Abstract
Seven mycoplasmal strains have been isolated from the genital tract, of which Mycoplasma hominis and Mycoplasma genitalium are the commonest.
M. genitalium has an unknown incubation period, but symptoms commonly develop within one to three weeks.
There is an estimated 2–2.5-fold increase in the risk of urethritis, cervicitis, pelvic inflammatory disease, infertility and preterm delivery for women infected with M. genitalium.
It can be found in the vagina, cervix and endometrium, and usually the infections are asymptomatic. Most studies have the organism in 10–30 per cent of women with clinical cervicitis.
M. genitalium infection is a sexually transmitted infection.
Mycoplasma genitalium
Introduction
Seven mycoplasmal strains have been isolated from the genital tract, of which Mycoplasma hominis and Mycoplasma genitalium are the commonest.
M. genitalium has an unknown incubation period, but symptoms commonly develop within one to three weeks.
There is an estimated 2–2.5-fold increase in the risk of urethritis, cervicitis, pelvic inflammatory disease, infertility and preterm delivery for women infected with M. genitalium.1
It can be found in the vagina, cervix and endometrium, and usually the infections are asymptomatic. Most studies have the organism in 10–30 per cent of women with clinical cervicitis.
M. genitalium infection is a sexually transmitted infection.
Clinical Presentations
Dysuria
Vaginal discharge
Urethral discharge
Pelvic pain
Possibly proctitis
Intermenstrual bleeding
Post-coital bleeding
Effect on Pregnancy
1. Preterm labour
2. Miscarriage
3. Chorioamnionitis
A meta-analysis demonstrated an approximately two-fold increased risk of cervicitis, preterm birth and spontaneous abortion in women infected with M. gentialium. [EL 1]
M. hominis was isolated from blood in approximately 13 per cent of women with postpartum and post-abortion fever.
It was found to be an independent risk factor for preterm delivery after 24 weeks of gestation.2
Diagnosis
M. genitalium is a slow-growing organism.
1. Culture can take up to six months, and only a few laboratories in the world are able to recover clinical isolates.
2. Nucleic acid amplification test (NAAT) is the preferred method for M. genitalium detection. It is only available in a few large medical centres and commercial laboratories.
Diagnosis is made by NAAT testing of urine, urethral, vaginal and cervical swabs and through endometrial biopsies, typically using in-house polymerase chain reaction (PCR) or assays intended for research use only.3
Treatment
M. genitalium lacks a cell wall, and thus antibiotics targeting cell wall biosynthesis (e.g. beta-lactams including penicillins and cephalosporins) are ineffective against this organism.
Due to diagnostic challenges, treatment of most M. genitalium infections occurs in the context of syndromic management for urethritis, cervicitis and PID.4
Urethritis and Cervicitis
A) First-Line Therapy
Single dose of 1 g azithromycin was more effective than doxycycline in two randomised urethritis treatment trials and is the preferred choice. [EL 1]
However, resistance to azithromycin appears to be rapidly growing as median cure rate used to be approximately 85 per cent, but in the most recent trial (278) was found to be in only 40 per cent.
Longer course of azithromycin (an initial 500 mg dose followed by 250 mg daily for four days) might be marginally superior. However, in some settings, approximately 50 per cent of all M. genitalium infections are caused by organisms that are already resistant to azithromycin, therefore no regimen has beneficial effect over others.
B) Second-Line Therapy
Moxifloxacin, a fourth-generation fluoroquinolone (400 mg daily for 14 days), has been successfully used to treat M. genitalium in men and women with previous treatment failures, with cure rates of 100 per cent in initial reports.
However, it has been used in only a few cases, and the drug has not been tested in clinical trials. Although generally considered effective, studies in Japan, Australia and the United States have reported moxifloxacin treatment failures after the seven-day regimen.5
Pelvic Inflammatory Disease
PID unresponsive to the standard treatment should be tested for M. genitalium where available. A regimen of moxifloxacin 400 mg/day for 14 days has been effective in eradicating the organism. Nevertheless, no data have been published that assess the benefits of testing women with PID for M. genitalium, and the importance of directing treatment against this organism is currently unknown.
Effective treatment reduces the risks of preterm labour and neonatal complications.6
Because of the increasing resistance among M. genitalium for macrolides and quinolones, treatment courses should be short and convenient in order to ensure compliance.
Patients with M. genitalium infection should observe abstinence from unprotected intercourse until both sexual partners have completed the treatment and are symptom-free.
Both sexual partners should be screened for other STIs.
If the partner does not get tested, the same treatment is offered as given to the index patient.
A test of cure should also be performed routinely for all patients, in view of the increasing prevalence of macrolide resistance, which may exist prior to initiation of therapy or can evolve during therapy with a macrolide.7
Contact Tracing
1. In heterosexuals there is a greater risk of PID and reproductive complications, which suggests a greater need to trace, test and treat infected contacts. The time period for contact tracing is unknown.
