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Thursday, 9 January 2014





OVERVIEW
Neisseria gonorrhoeae is a sexually transmitted organism that primarily infects the columnar epithelia of mucosal surfaces, causing urethritis in men and endocervicitis and urethritis in women. Other sites of primary infection include the rectum, pharynx, and conjunctiva, and vulvovaginitis can occur in prepubertal girls.
The most common complication is acute salpingitis, or pelvic inflammatory disease, in turn leading to infertility and ectopic pregnancy. Other complications are epididymitis, posterior urethritis, urethral stricture, Bartholin gland abscess, and perihepatitis. Bacteremia may occur, with production of characteristic cutaneous lesions, arthritis, and rarely endocarditis or meningitis. Neonatal conjunctivitis (ophthalmia neonatorum) formerly was a common cause of blindness.
CLINICAL MANIFESTATIONS
UROGENITAL GONORRHEA IN MALES.
Gonococcal urethritis in men ("clap") typically is characterized by purulent urethral discharge and dysuria. The usual incubation period is 2 to 6 days. Only a small minority of men who acquire urethral infection, generally estimated at 1 to 10% and varying with the auxotype/serotype class of the infecting strain, remain asymptomatic. Physical examination typically reveals purulent (yellowish) urethral exudate, usually apparent spontaneously but sometimes only expressed by compression of the urethra. Erythema of the meatus sometimes is present. Nongonococcal urethritis (NGU) typically presents with less copious and less purulent discharge and meatal erythema is rare. The diagnosis of gonococcal urethritis usually is suspected clinically, confirmed preliminarily by a Gram-stained smear showing leukocytes with intracellular Gram-negative diplococci, and made definitively when N. gonorrhoeae is identified by culture or other specific test.
Urethral stricture formerly was a common complication but now is rare. Even in the preantibiotic era, more strictures may have resulted from the use of caustic treatment regimens, such as urethral irrigation with antiseptic solutions like silver nitrate or potassium permanganate, than from gonorrhea itself. Acute epididymitis, although uncommon, is the most frequent complication of gonococcal urethritis today, but more common causes are C. trachomatis or, in men over 35 years old, Escherichia coli and other uropathogens. Epididymitis usually presents with unilateral testicular pain and swelling, often with fever. Posterior urethritis, typically presenting with pelvic or perineal pain and urinary retention (suggesting acute prostatitis), once was fairly common; it is uncertain whether true gonococcal prostatitis also occurred, but in any case the clinical syndrome now is rare.
LOWER GENITAL TRACT GONORRHEA IN FEMALES.
The primary site of infection in women is the endocervical canal, and N. gonorrhoeae is isolated from the cervix in 85 to 90% of women with gonorrhea. When symptoms are present, the dominant ones are vaginal discharge and abnormal vaginal bleeding, typically with scant intermenstrual bleeding, often following intercourse, or enhanced bleeding during menses (metrorrhagia). Dysuria also is frequent, and N. gonorrhoeae can be isolated from the urethra in up to 80% of women with gonorrhea, although it rarely is the only infected site except in women who have had hysterectomies.
The physical examination may be normal, but many women have evidence of cervicitis, with purulent or mucopurulent exudate and often with edema and easily induced bleeding (e.g., with gentle swabbing, sometimes mistakenly called "friability") in an area of endocervical ectopy. Many women with gonorrhea have simultaneous bacterial vaginosis or trichomonal vaginitis, with abnormal vaginal discharge. However, gonorrhea itself does not cause vaginitis, because N. gonorrhoeae does not infect the estrogen-influenced, glycogen-rich squamous epithelium of sexually mature women. As discussed later, microbiologic diagnosis usually rests on identification of N. gonorrhoeae in cervical secretions by culture or other specific test; the Gram stained smear is insensitive..
In uncomplicated infection, purulent exudate sometimes can be expressed from a Bartholin gland duct, near the vaginal introitus laterally, or from Skene's glands, adjacent to the urethral meatus. Bartholin gland abscess is an uncommon complication, presenting with a tender introital mass, and may involve superinfection with facultative and anaerobic bacteria. Gonococcal ophthalmia occasionally is seen in adults, usually as a result of autoinoculation in persons with anogenital gonorrhea. It presents with acute, purulent conjunctivitis that can result in corneal ulceration if not treated promptly.
PELVIC INFLAMMATORY DISEASE.
