Fmt. Behets et al., Genital ulcers: Etiology, clinical diagnosis, and associated human immunodeficiency virus infection in Kingston, Jamaica, CLIN INF D, 28(5), 1999, pp. 1086-1090
Individuals presenting consecutively with genital ulcers in Kingston, Jamai
ca, underwent serological testing for human immunodeficiency virus (HIV) in
fection, chlamydial infection, and syphilis. Ulcer material was analyzed by
multiplex polymerase chain reaction (M-PCR) analysis. DNA ti om herpes sim
plex virus (HSV), Haemophilus ducreyi, and Treponema pallidum was detected
ia 158 (52.0%), 72 (23.7%), and 31 (10.2%) of 304 ulcer specimens. Of the 3
04 subjects, 67 (22%) were HIV-seropositive and 64 (21%) were T. pallidum-s
eroreactive. Granuloma inguinale was clinically diagnosed in nine (13.4%) o
f 67 ulcers negative by M-PCR analysis and in 12 (5.1%) of 237 ulcers posit
ive by M-PCR analysis (P = .03). Lymphogranuloma venereum was clinically di
agnosed in eight patients. Compared with M-PCR analysis, the sensitivity an
d specificity of a clinical diagnosis of syphilis, herpes, and chancroid we
re 67.7%, 53.8%, and 75% and 91.2%, 83.6%, and 75.4%, respectively, Reactiv
e syphilis serology was 74% sensitive and 85% specific compared with M-PCR
analysis. Reported contact with a prostitute in the preceding 3 months was
associated with chancroid (P = .009), reactive syphilis serology (P = .011)
, and HIV infection (P = .007). The relatively poor accuracy of clinical an
d locally available laboratory diagnoses pleads for syndromic management of
genital ulcers in Jamaica. Prevention efforts should be intensified.