This chapter should be cited as follows:
Faraj PE, Louis L, Glob Libr Women's Med
ISSN: 1756-2228; DOI 10.3843/GLOWM.418573

The Continuous Textbook of Women’s Medicine Series – Gynecology Module

Volume 4

Benign gynecology

Volume Editor: Professor Shilpa Nambiar, Prince Court Medical Centre, Kuala Lumpur, Malaysia

Chapter

Common Infections of the Vulva, Vagina and Bartholin Gland

First published: January 2025

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TERMINOLOGY

We recognize that patients have diverse gender identities. In this chapter, we use the word ‘woman/en’ and 'female' to describe patients or individuals whose sex assigned at birth was female. We use these terms as used in the studies cited.

INTRODUCTION

Infections of the vulva, vagina or Bartholin gland have a significant impact on the patient’s quality of life and are a common reason for women to seek medical attention. Infections can be opportunistic, sexually transmitted, due to physiological changes or secondary to medication use. Such infections have variable presentations and can often be diagnosed on clinical examination, while others need laboratory investigations to differentiate from one another and guide treatment. Most are relatively easy to treat, others are protracted, and some require surgical management. This chapter describes the common infections encountered in gynecological visits and how they can be diagnosed and managed.

The common infections of the vulva discussed in this chapter are:

• lymphogranuloma venereum
• chancroid
• granuloma inguinale (donovanosis)
• syphilis (chancre, mucous patches and condylomata lata)
• infections caused by human papilloma virus (condylomata acuminata)
• infections caused by herpes simplex virus types 1 and 2
• shingles (herpes zoster)
• bullous impetigo

The common infections of the vagina discussed in this chapter are:

• bacterial vaginosis
• candidiasis
• trichomoniasis

In addition, the chapter also discusses the diagnosis and treatment of Bartholin gland cysts and abscesses.

LYMPHOGRANULOMA VENEREUM

Introduction

Lymphogranuloma venereum (LGV) is a genital ulcer disease that is caused by the L1, L2 and L3 biovars of Chlamydia trachomatis.¹ In the past, LGV was more commonly found in tropical and subtropical areas, but since 2003, LGV has become increasingly prevalent in high-income countries and other temperate areas due to the increase in the number of men who have sex with men, leading to increased cases of proctitis and in turn making them more susceptible to LGV.² The main risk factors are genital ulcers, previous sexually transmitted infections (STIs), unprotected sex and travel to endemic areas.³

Pathogenesis

LGV mainly affects lymphatic tissue, with the spread of the organism extending from the primary infection site to the draining lymph nodes and inducing a lymphoproliferative reaction. Areas of necrosis occur within these lymph nodes, causing abscess formation.⁴

Clinical manifestations

Three stages of LGV have been identified: primary, secondary and late LGV.

Primary infection

The primary infection has an incubation period lasting 3–12 days, and is characterized by a genital ulcer or a mucosal inflammatory reaction at the site of inoculation. These lesions spontaneously heal within a few days

Secondary infection

During the secondary stage, extension from the local site to regional lymph nodes occurs, and may lead to severe inflammation and systemic symptoms. The inguinal and femoral lymph nodes are most commonly involved; this stage of the disease may last up to 2–6 weeks.

Late LGV

After severe inflammation, fibrosis and strictures occur, which are characteristic of late LGV. This disease progression is noted in patients with untreated or under-treated earlier stages of LGV infection. Late complications may include genital elephantiasis, anal fistulae and strictures, frozen pelvis and infertility.⁴

Diagnosis

LGV is diagnosed in patients who present with consistent symptoms, risk factors, clinical findings and a positive result for C. trachomatis (identified using a nucleic acid amplification test on a swab from the affected area)⁴

Treatment of symptomatic patients

Antimicrobials are the drugs of choice for patients with symptomatic LGV, as they are curative and prevent further damage.¹ For non-pregnant patients, a course of doxycycline, 100 mg orally twice a day for 21 days, is recommended.¹ In cases of doxycycline intolerance or during pregnancy, azithromycin, 1 g orally once weekly for 3 weeks, or erythromycin, 500 mg four times daily for 21 days, is recommended. Use of azithromycin is the preferred option as patients are more likely to be compliant and it is known to have fewer side-effects.¹ In patients with inflamed lymph nodes, needle aspiration or incision and drainage may be required to avoid rupture or sinus tract formation.¹