The most common complication of gonorrhea is acute salpingitis, often accompanied by endometritis, collectively termed pelvic inflammatory disease (PID), which is estimated to occur in 10 to 20% of infected women. Chlamydia trachomatis is the dominant cause of PID in the United States, but gonorrhea remains a frequent cause; the proportion of cases due to either organism is directly related to their relative prevalences in the local population. Neither organism can be implicated in a substantial minority of patients; Mycoplasma genitalium may cause some cases. Regardless of the initiating infection, several other vaginal organisms, such as Mycoplasma hominis and various facultative and anaerobic Gram-positive and Gram-negative bacteria, often are implicated as co-pathogens. Low abdominal pain is the dominant symptom and often begins in proximity to a menstrual period; fever and other systemic manifestations such as malaise and anorexia are common. Often there are symptoms of lower genital tract infection, but their absence does not exclude the diagnosis of PID.
Examination usually discloses low abdominal tenderness, cervical motion tenderness, and bilateral adnexal tenderness, sometimes with a palpable mass. Most women have signs of cervicitis or vaginal infection. In a small proportion of cases, the abdominal or adnexal signs may be unilateral, causing confusion with appendicitis, ectopic pregnancy, and other conditions. Right upper quadrant abdominal tenderness sometimes is present due to Fitz-Hugh-Curtis syndrome, in which intra-abdominal extension of infection results in perihepatitis, which can mimic acute cholecystitis or viral hepatitis. Although Fitz-Hugh-Curtis syndrome usually is seen in conjunction with overt PID, sometimes perihepatitis occurs in the absence of other abdominal or pelvic findings, perhaps especially when caused by C. trachomatis . Severe PID may present with signs of generalized peritonitis. Laboratory studies often show elevation of the white blood cell count and erythrocyte sedimentation rate or C-reactive protein. However, these tests often are normal, and they are more useful in judging clinical severity than as diagnostic criteria.
The clinical diagnosis of PID is inexact. When laparoscopy showing visible salpingitis is used as the definitive test, the clinical diagnosis of PID is both insensitive and nonspecific; that is, many cases of PID lack classic signs and symptoms, and some women with clinically typical PID have no laparoscopic abnormality. The finding of plasma cells on endocervical biopsy, which can be performed by an aspiration technique with little pain or morbidity, has been used as a research tool and promoted as a useful aid to clinical diagnosis but is not yet in widespread use. Because the consequences of untreated PID may be severe, the U.S. Centers for Disease Control and Prevention (CDC) recommends that all sexually active women with uterine or adnexal tenderness and cervical motion tenderness be treated for PID if no other cause is readily apparent.
Fallopian tube scarring due to PID often results in infertility or ectopic pregnancy, and prior gonococcal and chlamydial infections probably are the most common antecedents of both complications. The incidence of tubal infertility has been estimated at 15% after one episode of PID and up to 50% after three attacks. The incidence of ectopic pregnancy is increased up to tenfold in women with previous salpingitis. However, most cases of tubal infertility and ectopic pregnancy attributable to STDs occur in women with neither a prior diagnosis of PID nor past symptoms suggestive of pelvic infection, indicating that subclinical infection-usually with C. trachomatis but perhaps with N. gonorrhoeae as well-can result in tubal scarring. Chronic pelvic pain, sometimes of disabling severity, also is a common consequence of PID. Each episode of PID, whether due to N. gonorrhoeae , C. trachomatis , or neither of these, significantly increases the risk of recurrent salpingitis. Many recurrent cases are associated with neither gonococcal nor chlamydial infection, suggesting that initial infection alters tubal clearance mechanisms or other defenses against ascending infection with vaginal bacteria.
RECTAL INFECTION.
Gonococcal infection of the rectum is common in women and in MSM. In women, most infections probably are acquired through perineal contamination with cervicovaginal secretions, but MSM and some women acquire infection by anal intercourse. In women with cervical gonorrhea, and among MSM with gonorrhea of any anatomic site, about 40% have rectal infection. Most infections are subclinical, but symptomatic proctitis occasionally occurs, presenting with anal pruritus, mucopurulent discharge (often recognized by the patient as exudate coating feces), and sometimes pain, tenesmus, and bleeding. Symptomatic proctitis seems to be more common among MSM than in women with rectal gonorrhea, suggesting that the size of the infecting inoculum or the trauma of anal intercourse may contribute to the clinical manifestations.
