Junral Di Translete Gonore
Junral Di Translete Gonore
Junral Di Translete Gonore
Cher yl K Walker
Richard L Sweet
Women’s Center for Health,
Department of Obstetrics and
Gynecology, University of California, Davis School of Medicine,
Sacramento, CA, USA
Correspondence: Cheryl K Walker Women’s Center for Health, Department of Obstetrics and Gynecology, University of California, Davis School of
Medicine,
4869 Y Street, Suite 2500, Sacramento, CA 95817, USA
Tel +1 916 734 6670
Fax +1 916 734 6666
email ckwalker@ucdavis.edu
Abstract: Gonorrhea is a set of clinical conditions resulting from infection with the sexually acquired bacterial pathogen Neisseria
gonorrhoeae. Acquisition may involve multiple mucosal sites in the lower female genital tract, including the urethra, cervix, Bartholin’s
and Skene’s glands, as well as the anorectal canal, pharynx, and conjunctivae. It may spread to the upper genital tract, uterine tubes,
abdominal cavity, and other systemic sites. Gonorrhea is the second most commonly reported sexually transmitted infection in the US
and rates are higher among women than men. Women and infants are affected disproportionately by gonorrhea, because early infection
may be asymptomatic and also because extension of infection is often associated with serious sequelae. Screening is critical for infection
identification and the prevention or limitation of upper genital tract spread, and horizontal and vertical transmission. Routine genital
screening is recommended annually for all sexually active women at risk for infection, including women aged , 25 years and older
women with one or more of the following risks: a previous gonorrhea infection, the presence of other sexually transmitted diseases,
new or multiple sex partners, inconsistent condom use, commercial sex work, drug use, or human immunodeficiency virus infection
with sexual activity or pregnancy. Pharyngeal gonococcal infections are common in adolescents, and direct culture screening is
necessary to identify affected individuals. Nucleic acid amplification tests (NAATs) are considered the standard for screening and
diagnosis. Although urine NAAT testing is most commonly used, there is growing support for vaginal swabs collected by providers or
patients themselves. Resistance to all antibiotics currently recommended for the treatment of gonorrhea has been documented and
complicates therapeutic strategies. The Centers for Disease Control and Prevention recommend treatment of gonorrhea with a single
class of drugs, ie, the cephalosporins.
Keywords: gonorrhea, women, infection, treatment, cephalosporins
Introduction
Gonorrhea refers to a set of clinical conditions involving infection with the sexually acquired bacterial pathogen, Neisseria
gonorrhoeae, identified microbiologically by its Gram negative intracellular diplococci. N. gonorrhoeae may be
acquired at multiple mucosal sites in the lower genital tract, including the urethra, cervix, Bartholin’s and Skene’s glands,
as well as through the anorectal canal, pharynx, and conjunctivae. It may spread to the upper genital tract, uterine tubes,
and abdominal cavity, as well as other systemic sites. With references to this condition dating back over 2000 years,
gonorrhea is an old disease, with humans serving as the sole natural host.
Geographic distribution
Dovepress
Prevalence
Gonorrhea is a common infection, with recent Centers for Disease Control and Prevention (CDC) figures estimating more
than 700,000 new cases in the US each year, only half of which are reported. In 2009, there were 301,174 cases of gonorrhea
reported in the US, a rate of 99.1 cases per 100,000 people, a 10.5% decrease from the previous year. Gonorrhea follows
chlamydial infections as the second most commonly reported sexually transmitted infection (STI) in the US.1
As a treatable STI, gonorrhea rates respond to public health interventions aimed at aggressive case finding and treatment, and
between 1975 and 1997, rates fell 74% in response to a national gonorrhea control program. Following the conclusion
of that program, gonorrhea rates have remained relatively stable.
Overall rates and comparisons between subpopulations must be understood within the context that reported case results
are greatly influenced by changes in public awareness, health care access, screening practices, resistance patterns, reporting
practices, outbreaks of other STIs, and budgetary limitations that hamper the abilities of public health officials to monitor
disease patterns accurately.1,2 In particular, rates of asymptomatic infections are subject to dramatic shifts based on alterations
in screening behaviors.3–6
Reported rates of gonorrhea and other STIs are commonly held to represent the tip of the iceberg of true infection prevalence,
in large part because roughly half of all gonococcal infections in women are asymptomatic. 7 Some have cautioned that
actual prevalence is likely to be roughly twice the reported rate.8 Problems that evolve from that paradigm are that many
infected individuals harbor untreated infection for protracted periods of time, greatly increasing the potential both for
transmission of infection to sex partners and development of complications due to more profound extension of the infection.1
Given the biased and incomplete nature of passive case reporting, active surveillance efforts are used to assess disease
burden in selected higher risk populations. In 2009, the median state specific gonorrhea test positivity among women aged
15–24 years in a subset of states, the District of Columbia, Puerto Rico, and the Virgin Islands, was ascertained through
screening efforts in various settings: family planning clinics 1.0% (range 0.0%–3.4%); prenatal clinics
1.2% (range 0.0%–5.5%); women entering the National Job
Training Program 1.6% (0.0%–5%); and women entering juvenile corrections facilities 2.9% (0.0%–13.4%).1
Prevalence in the US varies by geography and demographics, with the highest risk profile in adolescent black women residing
in urban locales in the South. The South has traditionally had the highest rates in the US, followed closely by the Midwest.
