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Kenneth H. Mayer, Tarquin K. Collis, Connie L. Thus, the appropriate diagnosis and treatment of STDs in this population are extremely important. Further research is needed to define effective management and screening strategies for STDs in men with HIV infection. Sexually transmitted diseases STDs can present ificant diagnostic difficulties when they occur in HIV-positive persons, and the appropriate treatment and follow-up of an HIV-positive patient with an STD occasionally differs from the standard clinical approach to treating HIV-negative patients.
The purpose of this review, therefore, is to describe the clinical presentations of and treatment options for the most common STDs in HIV-positive men: syphilis, herpes, human papillomavirus infection, gonorrhea, Chlamydia infection, and nonchlamydial, nongonococcal urethritis. Although there have been ificant strides in syphilis control nationally [ 4 ], outbreaks of syphilis among men who have sex with men MSM continue to occur [ 56 ].
Although cross-sectional studies have documented an association between HIV transmission and syphilis [ 7 ], data from prospective studies have been less consistent in defining a causal association between syphilis and incident HIV infection. Clinical manifestations. Numerous case reports indicate that syphilis can present in highly atypical and aggressive forms in HIV-positive persons; however, the frequency of such atypical presentations is unclear.
HIV-positive patients with syphilis may be more likely than HIV-negative persons to present with persistent chancres [ 12 ], ulcerative skin lesions [ 1314 ], gummatous disease [ 1516 ], and early ocular involvement [ 17 ]. In the late s, case reports documented accelerated courses of neurosyphilis and apparent cases of neurorelapse in patients with HIV infection [ 19—21 ]. The prospective study by Rolfs et al.
Thus, although concomitant HIV infection clearly broadens the scope of possible clinical presentations in patients with syphilis, the frequency of highly atypical or aggressive forms of syphilis among such patients appears to be lower than was originally thought. Serology and CSF interpretation.
Although the of serological tests for syphilis are generally accurate for patients with HIV infection, their interpretation should be approached with an understanding of their limitations in this setting.
However, this association may to a ificant extent reflect confounding by injection drug abuse, a known cause of biological false-positive. Indeed, in a study whose authors stratified MSM into those who did and those who did not abuse injection drugs, the association between biological false-positive and HIV seropositivity was present only among those who used injection drugs [ 25 ]. One group of investigators has reported that false-negative of nontreponemal tests due to the prozone phenomenon are more common in HIV-positive pregnant women [ 26 ]. The of treponemal tests for syphilis—the treponemal hemagglutination and microhemagglutination assays and the fluorescent treponemal antibody absorption tests—may also be affected by HIV serostatus.
Once positive, treponemal assays usually remain positive for life, but several retrospective studies [ 2728 ] and one prospective study [ 29 ] have indicated that HIV-positive patients with treated syphilis appear more likely to serorevert to negative treponemal test than are HIV-negative patients treated for syphilis. Although a positive result of a CSF VDRL test remains a specific, if not a particularly sensitive, means of diagnosing neurosyphilis, pleocytosis or elevated CSF protein levels must therefore be interpreted carefully in HIV-positive persons.
Unfortunately, attempts to develop testing methods that have increased sensitivity and specificity for neurosyphilis have made little progress; the detection of T. Treatment for syphilis. The CDC STD treatment guidelines [ 32 ] do not differ in treatment recommendations for early latent syphilis or neurosyphilis in patients with and those without concomitant HIV infection.
Because of occasional reports of failure of treatment for syphilis among HIV-positive patients [ 33 ], some have questioned the efficacy of standard therapies for syphilis in HIV-positive patients. However, prospective data do not support differential treatment recommendations for those with HIV infection. A recently published prospective study [ 30 ] of ceftriaxone 2 g iv once daily for 10 days suggests that ceftriaxone may prove an effective alternative to iv penicillin in treating HIV-positive patients with secondary syphilis and CNS involvement.
In the absence of proven benefit from alternative therapeutic regimens, the standard of care for treating patients with HIV and syphilis remains as follows: a single dose of 2. For those persons with neurosyphilis for whom iv therapy is not feasible and in whom good compliance can be assured, an alternative regimen is 2.
Close follow-up of HIV-positive patients to assess for treatment failure and the development of neurosyphilis is essential see below. Issues pertaining to the treatment of HIV-positive patients with syphilis have recently been reviewed [ 31 ], and the literature from which the guidelines were drawn has been summarized [ 34 ]. Despite the challenge of interpreting CSF abnormalities in patients with HIV infection, lumbar punctures should be performed before syphilis treatment for all HIV-positive patients with late latent syphilis or syphilis of unknown duration.
