Pediculosis Syphilis Flashcards
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T. pallidum bacteriology
small: 0.25 micrometers diameter (invisible to light microscopr)
Delicate: can’t survive outside hose
Motile: Flagellar “corkscrew” motion
Human-restricted in nature (can infect rabbits in lab)
cannot be grown in culture
Extremely infectious sexually
Virulence based on immune evasion
T. palidum pathogenesis
Transmitted by sexual contact (acquired), blood, transplacentally (congenital)
National plan to eliminate in US hit bumps: working among whites, women, not among MSM, slower among minorities
T. pallidum pathogenesis
Acquired:
penetrates mucous membranes or small abrasions, grows in blood vessel endothelium, enters lymphatics and bloodstream
CNS is invaded relatively early, though symptoms take years to develop: first CSF abnormalities, then meninges, then parenchyma of brain and spinal cord
Host raises antibodies: specific anti-treponemal, nonspecific reagin
Immunity is incomplete:
surface of spirochete nonimmunogenic
Spirochete down-regulates TH1 cells
T. pallidum pathogenesis
Primary syphilis
Painless chancre at site of transmission 3-6 wks later: highly infectious
Inflammatory infiltrate at site fails to clear organism
chancre heals 3-12 weeks
T. pallidum pathogenesis
Secondary syphillis
4-10wks, Spirochete multiplication -> systemic symptoms
fever, malaise, myalgias, arthralgias, lymphadenopathy
mucocutaneous lesions of variable types, condylomata lata, patchy alopecia (“moth eaten”)
High antibody titers
T. pallidum pathogenesis latent syphilis (end for 2/3)
organism remains
secondary symptoms resolve, may return intermittently over years
T. pallidum pathogenesis
Tertiary syphilis
1/3 untreated, fatalities possible
gummatous syphilis: grnulomatous lesions (“gummas”) w/rubbery necrotic center. Primarily liver, bones, testes
Cardiovascular syphilis (>10yrs) aneurysm of ascending aorta caused by chronic inflammation of vasa vasorum (the vessels of the vessels!)
Neurosyphilis:
syphilic meningitis: early (6mo)
Meningovascular syphilis: damage to blood vessels of meninges, brain, spinal cord
Parenchyma neurosyphilis:
Tabes dorsalis: damage to spinal cord -> impaired sensation, wide-based gait
Disruption of dorsal roots -> loss of pain and temperature sensation, areflexia
General paresis: damage to cortical brain tissue -> dementia
T. pallidum pathogenesis
Congenital
Treponemes readily cross placenta and infect fetus
Miscarriage/stillbirth/neonatal death 40-50%
Within first two years, surviving infants develop severe secondary syphilis
Syphilis and HIV
ulcerations of syphilis facilitate HIV infection
HIV immunosuppression accelerates syphilis course and reduces efficacy of treatment
Syphilis diagnosis: exam
Primary syphilis
“The great imitator”
Time course of symptoms: Primary syphilis approx. 3 weeks
Chancres are raised, red firm, buttonlike structure up to several cm, heal in 4-8 weeks, not painful unless superinfected
site may e genital or other intimate; local lymph node swells w/invasion
Syphilis diagnosis: exam
Secondary syphilis
begins 4-10wks after primary, peaks 3-4mo after infection
may be subtle
first-round rash is bilaterally symmetrical, with generalized nontender lymphadenopathy, round pink spots 5-10mm
Second batch of lesions appears days or weeks later, palms & soles, become necrotic
patchy alopecia
condylomata lata:
reddish-brown papular lesions on the penis or anogenital area
can coalesce into large elevated plaques up to 2-3 cm in diameter
lesions usually progress from red, painful, and vesicular to “gun metal grey”
sometimes confused with veneral warts
mild constitutional symptoms: malaise, headache, anorexia, nausea, aching pains in the bones, and fatigue, fever and neck stiffness, syphilitic meningitis
Syphilis diagnosis: exam
Tertiary syphilis
3-10yr after infection, years of inflammation
gumma Bone: deep boring pain worse at night. Skin hyperpigmented circle. Often on lower leg, asymmetric, few grouped close
Liver-jaundice
Cardiovascular sphilis aorta or other major arterial scarring; diastolic murmur with a tambour quality, secondary to aortic dilation with valvular insufficiency
meningovascular syphilis:
5-10 years after infection
Endarteritis affects small blood vessels of the meninges, brain, and spinal cord
CNS vascular insufficiency or stroke
Parenchymal neurosyphilis:
15-20 years after primary infection
parenchymal CNS invasion by T. pallidum
General paretic syphilis: widespread parenchymal invasion that causes individual cell death and brain atrophy
Tabes dorsalis: damage to the sensory nerves in dorsal roots, ataxia and loss of pain sensation, proprioception, deep tendon reflexes, deep ulcers of the feet
Dementia
Argyll-robertson pupil: Hallmark of neurosyphilis - one or both pupils fail to constrict in response to light
But does constrict to focus on a near object
T. pallidum diagnosis: exam
Imaging:
CT for gummas
Chest radiograph, angiograph for cardiovascular syphilis
CT and MRI for neurosyphilis
Lumbar puncture for neurosyphilis or syphilis+HIV
-VDRL, cell count, protein
-PCR for evidence of past infection
T. pallidum diagnosis: Lab
won’t culture, too small to gram stain
Swab moist cutaneous lesions for darkfield microscopy or IF
For neurosyphilis, use CSF for tests, specific but not sensitive
Serology:
First, nontreponemal serology screening using veneral disease research labratory (VDRL), rapid plasma reagin (RPR), or ICE syphilis recombinant antigen test
