The Causative Organism Known To Cause Syphilis Biology Essay

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Primary Syphilis occurs when T. pallidum enters mucous membranes or skin microabrasions and approximately three weeks later, it is mostly common that a single painless chancre will arise at the site of the primary infection. The site of infection is most commonly associated with the external genitals and without treatment the chancre will generally heal itself in one to four months (2). Diagnosis of primary syphilis is through examining a suspected chancre through dark-field microscopy, or through serology. However, when there is a chancre present, dark-field microscopy is the diagnosing technique of choice as it is the most specific (7). In dark-field microscopy, serous exudate is obtained from the lesion and it is then transferred onto a slide to examine with a microscope that has a dark-field condenser. Through this technique, the identification of T. pallidum is seen in a corkscrew form (2). This technique, whilst being cost effective and rapid its disadvantages appear to be that there is a requirement for special equipment, live T. pallidum in a fresh exudates and a technician with experience that is able to differentiate and identify the organism (4).

If individuals are not treated, secondary syphilis occurs as T. pallidum disseminates through the body and enters tissues (6). The clinical symptoms of secondary syphilis develop in the following few weeks to months after the appearance of the primary chancre. These symptoms are predominately associated with the skin but can occur in a variety of different manifestations ranging from fever, sore throat, muscle aches, weight loss, malaise, lymphadenopathy, diffuse rashes and condyloma latum present on the genitals or perineal (2, 3). The rashes associated with secondary syphilis can occur on all parts of the skin, particularly the soles and palms. Affected individuals may also obtain macular, maculopapular or pustular lesions commencing on the trunk and proximal ends. Secondary syphilis is diagnosed through nontreponemal and treponemal tests (2, 3, 9). Nontreponemal tests include the VDRL test and rapid plasma reagin test (RPR test), where the main underlying principle states that in syphilis infections there is an accumulation of non-specific antibodies that are made which respond to cardiolipin (2). These tests are quick and relatively simple to perform, but they lack sensitivity in detecting early primary syphilis (4). Treponemal-specific tests detect antibodies that are produced in response to presence of T. pallidum and act as a confirmatory test to those who yield a positive result in the nontreponemal tests. Treponemal tests include enzyme immunoassay (EIA) to detect antitreponemal IgG, T. pallidum hemaggluntination test (TPHA) for the titration and detection of antibodies and the fluorescent antibody-absorption test (FTA-abs) which uses specific antibodies for T. pallidum (2).

The following stage is separated into early and late latent syphilis. Early latent syphilis includes the first year after infection with the possibility of reoccurring secondary syphilis. If the infected individual does not revert back to primary or secondary syphilis within a year after infection, this is classed as late latent syphilis. During this time, serology tests are positive and this stage only ends if the patient is treated with antibiotics or once tertiary syphilis begins (2, 6).

The rare and final, but most severe stage is tertiary syphilis. This stage is further divided into gummatous syphilis, cardiovascular syphilis and neurosyphilis and occurs approximately 20 to 40 years after initial infection (2, 6). Gummas produce granulomatous-like lesions and cause local destruction, commonly present on the mucous membranes, skin and bones. In cardiovascular syphilis, there is degradation of the elastic tissue in the aorta eventually leading to aneurysm. Neurosyphilis can occur at any stage but can present as asymptomatic or with insomnia, changes in personality or vertigo. In late neurosyphilis, vascular lesions and neuronal deterioration can occur possibily resulting in symptoms such as hearing loss, hallucinations, memory loss, changes in personality, seizures and hyperactive reflexes (2, 6). Nontreponemal and treponemal specific tests are completed for tertiary and latent syphilis. TPHA is helpful to exclude neurosyphilis when there is a negative result as false positives may be obtained because IgG is able to cross the blood brain barrier (2).

Bacterial vaginosis (BV) is a very common genital tract problem for women (10). Garner and Dukes first introduced Bacterial vaginosis and the clinical symptoms which can present as an increase of vaginal discharge, with or without an unpleasant fishy odour through to asymptomatic symptoms (5). The vagina is a polymicrobial habitat, predominately made up of Lactobacillus spp., and when there is a change in this normal environment where anaerobes such as Mycoplasma hominis, Gardnerella vaginalis, and Bacteroides spp. begin to dominate, this is known as bacterial vaginosis (8, 11). As this disease presents as a polymicrobial manifestation and many of the different bacterial species are found in low numbers in normal, healthy women, culture is not usually helpful to aid in the diagnosis of this disease. The diagnosis of BV is completed through clinical symptoms and is composed of the Amsel’s criteria. In order to diagnose BV, this criteria states that three out of the four criteria have to be met, which includes: thin, grey homogenous vaginal discharge, vaginal pH > 4.5, presence of clue cells on vaginal smear and a fishy odour when 10% KOH is added (1, 12).

1. Amsel, R., P. A. Totten, C. A. Spiegel, K. C. S. Chen, D. Eschenbach, and K. K. Holmes. 1983. Nonspecific vaginitis: diagnostic criteria and microbial and epidemiological associations. Am J Med 74:14-22.

2. Brown, D. L., and J. E. Frank. 2003. Diagnosis and Management of Syphilis. Am Fam Physician 68:283-290.

3. Chapel, T. A. 1980. The signs and symptoms of secondary syphilis. Sexually transmitted diseases 7:161-164.

4. Cummings, M. C., S. A. Lukehart, C. Marra, B. L. Smith, J. Shaffer, L. R. Demeo, C. Castro, and W. M. McCormack. 1996. Comparison of Methods for the Detection of Treponema pallidum in Lesions of Early Syphilis. Sexually Transmitted Diseases 23:366-369.

5. Gardner, H. L., and C. D. Dukes. 1955. Haemophilus vaginalis vaginitis: a newly defined specific infection previously classified non-specific vaginitis. . American Journal of obstetrics and gynecology 69:962-976.

6. LaFond, R. E., and S. A. Lukehart. 2006. Biological Basis for Syphilis. Clinical Microbiology Reviews 19:29-49.

7. Larsen, S. A., B. M. Steiner, and A. H. Rudolph. 1995. Laboratory diagnosis and interpretation of tests for syphilis. Clinical Microbiology Reviews 8:1-21.

8. Mazzulli, T., A. E. Simor, and D. E. Low. 1990. Reproducibility of interpretation of Gram-stained vaginal smears for the diagnosis of bacterial vaginosis. Journal of Clinical Microbiology 28:1506-1508.

9. Mindel, A., S. J. Tovey, D. J. Timmins, and P. Williams. 1989. Primary and secondary syphilis, 20 years' experience. 2. Clinical features. Genitourinary Medicine 65:1-3.

10. Money, D. 2005. The laboratory diagnosis of bacterial vaginosis. Can J Infect Dis Med Microbiol 16:77-79.

11. Nugent, R. P., M. A. M. A. Krohn, and S. L. Hillier. 1991. Reliability of diagnosing bacterial vaginosis is improved by a standardized method of gram stain interpretation. J Clin Microbiol 29:297-301.

12. Spiegel, C. A., R. Amsel, and K. K. Holmes. 1983. Diagnosis of bacterial vaginosis by direct gram stain of vaginal fluid. J Clin Microbiol 18:170-177.

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