CHANCROID

Introduction

Chancroid is a rare infection in high-income countries, but has been noted to be a chief cause of genital ulcers in sub-Saharan Africa, Latin America and Southeast Asia. The true incidence of chancroid has been challenging to determine due to laboratories in endemic areas lacking the capability to microbiologically confirm this diagnosis.⁵

Pathogenesis

Haemophilus ducreyi, the causative agent of chancroid, is a small, fastidious, gram-negative rod that requires an enriched growth medium containing hemin and usually serum for successful cultivation.⁶ H. ducreyi is thought to gain access to tissue through microabrasions on the skin after sexual intercourse in adults. The dose of the inoculum is believed to be linked to the likelihood of papule formation.⁷ H. ducreyi has been found to secrete cytolethal distending toxins, which play a significant role in epithelial cell injury and the development of an ulcer.⁸

Clinical manifestation

Chancroid has an incubation period of 4–10 days. H. ducreyi infection manifests with an erythematous papule that rapidly evolves into a pustule and later erodes into an ulcer. Genital ulcers caused by H. ducreyi are painful and erythematous with well-demarcated borders. Ulcers can vary in size and number and tend to be more numerous and larger in patients with HIV.⁵ Lymphadenitis is less common in female patients compared to male patients with H. ducreyi infection. Involved lymph nodes appear 1–2 weeks after the initial appearance of the primary ulcer, and may undergo liquefaction and present as fluctuant buboes.⁵

Diagnostic criteria

Probable cases

Probable cases are clinically compatible cases with (1) no evidence of Treponema pallidum infection by darkfield microscopic examination of ulcer exudate or by a serological test for syphilis performed 7 or more days after the onset of ulcers and (2) either a clinical presentation of the ulcer(s) that is not typical of a disease caused by herpes simplex virus (HSV) or a culture that is negative for HSV.

Confirmed cases

Confirmed cases are clinically compatible cases that are laboratory-confirmed using either Gram staining to identify the typical small gram-negative rods in a chain, the so-called ‘school of fish’ (this method has poor sensitivity), by growth of H. ducreyi on special culture medium, leading to a definitive diagnosis, or by use of nucleic acid amplification tests, which may lead to a definitive diagnosis of H. ducreyi but have limited availability globally.⁹

Treatment

Treatment is recommended for patients with confirmed or suspected chancroid. When considering empirical treatment for chancroid based on clinical manifestation and epidemiology, the patient should receive treatment for both HSV and syphilis alongside the chancroid treatment. Once patients have started treatment, it is impossible to be certain about the duration of infectivity, and hence patients should abstain from sexual intercourse until the ulcers are fully healed. Patients should be strongly advised to use condoms during sexual intercourse thereafter. The drug of choice is azithromycin (1 g orally in a single dose) or ceftriaxone (250 mg intramuscularly). Alternatives include ciprofloxacin (500 mg orally twice a day for 3 days) or erythromycin (500 mg orally three times a day for 7 days).¹⁰ Any buboes (fluctuant lymphadenitis) should be drained; this is usually achieved by needle aspiration.

GRANULOMA INGUINALE

Introduction

Granuloma inguinale, also known as donovanosis, is a genital ulcerative disease that is caused by an intracellular gram-negative bacterium named Klebsiella granulomatis. The disease is less common in high-income countries, but cases have been described in India, South Africa and South America.¹¹

Clinical manifestation

Infection with K. granulomatis is characterized as painless, slowly progressive ulcerative lesions on the genitals or perineum without regional lymphadenopathy, with a risk of formation of subcutaneous granulomas (pseudo-buboes). The lesions tend to bleed as they are highly vascular, giving a beefy red appearance. Infections may extend to the pelvis and disseminate to intra-abdominal organs, bones or the mouth. Superimposed bacterial infections may occur, and they may co-exist with other STIs.¹¹

Diagnostic considerations

K. granulomatis is diagnosed by direct visualization of dark-staining Donovan bodies (small oval or rounded immobile cocci) on a tissue crush preparation or biopsy.¹¹

