syphilis

introduction

syphilis is a sexually transmitted infections (STDs/STIs) caused by the spirochete bacteria, Treponema pallidum
it was relatively common until the widespread use on penicillins in the 1950's when it became rare in Western cultures but has been gradually increasing with increased general sexual promiscuity and drug use in the 1980's but massive campaigns against HIV / AIDS and advice of safe sex reduced its prevalence in the 1990's. Unfortunately, it is again on the rise in line with massive rises in other sexually transmitted infections (STDs/STIs) as adherence to safe sex practices are no longer widespread.
cannot be cultivated in vitro and is too small to be seen under the light microscope, but can be detected using dark-field microscopy or direct immunofluorescence staining of fixed smears
rapidly penetrates intact mucous membranes or microscopic dermal abrasions
it can also be spread:
- from mother to baby in utero (“congenital syphilis”)
- via blood transfusions
- from breaks in the skin contacting syphilitic open skin lesions
incubation period from exposure to development of primary lesions 10-90 days with average of 3 weeks
pathology is characterised by obliterative endarteritis

high rate of spontaneous abortion and stillbirth
the first 2 years of life, symptoms are similar to severe adult secondary syphilis with widespread condylomata lata and rash
Snuffles” describes the mucopurulent rhinitis caused by involvement of the nasal mucosae
“saddle nose” (due to destruction of the nasal septum)
“saber shins” (due to inflammation and bowing of the tibia)
“Clutton’s joints” (due to inflammation of the knee joints)
“Hutchinson’s teeth” (in which the upper incisors are widely spaced and notched)
“mulberry molars” (in which the molars have too many cusps)
Tabes dorsalis and general paresis may develop
8th cranial nerve deafness and optic nerve atrophy may occur

the initial painless primary chancre lesion on the skin at site of initial transmission
the lesion has a punched-out base and rolled edges and is highly infectious

develops about 4-10 weeks after the appearance of the primary lesion as the bacteria spread throughout the body and multiply
clinical features can be diverse but usually include:
- malaise
- fever
- myalgias & arthralgias
- lymphadenopathy
- rash:
  - generalised mainly macular rash which may involve the palms, soles, and oral mucosae
  - can be pustular, annular, or scaling
  - wet mucous patches are the most contagious
- condylomata lata
  - painless, highly infectious gray-white lesions that develop in warm, moist sites such as genitalia/perianal areas
- patchy alopecia often with a “moth-eaten” appearance
immune reaction is at its peak

rare
slow inflammatory damage to tissues, especially to cardiovascular system and central nervous system
3 categories:
- gummatous syphilis:
  - gummas are painless rubbery granulomas which may affect any tissue but particularly, liver, bones, testes, and which break down with necrotic centres and may form ulcers
  - Treponema are rarely seen in these lesions
- cardiovascular syphilis
  - occurs at least 10 years after primary infection
  - ascending aortic aneurysm +/- aortic valve insufficiency
- neurosyphilis
  - various forms:
    - syphilitic meningitis
      - usually occurring within 6 months of the primary infection
      - cerebrospinal fluid (CSF): high protein, low glucose, high lymphocyte count, and positive syphilis serology
    - meningovascular syphilis
      - results in multiple infarctions and a range of neurologic features depending on areas infarcted
    - parenchymal neurosyphilis
      - Argyll-Robertson pupil:
        
        a pupil that does not react to light but does constrict during accommodation
      - tabes dorsalis
        
        develops as the posterior columns and dorsal roots of the spinal cord are damaged
        
        wide-based gait with impaired vibration and proprioceptive sensation, areflexia
      - general paresis
        
        damage to cerebral cortex causing dementia

VDRL and RPR serology tests:
- ~80% sensitive in primary syphilis
  - VDRL turn positive 1-2 weeks after chancre formation
- 100% sensitive in secondary syphilis
- 95-98% for detecting tertiary syphilis
- false positives may be an issue if:
  - collagen vascular disease
  - pregnancy
  - intravenous drug use
  - advanced malignancy
  - tuberculosis (TB)
  - malaria
  - viral
  - rickettsial diseases
- positive results should be confirmed by using treponemal tests such as:
  - fluorescent treponemal antibody-absorption (FTA-ABS)
  - quantitative VDRL/RPR
  - microhemagglutination assay T pallidum (MHA-TP)
  - T pallidum hemagglutination (TPHA)
  - T pallidum particle agglutination (TPPA)
  - in addition, Treponemal enzyme immunoassay (EIA) for immunoglobulin G (IgG) and immunoglobulin M (IgM) may be performed
- testing must be performed more than once in patients diagnosed with latent syphilis in order to exclude laboratory error
dark-field microscopy or direct immunofluorescence staining of fixed smears
- ~90% sensitive from swabs of moist cutaneous lesions