{"id":5123,"date":"2011-07-14T20:23:39","date_gmt":"2011-07-14T20:23:39","guid":{"rendered":"http:\/\/crashtext.org\/misc\/genital-infections-and-stds.htm\/"},"modified":"2013-02-02T23:55:01","modified_gmt":"2013-02-03T04:55:01","slug":"genital-infections-and-stds","status":"publish","type":"post","link":"https:\/\/crashingpatient.com\/ob-gyn\/genital-infections-and-stds.htm\/","title":{"rendered":"Genital Infections and STDs"},"content":{"rendered":"
CDC Guidelines<\/a> for\u00a0Genital Infections and STDs<\/p>\n HSV-1 can cause, but usually 2.<\/p>\n Vesicles on erythematous base.<\/p>\n Acyclovir 200 5ID x 10 days at first outbreak<\/p>\n For Recurrence, oral acyclovir 400 mg PO TID, but only if within 1-2 days of recurrence of lesions<\/p>\n gonorrhea\/chlamydia.\u00a0 Drain, can use word cath.<\/p>\n <\/p>\n We investigated the use of a rubber ring catheter (the Jacobi ring) in the treatment of Bartholin’s abscesses. The ring catheter was made from a 7-cm length of an 8\u0096French T tube threaded with a 20-cm length of 2-0 silk suture (Fig. 1). The catheter enters and exits the abscess through 2 separate incisions, forming a closed rubber ring when the suture ends are tied<\/p>\n <\/a><\/a><\/p>\n (Am J EM 2005 23(3):414)<\/p>\n <\/p>\n spirochette, treponema pallidum.<\/p>\n Can present c chancre, inguinal nodes (non painful, called buboes) or rash of 2nd. 1\u00b0-papule which ulcerates, then lymph nodes2\u00b0-6-20 weeks, maculopapular symmetrical rash on palms and soles.\u00a0 Condyloma Lata (flat warts) 3\u00b0-Tabes dorsalis.<\/p>\n <\/p>\n The diagnosis of syphilis is complicated by the fact that T. pallidum cannot be cultured in the laboratory. Thus, the disease must be identified by direct visualization of the organism in clinical specimens, or, more commonly, by serology. Serologic testing is by definition an indirect method of diagnosis since it relies upon a humoral immune response to infection. As such, it has inherent limitations. Darkfield microscopy \u0097 The quickest and most direct method for diagnosing primary and secondary syphilis is direct visualization of the spirochete from moist lesions by means of darkfield microscopy [4]. In order for this test to be useful, it must be performed by someone experienced in the identification of T. pallidum, and the proper equipment must be readily available so that the specimen can be examined promptly. In clinical practice, darkfield microscopy is generally limited to clinics that specialize in the diagnosis and treatment of sexually transmitted diseases (STDs).<\/p>\n Fluorescent antibody testing \u0097 An alternative method of identifying T. pallidum from lesions is direct fluorescent antibody testing (DFA-TP) [5]. This technique has the advantage of permitting the identification of the organism when smears cannot be examined immediately. It also avoids the problem of misidentifying other spirochetes as T. pallidum since it is specific for T. pallidum antigens. This test requires a fluorescence microscope and a trained and experienced technologist; it is not widely available in most clinics seeing patients with STDs. Polymerase chain reaction \u0097 Newer techniques involving molecular methods are beginning to be used for the diagnosis of early syphilis [6,7]. Potentially most interesting is a multiplex polymerase chain reaction (M-PCR) assay that can simultaneously detect Treponema pallidum, Hemophilus ducreyi (the etiologic agent of chancroid), and herpes simplex [8,9]. (See “Chancroid”). Another PCR test using sequences of the DNA polymerase I gene had a sensitivity and specificity of 95.8 and 95.7 percent, respectively, in 112 genital ulcer specimens; this test did not cross-react with nonpathogenic treponemal species or other spirochetes [10]. However, the application of such technology to STD clinics is not likely to occur in the near future. Serologic tests \u0097 Because of lack of availability of equipment, test reagents, or the skilled personnel required for direct visualization techniques or PCR, a substantial proportion of patients suspected of having syphilis must be diagnosed by alternative methods. In virtually all cases, this means serologic testing. There are two types of serologic tests for syphilis: nontreponemal tests such as the Venereal Disease Research Laboratory (VDRL) test and the Rapid Plasma Reagin (RPR) test, and treponemal tests such as the fluorescent treponemal antibody absorption (FTA-ABS) test, the microhemagglutination test for antibodies to Treponema pallidum (MHA-TP), and the Treponema pallidum particle agglutination assay (TPPA). Nontreponemal tests \u0097 Nontreponemal tests (also known as tests for reagin antibodies) are based upon the reactivity of serum from patients with syphilis to a cardiolipin-cholesterol-lecithin antigen. These tests measure IgG and IgM antibodies and are used as the screening test for syphilis in most settings. Positive tests are usually reported as a titer of antibody, and they can be used to