Diagnosis of rectal infection depends on isolation of N. gonorrhoeae by culture. The Gram-stained smear is insensitive and, in most examiners' hands, nonspecific. No other test is approved for diagnosis of rectal gonorrhea, although preliminary data suggest that some DNA amplification tests may give accurate results. The differential diagnosis of symptomatic proctitis includes other traditional STDs, especially herpes, syphilis, and chlamydial infection, including lymphogranuloma venereum, as well as ulcerative colitis, Crohn's colitis, anal fissure, rectal lacerations, and proctocolitis due to Shigella , Campylobacter , Yersinia enterocolitica , and other enteric pathogens.
PHARYNGEAL INFECTION.
Pharyngeal gonococcal infection results from orogenital exposure, is more efficiently acquired by fellatio than cunnilingus, and is found in about 5% of heterosexual men, 5 to 10% of women, and 10 to 20% of MSM with gonorrhea. Asymptomatic infection is the rule, although rare cases present with exudative pharyngitis and cervical lymphadenopathy. Isolated pharyngeal infection is rare, complications occur infrequently if ever, and most cases resolve spontaneously within a few weeks or in response to therapy for genital or rectal infection. In addition, transmission of pharyngeal infection to other sites is inefficient. For these reasons, testing persons at risk for pharyngeal gonococcal infection is optional, although most providers routinely test MSM. Culture is the only approved test.
GONORRHEA IN CHILDREN.
Infants born to mothers with gonorrhea may develop gonococcal conjunctivitis, or ophthalmia neonatorum. Formerly a common cause of blindness, gonococcal ophthalmia now is rare in industrialized countries, owing both to improved gonorrhea control and to routine use of neonatal ocular prophylaxis with topical antibiotics or 1% silver nitrate. Neonates also may acquire pharyngeal or rectal infection and, rarely, gonococcal pneumonia or sepsis. Neonatal vaginal infection is uncommon, because under the influence of maternal estrogen, the glycogen-rich squamous epithelium of the neonatal vagina is resistant to gonococcal infection, just as N. gonorrhoeae does not cause vaginitis in sexually mature women. From the neonatal period through 1 year of age, most cases present with conjunctivitis or vaginitis resulting from accidental contamination from an adult. After age 1, almost all childhood gonorrhea is the result of sexual abuse by an adult. Beyond the neonatal period, purulent vaginitis is the most common manifestation of gonorrhea or chlamydial infection in girls, and rectal or pharyngeal infection is the most common manifestation in prepubertal boys. Culture is the test of choice for all childhood gonorrhea, because nonculture tests have not been validated and because forensic considerations may dictate preservation of an isolate.
DISSEMINATED GONOCOCCAL INFECTION.
Disseminated gonococcal infection (DGI) usually is manifested by various combinations of polyarticular tenosynovitis, dermatitis due to focal septic embolization, and septic arthritis. DGI has been estimated to occur in 1 to 3% of adults with gonorrhea, but the risk depends on the likelihood of infection with particular strains of N. gonorrhoeae and probably is well under 1% in most geographic areas. Women may be somewhat more susceptible to DGI than men, and onset often occurs in association with menstruation. Severity varies from a mild illness with slight joint discomfort, few skin lesions, and little or no fever, to a fulminant illness with overt polyarthritis, high fever, and prostration. Most women and many men with DGI have no symptoms of genital gonorrhea, because the same auxotype/serotype classes of N. gonorrhoeae are associated with both resistance to serum bactericidal activity and the propensity to cause subclinical genital infection.
The early stage of DGI is sometimes called the arthritis-dermatitis syndrome, the main symptoms of which are polyarthralgias, skin lesions, and fever. Physical examination usually reveals tenosynovitis of two or more joints, most commonly the wrists, ankles, hands, and feet and less commonly the knees or elbows. Axial skeletal involvement is rare, a feature that can help differentiate DGI from Reiter's syndrome and other kinds of reactive arthritis. Skin lesions are few in number (usually <30) and normally are limited to the extremities. The individual lesions tend to evolve over several days from papules to pustules, often with a hemorrhagic component, so that lesions at various stages typically are present simultaneously. Bullae, petechiae, or overtly necrotic lesions that mimic ecthyma gangrenosum occasionally are seen. Although other conditions (e.g., bacterial endocarditis, meningococcemia) can cause similar lesions, the rash is sufficiently typical that it should strongly suggest DGI when seen in a sexually active young person.
