Background

The identification of the causative agent of chancroid, Haemophilus ducreyi, was first reported in 1889 by August Ducrey, as a short streptobacillary rod with rounded ends, following experiments in which he autoinoculated patients' forearms with pus from their genital ulcers.¹ Bezancon et al subsequently inoculated the forearms of human volunteers with culture purified organisms and produced characteristic soft chancres from which the same organism was re-isolated.² This observation definitively identified H ducreyi as the causative organism of chancroid by fulfilling Koch's postulates.

Chancroid is a major cause of genital ulcer disease (GUD) in many resource poor countries of Africa, Asia, and Latin America although it remains relatively uncommon in the United States and Western Europe.^{3, 4} Tender inguinal lymphadenopathy or bubo formation is a characteristic feature in up to 50% of chancroid patients.⁵ Genital ulcers may caused by other sexually transmitted agents apart from H ducreyi, including Treponema pallidum, Chlamydia trachomatis serovars L1-L3, Calymmatobacterium granulomatis, and herpes simplex virus (HSV). It is therefore important to use appropriate diagnostic techniques in the management of patients presenting with the genital ulcer syndrome so that adequate treatment can be administered. In resource poor settings, where diagnostic facilities are not readily available, the World Health Organisation advocates the use of a syndromic management approach for the management of genital ulcer disease.⁶ Prospective and cross sectional case-control studies in Africa have provided substantial evidence that chancroid, either as a constituent of the GUD syndrome or as an aetiological diagnosis, is a risk factor for the heterosexual spread of human immunodeficiency virus (HIV).^7–9 The few clinical studies published to date suggest that HIV seropositive men have increased numbers of genital ulcers which are slow to heal^{10, 11} and there are reports …