follow the response to treatment in many patients. These tests are relatively inexpensive and easy to perform. Treponemal tests \u0097 Treponemal tests are more complex and are usually used as confirmatory tests when the nontreponemal tests are reactive. These tests all use T. pallidum antigens and are based upon the detection of antibodies directed against treponemal cellular components. These tests are qualitative and are reported as reactive or nonreactive [4]. Algorithm for screening and testing \u0097 Serologic testing to diagnose syphilis is performed in two settings: screening of patients at increased risk and evaluation of patients with suspected disease. The United States Preventive Services Task Force (USPSTF) issued updated guidelines for syphilis screening in the summer of 2004 [11]. A review of recent evidence increased the strength of support for the strategy of screening all pregnant women and people at higher risk of acquiring syphilis (MSM who engage in high risk behaviors, commercial sex workers, persons who exchange sex for drugs, and those in adult correctional facilities). The task force recommended against routine screening of asymptomatic persons who are not at increased risk of syphilis, since most positive tests in this setting represent false positive and can lead to unnecessary anxiety for patients as well as increased costs and potential harm from inappropriate antibiotic use. The use of a single serologic test to diagnose syphilis is generally inadequate because of the potential for false-positive results [12]. It is highly unlikely that any one patient will have false positive tests using both reagin and treponemal techniques. Thus, the usual testing algorithm is to screen with a nontreponemal test such as the VDRL; a reactive specimen is then confirmed as a true positive with a treponemal test such as the FTA-ABS. An understanding of the proper interpretation of these tests is essential to their effective use. In addition to false positive tests, false negative results may also complicate serologic diagnosis. False positive and negative tests \u0097 Both acute and chronic false positive tests for syphilis (sometimes referred to as “biologic false positive tests”) can occur with both nontreponemal and treponemal tests; the false positive rate for treponemal tests is approximately one percent in the general population [4]. Some are of short duration and are generally attributed to coexisting events such as febrile illnesses and immunizations. Test abnormalities attributed to these conditions typically last for six months or less. Chronic false positive tests are associated with a variety of conditions including autoimmune disorders (particularly systemic lupus erythematosus), intravenous drug use, chronic liver disease, and HIV infection (show table 1) (see “Syphilis serology in HIV-infected patients” below). Probably the most common cause of a false negative syphilis serologic test is performance prior to the development of diagnostic antibodies (show figure 2). Twenty to 30 percent of patients presenting with a chancre will not yet have developed a reactive serologic test for syphilis [13]. The second major cause of false negative tests is the prozone reaction. This phenomenon affects nontreponemal tests and occurs in less than 2 percent of samples, almost always during secondary syphilis when antibody titers are the highest. It is thought to be due to a mismatch between concentrations of antigen and antibody. Laboratory technologists may suspect its presence when an apparent nonreactive test exhibits a rough or granular appearance [14]. When such a specimen is diluted, reactivity becomes apparent at higher titers. MONITORING THE RESPONSE TO THERAPY \u0097 Once syphilis has been diagnosed, the response to treatment can be assessed by changes in the titer of reagin antibodies. It is important that the same testing method (eg, RPR or VDRL) be used for all follow-up examinations since titers may vary by 1 to 2 dilutions if different tests are used. The response to treatment is not uniform among all patients, and it may be difficult to decide when retreatment or further work-up (such as cerebrospinal fluid examination) is needed. Several factors may influence the rate at which titers decline following therapy, including prior episodes of syphilis, the duration of infection prior to therapy, and the pretreatment antibody titer [1,15]. The results are usually expressed as a change in titer. In one series of 882 patients, most of whom had primary syphilis, the following reductions in reagin antibody titers were noted after recommended antibiotic therapy: Among patients with primary and secondary syphilis, a fourfold decline by six months and an eightfold decline by 12 months Compared to those with primary and secondary syphilis, the rate of decline was slower among patients with early latent syphilis \u0097 fourfold decline by 12 months Although it has been widely thought that, once positive, treponemal