HAEMOPHILUS DUCREYI: CHANCROID

Chancroid is an acute STI characterized by

A painful ulcer at the site of inoculation, usually on the external genitalia
The development of suppurative regional lym-phadenopathy.
STI most strongly associated with increased risk for HIV/AIDS
transmission.Synonyms: Soft chancre, ulcus molle, chancre mou.ICD-9 : 099.0
ICD-10 : A57

ETIOLOGY AND EPIDEMIOLOGY Etiology

H. ducreyi , a gram-negative
strepto-bacillus. Epidemiology
In the United States, chancroid usually occurs
in discrete outbreaks, although the disease is endemic in some areas. Sex
Young males. Lymphadenitis more com-mon in males. Risk Factors
Transmission mainly heterosexual Males > females 3:125:1
Prostitution significant Strongly associated with illicit drug use.
Transmission
Most likely during sexual inter-course with partner who has H.
ducreyi genital ulcer. Chancroid is a cofactor for HIV/AIDS transmission; high
rates of HIV/AIDS infec-tion among those who have chancroid. 10% of individuals
with chancroid have syphilis or genital herpes.

Demography
Uncommon in industrialized nations. Endemic in tropical and
subtropical developing countries, especially in poor, urban, and seaport
populations.
PATHOGENESIS Primary infection develops at the site of inoculation (break in epithelium), followed by lymphadenitis. The genital ulcer
is characterized by perivas-cular and interstitial infiltrates of macro-phages and
of CD4+ and CD8+ lymphocytes, consistent with a delayed-type hypersensitivity, cell-mediated immune response. CD4+ cells and macrophages in the
ulcer may explain the facilitation of transmission of HIV/AIDS in patients with
chancroid ulcers.
CLINICAL MANIFESTATION Incubation period is 47 days.
Skin Lesions Primary lesion: tender papule with erythema-tous halo that
evolves to pustule, erosion, and ulcer. Ulcer is usually quite tender or painful .
Its borders are sharp, undermined, and not indurated (Figs. 30-27 and 30-28).
Base is friable with granulation tissue and covered with gray to yellow exudate.
Edema of prepuce common. Ulcer may be singular or multiple, merging
to form large or giant ulcers (>2 cm) with serpiginous shape. Distribution
Multiple ulcers (Fig. 30-28) develop by autoinoculation. Male: prepuce,
frenulum, coronal sulcus, glans penis, shaft. Female: fourchette, labia,
vestibule, clitoris, vaginal wall by direct extension from introi-tus, cervix, perianal.
Extragenital lesions: breast, fingers, thighs, oral mucosa. Bacterial
superinfection of ulcers can occur.
General Findings
Painful inguinal
lymphad-enitis (usually unilateral) occurs in 50% of patients 721 days after
primary lesion. Ulcer may heal before buboes occur. Buboes oc-cur with overlying
erythema and may drain spontaneously.
DIFFERENTIAL DIAGNOSIS Genital

Ulcer
Genital herpes, primary syphilis, lymphogranuloma venereum (LGV),
donova-nosis, secondarily infected human bites, trau-matic lesions. Tender
Inguinal Mass
Genital herpes, second-ary syphilis, LGV, incarcerated hernia,
plague, tularemia.
LABORATORY EXAMINATIONS Gram Stain
Of scrapings
from ulcer base or pus from bubo, usually not helpful. Culture
Special growth
requirements; isola-tion difficult. Using special media, sensitivity is no higher than
80%. Serologic Tests
None available. Patients should have HIV/AIDS serology
at time of diagnosis. Patients should also be tested 3 months later for both
syphilis and HIV/AIDS infection if initial results are negative. Dermatopathology
May be helpful. Organism rarely demonstrated. PCR
Detects H. ducreyi DNA
sequences.
FIGURE 30-27 ChancroidPainful ulcer with marked surrounding
erythema and edema. (Courtesy of Prof. Alfred

DIAGNOSIS Combination of painful ulcer with tender lym-phadenopathy (onethird of patients) is sug-gestive of chancroid and, when accompanied by
suppurative inguinal lymphadenopathy, is almost pathognomonic. Definitive
Diagnosis
Made by isolation of H. ducreyi on special culture media (not widely
available). Sensitivity 80%. Probable Diagnosis
Made if patient has fol-lowing
criteria: Painful genital ulcers No evidence of T. pallidum infection by
dark-field examination of ulcer exudate or by STS performed at least 7 days after
onset of ulcers Clinical presentation, appearance of genital ulcers, and
lymphadenopathy, if present, are typical for chancroid and a test for HSV is
negative.
COURSE AND PROGNOSIS Patients should be reexamined 3
7 days after initiation of therapy. If treatment is successful, ulcers improve
symptomati-cally within 3 days and improve objectively within 7 days after
therapy is begun. If no clinical improvement is evident, diagnosis may be
incorrect, co-infection with another STI agent exists, the patient is HIV/AIDSinfected, treatment was not taken as instructed, or the H. ducreyi strain causing
infection is resistant to the pre-scribed antimicrobial. The time required for
complete healing is related to the size of the ulcer; large ulcers may require 14
days. Complete resolution of fluctuant lymphadenopathy is slower than that of
ulcers and may require needle aspiration through adjacent intact skineven
during successful therapy. In HIV/AIDS, healing may be slower, and
treatment failures may occur; longer treat-ment regimens may be advisable.
MANAGEMENT
Antimicrobial Therapy
Azithromycin 1 g PO in a
single dose, or Ceftriaxone 250 mg IM in a single dose, or
Ciprofloxacin
500 mg PO twice a day for 3 days, or Erythromycin base 500 mg PO four
times a day for 7 days. Management of Sex Partners
Sex partners should be
referred for evaluation and treat-ment. FIGURE 30-28 ChancroidMultiple, painful,
punched-out ulcers with undermined borders on the vulva occurring after
autoinoculation.