Uro LBM 4

Ulcus Herpes Genital

Etiology : Herpes Simplex Virus (HSV), HSV-2>HSV1
HSV infection is transmitted through close contact with
a person shedding virus at a peripheral site, mucosal
surface, or secretion.
Infection occurs via inoculation onto susceptible
mucosal surface or break in skin.
Subsequent to primary infection at inoculation site, HSV
ascends peripheral sensory nerves and enters sensory
or autonomic nerve root ganglia, where latency is
established.
Latency can occur after both symptomatic and
asymptomatic primary infection.
Recrudescences may be clinically symptomatic or
asymptomatic.
 Clinical Manifestations
3 stages : Primary, Laten, Recurrent
Incubation Period : 2-20 days (average : 20)
Primary : mostly asymptomatic, Those with
symptoms report fever, headache, malaise,
myalgia, peaking within the first 34 days after
onset of lesions, resolving during the subsequent
34 days.
Tender inguinal lymphadenopathy occurs during
second and third weeks. Deep pelvic pain
associated with pelvic lymphadenopathy.
 Primary Characteristic
An erythematous plaque is often noted initially,
followed soon by grouped vesicles, which may evolve
to pustules; these become eroded as the overlying
epidermis sloughs.
Erosions are superficial; may enlarge to ulcerations;
classic findings described below may be crusted or
moist. These epithelial defects heal in 24 weeks,
often with resulting postinflammatory hypo- or
hyperpigmentation, uncommonly with scarring.
 Latency : no clinical manifestation present.
HSV found inactive in dorsal ganglion.
 Recurrent :
Reactivation of dormant HSV in dorsal ganglion
due to various factors.
New symptoms may result from old infections.
Most individuals with GH do not experience
classic findings of grouped vesicles on
erythematous base.
Dysuria, sciatica, rectal discomfort.
 Recurrent characteristic :
Usually milder than primary stage, but shown
similar characteristic
Local prodromal symptom (itching, burning,
fissure, redness, irritation) prior to eruption of
vesicles.
Last about 7-10 days
 Tzanck tes Giemsa datia cell with
multiple nuclei, intranuclear inclusion body
No lession HSV antibody
 Differential Diagnosis
Oral Impetigo vesikobulosa
Genital
Ulkus Durum
Ulkus mole
Ulkus mikstum
 Treatment
No specific effective therapy to prevent
recurrent episodes.
Idoksuridin, Acyclovir topical
Acyclovir oral 5x200mg for 5 days better
result
Lupidon H (HSV-1) & Lupidon G (HSV-2)
prevent recurrent episodes.
Levamisol & isoprinosin as imunostimulator.
 Ulcus Molle / Chancroid
Etiology : H. ducreyi , a gram-negative streptobacillus.
Primary infection develops at the site of inoculation
(break in epithelium), followed by lymphadenitis.
The genital ulcer is characterized by perivascular and
interstitial infiltrates of macrophages 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 erythematous halo
that evolves to pustule, erosion, and ulcer. Ulcer is
usually quite tender or painful . Its borders are sharp,
undermined, and not indurated. 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.
 General Findings
Painful inguinal lymphadenitis (usually unilateral)
occurs in 50% of patients 721 days after primary
lesion. Ulcer may heal before buboes occur.
Buboes occur with overlying erythema and may
drain spontaneously. (buboes/bubo)
 Differential Diagnosis
Genital Ulcer : Genital herpes, primary
syphilis, lymphogranuloma venereum (LGV),
donovanosis, secondarily infected human
bites, traumatic lesions.
Tender Inguinal Mass : Genital herpes,
secondary 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; isolation
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.
 Diagnosis
Combination of painful ulcer with tender
lymphadenopathy is suggestive 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 following
criteria:
Painful genital ulcers
No evidence of T. pallidum infection by darkfield
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.
 Treatment
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.
 Syphillis
Etiologic agent: Treponema pallidum A chronic
systemic infection transmitted through skin and
mucosa, with manifestations in nearly every organ
system.
Manifestations:
A painless ulcer or chancre on the mucocutaneous site of
inoculation
Associated with regional lymphadenopathy (chancriform
syndrome: distal ulcer associated with proximal
lymphadenopathy)
Shortly after inoculation, syphilis becomes a systemic
infection with characteristic secondary and tertiary stages.
 Congenital Syphillis
Transmission During gestation or intrapartum.
Risk of transmission: Early maternal syphilis, 75
95%; >2 years duration, 35%. Pathogenesis
Lesions usually develop after fourth month of
gestation, associated with fetal immunologic
competence.
Pathogenesis depends on immune response of
fetus rather than toxic effect of spirochete.
Adequate treatment before sixteenth week of
pregnancy prevents fetal damage. Untreated:
fetal loss up to 40%.
 Early Manifestations
Appear before 2 years of age, often at 210 weeks.
Infectious, resembling severe secondary syphilis in
adult.
Cutaneous: Bullae, vesicles on palms and soles,
superficial desquamation, petechiae, papulosquamous
lesions
Mucosal: Rhinitis/snuffles (23%); mucous patches,
condylomata latum.
Bone changes: osteochondritis, osteitis, periostitis.
Hepatosplenomegaly, jaundice, lymphadenopathy.
Anemia, thrombocytopenia, leukocytosis.
 Late Manifestations
Appear after 2 years of age. Noninfectious.
Similar to late acquired syphilis in adult.
Cardiovascular syphilis.
Interstitial keratitis
Eighth nerve deafness.
Recurrent arthropathy; bilateral knee effusions
(Clutton joints). Gummatous periostitis results in
destructive lesions of nasal septum/ palate.
Asymptomatic neurosyphilis in 33% of patients;
clinical syphilis in 25%.
 Residual Stigmata
Hutchinson teeth (centrally notched, widely spaced,
pegshaped upper central incisors; mulberry molars
(multiple poorly developed cusps).
Abnormal facies: frontal bossing, saddle nose, poorly
developed maxillae, rhagades (linear scars at angles of
mouth, caused by bacterial superinfection of early
facial eruption).
Saber shins.
Nerve deafness
Old chorioretinitis, optic atrophy, corneal opacities due
to interstitial keratitis.
Etiology : Chlamydia trachomatis
 Clinical manifestations
Painless, progressive,
ulcerative lesions of the
genital and perianal areas.
Highly vascular (i.e., a beefy
red appearance) and bleed
Etiology : Donovania easily on contact.
granulomatis, No regional
Calymmatobacterium lymphadenopathy. Large
granulomatis, an subcutaneous nodule may
encapsulated intracellular mimic a lymph node, i.e.,
gramnegative rod; closely pseudobubo.
related to Klebsiella spp