State reported gonorrhea rates fell in 84% of states between 2008 and 2009. In 2009, gonorrhea rates per 100,000 population
by state ranged from 7.2 in Utah to 246.4 in Mississippi. The majority of people with gonorrhea reside in urban locations,
with 60% of gonorrhea cases reported by the 50 most populous metropolitan areas that report to the CDC in 2009.
Gender
Traditionally, men were more likely to have gonorrhea, but rates equilibrated by 1996 and have remained similar since then.
In 2009, the gonorrhea rate among women was higher than the rate among men, and the most common reporting source for
women was private physicians/health maintenance organizations (30.9%), followed by STI clinics (16.7%), family planning
clinics (9.1%), other health department clinics (8.1%), and emergency rooms (5.8%).
education
Education has been inversely correlated to behavioral risk taking associated with the acquisition of STIs in
adolescents.9–13 A recent study of self reported STIs, including gonorrhea, chlamydia, and trichomoniasis, among young adult
women confirmed that education is associated with decreased engagement in sexual risk behaviors and lower rates of STI
diagnosis, but that those associations varied across racial strata, with college educated black women reporting higher rates
of STI compared with white women who had not completed high school.8
Clinical manifestations
Women and infants are affected disproportionately by gonorrhea, because early infection may be asymptomatic or
subclinical and also because extension of infection is often
198
submit your manuscript | www.dovepress.com
Dovepress
International Journal of Women’s Health 2011:3
Dovepress
Gonorrhea infection in women
associated with serious sequelae. The simplest gonococcal infections in women involve mucosal surfaces of the
endocervix, urethra, anus, or pharynx. Most such infections are either silent or generate only mild symptoms, including
discharge and mild irritation, that may or may not be appreciated until the infection spreads to the upper genital tract.
Pharyngeal infections are nearly always asymptomatic. When an etiologic organism is isolated in the presence of cervicitis, it is
typically Chlamydia trachomatis or N. gonorrhoeae.
Because cervicitis might be a sign of upper genital tract infection, women who seek medical treatment for a new episode
of cervicitis should be assessed for pelvic inflammatory disease. An estimated 10%–20% of women with gonorrrhea or
chlamydia may develop pelvic inflammatory disease if their infection is not identified and they do not receive adequate
treatment.14 Among women with pelvic inflammatory disease, uterine tubal scarring can cause involuntary infertility in 20% of
women, ectopic pregnancy in 9%, and chronic pelvic pain in 18%.15 Some cases of pelvic inflammatory disease have a severe
presentation with abdominal pain and fever, and may result in tubo ovarian abscesses and systemic infection. As with
uncomplicated gonococcal infection, many women with pelvic inflammatory disease are asymptomatic or have subtle signs
and symptoms of ongoing damage to uterine tubes, resulting in treatment delays in approximately 85% of women with pelvic
inflammatory disease and enhancing the chance for long term sequelae.15,16
Gonorrhea can become disseminated, with bacteremia leading on occasion to chronic joint infections and sepsis.
Disseminated gonorrhea frequently results in petechial or pustular acral skin lesions, asymmetrical arthralgia, tenosynovitis, or
septic arthritis. The infection is complicated occasionally by perihepatitis and rarely by endocarditis or meningitis.
Finally, gonorrhea is highly transmissible, both to sexual contacts and at birth. Infections in the neonate include
conjunctivitis, blindness, sepsis, and joint infections.