Treatment

Treatment is aimed at halting the progression of the lesions, and healing becomes visible from the ulcer margins proceeding inwards. Various antimicrobial regimens have proven to be effective. Achieving granulation and re-epithelialization of the ulcers requires prolonged therapy, with a risk of recurrence 6–18 months later.¹¹ The recommended regimen is azithromycin 1 g orally once weekly or 500 mg daily for >3 weeks and until all lesions have completely healed. Alternative regimens include doxycycline (100 mg orally twice a day), erythromycin (500 mg orally four times a day) or one trimethoprim/sulfamethoxazole double-strength tablet (160 mg/800 mg) orally twice a day, for >3 weeks and until all lesions have completely healed. Adding another antibiotic to these regimens may be considered if improvement is not evident within the first few days of therapy. In addition to antibiotic treatment, HIV testing should be offered to all persons diagnosed with granuloma inguinale.¹²

SYPHILIS (CHANCRE, MUCUS PATCHES AND CONDYLOMATA LATA)

Syphilis is discussed only briefly here, focusing on its clinical manifestation in relation to vulval disease. The GLOWM chapter on syphilis provides more detailed coverage of the disease.¹³ Syphilis is an infection that is caused by Treponema pallidum, a corkscrew-shaped organism with tightly wound spirals.^14,15 The majority of new syphilis cases in adults are sexually acquired. In 2016, the World Health Organization estimated that there were 6.3 million new cases worldwide and 19.9 million cases in those aged between 15 and 49 years. The highest prevalence was reported in the Western Pacific region, followed by the African and American regions.¹⁶

Transmission

Transmission of T. pallidum occurs after direct contact with the infectious lesions. This may occur during sex or via vertical transmission to the fetus. Sexual transmission requires direct contact with infected lesions such as chancre in primary syphilis or condylomata lata in secondary syphilis. These lesions are highly infectious in comparison to intact cutaneous lesions.^15,17 Primary syphilis can develop wherever inoculation occurs. Therefore, syphilis may be acquired anywhere after contact with a person who has active lesions on the oral cavity, genitalia or breasts.

Stages of disease

Depending on the stage of the disease, syphilis has a wide range of clinical manifestations. The stages of syphilis may be divided into early and late. Early syphilis occurs within weeks to months after the initial infection, and comprises both primary and secondary syphilis. The patient may be asymptomatic within 12 months of acquiring syphilis, and this is termed early latent syphilis. Late syphilis occurs in untreated patients as they progress to develop late latent disease or tertiary syphilis. Central nervous system manifestations may occur at any time after initial infection.¹⁵

Clinical manifestations

Chancre, a localized painless skin lesion, is the initial clinical manifestation after T. palladium infection. The incubation period prior to the appearance of chancre ranges from 3–90 days.^15,18 Chancre develops from a papule at the site of inoculation that ulcerates and forms a raised indurated margin. The base of the ulcer is generally non-exudative and is associated with bilateral, regional lymphadenopathy. The chancre usually presents on the genitalia, but may be found on the posterior pharynx, anus or vagina. It can take up to 3–6 weeks for chancre to heal spontaneously without treatment, and such healing is believed to be possible due to local immune responses.^15,18 As chancre is painless, patients are less likely to seek treatment and continue to transmit the disease unknowingly. After the initial local infection and formation of the chancre, widespread spirochete dissemination occurs. This leads to the development of secondary syphilis, late syphilis and neurosyphilis.^15,18

Whitish erosions, called mucous patches, form during secondary syphilis, and can be found inside the mouth, vulva and vagina. Condylomata lata are smooth, raised, sharply margined, large and flat-topped lesions that may develop nearby or in moist and warm areas such as the mouth and perineum. They may be skin-colored, yellow, pink or white. Condylomata lata occur proximal to the primary chancre, reflecting direct spread of the organism.¹⁵

Diagnosis

T. pallidum is an organism that cannot be cultured in the laboratory, and is identified through direct visualization using dark-field microscopy or through direct fluorescent antibody testing. Other laboratory tests that are available include a specific treponemal enzyme immunoassay to screen for and quantify cardiolipin, and non-treponemal tests, such as rapid plasma reagin and venereal disease research laboratory tests, that help to assess the need for and response to treatment.¹⁹