However, abnormal of testing of CSF during early syphilis are not very specific predictors of those at risk to develop neurosyphilis, and thus routine lumbar puncture for HIV-positive persons with early syphilis is not recommended in the most recent CDC STD treatment guidelines [ 32 ]. Responses to therapy in patients with HIV and syphilis may also prove difficult to interpret. Although some studies have demonstrated a normal decline in titers of serum nontreponemal tests after therapy for syphilis in patients with HIV [ 293536 ], other studies have shown delayed serological responses in coinfected patients [ 182437 ].
In addition, 2 studies have demonstrated that the reversion of CSF abnormalities may be delayed in some HIV-positive patients with neurosyphilis [ 3738 ], although in these studies, the majority of patients with persistently abnormal CSF parameters showed no evidence of clinical treatment failure. Therefore, the clinical relevance of a delayed serological or CSF response to therapy in patients with HIV who have been treated for syphilis is unclear.
However, frequent clinical and serological evaluation of patients with HIV who have been treated for syphilis is clearly prudent; current CDC STD treatment guidelines suggest evaluations at 3, 6, 9, 12, and 24 months after therapy for HIV-positive patients with early syphilis and at 6, 12, 18, and 24 months after therapy for those with latent syphilis or syphilis of unknown duration [ 32 ].
Failure to show a 4-fold 2 dilutional decline in serum nontreponemal test titer at 6—12 months in patients with early syphilis or 12—24 months in patients with late latent syphilis or syphilis of unknown duration should prompt an examination of the CSF. In patients with neurosyphilis and HIV infection, serial lumbar punctures at 6-month intervals should be done after therapy.
Despite the ificant potential for increased transmissibility of HIV in those with HSV infection, epidemiological data regarding herpes and HIV transmission remain conflicting [ 5253 ]. Clinical manifestations and HSV shedding. In the majority of cases, these infections are due to HSV-2, although HSV-1 has recently been shown to for an increasing proportion of initial herpetic infections in MSM [ 54 ].
Nongenital manifestations of HSV infection include oral ulcers and herpetic whitlow. Primary HSV infections typically follow an incubation period of 2—4 days and may be accompanied by painful regional lymphadenopathy. Skin lesions due to HSV may present in different stages, including pustules, vesicles, shallow painful ulcers, and crusted lesions. HSV urethritis most often presents as dysuria and clear urethral discharge. Patients with symptomatic herpes proctitis usually describe anorectal pain especially with bowel movements or receptive anal intercourse and bloody or purulent anal discharge [ 5556 ]; there may be accompanying sacral radiculopathy and urinary retention, which help in distinguishing HSV from other causes of proctitis.
In the absence of herpetic vesicles, which may be absent or difficult to visualize, the findings on anoscopic examination are nonspecific. Genital HSV recurrences in persons with advanced HIV infection can be severe, producing disfiguring lesions that may show a slow response to therapy.
Interestingly, subclinical shedding was more common than clinically apparent shedding even on the penile shaft, an area easily examined for the presence of visible lesions. In a prospective study of men with more advanced HIV infection, the median duration of lesions was 11 days [ 58 ]. Although the frequencies of HSV shedding [ 57 ] and HSV ulceration [ 5960 ] appear to be higher among HIV-positive men with lower CD4 cell counts, both shedding and ulceration vary considerably among men with similar CD4 cell counts.
Diagnosis and treatment of herpes. To confirm the diagnosis of anogenital herpes, fluorescent antibody staining and culture of swabs or biopsy specimens should be done. The sensitivity of culture in the diagnosis of HSV depends on the stage of the lesion, and lower yields should be expected when culturing specimens from lesions that have already crusted over.
To diagnose HSV infection in asymptomatic persons with latent HSV-2 infection, commercially available type-specific serological assays are now available [ 61 ]. Although the best use of of type-specific serological tests in the clinical setting is still unclear [ 6263 ], it is likely that their use as a screening tool for both patients with and those without HIV infection will be demonstrated. The CDC STD treatment Im looking for a possible ltr with hpv or hsv woman [ 32 ] recommend that persons with HIV infection receive the same the acyclovir regimens for primary and recurrent herpes and for different sites of infection: mg of oral acyclovir 5 times a day or, more commonly, mg of oral acyclovir t.
The only placebo-controlled study of herpes proctitis—a study of immunocompetent adults—used mg of oral acyclovir 5 times a day [ 64 ], and therefore some practitioners prefer to treat herpes proctitis in all patients with higher dosages of acyclovir i.
