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Pelvic inflammatory disease (PID) is an often-serious consequence of gonococcal and chlamydial infection. An estimated 1 million women in the United States are treated each year for this condition, and at least one-fourth of these women will suffer one or more serious sequelae, including infertility, ectopic pregnancy, and major abdominal/pelvic surgery. It has been estimated that the cost of these sequelae will be $3.5 billion per year [1] by 1990. Since the early 1970s viagra sales, the Centers for Disease Control (CDC) has recommended therapeutic regimens for PID as part of the treatment guidelines for sexually transmitted diseases (STDs). In this report we will review the current understanding of PID as a clinical syndrome, the 1985 CDC recommendations and their rationale, and the advances that have been made in the understanding of the diagnosis and treatment of PID since 1985. We will also make further recommendations for PID treatment regimens.

Clinical Background. PID is an entity that has escaped consistent definition. In the 1985 Low price viagra STD treatment guidelines published by the CDC [2), PID was defined as “the acute clinical syndrome (unrelated to pregnancy or surgery) attributed to the ascent of microorganisms from the vagina and endocervix to the endometrium, fallopian tubes, and/or contiguous structures.” viagra online cheap Important gaps in our understanding of the pathophysiology of PID still exist.

PID is a syndrome that may include endometritis, order generic viagra, salpingitis, oophoritis, tubo-ovarian abscess, and pelvic peritonitis. Infection of the fallopian tubes is the hallmark of PID. In some women, infection of the fallopian tubes and contiguous structures leads to the formation of tubo-ovarian abscesses. viagra online cheap In contrast to what is known or suspected regarding abscesses elsewhere within the body, tubo-ovarian abscesses often respond to antibiotic therapy without surgical intervention. The exact mechanism by which microorganisms infect the upper genital tract is unknown. One unifying hypothesis regarding the pathogenesis of acute PID suggests that it usually starts as a cervical infection with Neisseria gonorrhoeae and/or Chlamydia trachomatis, with subsequent alteration in the cervicovaginal microenvironment as a result of the consumption of nutrients and the production of metabolic waste products. These changes cause others, including alterations in vaginal pH and the availability of oxygen, which result in overgrowth of endogenous and anaerobic flora. The original cervical pathogens and/or endogenous organisms then ascend into the upper genital tract [3] viagra online cheap. This hypothesis would explain the polymicrobial nature of PID.
With an estimated 4 million cases occurring annually in the United States, infections caused by Chlamydia trachomatis are the most frequent cause of bacterial sexually transmitted disease overnight shipping viagra in the United States [1,2). The health care costs of C trachomatis infections in the United States are estimated to exceed $2 billion annually (3). Given their significant morbidity and long-term sequelae in women and newborns, infections caused by C. trachomatis are a major public health problem.

Recommendations for viagra online cheap treatment of C. trachomatis infections [4,5] have traditionally been developed from historical and anecdotal experience, data from in vitro susceptibility testing, and results of published trials. Principles that have been generally accepted in the design of therapy for C. trachomatis infections are that (1) clinically relevant antimicrobial resistance has not been identified in C trachomatis, (2) therapy of extended duration (>5 days) is necessary to effectively eradicate the slow-growing organisms [5, viagra online cheap, 61, and (3) clinical efficacy generally parallels in vitro susceptibility [6]. Relatively few antibiotics are effective for the treatment of chlamydial genitourinary infections, however, and many cause adverse reactions [5, 6].

Suppression of chlamydial infection may conceivably occur during antimicrobial therapy without complete eradication; this possibility is of particular concern with p-lactam agents. Assessment of viagra online cheap efficacy immediately after therapy thus may falsely indicate cure. Microbiologic evaluation at a longer interval after completion of therapy may better detect the presence of continued infection, although exogenous reinfection will be difficult to distinguish from suppressed infection. Treatment trials to assess antimicrobial efficacy, optimally utilizing cell culture rather than nonculture diagnosis to determine microbiologic cure, should include examinations at intervals up to 4-6 weeks following therapy [7].

In vitro testing of antimicrobial susceptibility in chlamydial cell culture may reveal MICs that differ among various laboratories and testing methods [8, 9]. In general, however, consistent data are obtained for most antimicrobial classes with all strains of C. trachomatis (5,6,9] cheap online generic viagra. Tetracyclines, rifampin, and erythromycins show excellent antichlamydial activity in vitro [5, 10]. viagra online cheap MICs of sulfonamides may approach levels barely achievable in vivo [6J, whereas the cephalosporins are inactive against C. trachomatis [5]. In vitro studies have suggested that resistance to rifampin may evolve during therapy cheap generic overnight viagra (10-13], although as yet such resistance has not been demonstrated clinically [10]. The presence of subinhibitory levels of erythromycin and oxytetracycline with rifampin appears to inhibit the emergence of resistance to rifampin in vitro (13]. Therapy with such a combination might prevent the emergence of rifampin resistance in a clinical situation [13] viagra online.

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