The preferred treatment of primary and secondary syphilis is with penicillin G benzathine, 2.4 million units, intramuscularly, as one dose. Alternative antimicrobials are available, such as doxycycline, ceftriaxone, tetracycline and amoxicillin. After treatment, the patient should be invited for a clinical examination and a non-treponemal serological test at 6 and 12 months. Titers should be checked regularly for patients with HIV or if the risk of reinfection is a concern.²⁰

CONDYLOMATA ACUMINATA

Introduction

Human papillomavirus (HPV), the causative organism of condylomata acuminata, is a common cause of various cutaneous and mucosal infections. Individuals with anogenital HPV infection may present with condylomata acuminata, also known as anogenital warts. Around 200 types of HPV exist, but the vast majority of condylomata acuminata is caused by the HPV subtypes 6 or 11, which have low oncogenic potential. Condylomata acuminata manifest as soft plaques or papules in the anogenital area. HPV belongs to the family Papillomaviridae, and is a non-enveloped double-stranded DNA virus.²¹ Genital HPV types are divided into low- or high-risk types based on their associated risk for cancer. The low-risk types HPV 6 and 11 are detected in 90% of anogenital warts. Co-infection with high-risk strains is also common.²² HPV infection is the commonest sexually transmitted disease in the world.²² At least 75% of adults in the USA who are sexually active have been infected with at least one HPV type.²³ However, HPV infection rates are trending downwards after implementation of the HPV vaccination program. The impact of condylomata acuminata on the patient’s mental health is significant in the presence of fertility and malignancy concerns.

Transmission/risk factors

HPV transmission is through direct contact with infected skin or mucosal surfaces. Micro-abrasions allow the virus to invade the epidermal basal layer of cells. Sexual contact accounts for almost all anogenital HPV infections. Transmission can occur in the absence of warts, but they are known to be highly infectious due to a high viral load.

The primary risk factor for the acquisition of HPV infection is sexual activity, and the infection may be transmitted by skin-to-skin contact alone. Immunosuppressed patients (i.e. HIV-infected and diabetic patients) are at risk of developing larger anogenital warts that may also be resistant to condylomata acuminata treatment. Higher recurrence and malignant transformation rates are also reported in these patient groups.²⁴

Clinical manifestations/clinical course

Anogenital warts are typically found on the perineum, anal and perianal skin, vulva, groin and/or suprapubic skin, but may also involve the cervix, urethra and anal canal. These epidermal manifestations may present as single or multiple eruptions. The shape varies from flat to dome-shaped, cauliflower-shaped, fungating, cerebriform, pedunculate, filiform, plaque-like, smooth, verrucous or lobulated. The color of the warts varies from skin-colored to white, brown, erythematous, violaceous or hyper-pigmented lesions. Anogenital warts are generally painless and do not cause any symptoms, but, in some instances, may present with pruritus, burning, bleeding, pain, vaginal obstruction, dyspareunia or vaginal discharge. With regard to size, the lesions range from 1 mm to multiple cm in diameter.²⁵ Extensive condylomata acuminata can cause disfigurement of the anogenital area. On dermoscopy, papillomatosis is always present, with morphological features that vary from a finger-like to a knob-like pattern, and the vascular arrangement may be glomerular to dotted.²⁶

After the appearance of anogenital warts, they may increase in size and number or resolve spontaneously within 4 months (in one-third of the cases). Recurrence after resolution of warts may occur depending on the patient’s medical condition, immune status and viral load in the latently infected cells.

Diagnosis

Clinicians can diagnose condylomata acuminata on physical examination in most cases based on the typical features mentioned above. When assessing genital warts, all areas in which they are likely to appear should be inspected carefully, and one should also look for signs of possible co-existing STIs. Performing a vulvoscopy should be considered in the presence of diagnostic uncertainty. STI screening should be offered to those who present with genital warts and are with a new partner, in non-monogamous relationships or less than 25 years old. Features that may suggest another diagnosis include pinpoint papules (lichen nitidus), keratotic plugs and hyperpigmentation (seborrheic keratosis), umbilicated papules (molluscum contagiosum), yellowish color (Fordyce spots), moist surface (condylomata lata of syphilis), violaceous color (lichen planus) and ulceration (other infection or malignancy).

A biopsy is not routinely performed prior to treatment but is indicated in cases in which the diagnosis of condylomata acuminata is uncertain, in the presence of atypical features, in postmenopausal/immunocompromised patients or for lesions that are refractory to medical therapy.

