Volume 3 Issue 10 October, 2013
Consultation Liaison Psychiatry Focus: ‘Microbiology’
The Austrian psychiatrist Julius Wagner Ritter von Jauregg tried inoculation of malaria parasites in the case of
dementia paralytica caused by neurosyphilis, which successfully cured not only associated severe mental illness but also syphilis. In 1927, this discovery earned him the Nobel Prize in Physiology and Medicine. Syphilis is a sexually transmitted infection caused by a spirochete Treponema pallidum. The first case of syphilis occurred in Europe around the year 1493. The term “syphilis” was first described by the Italian physician and poet Giralomo Fracastoro in his epic noted poem titled “Syphilis sive morbus gallicus”. In 1905, Schaudinn and Hoffmann discovered Treponema pallidum in tissue of patients with syphilis. In scientific reports around the 19th century specific forms of neurosyphilis were grouped under the multicausal term “Paralytic Dementia”. The rising incidence of neurosyphilis the potentially devastating infection of the central nervous system by the spirochete Treponema pallidum, despite widely available curative treatment is a concern.
Syphilis has several clinical manifestations, making laboratory testing a very important aspect of diagnosis.
Syphilis progresses through distinct primary, secondary, latent and tertiary stages. The ulcers that appear in primary and secondary syphilis are rich in treponemes; venereal transmission occurs through direct contact with these lesions. The stage of the disease at which the patient presents has implications for diagnosis and treatment. In primary syphilis, after sexual activity, in 1 to 3 weeks time a single painless indurated ulcer appears on the genitalia. This ulcer heals in 3 to 6 weeks time spontaneously. After 2 to 24 weeks, in 50% patients secondary syphilis manifests with fever, malaise, loss of appetite and widespread skin rashes. This is the time when patient seeks treatment. After this, disease becomes
subclinical if not treated and after 10-25 years, manifests as tertiary syphilis with the involvement of CNS, CVS, bones,
eyes, many organs with gummas. In some stages, the disease may be asymptomatic, and there are problems in
diagnosing very early syphilis, neurosyphilis, asymptomatic congenital syphilis and syphilis in intravenous drug users and persons coinfected with serologically cross-reacting agents and HIV.
The etiological agent, Treponema pallidum, cannot be cultured, and there is no single optimal alternative test.
Serological testing is the most frequently used approach in the laboratory diagnosis of syphilis. Direct diagnostic
methods include the detection of T pallidum by microscopic examination of fluid or smears from lesions (Dark ground
microscopy or Fluorescence staining), histological examination of tissues or nucleic acid amplification methods such as
polymerase chain reaction (PCR). Indirect diagnosis is based on serological tests for the detection of antibodies.
Serological tests fall into two categories: nontreponemal tests for screening (VDRL or RPR) and treponemal tests
(TPHA/TPA or FTA-Abs) for confirmation. A confirmed serological test result is indicative of the presence of treponemal
antibodies but does not indicate the stage of disease and, depending on the test, may not differentiate between past
and current infection. Despite their shortcomings and the complexity of interpretation, serological tests are the
mainstay in the diagnosis and follow-up of syphilis. The discovery of penicillin was a caesura, ending malariotherapy and leading many to regard syphilis as a night-extinct illness, but this turned out to be an illusion. Syphilis is returning in new forms in tandem with the AIDS epidemic. Written-off endlessly by its obituarists, syphilis abides.