antibody tests remain so for life, reversion to nonreactive tests occurred in 24 percent by FTA-ABS and 13 percent by MHA-TP. This may be more likely to occur in patients with HIV infection (see “Syphilis serology in HIV-infected patients” below). TESTING FOR NEUROSYPHILIS \u0097 The major morbidity of syphilis occurs during its tertiary phase, a period that includes neurosyphilis. (See “Pathophysiology and natural history of syphilis”). T. pallidum disseminates widely after initial infection, and examination of the cerebrospinal fluid (CSF) during primary and secondary syphilis reveals a high incidence of central nervous system involvement [1,16]. These abnormalities resolve in most patients even without therapy, but the presence of an abnormal CSF during latent syphilis identifies a group of patients at increased risk for symptomatic neurosyphilis [17]. Thus, the identification of asymptomatic neurosyphilis is important to the proper management of persons with reactive syphilis serologies. Cerebrospinal fluid examination \u0097 Patients with reactive syphilis serologic tests must be assessed carefully for varied signs and symptoms of neurosyphilis. The diagnosis of asymptomatic neurosyphilis can be challenging. Up to 25 percent of patients with late neurosyphilis have nonreactive serum reagin antibody tests, presumably due to a loss of the antibody response to T. pallidum over time; in comparison, the serum treponemal tests (eg, FTA-ABS) usually remain reactive [1]. (See “Late syphilis”). Lumbar puncture with CSF examination is essential if there is any clinical evidence to suggest neurosyphilis. Current Centers for Disease Control and Prevention (CDC) recommendations suggest that CSF examination should be performed in persons with latent syphilis and any of the following (show table 2) [12]: Ophthalmic signs or symptoms Evidence of active tertiary syphilis Treatment failure (including failure of nontreponemal tests to fall appropriately) HIV infection with late latent syphilis or syphilis of unknown duration The optimal approach in patients with none of these findings is uncertain. In an analysis of CSF findings from 326 patients with syphilis (none of whom had previously been diagnosed with neurosyphilis), a serum RPR 1:32 increased the probability of neurosyphilis (defined as more than 20 white cells\/\u00b5L or a positive CSF VDRL) more than 10-fold in patients without HIV infection and six-fold in those with HIV [18]. Furthermore, among HIV-infected patients, a CD4 count <350 cells\/\u00b5L was associated with a 3-fold increased likelihood of neurosyphilis. Although these findings are not definitive, it seems reasonable to conclude that the presence of one or both of these risk indicators should be a factor in the decision as to whether or not lumbar puncture should be performed in patients with no neurologic symptoms. CSF analysis in patients suspected of neurosyphilis should include a cell count, protein concentration, and determination of the CSF-VDRL titer. Abnormalities variably present in those with neurosyphilis include a moderate mononuclear pleocytosis (usually in the range of 10 to 400 cells\/\u00b5L) and an elevated protein concentration (usually in the range of 45 to 200 mg\/dL). Sensitivity and specificity of CSF-VDRL \u0097 Assessing for an antibody response in the spinal fluid by means of the CSF-VDRL test is a highly specific test; even blood contamination will not create a falsely reactive CSF-VDRL unless the degree of contamination is sufficient to produce visibly blood-tinged CSF [19]. Unfortunately, the CSF-VDRL is quite insensitive, being reactive in as few as 30 percent of individuals with neurosyphilis [1,16]. Thus, a reactive CSF-VDRL is considered diagnostic but a nonreactive CSF-VDRL does not exclude neurosyphilis. Treponemal tests are not usually recommended for CSF samples, although they may be useful in ruling out neurosyphilis. A nonreactive FTA-ABS test in CSF appears to exclude the diagnosis [20]. SYPHILIS SEROLOGY IN HIV-INFECTED PATIENTS \u0097 Shortly after the HIV epidemic became widespread in the mid-1980s, there was a resurgence of syphilis in the United States, ultimately reaching levels that not been seen since the prepenicillin era [21]. During this period of two intersecting epidemics, reports suggested that HIV interacted with syphilis in ways that potentially influenced many features of the disease, including a variety of aberrant serologic manifestations. Most of these data were in the form of case reports or small series and included seemingly paradoxical events. HIV-positive patients with syphilis often have higher titers of reagin antibodies than HIV-uninfected individuals [22]. However, some patients with very late stage HIV infection have delayed or absent serologic responses to syphilis (ie, false negative tests) [23,24] or are more likely to lose their reactivity after appropriate therapy [25,26]. This variability is thought to reflect abnormally active B-cell function