Valacyclovir 1 g b. Although high doses of valacyclovir i. Acyclovir-resistant herpes. Infection with acyclovir-resistant HSV is a well-documented clinical problem in the treatment of a small minority of HIV-positive patients [ 6667 ] and has also been described in persons with other forms of immunocompromise [ 6869 ].
The prevalence of acyclovir-resistant herpes in persons with HIV is not known but appears low; in a recent study of HIV-positive MSM, the prevalence of acyclovir resistance was 1. Although routine susceptibility testing of HSV isolates from patients with HIV is not warranted, antiviral susceptibilities should be determined if lesions fail to respond to standard therapy. Acyclovir-resistant herpes among patients with HIV has been caused primarily by thymidine kinase-deficient HSV mutant strains [ 666770 ], which are also resistant to valacyclovir, famciclovir, and ganciclovir.
Although thymidine kinase-deficient mutant strains are capable of causing severe disease in patients with HIV [ 71 ], these strains do not appear to have intrinsically increased virulence compared with wild type viruses when studied in vitro and in animal models [ 70 ]. Thus, the aggressive clinical presentations of some acyclovir-resistant HSV infections most likely reflect the severe degree of immunodeficiency in the affected hosts rather than HSV-specific factors. Treatment options for acyclovir-resistant herpes in patients with HIV have been recently reviewed [ 65 ]. Human papillomavirus HPV infection is considered to be the most common sexually transmitted disease in the United States [ 7273 ] and is often subclinical.
More than 70 genotypes of HPV are recognized at present; those most commonly associated with anogenital infections include both HPV types considered low-risk for inducing malignant transformation types 6 and 11 and high-risk types types 16, 18, 31, and HPV is spread between male partners primarily through insertive or receptive anal sex.
Other possible routes of transmission include oral sex [ 83 ], finger-genital contact [ 84 ], and contact with the scrotal surface [ 73 ]. Circumcision status does not appear to affect the risk for genital HPV infection [ 85—87 ]. Anogenital warts most commonly present as verrucous, papular lesions condylomata acuminata. Keratotic warts, which have a thickened layer that more closely resembles common plantar or palmar warts, smooth papular warts small, skin-colored papulesand flat warts are other well-described variants.
In the perianal region, condylomata acuminata may be pedunculated. Warts can occur anywhere in the anogenital area, including on the scrotum and in the urethral meatus, anal canal, or crural folds. Anogenital warts do not usually cause symptoms, although itching, trauma-induced bleeding, and, less commonly, superinfection can occur. Patients with perianal warts may mistakenly diagnose themselves as having hemorrhoids.
Some investigators have found that the clinical appearance and distribution of anogenital warts in subjects with HIV infection do not appear to differ substantially from those without HIV [ 8889 ], whereas others report multiple anatomic sites of anal HPV infection to be more common [ 90 ].
Intra-anal manifestations of HPV infection are of particular importance, given the association of HPV with anal dysplasia see below. Warts in the anal canal are usually acuminate or papular in appearance, occur at or near the dentate line Im looking for a possible ltr with hpv or hsv woman 8889 ], and often demonstrate characteristically dilated surface vessels most easily visualized with a colposcope [ 88 ].
Other intra-anal manifestations that have been described are macular white patches and circumferential rings of warts [ 88 ]. Clinical appearance cannot reliably distinguish between anal condylomata with and those without intraepithelial neoplasia [ 8891 ]. The majority of intra-anal HPV infections among HIV-positive MSM are subclinical [ 74 ], and high-grade anal dysplasia has been demonstrated in biopsy specimens from completely normal-appearing rectal mucosa in both men with and men without HIV infection [ 92 ].
Intraoral manifestations of HPV infection include condylomata acuminata, verruca vulgaris solitary white lesionssquamous papillomas pedunculated lesions, generally on the soft palateand focal epithelial hyperplasia or Heck's disease painless soft papules on the buccal or labial mucosa resembling flat warts [ 94 ].
HPV-associated dysplasia and malignancy.
Data are conflicting as to whether the incidence of anal cancer is increased among HIV-positive men, and the mechanisms underlying the pathogenesis of anal intraepithelial neoplasia AIN and anal cancer remain poorly understood. However, reflecting the known relationship between HPV infection, cervical intraepithelial neoplasia, and cervical cancer, it appears that HPV infection with carcinogenic types is the primary factor responsible for the development of AIN, the precursor of anal squamous cell cancer.