Screening
Because gonorrhea is often asymptomatic in women, screening is critical for the identification of infection and the prevention or
limitation of upper genital tract spread, and horizontal and vertical transmission. Data from a randomized controlled trial of
chlamydia screening in a managed care setting suggest that such screening programs can reduce the incidence of pelvic
inflammatory disease by as much as 60%.17
Because the prevalence of gonorrhea varies widely among communities and populations, targeted rather than
widespread screening is recommended by the US Preventive Services Task Force and the CDC. Routine genital screening for
N. gonorrhoeae is recommended annually for all sexually active women at risk for infection, including women aged , 25
years and older women with one or more of the following risks: a previous gonorrhea infection, the presence of other STIs,
new or multiple sex partners, inconsistent condom use, commercial sex work, drug use, or human immunodeficiency virus
infection with sexual activity.18 Pharyngeal gonococcal infections are common in some segments of the population, especially
adolescents, and pharyngeal culture screening is responsible for identification of up to one quarter of infected adolescent women
who would likely be missed with traditional genital tract screening.19–23
All pregnant women at risk for gonorrhea or living in an area in which the prevalence of N. gonorrhoeae is high should be
screened at the first prenatal visit for N. gonorrhoeae.18
Pregnant women who test positive should be retested within approximately 3–6 months, and those who remain at high risk
for gonococcal infection, including adolescents, should be retested also during the third trimester.24
Specific testing for N. gonorrhoeae is recommended because of the subtle and nonspecific nature of presentation in most
women as well as the availability of highly sensitive and specific testing modalities. Although there are three ways to
diagnose gonorrhea, ie, traditional culture, nucleic acid hybridization, and nucleic acid amplification tests (NAATs),
NAATs are considered the standard for screening and diagnostic purposes currently. Culture requires collection of actual
cells from infected mucosal surfaces, and is the only methodology approved for detection of N. gonorrhoeae from both
genital (endocervical, urethral) and nongenital (anorectal, pharyngeal, and conjunctival) mucosal surfaces. Cultures can
provide antimicrobial susceptibility results, and should be the test of choice in cases of suspected or documented treatment
failure. Nucleic acid hybridization tests detect gonococcal DNA and some brands also test for chlamydial DNA; they are
recommended for use on specimens collected from genital tract surfaces, including genital tract, vagina, and urine. The
principal types of NAATs, ie, transcription mediated amplif ication, polymerase chain reactions, and strand displacement
amplification, detect and copy gonococcal DNA to enhance detection. NAATs are approved by the US Food and Drug
Administration for use with urine, urethral, and endocervical samples, and some are cleared for use on vaginal
swabs, but none are approved for use in specimens from the
Dovepress
199
Walker and Sweet
rectum, oropharynx, or conjunctivae due to concerns that specificity could be compromised by cross reaction with
nongonococcal Neisseria species. NAATs have demonstrated improved sensitivity and specificity compared with culture
for the detection of N. gonorrhoeae at rectal and oropharyngeal sites among men.21,22,25,26 Numerous public and private
laboratories have established performance specifications for using NAAT with vaginal, rectal, and pharyngeal swab
specimens, thereby allowing results to be used for clinical management. Under these circumstances, NAATs are preferred
for rectal, oropharyngeal, and conjunctival specimens. Liquid based cervical cytology specimens appear to hold promise for
NAAT testing, although test sensitivity using these specimens might be lower than those resulting from the use of cervical
swab specimens.27
Although the standard female genital screening tool at most public health clinics is urine NAAT testing, there is growing
support for vaginal swabs collected by providers and patients in clinical and nonclinical settings. Vaginal swab specimens
perform at least as well as with other approved specimens using NAATs, and women find this screening strategy highly
acceptable.31,32 In a study of women using long acting contraception who remain at risk of STI acquisition, those randomized
to self collected vaginal swabs were more likely to complete screening than the women in the traditional clinical screening
group.33 Another study showed that women recruited by the Internet demonstrated higher positivity of chlamydia than those
attending a family planning clinic, providing an important at risk market for self collected vaginal swabs.34 Finally, as a
practical matter, swabs reduce biological waste associated with urine testing.
In symptomatic women, the finding of .10 white blood cells per high powered field in vaginal fluid in the absence of
trichomoniasis, may reflect endocervical inflammation caused by C. trachomatis or N. gonorrhoeae,28,29 and should increase
motivation for empiric treatment.
Due to high prevalence of gonorrhea in juvenile detention and jail facilities, the CDC recommends universal screening at
intake of adolescent and adult women up to 35 years of age or on the basis of local institutional prevalence data.1
Routine testing of inmates has the potential to diagnose a large portion of STIs in the community. When the Cook
County Jail in Chicago stopped offering routine chlamydia and gonorrhea testing to all male inmates, approximately
90% fewer detainees were diagnosed with either disease and citywide diagnosis in males and females decreased
by 9.3% for chlamydia and 12.9% for gonorrhea.5 Failure
Dovepress
to perform universal screening in high risk populations represents a missed opportunity to uncover substantial numbers
of infections. When New York City began routine testing for chlamydia and gonorrhea among incarcerated men less than
35 years of age, the citywide diagnosis of chlamydia and gonorrhea increased by 59% and 4%, respectively. 6 Kahn
examined the link between incarceration and sexually transmitted infections from a social network perspective in
Brooklyn, NY (n = 343) and found that acquisition of an STI was highly associated with a history of incarceration.30
Persons with gonorrhea should be tested for other STIs. Outside of the neonatal period, evidence of gonococcal infection
at any site is considered virtually 100% indicative of sexual contact.35
Management
Antimicrobial resistant N. gonorrhoeae Gonor rhea treatment is complicated by the ability of N.