Treatment

Treatment of vulvovaginal warts is mainly symptomatic, aiming to alleviate bothersome physical discomfort or psychological distress. Vulvovaginal warts are not known to pose a serious risk to health or fertility. Treatment is not indicated for asymptomatic genital warts that are diagnosed incidentally on genital examination. There is no evidence to support treatment of asymptomatic genital warts solely to eliminate infectivity and transmission to a sexual partner.

Prolonged treatment, with regular follow-up for 3–16 weeks, is key to achieving clearance of warts in 35–100% of patients.²⁷ This still does not guarantee eradication of all HPV-infected cells due to the clinical and histological presence of HPV-infected cells beyond the treated areas. Therefore, recurrence and transmission to sexual partners are still possible after the resolution of warts. Most genital warts are cleared within 2 years in immune-competent patients.²⁸

There are no consistent data that support medical vs surgical management of genital warts for all types of patients and all types of warts. Treatment choice should be based on the number, location and size of the warts, and the patient’s characteristics and preferences. Surgical therapy is usually offered to patients who have not responded to medical therapy or those with extensive and bulky lesions. Surgical management tends to be quick and has a high clearance rate, but no difference in recurrence rates has been demonstrated in comparison with medical therapy.²⁷

All therapy options available have been shown to be associated with localized discomfort, itching, erosions, pain and burning due to epithelial disruption.²⁷ Complications commonly associated with treatment include hyper- or hypopigmentation, chronic vulvar pain and scarring.²⁹ Single-line medical therapy is usually tried first. If complete clearance of warts has not been achieved within 3–12 weeks, another medical treatment may also be administered. Medical therapy can be grouped into two main categories: cytodestructive therapies (podophyllin, trichloroacetic acid, bichloracetic acid and fluorouracil) and immune-mediated therapies (imiquimod, sinecatechins, interferons, Bacillus Calmette–Guérin and HPV vaccine). Medical therapy is most useful in patients with limited disease. Podophyllotoxin, sinecatechins, imiquimod and topical interferon may be self-administered at home. Vulvar warts may be treated with all available medical treatment options, while vaginal warts may be treated with bichloracetic acid, interferons and trichloroacetic acid. Trichloroacetic acid is the preferred treatment option in pregnant patients, as it is not systemically absorbed and has no known fetal effects. Cytodestructive therapies are avoided in pregnancy.

Surgical therapy includes cryoablation (liquid nitrogen or nitrous oxide), laser ablation (carbon dioxide laser), electrocautery, ultrasonic aspiration using a cavitron ultrasonic aspirator, and excision. In cases of extensive disease, excision and ablation are commonly used together. The choice of surgical method depends on surgical experience, equipment availability and personal preference. The surgeon should be cautious when surgically managing vaginal warts, as deep vaginal tissue destruction can lead to fistula formation.

Surgical management can be offered to pregnant women and used on both the vulva and vagina. It requires fewer patient visits than medical management, even though repeat procedures may be needed, as with cryotherapy. Hypo- or hyperpigmentation is a disadvantage with ablative therapies and may affect patient choice. All surgical treatments require some form of anesthesia and often require access to an operating theater. A biopsy should be obtained prior to surgery if malignancy is suspected or in cases of uncertain diagnosis. A biopsy sample should be obtained before any surgical therapy, as obtaining a histological specimen is impossible after all surgical procedures except excision.

In cases of limited vulvar disease with five or fewer small warts, patients who can comply with self-administered therapy can be started on imiquimod or podophyllotoxin.³⁰ Patients who fail to complete self-administered therapy or cannot comply are best managed with trichloroacetic acid or cryotherapy.²⁷ Trichloroacetic acid alongside imiquimod is considered an effective combination to manage patients for whom cryotherapy failed as a monotherapy.³¹

In cases of limited vaginal disease, trichloroacetic acid is the preferred medical therapy. In cases for which surgical management is indicated, laser ablation is considered the best option due to its ability to reach the lesions within the vagina and the ability to control the depth of treatment. Surgical therapy is used in cases of extensive lesions (>20 cm²) and bulky disease. Recurrence is managed with the initial treatment that resulted in clearance of the condyloma.¹²

