last for months, causing permanent scarring.[17]

The reasons why H ducreyi is so infectious are incompletely understood. There are a number of proposed virulence factors that mediate the initial infection (pili and outer membrane proteins), cause tissue damage (haemolysins, heat shock proteins, lipopolysaccharide), and enable evasion of and resistance to host defences (lipopolysaccharide, resistance to alpha- and beta-defensins).[2][33][37][38][39][40]

Circumcision is protective against infection. This may be because the moist area under the foreskin is conducive to replication. Additionally, the epithelium lining the inner surfaces of the foreskin and frenulum is less cornified and more susceptible to abrasions, particularly during intercourse, therefore providing more entry sites for the organism.[15][23][24]​​​

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