Smoking, which has been associated with invasive anal cancer [ 96 ], has also been linked to the presence of abnormal anal cytology independent of CD4 cell count [ 97 ]. Treatment of anogenital warts. The treatment of anogenital warts in patients with HIV can pose difficulties both because of the large and size of lesions that may be present and because of the high rate of recurrence after treatment.
To date, however, few data exist that specifically address the comparative efficacy of treatment modalities for anogenital warts in HIV-positive persons. The CDC STD treatment guidelines do not specify different treatment approaches for HPV infections in HIV-positive patients, except to recommend that more frequent biopsies of lesions may be advisable, given the potentially increased risk of squamous cell cancer [ 32 ]. Several excellent reviews of treatment options for anogenital warts in immunocompetent patients have recently been published [ 9398 ].
Preliminary clinical experience with topically applied cidofovir for patients with HIV and genital warts has been promising [ 99 Im looking for a possible ltr with hpv or hsv woman, ] and merits further study. Oral warts in patients with HIV may be difficult to treat, are generally approached with cryotherapy or surgical excision, and show a high rate of recurrence following therapy [ ]. Although some clinicians advocate a more aggressive, excision-based approach to HPV therapy in patients with HIV infection [ ], it remains to be seen whether this approach in improved outcomes.
It remains to be seen whether HAART will lead to regression of anal dysplasia or whether aggressive antiretroviral therapy may paradoxically increase the incidence of anal cancer by prolonging the life span of patients with HIV infection. Patients with HPV infection should nonetheless be counseled that condom use is clearly of benefit in preventing the transmission of other STDs, including HIV, and may help prevent superinfection of or bleeding from denuded or friable surfaces during treatment for anogenital warts.
Smoking cessation counseling should be offered to HIV-positive patients with anal HPV infection who smoke, given that this population may be at particularly increased risk for anal dysplasia and anal cancer. Screening and treatment for anal dysplasia. Because the natural history of anal dysplasia is incompletely understood, and because the best means of screening for anal intraepithelial neoplasia is not known, practice guidelines for the diagnosis and management of HPV-associated anal dysplasia have not yet been established.
Although a recent study has shown that performing anal Pap smears on MSM every 1—2 years would be as cost-effective as screening for cervical cancer, as measured by quality-adjusted life expectancy benefits [ ], most experts agree that further research on the natural history and treatment of anal dysplasia is needed before anal Pap smears become part of the general medical care of HIV-positive MSM.
The clinical utility of HPV typing also remains unestablished; however, knowledge of HPV types in a given lesion or patient is unlikely to affect treatment decisions at present, and thus routine typing is not currently recommended. Until the utility of routine screening for anal dysplasia is established, clinicians should have a low threshold both for performing anoscopic examinations of patients with symptoms referable to the anal canal and for performing biopsies of suspect lesions. Appropriate treatment for persons found to have high-grade anal intraepithelial neoplasia remains unclear, but surgical removal [ ] or ablation of lesions by cautery or laser [ 88 ] have been suggested.
Such decisions clearly need to be made on a case-by-case basis; for example, pursuing aggressive therapy for high-grade dysplasia may be most appropriate for those patients with a reasonable life expectancy [ ]. Unless symptoms are present, men found to have low-grade anal neoplasia should be followed closely but not treated.
Although gonorrhea remains prevalent among MSM, relatively little has been published in recent years about the epidemiology or clinical presentations of gonorrhea in MSM or in subjects with HIV. Gonorrhea can be transmitted by insertive or receptive anal intercourse and, less efficiently, by fellatio [ ].
Recent evidence, including a well-documented outbreak of gonorrhea among young MSM in Australia [ ]; coincident increases in the cases of rectal gonorrhea, hepatitis B virus infection, and HIV infection among MSM in England and Wales [ ]; and recently described increases in unprotected anal intercourse and rectal gonorrhea in San Francisco [ ], underscores the fact that anogenital gonorrhea remains an important marker of high-risk sexual behavior among MSM. Epidemiological data are conflicting as to whether gonorrhea plays a role in increasing the transmissibility of HIV Some studies have shown an association with increased acquisition of HIV infection [ — ], whereas others have found no ificant association .
Substantive data do, however, link gonorrhea to increased HIV shedding in semen: Cohen et al. The effect of rectal gonorrhea on the rectal shedding of HIV is not known but is currently under study.Im looking for a possible ltr with hpv or hsv woman
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Cervical Intraepithelial Neoplasia Is Associated With Genital Tract Mucosal Inflammation