during early HIV infection and B-cell failure during late stage HIV infection. Presumably due to HIV-induced abnormalities in B-cell function, HIV-infected individuals who do not have syphilis have a greater incidence of falsely reactive nontreponemal tests than those without HIV infection [27-29]. In two series of HIV-infected patients, for example, the rate of false positive tests was higher than controls for both VDRL (6.8 versus 0.2 percent) and RPR (11 versus 0.8 percent) [28,29]. (See “Screening laboratory tests in HIV-infected patients”). Interestingly, subsequent analysis of some of the HIV-infected persons with apparent false positive nontreponemal tests suggested that a proportion of such cases actually were due to failure of the treponemal test (FTA-ABS) to detect true infection [30]. In one series of 35 patients who had at least one positive RPR test with a nonreactive FTA-ABS, five converted to a reactive FTA-ABS test; in addition, some patients who remained nonreactive by FTA-ABS had antibodies to T. pallidum membrane antigens. Thus, patients may represent false negative FTA-ABS reactions in HIV-infected patients with latent syphilis rather than biologically false positive nontreponemal tests in persons who do not have syphilis. The rate of decline of nontreponemal titers following successful therapy may be influenced by HIV coinfection, falling more slowly in those with HIV infection [31-33]. In a large, randomized prospective study of persons with early syphilis, for example, the group coinfected with HIV had a higher rate of serologically defined treatment failure [32]. However, in this and other studies, all but one patient responded clinically to treatment, suggesting that the significance of the diminished serologic response may be minimal [32,33]. In contrast to these findings, a prospective trial of therapy in 525 patients with syphilis found that the presence of HIV infection did not influence the performance of treponemal tests [34]. The conflicting data illustrate the difficulty of having to rely upon serologic tests for the diagnosis of any infectious disease. SUMMARY \u0097 It appears that serologic tests perform reasonably well for the vast majority of persons suspected of having syphilis, even those who are also HIV-infected. While clinicians should remain vigilant for exceptional cases, the management strategies outlined in published guidelines appear to be reasonable and appropriate for all patients [12]. <\/a><\/p>\n Second, Isaac Asimov wrote in Limericks,<\/em> under “Luetic Lament,”:<\/p>\n There was a young man of Back Bay Who thought syphilis just went away. And thought that a chancre Was merely a canker Acquired in lascivious play. Now first he got acne vulgaris, The kind that is rampant in Paris It covered his skin From forehead to shin And now people ask where his hair is. With symptoms increasing in number, His aorta’s in need of a plumber His hear is cavorting His wife is aborting And now he’s acquired a gumma. Consider his terrible plight – His eyes won’t react to the light His hands are apraxic. His gait is ataxic. He’s developing gun-barrel sight. His passions are strong as before But his penis is flaccid, and sore. His wife now has tabes And sabre-shinned babies She’s really worse off than a whore. There are pains in his belly and knees. His sphincters have gone by degrees. Paroxysmal incontinence, With all its concomitants, Brings on quite unpredictable pees. Though treated in every known way, His spirochetes grow day by day. He’s developed paresis, Converses with Jesus, And thinks he’s the Queen of the May.”<\/p>\n <\/p>\n <\/p>\n caused by chlamydia.\u00a0 Vesicle or pustule to large lymph nodes that can ulcerate.<\/p>\n Hemophilius Ducreyi, small papule that ulcerates and is painful.\u00a0 Small bubo can develop<\/p>\n C granulomatous.\u00a0 Painless papule to large ulcer<\/p>\n HPV,\u00a0 Padofilox .5% BID x 3 days<\/p>\n <\/p>\n Work-up for lesion (physical exam usually not sufficient):<\/p>\n dab a drop of vaginal mucus on a slide, add one drop of .9% NaCl and cover slide.\u00a0 Examine under 400x magnification.\u00a0 Swimming protozoa are trich, clue cells (epithelial cell covered by bacteria) are bacterial vaginosis, pseudohyphae and spores (spaghetti and meatballs) are candida.\u00a0 If epithelial cells obscure the view, add 10% KOH and smell whether this has the scent of stale fish (trich or bact vaginosis), reexamine under the microscope.<\/p>\n Discharges are characterized by color (clear, white,green, gray, yellow), consistency (thin, thick, curdlike), andamount (more or less than usual). We could locate no scale thatallows the patient to quantify precisely the amount of her discharge.<\/p>\n<\/span>Genital Lesions<\/span><\/h2>\n
Herpes<\/h4>\n
Bartholin Cyst\/Abscess<\/h4>\n
Jacobi Ring<\/h4>\n
Syphilis<\/h4>\n
Lymphogranuloma Venerum<\/h4>\n
Chancroid<\/h4>\n
Granuloma Inguinale<\/h4>\n
Condyloma Acuminata<\/h4>\n
\n
<\/span>Genital D\/C<\/span><\/h2>\n
<\/h4>\n