Blood cultures are often positive for N. gonorrhoeae , but they are insensitive and bacteremia is intermittent, so that several cultures should be obtained to maximize the likelihood of isolation. All or most of the clinical manifestations appear to be related directly to bacteremic dissemination of the organism, even though it often cannot be isolated from blood, skin lesions, or synovial fluid. The leukocyte count usually is elevated but may be normal. The leukocyte count in synovial fluid, when obtained, usually is less than 20,000/mm 3 . Liver function tests often show transaminase elevations suggestive of mild hepatitis. Circulating immune complexes sometimes are present, but it is uncertain whether they contribute to the clinical manifestations.
The arthritis-dermatitis syndrome often subsides spontaneously, or it may evolve over several days into a second stage of septic arthritis, usually involving only one or two joints, with positive synovial fluid culture for N. gonorrhoeae . Skin lesions often have resolved by this time, and blood cultures nearly always are negative. However, sequential evolution from the arthritis-dermatitis syndrome to septic arthritis often is not observed, so that some patients present with one or two inflamed joints, most commonly the elbow, wrist, knee, or ankle, without prior symptoms. The physical examination and laboratory findings are typical for septic arthritis. The involved joint is swollen and warm, often with overlying erythema, with an overt synovial effusion that usually contains more than 40,000 leukocytes/mm 3 . Degenerative arthritis or frank joint destruction can result if treatment is delayed, and contiguous osteomyelitis can occur. Other manifestations of DGI are bacterial endocarditis and, very rarely, meningitis or myocarditis. In the preantibiotic era, N. gonorrhoeae caused up to 10% of all bacterial endocarditis but is now a rare cause. Gonococcal endocarditis usually involves the aortic valve and often progresses rapidly with valve destruction and congestive heart failure.
Young, sexually active persons with arthritis, tenosynovitis, or papulopustular skin lesions should be tested for N. gonorrhoeae at all potentially exposed anatomic sites. The diagnosis of DGI is secure when gonococci are recovered from the blood, a skin lesion, or synovial fluid but often is made presumptively when anogenital or pharyngeal gonorrhea is present in a patient with a typical clinical syndrome that responds promptly to antibiotics. The differential diagnosis includes Reiter's syndrome and other forms of reactive arthritis, meningococcemia, other kinds of septic arthritis, rheumatoid arthritis, systemic lupus erythematosus, and other rheumatologic conditions and infectious diseases. Reiter's syndrome, which usually is triggered by sexually acquired chlamydial infection, is the principal consideration in young adults. The skin lesions of the two conditions, when present, usually are distinct, and conjunctivitis and spinal involvement both are rare in DGI.

LABORATORY FINDINGS
GRAM-STAINED SMEARS.
The Gram-stained smear is positive when polymorphonuclear neutrophils are observed to contain intracellular Gram-negative diplococci of typical morphology. Methylene blue and other stains are standard in some countries and probably have performance characteristics similar to those of the Gram stain but are rarely used in the United States. The Gram-stained smear is 90 to 98% sensitive in the diagnosis of symptomatic gonococcal urethritis in men and the specificity is greater than 95%, so that confirmation by culture or another test is optional. However, the sensitivity is only around 50% for cervical or rectal infection and for asymptomatic urethral gonorrhea. Although the test is often considered highly specific for such infections, the actual performance varies with the skill and experience of the examiner, and rectal and cervical smears are unreliable in many clinical settings. Smears are both insensitive and nonspecific for pharyngeal gonococcal infection and are not recommended.
CULTURE.
Isolation of N. gonorrhoeae by culture, usually using antibiotic-containing selective media, is the historic mainstay of gonorrhea diagnosis. Ideally, growth media should be inoculated directly and placed promptly into a humid atmosphere with increased carbon dioxide, such as a candle-extinction jar. However, standard transport systems (e.g., Culturette) are acceptable if specimens are kept moist, not refrigerated, and processed within 6 hours. When testing specimens not likely to be colonized by competing flora (e.g., synovial fluid), nonselective chocolate agar should be used.
NUCLEIC ACID AMPLIFICATION TESTS.