HERPES SIMPLEX VIRUS

Introduction

Genital herpes simplex is a sexually transmitted viral infection that is widespread globally and is considered a major public health problem. Most genital herpes is attributed to HSV‑2, but infection with HSV‑1 leads to clinically similar disease with an increased incidence of disease.³² HSV establishes a latent state that leads to viral reactivation and local disease recurrence. Significant morbidity and mortality have been documented after perinatal transmission of HSV,³³ and it has been linked with increased HIV transmission.³⁴

HSV infection is considered a primary infection when an infection is confirmed in a patient without pre-existing antibodies to HSV. When the acquisition of genital HSV‑1 occurs in a patient with pre-existing antibodies to HSV‑2 or vice versa, this is considered a non-primary HSV infection. Recurrent HSV infection is when reactivation of genital HSV occurs and is confirmed as being the same type as previously identified in the patient. Most cases of recurrence are caused by HSV‑2.³⁵

Epidemiology

Most HSV is transmitted by asymptomatic persons and those unaware of the presence of the disease.²⁹ Patients are three times more likely to have asymptomatic HSV‑2 infection if previously infected with HSV‑1.³⁶ It is estimated that 192 million people were infected with genital HSV‑1 and that between 596 and 656 million were infected with both genital HSV‑1 and HSV‑2 worldwide in 2016.³⁷

Viral shedding and transmission

Intermittent viral shedding can occur, in the absence of lesions, after resolution of the primary infection.^38,39 A prospective study on a university student population reported a transmission rate of 70% after sexual contact with an asymptomatic partner.⁴⁰ The risk of transmission was higher for male source partners compared with female source partners, and the rate of genital herpes acquisition was higher in patients lacking HSV‑1 and HSV‑2 antibodies.⁴⁰

HSV‑2 and risk of HIV transmission

There is a strong link between genital ulcers caused by HSV‑2 and an increased risk of co-infection with HIV‑1 (human immunodeficiency virus type 1). One study found a risk of acquiring HIV infection from patients with HSV‑2 seroconversion within 6 months of 22.6%, compared with 3.6% in those who are seronegative.⁴¹

Clinical manifestation

The clinical manifestations of genital HSV vary widely depending upon whether the infection is primary, non-primary or recurrent.

Primary infection

Primary HSV infection has a mean incubation period of 4 days before development of genital herpes, and tends to resolve after a mean of 19 days, with highly variable clinical manifestations.⁴² These range from severe symptoms with painful genital ulcers, dysuria, fever, tender local inguinal lymphadenopathy and headache, to mild, subclinical or entirely asymptomatic,⁴³ with no difference between HSV‑1 and HSV‑2.⁴⁴

The characteristic skin lesions start as clustered 2–4-mm vesicles with underlying erythema that progress to vesicopustules, erosions and ulcerations. Vesicles and pustules may exhibit a central depression, while erosions and ulcerations often have scalloped borders. In one review, patients with primary HSV infections had multiple bilateral, ulcerating, pustular lesions.⁴² Overall, 67% showed systemic symptoms, including fever, headache, malaise and myalgias, 98% showed local pain and itching, 63% showed dysuria and 80% showed tender lymphadenopathy.⁴³

Non-primary infection

Due to the presence of antibodies against one of the HSV types, non-primary first-episode infections cause fewer lesions and fewer systemic symptoms than primary infections.⁴³

Recurrent infection

Recurrent infection tends to start with prodromal symptoms such as tingling and shooting pains in the legs, hips or buttocks before eruption of the lesions. Recurrence of genital herpes is common, and tends to be less severe than both primary and non-primary infections. Lesions last a mean of 10 days, with viral shedding occurring for 2–5 days. Immunosuppressed patients are more likely to suffer from a higher recurrence rate.⁴³

Patients with HIV tend to have severe episodes that are prolonged, and are at higher risk for developing drug-resistant HSV.

Diagnosis

Given the variation in clinical manifestations of genital herpes, laboratory testing should be used to confirm the diagnosis. Cell culture and PCR are the preferred tests for those presenting with active genital herpes lesions. Viral culture of sampled vesicle fluid has a sensitivity of 50%. PCR is the most sensitive method and is able to differentiate between HSV‑1 and HSV‑2.