2. Usual testing method: nucleic acid amplification testing on first-pass urine in men (urethral swab less sensitive) and first-pass urine, high vaginal or cervical swab in women.
3. It is sexually transmitted, with possible infection due to oral sex.
4. Duration of potential infectivity is unknown, but persistent infection occurs in 25 per cent of cases, which may persist to more than 12 months. Infections up to two to three years have been reported.8
Ureaplasma
Ureaplasma parvum (serovars 1, 3, 6 and 14) and Ureaplasma urealyticum (serovars 2, 4, 5 and 7–13) lack cell walls, hydrolyse urea to generate adenosine triphosphate (ATP), have limited biosynthetic functions and adhere to human mucosal surfaces of the genitourinary tract in adults and respiratory tract in newborns.
These organisms can be detected in vaginal flora in 40–80 per cent of healthy women, and their presence has been causally linked to infertility and other fetal implications.
Fetal Implications
Vertical transmission from mothers to their infants occurs in utero or during delivery.
1. Early pregnancy loss
2. Stillbirth, preterm birth
3. Neonatal morbidities
The clinical history of patients with urogenital or extragenital infections because of Ureaplasma species is syndrome-specific, not organism-specific. Usually there are no distinguishing features to indicate the microbiologic aetiology of these infections.9
Because of lack of facilities to diagnose Ureaplasma infections in many clinical settings, many clinicians are unfamiliar with aetiologic agents. Identification of these organisms may be achieved only as a last resort, especially if initial treatment with ineffective drugs is unsuccessful.
Signs and Symptoms in Adults
Urethritis
Pyelonephritis
Cystitis
Urinary calculi
Endometritis or chorioamnionitis
Infectious arthritis
Surgical and non-surgical wound infections
Bacteraemia
Pneumonia
Meningitis
Neonatal Implications
Neonates, particularly if preterm, are especially vulnerable to dissemination of infectious organisms (acquired in utero or at birth) in the bloodstream and, ultimately, the central nervous system.
Usually there are no characteristic signs and symptoms to predict the type of organism present. Subtle manifestations, such as temperature instability, blood pressure fluctuations, heart rate and respiratory efforts, may be the only signs that an infection is present.
Consider Ureaplasma species if signs and symptoms of infection are present; if the neonate does not respond to beta-lactam drugs; and if cultures from blood, the lower respiratory tract and cerebrospinal fluid (CSF) do not reveal a more common microbiological cause.
Radiographic evidence of pneumonitis in the absence of a proven bacterial or viral cause and mononuclear or polymorph nuclear pleocytosis (an abnormal increase in the amount of lymphocytes in the CSF with a negative Gram stain and culture result are consistent with Ureaplasma infection.
Although these organisms have been considered of low virulence, in vitro and in vivo experimental models have provided extra evidence that perinatal morbidities in premature babies (such as bronchopulmonary dysplasia, intraventricular haemorrhage and necrotising enterocolitis) do exist.10
Diagnosis
1 Culture Methods
Since Ureaplasma species hydrolyse urea and use it for a substrate for ATP generation, the organisms require media containing urea such as 10B broth and A8 agar. In experienced laboratories, the detection limit for culture methods is 100–1000 viable organisms.
For females, urine, cervical swabs or vaginal swabs are acceptable.
2 Polymerase Chain Reaction, Molecular Techniques (PCR)
This is more sensitive than culture for detection (<100 genome copies) of non-viable as well as viable ureaplasmas.11
Antimicrobial Therapy
1. Erythromycin ethylsuccinate
Dose: oral 800 mg tablets, eight-hourly for seven days
2. Clarithromycin
(USA only) Dose: suspension, 500 mg oral 12-hourly for 7–14 days
3. Azithromycin
Dose: 1 g orally in a single dose12
Chancroid (Haemophilus ducreyi Infection)
Background
Chancroid is a bacterial sexually transmitted disease (STD) caused by Haemophilus ducreyi infection. It is characterised by painful necrotising genital ulcers that may be accompanied by inguinal lymphadenopathy. It is a highly contagious but curable disease.
Clinical manifestations include genital ulcers and inguinal lymphadenopathy.13
Chancroid was previously highly prevalent in many areas of the world. Because of collaborative efforts and increasing social awareness, along with subsequent changes in sexual practices, improved diagnosis and treatment options, it has been eradicated as an endemic disease in industrialised countries.14
In 2000, the proportion of chancroid among genital ulcerative diseases decreased from 69 per cent to 15 per cent.
It remains prevalent in certain underdeveloped regions such as Asia, Africa and the Caribbean. In these areas, outbreaks occur in cities among workers in the sex trade.
Individuals travelling to these high-risk areas are at risk of contracting the disease.
In addition, individuals from high-risk areas who travel to other countries to work in the sex industry remain a source of outbreaks in the industrialised world.