In many laboratories, culture is rapidly being supplanted by nucleic acid amplification tests (NAATs), including ligase or polymerase chain reaction, transcription-mediated amplification, and the DNA strand displacement assay. The NAATs for N. gonorrhoeae are only slightly more sensitive than culture, but they are more expensive, do not preserve an isolate for antimicrobial susceptibility testing, and have not been validated for rectal or pharyngeal specimens. In addition, even a highly specific nonculture test may have a low positive predictive value when used in a population with a low prevalence of infection, so that many results will be falsely positive when persons at low risk are tested. This may be a particular problem when an NAAT for N. gonorrhoeae is "bundled" with a test for C. trachomatis for a single price and used to test persons at substantial risk for chlamydial infection but at low risk for gonorrhea, a common occurrence. On the other hand, the NAATs retain excellent sensitivity when used to test voided urine or self-obtained vaginal swabs and offer more convenient specimen management than culture, and the combination assays for N. gonorrhoeae and C. trachomatis may facilitate screening for both STDs in some settings.
Other nonculture tests, based on nonamplified DNA probe technology or immunochemical detection of gonococcal antigens, are substantially less sensitive and probably are less specific than culture or the NAATs, and they cannot be used to test urine or anatomic sites other than the urethra or cervix. Although some such tests have been used commonly in recent years, they have little clinical use today and are not recommended.

TREATMENT
ANTIMICROBIAL SUSCEPTIBILITY.
At first exquisitely susceptible to most antimicrobial agents, N. gonorrhoeae strains with clinically significant antimicrobial resistance began to evolve almost immediately after the introduction of treatment with the sulfonamides and then penicillin. Today, gonococci with chromosomal or plasmid-borne mutations that confer relative or absolute resistance to the penicillins, tetracyclines, and sulfonamides-to which all strains initially were susceptible-are prevalent worldwide, and none of these drugs remains acceptable as empirical therapy anywhere in the world. However, the prevalences of specific kinds of resistance vary widely between geographic areas and populations. For example, compared with heterosexual men and women, MSM more commonly are infected with relatively resistant gonococci. Infection of the rectum is required for propagation of gonorrhea among MSM, and the rectal environment selects for mutations that reduce permeability of the organism's outer membrane to toxic fecal bile salts and fatty acids, and the same membrane changes also reduce permeability to β-lactam antibiotics, tetracyclines, and macrolides. The prevalence of β-lactamase (penicillinase) plasmids, conferring absolute resistance to penicillin and ampicillin-formerly the worldwide mainstays of therapy-varies from around 10% of gonococci in the United States and western Europe to almost 50% in some developing countries.
Despite these trends, virtually all gonococci remain susceptible to the newer cephalosporins, and until recently the fluoroquinolones were uniformly active. However, N. gonorrhoeae strains with clinically significant resistance to the fluoroquinolones began to emerge in the late 1980s, primarily in east Asia and Pacific island nations, and by the mid-1990s, these drugs had lost their utility for gonorrhea in the Philippines, Japan, and parts of southeast Asia. For several years, fluoroquinolone-resistant strains were isolated only sporadically in North America and Europe. However, by 2002 such strains accounted for 20% of all gonorrhea in Hawaii, in 2001 they appeared in rapidly rising numbers in California, and sporadic cases have been reported elsewhere. Thus, the fluoroquinolones no longer are recommended for empiric treatment of gonorrhea in California and Hawaii, and soon they probably will be unacceptable as routine therapy throughout North America. Clinicians who treat patients for gonorrhea and other STDs should keep abreast of regional trends in resistance and therapeutic recommendations.
PRINCIPLES OF TREATMENT.
Unlike most bacterial infections, uncomplicated gonorrhea infection almost always responds to single dose treatment with an appropriate antibiotic. Because of the need to immediately curtail transmission, therapy usually is selected before the diagnosis is confirmed, and even when N. gonorrhoeae is isolated by culture, antimicrobial susceptibility testing usually is not done. Accordingly, treatment is determined solely by local or regional patterns of gonococcal antimicrobial susceptibility. (However, susceptibility testing should be used to guide the treatment of gonococcal endocarditis or meningitis.) Five to 10% of MSM, 10 to 20% of heterosexual men, and 20 to 40% of women with gonorrhea also are infected with C. trachomatis , so that routine treatment for chlamydial infection is advised in addition to specific therapy for gonorrhea. At one time it was considered important that gonorrhea therapy be effective against syphilis, but incubating or active syphilis now is rare in persons with gonorrhea, and data show that the use of antibiotics without activity against Treponema pallidum does not influence the incidence of syphilis.
TREATMENT REGIMENS.