36
gonorrhoeae to develop resistance to antimicrobial therapies. In 1986, the CDC developed a national surveillance
program called the Gonococcal Isolate Surveillance Project to monitor gonococcal isolate resistance patterns in the US
among selected STI clinics in approximately 25–30
Gonococcal Isolate Surveillance Project sentinel sites and
4–5 regional laboratories.
Penicillin was the original treatment choice for gonococcal infections until the discovery in 1976 of resistance mediated
by plasmid production of β lactamase.37 Rates of penicillinase producing N. gonorrhoeae have risen steadily since
then, and chromosomal mediated resistant N. gonorrhoeae has emerged to tetracycline, cephosporins, spectinomycin, and
aminoglycosides. 38 Newer f indings include plasmid mediated tetracycline resistance resulting from acquisition of a tet M
gene38–40 and fluoroquinolone resistance.1,41
Treatment with quinolones used to be the mainstay of N. gonorrhoeae treatment in the US, but resistant strains spread
throughout the US and the world,42 leading to removal of that class of drugs from recommendations for the treatment of gonorrhea
and pelvic inflammatory disease in April 2007.43
Provider compliance has been excellent, with the proportion of Gonococcal Isolate Surveillance Project patients treated with
fluoroquinolones (ciprofloxacin, ofloxacin, or levofloxacin) at 0.5% and the proportion treated with cephalosporins at 96.2% in
2009. By 2009, 23.5% of isolates collected from Gonococcal Isolate Surveillance Project sites were resistant
to penicillin, tetracycline, or ciprofloxacin.1
200
submit your manuscript | www.dovepress.com
Dovepress
International Journal of Women’s Health 2011:3
Dovepress
Gonorrhea infection in women
Decreased susceptibility has been documented to azithromycin in US isolates of N. gonorrhoeae, 1 and resistant
strains have been documented internationally. 44–47
Most of the treatment failures resulting from use of oral cephalosporins have been reported from Asian and
European countries, 48–51 although one possible case was reported in Hawaii in 2001.52 To ensure appropriate antibiotic
therapy, clinicians should ask patients testing positive for gonorrhea about recent travel to and sexual activity in these
countries. Two cases of suspected treatment failure with ceftriaxone have been reported. 53 Decreased susceptibility of
N. gonorrhoeae to cephalosporins and other antimicrobials is expected to continue to spread; therefore, state and local
surveillance for antimicrobial resistance is crucial for guiding local therapy recommendations. 36
The CDC website (http://www.cdc.gov/std/gisp) and state health departments can provide the most current
information.
Antimicrobial regimens
While gonorrhea is a bacterial infection that responds to a number of antibiotics, resistance to all antibiotic treatments
currently recommended for the treatment of gonorrhea has been documented and complicate therapeutic strategies. The
CDC released new STI treatment guidelines in 2010, with evidence based antibiotic regimens designed to treat gonorrhea
by anatomic site of infection (Table 1).35 The recommended treatment of gonorrhea has been limited to a single class of
drugs, the cephalosporins. The regimens listed in Table 1 are recommended for treatment of uncomplicated lower genital tract
and anorectal gonococcal infection in women. Treatment should be administered or dispensed at the time of diagnosis to
maximize patient adherence. Patients should be instructed to abstain from sexual intercourse until therapy is completed and
until they and their sex partners no longer have symptoms.
Dovepress
201
Walker and Sweet
Dovepress
Special populations
Pregnant women and women who are HIV infected and diagnosed with gonorrhea should be treated according to standard
recommendations.
Allergic reactions
Up to 10% of individuals with a history of penicillin allergy develop an adverse reaction to first generation
cephalosporins, and fewer react to third generation cephalosporins. 67 Cephalosporin use should be avoided only
202
submit your manuscript | www.dovepress.com
Dovepress
International Journal of Women’s Health 2011:3
Dovepress
Gonorrhea infection in women
in those with a history of a severe reaction to penicillin (eg, anaphylaxis, Stevens Johnson syndrome, and toxic epidermal
necrolysis), 68 and further treatment decisions should be made in consultation with an infectious disease specialist.