Serology is beneficial for identifying type-specific antibodies to HSV, which develop after the infection and persist indefinitely. Serology has aided in the increased accuracy of epidemiological studies. Alongside PCR, it may help to diagnose a history of previous genital herpes in symptomatic patients or those with atypical presentation, to determine the susceptibility of a sexual partner of a patient with documented genital HSV infection, and to identify asymptomatic HSV infection in pregnant women who are at risk of shedding at the time of delivery, with potential transmission to the infant.⁴⁵

Treatment

Topical therapy has shown only marginal benefits as a treatment for genital herpes, and thus has no role in treating genital herpes, especially in patients who are taking oral antivirals. Parenteral therapy with intravenous antivirals is reserved for patients with complications such as urinary retention, meningitis, or severe clinical manifestations of HSV infection.

Treatment of the first episode

Antiviral therapy should be started as soon as possible after lesion appearance, and within 72 h of the appearance of newly developing lesions. Use of oral antiviral therapy decreases the duration and severity of the disease by days to weeks. Oral antivirals do not eradicate the latent virus; therefore, the risk of recurrence is high.

The 2015 US Centers for Disease Control and Prevention (CDC) guidelines recommend any of the following oral treatment options:²⁹

• acyclovir: 400 mg three times daily or 200 mg five times daily
• famciclovir: 250 mg three times daily
• valacyclovir: 1000 mg twice daily (best for patient compliance)

Therapy should be administered for 7–10 days but could be extended for a further week if new lesions are still developing.²⁹

Treatment of recurrent infection

Treatment is determined on a case-to-case basis, and patient preference should be the main factor regarding the choice of therapy. Episodic therapy involves self-administered antiviral therapy for individual outbreaks as they arise. This is the preferred option for patients with infrequent/less severe recurrence and those who are not sexually active. Options include:

• acyclovir: 800 mg three times daily for 2 days, 800 mg twice daily for 5 days, or 400 mg three times daily for 5 days
• famciclovir: 1000 mg twice daily on one day, 125 mg twice daily for 5 days, or 500 mg once, followed by 250 mg twice daily for 2 days
• valacyclovir: 500 mg twice daily for 3 days or 1000 mg once daily for 5 days²⁹

Chronic suppressive therapy

Chronic suppressive therapy may be used for those with very frequent/severe recurrences and/or those who wish to reduce the risk of transmission to their HSV-uninfected sexual partner. Options include:

• acyclovir: 400 mg twice daily
• famciclovir: 250 mg twice daily
• valacyclovir: 500 mg once daily or 1000 mg once daily²⁹

HERPES ZOSTER

In this section, we discuss varicella zoster virus (VZV) as it pertains to genital herpes zoster. Further details of the disease are provided in the chapter on herpes, varicella and rubella on the GLOWM website.⁴⁶ 

Introduction

Herpes zoster is defined as the reactivation, within the sensory ganglion, of latent VZV infection. This reactivation leads to a painful, unilateral vesicular skin eruption that follows a restricted dermatomal distribution. The CDC has estimated that 30% of the population in the USA will have at least one episode of herpes zoster in their lifetime.⁴⁷ Its incidence has been growing globally in the older population, but less so in the younger population, which has been attributed to the global childhood immunization program.⁴⁸ The immune status of the host has a significant influence on the natural history of herpes zoster. Risk factors for reactivation of VZV include disease-related immunocompromise, age-related immunosenescence and iatrogenic immunosuppression.

Clinical presentation

In general, the first sign of herpes zoster is a burning or tingling type of pain. It starts in a specific location and spreads unilaterally, in most cases, along the dermatome of the infected ganglion. Systemic symptoms such as headache, fever and malaise may accompany the rash. Round/oval inflamed pink plaques are present at the sight of reactivation; between one and five vesicles appear on these pink plaques within 2 days and these have the potential to become pustular. The eruption continues for several days, and the vesicles tend to coalesce and form large bullae.⁴⁹ In the anogenital region, the blisters extend unilaterally from the buttocks to the labia majora and minora. The roof of the blisters may break down easily, leading to painful grouped erosions that are open with a loose scale on the surrounding area. These erosions finally crust over and heal, but may cause scarring and ulcerations.⁴⁹

Diagnosis

Diagnosis of herpes zoster is usually based on clinical examination. VZV is differentiated from HSV by the fact that vesicles caused by VZV follow a specific dermatome, while those caused by HSV cross the midline and are more limited. PCR, viral cultures and immunofluorescence may be used to differentiate between VZV and HSV.

