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28 Cards in this Set

  • Front
  • Back
what is STD?
infections which are primarily sexually transmitted
syndromic classification of STD
genital ulcer
urethritis/cervicitis
vaginitis/vaginosis
exophytic processes
extoparasitic infectinos
systemic STD syndromes
agents of genital ulcer diseases
syphilis (T. pallidum)
genital herpes (HSV)
chancroid (H ducreyi)
lymphogranuloma venereum (chlamydia)
rare: granuloma inguinale
characteristics of t. pallidum
syphilis
spirochete. can't be cultured
humans sole host
pathogenesis of syphilis
penetrates skin and mucous membrane
attaches to epithelial cells, replicate w/o visible inflammation
travels to regional lymph nodes and body via blood stream
activate lymphocytes / macrophages
1' lesion (chancre) develops at site of inoculations (~ 2 wks from exposure to Sx)
stages of syphilis
1' infection : painless ulcer (chancre)
2' infection: rash, condyloma lata, systemic Sx
3' infection: neurological, CV, ophthalmologic, osseous
congenital: fetal demise, mental retardation, long term disability
latent phase after secondary 2-20 yrs. 1/3 go into 3' infection
what is chancre?
hallmark of 1' infection
painless
indurated, indolent
rasied border, punched out appearance
red, smooth base
scant serous secretion
clinical presentation of chancre
often solitary. multiple lesion possible
develop anywhere in the genital tract, oropharyngeal area, or other body site of initial contact
clinical presentation of syphilis
onset approx 3 weeks after exposure
chancre heals spontaneously 1-6 wks
secondary Sx occur 3-6 wks after chancre appears and may persist
rash ultimately resolves, but infection is lifelong w/o Tx
latent syphilis manifestation
positive blood test, no clinical Sx
manifestation of 3' syphilis
neurosyphilis
aortitis
gumma
manifestation of congenital syphilis
"snuffles" - chronic runny nose
hutchinson's incisors - notched central incisors
Dx of syphilis
darkfield examination
serologic tests - RPR or VDRL (screening tset) TP-PA, FTA-ABS (confirmatory tests)
Tx of syphilis
penicillin (needs to be injected)
oral tetracycline are alternative but not preferred
azithromycin has activity but resistance is widespread
where does HSV -1 and HSV-2 manifest?
HSV1- mouth lips
HSV2- genital
pathogenesis of HSV
transmission - close contact w/ a person shedding virus.
HSV ascends peripheral sensory nerves, enters nerve root ganglia
lifelong persistent infection
Sx of initial HSV infection
1-3 weeks of viral shedding and Sx
systemic Sx - fever, headache, pharyngitis, malaise, myalgia
local Sx - pain itching dysuria, vaginal, urethral discharge, tender inguinal adenopathy
recurrent infection of HSV
HSV-1 less likely
HSV-2 80% recur within 12 months
sign/Sx localized to genitals
50% experience prodrome - tingling, itching, headache
papule and vesicles form
no scarring
what is subclinical infection of HSV?
unrecognized lesions which persons can be taught to identify. they are shedding virus
Dx of HSV
PCR (standard)
culture
HSV antigen
cytology
serology
Tx of herpes
oral acyclovir
famciclovir
what causes chancroid?
Haemophilus ducreyi
characteristics of H. ducreyi
gram negative bacillus. facultative anaerobe
requires hemin for growth
break in skin required for infection
induces pyogenic inflammatory response
endemic in NYC, new orleans
presentation of chancroid
genital ulcer (4-7 days after exposure)
** painful. soft ragged border "serpiginous"
dusky base w/ exudate
multiple lesions often

inguinal adenopathy
- occurs in 50%
Dx of chancroid
clinical presentation/ Hx
gram stain
culture
Tx of chancroid
ceftriaxone - drug of choice

macrolide (azithro) or fluoroquinolone (cipro) as alternative
lymphogranuloma venereum is caused by?
chlamydia trachomatis serotype L1, L2, L3
transient ulcer -> heaped up inguinal lymph nodes
caused by klebsiella granulomatis
painless progressive ulcerations which bleed easily on contact
granuloma inguinale (donovanosis)