Jumat, 16 Juli 2010

Diagnosis Penyakit Menular Seksual

Specimen Collection Technique is Vital for Most Chlamydia Tests

Traditional tests for chlamydia, including unamplified nucleic acid hybridization, enzyme immunoassay, direct fluorescent antibody, and cultures, have a sensitivity for detection of C trachomatis ranging from about 50% to 85%, and this level of performance is achieved only when optimal swab specimens are collected. Collection technique is vital, since a positive result is dependent on swab samples that have a sufficient number of chlamydial organisms (which usually means a sufficient number of columnar epithelial cells for isolation of the intracellular organism C trachomatis) and, in women, minimal cervical mucus (which can interfere with assays).

In contrast, nucleic acid amplification tests (NAATs), such as the Gen-Probe Aptima Combo 2, the Becton Dickinson ProbeTec, and the Roche Amplicor assays, are the most sensitive currently available tests for C trachomatis detection, with sensitivities approaching 90% to 95%. Collection technique is less important for NAATs, since only a few organisms must be present for a positive test result and easier-to-collect specimen types, such as those from urine, tampons, and vaginal swabs, can be used.
Women Who Have Had a Hysterectomy Can Still Acquire Chlamydialor Gonococcal Urethritis; Several Testing Options Are Available.

After hysterectomy, the urethra is the usual site of infection with C trachomatis or N gonorrhoeae. Infected patients are usually asymptomatic, although some will present with an acute urethral syndrome (dysuria and frequency without significant bacteriuria). While signs of urethritis (discharge, swelling, or meatal redness) are infrequent in women with chlamydial urethritis,[10] those with gonococcal urethritis may occasionally have purulent exudate that can be expressed from the urethra, the periurethral glands, or the Bartholin gland duct.[11]

For urethral sampling, swabs should gently be inserted 1 to 2 cm into the urethra and rotated in one direction for one revolution or less to obtain sufficient materials for chlamydial testing using culture or nonculture methods. Vaginal swabs are not appropriate for chlamydia culture, even in women who have undergone hysterectomy, since the squamous epithelial cells lining the vagina are not considered susceptible to C trachomatis, which typically infects columnar epithelial cells. NAATs can be performed on urine specimens as an alternative in hysterectomized women. These tests are preferable in most settings because of their sensitivity and because of the ease of collection of specimens.
Assessment of PH Helps Distinguish Among Causes Of Vaginal Discharge.

Both infectious and noninfectious conditions may influence the pH of the vaginal environment, which under normal conditions has a pH of 4.5 or lower. A simple yet accurate test strip method to measure pH is a reliable indicator in helping to distinguish the different causes of vaginal discharge. In the setting of nonbloody vaginal discharge and absence of mucopurulent cervical discharge, a vaginal pH higher than 4.5 is indicative of bacterial vaginosis or trichomoniasis, while a vaginal pH of 4.5 or lower is suggestive of vulvovaginal candidiasis (VVC). Menses and semen may both raise the pH of vaginal secretions and confound the interpretation of vaginal pH. With most other noninfectious causes of vaginal discharge, the pH will be 4.5 or lower.
Always Perform RPR or VDRL tests Before Treating Syphilis.

No matter what stage of syphilis is being treated and whether there is other laboratory evidence to establish the diagnosis (eg, treponemes seen on darkfield microscopy), a nontreponemal test should be performed before initiating treatment when possible; however, treatment should not be held up while awaiting test results. Nontreponemal titers establish a baseline for follow-up after therapy. Samples becoming nonreactive on a nontreponemal test following treatment are clear evidence of successful therapy; if the patient subsequently tests positive, this represents a new infection. A 4-fold decrease in nontreponemal titers documents an appropriate response to therapy, and even if titers do not become nonreactive (serofast state), most patients have a clinical cure. Rising nontreponemal titers following treatment signify treatment failure and the need for further therapy and further evaluation.
Reactivation of Genital Herpes Often Presents with Atypical Findings. Other Than Genital Warts, All Genital Lesions Should Evoke Suspicion of Herpes

While some primary genital herpes infections may be subclinical, and the classic presentation is one of genital lesions that appear as pustules, vesicles, or ulcers depending on the duration of infection, this presentation is seen in only a minority of patients who acquire genital herpes; other less "typical" presentations are common. Initial presentations are highly variable and may be quite subtle. Similarly, in reactivation of genital herpes, the clinical spectrum of lesions is variable and even more diverse. Subclinical disease or classic herpes lesions that are decreased in number and area of involvement can occur, as can other lesions, including small linear fissures or ulcerations, areas of excoriation, and nonconcentric ulcers without an erythematous base.[3] These lesions are sometimes misdiagnosed as being caused by trauma, yeast, or a noninfectious dermatitis. All genital lesions, other than genital warts, should be evaluated for herpes because of the diverse spectrum of clinical lesions seen in genital herpes and the high prevalence of this STD.
HSV Resistance to Antiviral Agents is Rare, But It Should Be Considered When Genital Herpes Lesions Persist or Recur