Follow up
Women treated with any of the recommended or alternative regimens for an uncomplicated episode of N. gonorrhoeae do
not need a test of cure 3 weeks after completing therapy,
but should be retested 3 months after treatment or the next time they seek medical care irrespective of partner treatment.69
Because reinfection within a few months is common,70–72 patient education regarding safer sexual practices and partner referral
is warranted. If symptoms persist following treatment, women should be tested for other pathogens and reevaluated by culture for
N. gonorrhoeae; any gonococci isolated should be tested for antimicrobial susceptibility.
Sex partners of patients with N. gonorrhoeae infection
whose last sexual contact with the patient was within
Dovepress
203
Walker and Sweet
Dovepress
60 days of the onset of symptoms or diagnosis of infection in the patient shoul d b e eva l u a t e d a n d t r e a t e d f o r N.
gonorrhoeae and C. trachomatis. If a patient’s last sexual intercourse was .60 days before onset of symptoms or diagnosis,
the patient’s most recent sex partner should be treated. For those whose partners’ treatment cannot be ensured or is unlikely,
delivery of antibiotic therapy for gonorrhea (as well as for chlamydia) by the patients to their partners should be considered,
accompanied by efforts to educate partners about symptoms and to encourage partners to seek clinical evaluation.73,74
Suspected treatment failure is less common than reinfection, but has been reported, especially among persons
receiving regimens other than the 250 mg dose of ceftriaxone.49,53,56–58 Clinicians of patients with suspected treatment
failure or persons found to harbor a resistant strain should consult an infectious disease specialist, conduct culture and
susceptibility testing of relevant clinical specimens, retreat with at least 250 mg of ceftriaxone intramuscularly or
intravenously, ensure partner treatment, and report the situation to the CDC through state and local public health authorities.35
Disclosure
The authors report no conflicts of interest in this work.
References
1. Centers for Disease Control and Prevention. Sexually Transmitted
Disease Surveillance 2009. Atlanta: US Department of Health and Human Services; 2010. Available from: http://www.cdc.gov/std/stats09/ surv2009-
Complete.pdf. Accessed June 17, 2011.
2. Centers for Disease Control and Prevention. Gonorrhea – United States,
1998. MMWR Morb Mortal Wkly Rep. 2000;49:538–542.
3. Majdzadeh R, Pourmalek F. A conditional probability approach to surveillance system sensitivity assessment. Public Health. 2008;122:
53–60.
4. Bernstein KT, Marcus JL, Nieri G, Philip SS, Klausner JD. Rectal gonor- rhea and chlamydia reinfection is associated with increased risk of HIV
seroconversion. J Acquir Immune Defic Syndr. 2010;53:537–543.
5. Broad J, Cox T, Rodriguez S, et al. The impact of discontinuation of male STD screening services at a large urban county jail: Chicago, 2002–2004. Sex
Transm Dis. 2009;36(Suppl 2):S49–S52.
6. Pathela P, Hennessy RR, Blank S, Parvez F, Franklin W, Schillinger JA.
The contribution of a urine-based jail screening program to citywide male
Chlamydia and gonorrhea case rates in New York City. Sex Transm Dis.
2009;36(Suppl 2):S58–S61.
7. Hook EW, III, Handsfield HH. Gonococcal infections in the adult.
In: Holmes KK, Sparling PF, Stamm WE, et al, editors. Sexually Trans- mitted Diseases. 4th ed. New York: McGraw-Hill; 2008.
8. Annang L, Walsemann KM, Maitra D, Kerr JC. Does education matter?
Examining racial differences in the association between education and STI diagnosis among black and white young adult females in the US. Public
Health Rep. 2010;125(Suppl 4):110–121.
9. Halpern CT, Joyner K, Udry JR, Suchindran C. Smart teens don’t have sex (or kiss much either). J Adolesc Health. 2000;26:213–225.
10. Zweig JM, Phillips SD, Lindberg LD. Predicting adolescent profiles of risk: looking beyond demographics. J Adolesc Health. 2002;31:
343–353.
11. Ford CA, Pence BW, Miller WC, et al. Predicting adolescents’ longitudinal risk for sexually transmitted infection: results from the National
Longitudinal Study of Adolescent Health. Arch Pediatr Adolesc Med. 2005;159:657–664.
12. Ohannessian CM, Crockett LJ. A longitudinal investigation of the relationship between educational investment and adolescent sexual activity. J
Adolesc Res. 1993;8:167–182.
13. Scott-Jones D, White AB. Correlates of sexual activity in early adolescence. J Early Adolesc. 1990;10:221–238.
14. Haggarty CL, Gottlieb S, Taylor BD, Low N, Xu F, Ness RB. Risk of sequelae after Chlamydia trachomatis genital infection in women. J Infect
Dis. 2010;201(Suppl 2):S134–S155.
