CLINICAL AND IN-SITU CELLULAR-RESPONSES TO HAEMOPHILUS-DUCREYI IN THEPRESENCE OR ABSENCE OF HIV-INFECTION

We aimed to determine if the clinical and histological features of cha ncroid are altered by HIV infection. Male patients presenting to the N airobi special treatment clinic with a clinical diagnosis of chancroid were eligible for the study. A detailed history, physical examination , swabs for Haemophilus ducreyi culture and blood for HIV serology, sy philis serology and CD4 counts were obtained from all patients. Punch biopsies from an ulcer were obtained from 10 patients and either fixed in 10% formalin or snap frozen in Optimum Cutting Temperature (OCT) m edium compound at -70 degrees C. Patients were treated with erythromyc in and followed for 3 weeks. Chi-square and Student's t-test were used to determine if the clinical and laboratory features of chancroid dif fered between HIV-seropositive and seronegative individuals. Cox regre ssion survival analysis was used to determine if HIV infection altered cure rates of chancroid at 21 days. Immunohistochemical staining was performed using lymphocytic and macrophage markers and tissue sections were analysed by 2 pathologists in a blinded manner. Between February and November 1994, 109 HIV-seropositive and 211 HIV-seronegative indi viduals were enrolled in the study. HIV patients had ulcers of longer duration than HIV-seronegative patients (P=0.03). Although cure rates were similar at 3 weeks, HIV patients had lower cure rates at 1 week ( 23% v 54%, P=0.002). A dense interstitial and perivascular inflammator y infiltrate extending from the reticular to deep dermis was present i n all biopsies. This consisted of equal amounts of CD4 and CD8 T-lymph ocytes as well as macrophages. The histological and immunohistochemica l picture was identical for HIV-positive and negative patients. HIV in fection slows the healing rates of chancroid ulcers despite appropriat e antibiotic therapy. This clinical difference cannot be attributed to an altered histopathological response to HN infection. Additional stu dies are needed to elucidate the mechanisms responsible for this findi ng.