In most published studies, fewer than 1% of HSV isolates from immunocompetent patients were acyclovir-resistant in vitro,[12] and resistant isolates have not always been associated with clinical failure in those receiving acyclovir therapy.[13] A greater proportion of acyclovir-resistant isolates are found in immunocompromised patients, especially those who have received multiple courses of therapy for established herpesvirus infections.[3] Persisting genital herpes unresponsive to acyclovir in patients with advanced HIV disease correlates well with in vitro resistance.[14] When genital herpes lesions persist or recur in a patient receiving antiviral therapy, HSV resistance should be suspected and a viral isolate obtained by culture for susceptibility testing. In general, acyclovir-resistant strains will be resistant to valacyclovir and to famciclovir, since each of these medications has the same mechanism of action.[3] In this situation, alternative therapies should be discussed with a specialist.
Coliform Bacteria Cause Some Cases of Nongonococcal Urethritis (NGU) in MSM.

Numerous organisms, including bacterial, viral, and protozoan pathogens, have been reported to be associated with NGU. While C trachomatis and Ureaplasma urealyticum are responsible for many cases of nongonococcal urethritis in men irrespective of type of sexual activity, coliform bacteria will cause some cases of NGU in MSM who practice insertive anal intercourse.[15] Of the CDC-recommended agents for NGU, doxycycline and the fluoroquinolones will provide better antimicrobial coverage against coliforms than azithromycin and should be considered for empiric therapy for NGU in this group of MSM when gram-negative rods are seen on Gram stain or if the infection does not respond to a single dose of azithromycin.

REFERENSI
1. Cates W Jr. Estimates of the incidence and prevalence of sexually transmitted diseases in the United States. Sex Transm Dis. 1999;26(4 suppl):S2-S7.
2. Fleming DT, McQuillan GM, Johnson RE, et al. Herpes simplex virus type 2 in the United States, 1976 to 1994. N Engl J Med. 1997;337:1105-1111.
3. Corey L, Wald A. Genital herpes. In: Holmes KK, Sparling PF, Mårdh P, et al, eds. Sexually Transmitted Diseases. New York: McGraw Hill; 1999:285-312.
4. Centers for Disease Control and Prevention. Sexually transmitted diseases treatment guidelines 2002. MMWR. 2002;51:1-78.
5. Suchland RJ, Geisler WM, Stamm WE. Methodologies and cell lines used for antimicrobial susceptibility testing of Chlamydia spp. Antimicrob Agents Chemother. 2003;47:636-642.
6. Centers for Disease Control and Prevention. 2001 Sexually transmitted disease national surveillance report. Available at: http://www.cdc.gov/std/stats/TOC2001.htm.
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13. Fife KH, Crumpacker CS, Mertz GJ, et al. Recurrence and resistance patterns of herpes simplex virus following cessation of ≥ 6 years of chronic suppression with acyclovir. J Infect Dis. 1994;169:1338-1341.
14. Safrin S, Elbeik T, Phan L, et al. Correlation between response to acyclovir and foscarnet therapy and in vitro susceptibility result for isolates of herpes simplex virus from human immunodeficiency virus-infected patients. Antimicrob Agents Chemother. 1994;38:1246-1250.
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16. Wright RA, Judson FN. Penile venereal edema. JAMA. 1979;241:157-158.
17. Amsel R, Totten PA, Spiegal CA, et al. Nonspecific vaginitis: diagnostic criteria and microbial and epidemiologic associations. Am J Med. 1983:74:14-22.
18. Edwards L. Genital dermatoses. In: Holmes KK, Sparling PF, Mårdh P, et al, eds. Sexually Transmitted Diseases. New York: McGraw Hill; 1999:900.
19. Ferenczy A, Richart RM, Wright TC. Pearly penile papules: absence of human papillomavirus DNA by polymerase chain reaction. Obstet Gynecol. 1991;78:118-122.
20. Kiviat NB, Critchlow CW, Holmes KK, et al. Association of anal dysplasia and human papillomavirus with immunosuppresion and HIV infection among homosexual men. AIDS. 1993;7:43-49.
21. Kiviat NB, Koutsky LA, Paavonen J. Cervical neoplasia and other STD-related genital tract neoplasias. In: Holmes KK, Sparling PF, Mårdh P, et al, eds. Sexually Transmitted Diseases. New York: McGraw Hill; 1999:811-831.
22. Koutsky LA, Kiviat NB. Genital human papillomavirus. In: Holmes KK, Sparling PF, Mårdh P, et al, eds. Sexually Transmitted Diseases. New York: McGraw Hill; 1999:347-359.

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