15. Westrom L, Joesoef R, Reynolds G, Hagdu A, Thompson SE. Pelvic inflammatory disease and fertility: a cohort study of 1,844 women with
laparoscopically verified disease and 657 control women with normal laparoscopy. Sex Transm Dis. 1992;9:185–192.
16. Hillis SD, Joesoef R, Marchbanks PA, Wasserheit JN, Cates W Jr, Westrom L. Delayed care of pelvic inflammatory disease as a risk factor
for impaired fertility. Am J Obstet Gynecol. 1993;168:
1503–1509.
17. Scholes D, StergachisA, Heidrich FE,Andrilla H, Holmes KK, Stamm WE.
Prevention of pelvic inflammatory disease by screening for cervical chlamydial infection. N Engl J Med. 1996;34:1362–1366.
18. US Preventive Ser vices Task Force. Screening for gonor rhea:
recommendation statement. Ann Fam Med. 2005;3:263–267.
19. Giannini CM, Kim HK, Mortensen J, Mortensen J, Marsolo K, Huppert J.
Culture of non-genital sites increases the detection of gonorrhea in women. J Pediatr Adolesc Gynecol. 2010;23:246–252.
20. Mayer KH, Klausner JD, Handsfield HH. Intersecting epidemics and educable moments: sexually transmitted disease risk assessment and screening
in men who have sex with men. Sex Transm Dis. 2001;28:
464–467.
21. Schachter J, Moncada J, Liska S, et al. Nucleic acid amplification tests in the diagnosis of chlamydial and gonococcal infections of the oropharynx
and rectum in men who have sex with men. Sex Transm Dis.
2008;35:637–642.
22. Mimiaga MJ, Mayer KH, Reisner SL, et al. Asymptomatic gonorrhea and chlamydial infections detected by nucleic acid amplification tests among
Boston area men who have sex with men. Sex Transm Dis. 2008;
35:495–498.
23. Linhart Y, Shohat T, Amitai Z, et al. Sexually transmitted infections among brothel-based sex workers in Tel-Aviv area, Israel: high prevalence
of pharyngeal gonorrhoea. Int J STD AIDS. 2008;19:
656–659.
24. Aggarwal A, Spitzer RF, Caccia N, Stephens D, Johnstone J, Allen L.
Repeat screening for sexually transmitted infection in adolescent obstetric patients. J Obstet Gynaecol Can. 2010;32:956–961.
25. Bachmann LH, Johnson RE, Cheng H, et al. Nucleic acid amplification tests for diagnosis of Neisseria gonorrhoeae oropharyngeal infections. J Clin
Microbiol. 2009;47:902–907.
26. Bachmann LH, Johnson RE, Cheng H, et al. Nucleic acid amplification tests for diagnosis of Neisseria gonorrhoeae and Chlamydia trachomatis rectal
infections. J Clin Microbiol. 2010;48:1827–1832.
27. Chernesky M, Freund GG, Hook E III, et al. Detection of Chlamydia trachomatis and Neisseria gonorrhoeae infections in North American women by
testing SurePath liquid-based Pap specimens in APTIMA assays. J Clin Microbiol. 2007;45:2434–2438.
28. Steinhandler L, Peipert JF, Heber W, et al. Combination of bacterial vaginosis and leukorrhea as a predictor of cervical chlamydial or gono- coccal
infection. Obstet Gynecol. 2002;99:603–607.
29. Geisler WM, Yu S, Venglarik M, et al. Vaginal leucocyte counts in women with bacterial vaginosis: relation to vaginal and cervical infections.
Sex Transm Infect. 2004;80:401–405.
204
submit your manuscript | www.dovepress.com
Dovepress
International Journal of Women’s Health 2011:3
Dovepress
Gonorrhea infection in women
30. Khan MR, Epperson MW, Mateu-Gelabert P, Bolyard M, Sandoval M, Friedman SR. Incarceration, sex with an STI- or HIV-infected partner, and
infection with an STI or HIV in Bushwick, Brooklyn, NY: a social network perspective. Am J Public Health. 2011;101:
1110–1117.
31. Schachter J, Chernesky MA, Willis DE, et al. Vaginal swabs are the specimens of choice when screening for Chlamydia trachomatis and Neisseria
gonorrhoeae: results from a multicenter evalua- tion of the APTIMA assays for both infections. Sex Transm Dis.
2005;32:725–728.
32. Doshi JS, Power J, Allen E. Acceptability of chlamydia screen- ing using self-taken vaginal swabs. Int J STD AIDS. 2008;19:
507–509.
33. Graseck AS, Secura GM, Allsworth JE, Madden T, Peipert JF.
Home compared with clinic-based screening for sexually transmitted infections: a randomized controlled trial. Obstet Gynecol. 2010;116:
1311–1318.
