By Disease Name > Syphilis

Syphilis

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Primary syphilis

chancre:  clean, well made, rolled border, painless
serology becomes positive » 3 weeks after chancre (4-6 weeks after infection)
therefore diagnose primary syphilis by dark field examination
generally heals within 4 to 6 weeks
ddx:  see GENITAL ULCERS

 

Secondary syphilis

6 weeks to 6 months after contact

Manifestations

healing primary chancre is still present in 15% of cases
generalized non-tender lymphadenopathy (cervical, epitrochlear, inguinal)

 

Dermatologic:

often PR or guttate psoriasis appearing lesions; non-pruritic
moth eaten alopecia (eyebrows also)
check for mucous patches:
ddx:  white sponge nevus, LP, SCC, oral hairy leukoplakia, thrush, leukoplakia, blistering disease
dark-field exam useless in specimens from the mouth (because of nonpathogenic spirochetes)
split papules (commisures of lips, side of nose, post-auricular)
when the papular lesions occur in most intertriginous areas, they are known as condyloma lata same lesions in the mouth = mucous patches etc...
lues cornee

 

DISTINCT PRESENTATIONS

hmtoggle_plus1Rupioid Syphilis
rupioid = “dirty”;  secondary syphilis
heaped up, ostraceous (oyster shell) scale

 

hmtoggle_plus1Annular Syphilide
classically:  black patient, face
“nickels and dimes” on face of patient with secondary syphilis
histology:  lichenoid and granulomatous with plasma cells

 

TREATMENT: primary or secondary (non-HIV) syphilis pencillin G 2.4 million units IM X 1

 

Prozone phenomenon:

cause of false negativity in RPR, VDRL etc…
titer of antibody is too high, and therefore no flocculation will occur until higher dilutions

 

Jarcisch Herxheimer Reaction:

flu-like symptoms occurring 2-6 hours after treatment with PCN (most often seen in secondary syphilis)
symptoms are controlled with NSAID's or aspirin

 

 

hmtoggle_plus1Tertiary syphilis:
4 to 20 years after infection
1/3 of untreated cases progress to tertiary syphilis
tertiary syphilis can be mucocutaneous, osseous, visceral or neural
tertiary lesions are caused by obliterative small-vessel endarteritis (usually involves the vasa vasorum of the ascending aorta and, less often the CNS)

Neurosyphilis

 

Meningovascular:

invasion of the CNS by T. pallidum occurs during the first weeks or months of infection
syphilitic meningitis is therefore seen in secondary syphilis; presenting as an aseptic meningitis
meningovascular syphilis is an endarteritis with focal neurologic signs

 

Parenchymatous:

a result of the arteritis that occurs in tertiary syphilis
these are late complications of late untreated neurosyphilis

Tabes dorsalis

dorsal columns and posterior roots affected (particularly affecting the lower extremities)
dorsal columns = proprioception and stereognosis
ataxia
posterior roots =  peripheral sensory nerves entering spinal cord
posterior root irritation à shooting or lightening pains
paresthesia à secondary injuries and infection: Charcots joints (from trauma)
areflexia

 

General paresis

parenchymatous degeneration of brain substance
Argyll Robertson pupils (+ accommodate, (-) light;  i.e. like a prostitute, they accommodate but do not react)

gumma

starts as a deep firm swelling that eventually breaks down to form an ulcer
destructive, hypersensitivity reaction

cardiovascular disease

 

Congenital syphilis:

early until 2 years (snuffles, diaper dermatitis, peri-orificial inflammation, palms and soles, blisters this is the only time that syphilis is vesicular)
“snuffles” (syphilitic rhinitis) purulent/ hemorrhagic nasal discharge
late after 2 years (stigmata)
Hutchinsons teeth upper incisors that are peg shaped and notched
Mulberry molars dome shaped molars with numerous cusps
Higoumenakis sign unilateral irregular enlargement of the clavicle  (secondary to previous periostitis)
Saddle nose
Saber shins anterior bowing and thickening of midportion of the tibia (secondary to previous periostitis)
Rhagades depressed linear lines that radiate form the orifice like spokes of a wheel
diagnosis: IgM FTA-ABS (all other tests measure IgG)