. In most settings, ceftriaxone 125 mg intramuscularly or an oral cephalosporin, such as cefpodoxime 400 mg, should be given. Cefixime 400 mg, heretofore the oral treatment of choice, is no longer available in the United States. Cefuroxime 1.0 g also is an option, but might be slightly less effective than other regimens for gonococcal urethritis. Cefpodoxime and cefuroxime may be less effective for pharyngeal gonococcal infection than ceftriaxone or cefixime. Single-dose oral therapy with ciprofloxacin, ofloxacin, or levofloxacin is highly effective for genital, rectal, or pharyngeal infection due to susceptible strains, but should not be used for gonorrhea acquired in geographic areas where fluoroquinolone-resistant strains are prevalent. Other fluoroquinolones have no advantage over the recommended ones. Spectinomycin can be used in the rare circumstance when neither a cephalosporin nor a fluoroquinolone can be given (e.g., a pregnant woman with severe allergy to penicillin or other β-lactam antibiotics). Another option is azithromycin 2 g orally in a single dose; 1 g is insufficient. The patient always should be directly observed taking single-dose oral therapy; studies show that when persons with bacterial STDs are given prescriptions, many fail to take the drug properly or even to fill the prescription.
All persons with gonorrhea should be routinely treated with an oral regimen active against C. trachomatis , usually azithromycin in a single dose of 1 g or doxycycline 100 mg twice daily for 7 days. Some experts and the CDC advise that co-therapy may be deleted if chlamydial infection has been excluded by specific testing. However, no test for C. trachomatis is 100% sensitive, and co-treatment often is warranted regardless of such testing. Also, even though neither doxycycline nor 1 g of azithromycin is sufficiently effective for use as sole therapy for gonorrhea, in most settings either regimen will cure about 90% of patients, perhaps further reducing the small chance of treatment failure and diminishing selection pressure for antibiotic-resistant N. gonorrhoeae . Indeed, one reason that fluoroquinolone-resistant gonococci have spread from Asia to North America more slowly than did β-lactamase-producing strains 15 years earlier may be that co-therapy was less commonly used in the early 1980s than in the 1990s.
Women with acute PID should be treated with antibiotics active against N. gonorrhoeae , C. trachomatis , and a broad range of facultative and anaerobic pathogens, regardless of whether gonococcal or chlamydial infection is documented. Recommended oral regimens are ofloxacin (400 mg twice daily) or levofloxacin (500 mg once daily), plus metronidazole (500 mg twice daily), for 14 days; or a single dose of one of the parenteral cephalosporins, such as ceftriaxone (250 mg IM), followed by doxycycline (100 mg twice daily), with or without metronidazole (500 mg twice daily), for 14 days. For hospitalized patients or others who require parenteral therapy, the CDC recommends cefoxitin or cefotetan plus doxycycline; or clindamycin plus gentamicin. Other options include ofloxacin or levofloxacin, with or without metronidazole; and ampicillin/sulbactam plus doxycycline. For all of these regimens, parenteral therapy is continued until improvement is observed, after which oral therapy is prescribed to complete 14 days total treatment.
Most persons with DGI should be hospitalized and treated with a parenteral third-generation cephalosporin, such as ceftriaxone, cefotaxime, or ceftizoxime, or with ciprofloxacin, ofloxacin, or levofloxacin if antimicrobial susceptibility testing shows the infecting strain to be sensitive. Joint irrigation or drainage appears not to be necessary for septic arthritis, although repeated aspiration of synovial fluid may speed improvement. Oral treatment (e.g., cefixime or a fluoroquinolone) usually can be substituted after improvement begins, then continued to complete 7 days' therapy. More prolonged parenteral treatment and higher doses are indicated for treatment of gonococcal meningitis or endocarditis. Gonococcal epididymitis, bartholinitis, and other localized complications usually should be treated for 7 to 14 days with drugs active against both N. gonorrhoeae and C. trachomatis . Gonococcal conjunctivitis in adults can be managed with a single dose of ceftriaxone 1 g intramuscularly, optionally with saline lavage.
MANAGEMENT OF SEX PARTNERS.
Failure to ensure treatment of patients' sex partners contributes to continued transmission of gonorrhea and often results in reinfection of the index case. Most persons with genital discharge, lesions, or dysuria cease sexual activity and seek treatment; therefore, gonorrhea and other STDs are selectively transmitted by persons with subclinical infection or with ignored symptoms. Accordingly, most patients' source contacts-the partners from whom they acquired infection-do not spontaneously seek health care, and active efforts are necessary to bring them to treatment. For some gonorrhea patients, such as those with PID, DGI, or childhood



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