34. Gaydos CA, Barnes M, Aumakhan B, et al. Chlamydia trachomatis age- specific prevalence in women who used an internet-based self-screening program
compared to women who were screened in family planning clinics. Sex Transm Dis. 2011;38:74–78.
35. Centers for Disease Control and Prevention. Sexually transmitted disease treatment guidelines. 2010. Available from: http://www.cdc.
gov/std/treatment/2010/STD-Treatment-2010-RR5912.pdf. Accessed June 17, 2010.
36. Workowski KA, Berman SM, Douglas JM Jr. Emerging antimicro- bial resistance in Neisseria gonorrhoeae: urgent need to strengthen prevention
strategies. Ann Intern Med. 2008;148:606–613.
37. Phillips I. Beta-lactamase producing penicillinase-resistant gonococcus.
Lancet. 1976;2:656.
38. Centers for Disease Control and Prevention. Sentinel surveillance system for antimicrobial resistance in clinical isolates of Neisseria gonorrhea.
MMWR Morb Mortal Wkly Rep. 1987;36:585.
39. Centers for Disease Control and Prevention. Tetracycline-resistant Neisseria gonorrhea – Georgia, Pennsylvania, New Hampshire. MMWR Morb
Mortal Wkly Rep. 1985;34:563.
40. Morse SA. High-level tetracycline resistance is the result of acquisition of streptococcal tet-M determinant. Antimicrob Agents Chemother.
1986;30:664.
41. Fox KK, Knapp JS, Holmes KK, et al. Antimicrobial resistance in Neisseria gonorrhoeae in the United States, 1988–1994: the emergence of
decreased susceptibility to the fluoroquinolones. J Infect Dis.
1997;175:1396–1403.
42. Tapsall JW. What management is there for gonorrhea in the postqui- nolone era? Sex Transm Dis. 2006;33:8–10.
43. Centers for Disease Control and Prevention. Update to CDC’s sexually transmitted diseases treatment guidelines, 2006: fluoroquinolones no longer
recommended for treatment of gonococcal infections. MMWR Morb Mortal Wkly Rep. 2007;56:332–336.
44. Palmer HM, Young H, Winter A, et al. Emergence and spread of azithromycin-resistant Neisseria gonorrhoeae in Scotland. J Antimicrob Chemother.
2008;62:490.
45. Chisholm SA, Neal TJ, Alawattegama AB, et al. Emergence of high- level azithromycin resistance in Neisseria gonorrhoeae in England and Wales. J
Antimicrob Chemother. 2009;64:353.
46. Starnino S, Stefanelli P; Neisseria gonorrhoeae Italian Study Group: azithromycin-resistant Neisseria gonorrhoeae strains recently isolated in Italy. J
Antimicrob Chemother. 2009;63:1200.
47. Deguchi T, Nakane K, Yasuda M, Maeda S. Emergence and spread of drug resistant Neisseria gonorrhoeae. J Urol. 2010;184:851–858.
48. Takahata S, Senju N, Osaki Y, Yoshida T, Ida T. Amino acid substitu- tions in mosaic penicillin-binding protein 2 associated with reduced susceptibility
to cefixime in clinical isolates of Neisseria gonorrhoeae. Antimicrob Agents Chemother. 2006;50:3638–3645.
49. Yokoi S, Deguchi T, Ozawa T, et al. Threat to cefixime treatment for gonorrhea. Emerg Infect Dis. 2007;13:1275–1277.
50. Pandori M, Barry PM, Wu A, et al. Mosaic penicillin-binding protein 2 in Neisseria gonorrhoeae isolates collected in 2008 in San Francisco, California.
Antimicrob Agents Chemother. 2009;53:4032–4034.
51. Unemo M, Golparian D, Syversen G, Vestrheim DF, Moi H. Two cases of verified clinical failures using internationally recommended first-line cefixime
for gonorrhoea treatment, Norway, 2010. Euro Surveill. 2010;
15:19721.
52. Wang SA, Lee MVC, O’Connor N, et al. Multidrug-resistant Neisseria gonorrhoeae with decreased susceptibility to cefixime – Hawaii, 2001. Clin Infect
Dis. 2003;37:849–852.
53. Tapsall J, Read P, Carmody C, et al. Two cases of failed ceftri- axone treatment in pharyngeal gonorrhoea verified by molecular microbiological
methods. J Med Microbiol. 2009;58(5):683–687.
54. Moran JS, Levine WC. Drugs of choice for the treatment of uncomplicated gonococcal infections. Clin Infect Dis. 1995;20(Suppl 1):S47–S65.
55. Newman LM, Moran JS, Workowski KA. Update on the management of gonorrhea in adults in the United States. Clin Infect Dis. 2007;44(Suppl 3): S84–S101.
56. Lo JY, Ho KM, Leung AO, et al. Ceftibuten resistance and treat- ment failure of Neisseria gonorrhoeae infection. Antimicrob Agents Chemother.
2008;52:3564–3567.
57. Deguchi T, Yasuda M, Yokoi S, et al. Treatment of uncomplicated gonococcal urethritis by double-dosing of 200 mg cefixime at a 6-h interval. J
Infect Chemother. 2003;9:35–39.
58. Muratani T, Akasaka S, Kobayashi T, et al. Outbreak of cefozopran (penicillin, oral cephems, and aztreonam)-resistant Neisseria gonor- rhoeae in
Japan. Antimicrob Agents Chemother. 2001;45:3603–3606.
59. Waters LJ, Boag FC, Betournay R. Efficacy of azithromycin 1 g single dose in the management of uncomplicated gonorrhoea. Int J STD AIDS.
2005;16:84.
60. McLean CA, Wang SA, Hoff GL, et al. The emergence of Neisseria gonorrhoeae with decreased susceptibility to azithromycin in Kansas City,
Missouri, 1999 to 2000. Sex Transm Dis. 2004;31:73–78.
61. Unemo M, Golparian D, Hestner A. Ceftriaxone treatment failure of pharyngeal gonorrhoea verified by international recommendations, Sweden,
July 2010. Euro Surveill. 2011;16:19792.
62. Ota KV, Fisman DN, Tamari IE, et al. Incidence and treatment outcomes of pharyngeal Neisseria gonorrhoeae and Chlamydia trachomatis infec- tions in
men who have sex with men: a 13-year retrospective cohort study. Clin Infect Dis. 2009;48:1237–1243.
63. Haimovici R, Roussel TJ. Treatment of gonococcal conjunctivitis with single-dose intramuscular ceftriaxone. Am J Ophthalmol. 1989;107:
511–514.
64. Haggerty CL, Ness RB, Amortegui A, et al. Endometritis does not predict reproductive morbidity after pelvic inflammatory disease. Am J Obstet
Gynecol. 2003;188:141–148.
65. Lyss SB, Kamb ML, Peterman TA, et al. Chlamydia trachomatis among patients infected with and treated for Neisseria gonorrhoeae in sexually transmitted
disease clinics in the United States. Ann Intern Med. 2003;
139:178–185.
66. Sathia L, Ellis B, Phillip S, et al. Pharyngeal gonorrhoea – is dual therapy the way forward? Int J STD AIDS. 2007;18:647–648.
67. Yates AB. Management of patients with a history of allergy to beta- lactam antibiotics. Am J Med. 2008;121:572–576.
68. Pichichero ME. A review of evidence supporting the American Academy of Pediatrics recommendation for prescribing cephalosporin antibiotics for
penicillin-allergic patients. Pediatrics. 2005;115:1048–1057.
69. Hosenfeld CB, Workowski KA, Berman S, et al. Repeat infection with chlamydia and gonorrhea among females: a systematic review of the literature.
Sex Transm Dis. 2009;36:478–489.
70. Peterman TA, Tian LH, Metcalf CA, et al. High incidence of new sexu- ally transmitted infections in the year following a sexually transmitted infection:
a case for rescreening. Ann Intern Med. 2006;145:564–572.
71. Fung M, Scott KC, Kent CK, et al. Chlamydial and gonococcal reinfec- tion among men: a systematic review of data to evaluate the need for retesting.
Sex Transm Infect. 2007;83:304–309.
International Journal of Women’s Health 2011:3 submit your manuscript | www.dovepress.com
Dovepress
205
Walker and Sweet
72. Kissinger PJ, Reilly K, Taylor SN, et al. Early repeat Chlamydia trachomatis and Neisseria gonorrhoeae infections among heterosexual men. Sex
Transm Dis. 2009;36:498–500.
73. Golden MR, Whittington WL, Handsfield HH, et al. Effect of expe- dited treatment of sex partners on recurrent or persistent gonorrhea or chlamydial
infection. N Engl J Med. 2005;352:676–685.
Dovepress
74. Kissinger P, Mohammed H, Richardson-Alston G, et al. Patient- delivered partner treatment for male urethritis: a randomized, controlled trial. Clin
Infect Dis. 2005;41:623–629.
Endocrine and autoimmune syndromes; Sexual and reproductive health; Psychological and psychosocial conditions. The manuscript management
system is completely online and includes a very quick and fair peer review system. Visit http://www.dovepress.com/ testimonials.php to read
real quotes from published authors.
Submit your manuscript here: http://www.dovepress.com/international journal of womens health journal
206
submit your manuscript | www.dovepress.com
Dovepress
International Journal of Women’s Health 2011:3