Treatment of uncomplicated herpes zoster

Treatment of VZV aims to reduce the duration and severity of pain, enhance healing of the lesions, reduce the risk of chronic pain (post-herpetic neuralgia), reduce the risk of transmission by decreasing viral shedding, and prevent new lesions from forming.⁵⁰ Patients with encrusted lesions are unlikely to benefit from antivirals. Nucleoside analogs such as famciclovir, acyclovir and valacyclovir have been used to treat herpes zoster and are taken for 7 days. Patients who present within 72 h of the onset of clinical symptoms may benefit from antivirals, which have proven to be most effective in older patients who suffer more from post-herpetic neuralgia.^50,51 For patients who present more than 72 h after the onset of clinical symptoms, antivirals are considered beneficial if there is ongoing development of new lesions.⁵¹ Analgesia is an integral part of managing herpes zoster, and should be discussed with patients. Use of acyclovir is an option during pregnancy.⁵⁰ Superimposed bacterial infections with Staphylococcus and Streptococcus may be present, and antimicrobials can be prescribed alongside antivirals.

Reducing transmission may be achieved by providing advice on appropriate hygiene, such as covering the rash and washing hands regularly. Contact with pregnant women who have not had VZV or who are not immunized should be avoided, as well as contact with premature babies and immunocompromised persons.⁵²

BULLOUS IMPETIGO

Introduction

Impetigo is a superficial bacterial skin infection that is contagious. Bullous impetigo is caused by Staphylococcus aureus, and less commonly by streptococcal species (mainly group A). According to the World Health Organization, approximately 111 million children in developing countries have bullous impetigo at any given time.⁵³ It is more commonly found in crowded low-income areas, populations with poor hygiene, and areas with humid and warm conditions. A diagnosis of bullous impetigo in adults should prompt investigations for HIV if demographic risk factors are present.

Clinical features

Anogenital impetigo is seen on the keratinized skin of the labia, mons pubis and upper inner thighs. It appears as fragile, thin-walled vesicles and bullae that break down and leave round erosions. The erosions are known to have variable honey-colored crusting and scales. Folliculitis often occurs and presents as red papulae or pustules. In cases in which the bullae remain intact for several days, white blood cells accumulate within, and the blister fluid becomes yellow–white in color.⁵⁴

Diagnosis

The diagnosis of bullae impetigo is confirmed by growth of S. aureus or streptococcal species in cultures from swabs obtained from blister fluid or the surface of erosions.

Treatment and prevention

Whether topical or oral, antibiotic therapy aims to cover both S. aureus and streptococcal species. Oral antibiotics are reserved for cases with multiple lesions, while topical treatment with mupirocin or retapamulin can be used for patients with few lesions.⁵⁵ Prevention may be achieved by treatment with antibiotics, covering the lesions and good hand hygiene, and by washing linens, towels and clothes daily while also avoiding sharing them with other members of the household.

BACTERIAL VAGINOSIS

Introduction

Bacterial vaginosis is the commonest cause of abnormal vaginal discharge, accounting for 50% of cases in female patients of childbearing age.⁵⁶ Bacterial vaginosis has been linked to an increased rate of preterm birth and susceptibility to STIs. Symptoms range from bothersome to none at all. Bacterial vaginosis is characterized by:⁵⁶

• a shift in the vaginal microbiota from Lactobacillus species toward other bacteria
• production of volatile amines
• an increase in the vaginal pH to more than 4.5

Pathogenesis and microbiology

Dysbiosis and altered vaginal microbiota

Complex changes to the vaginal microbiota lead to bacterial vaginosis. The main bacteria identified in women with bacterial vaginosis are Bacteroides species, Prevotella species, Gardnerella vaginalis, Porphyromonas species, Mycoplasma hominis, Peptostreptococcus species, Clostridiales species, Megasphaera, Mobiluncus and Sneathia species and Ureaplasma urealyticum.⁵⁷

Production of amines

The hydrogen peroxide-producing lactobacilli play a crucial role in preventing the overgrowth of anaerobes in the vaginal microbiota. The loss of lactobacilli leads to an increase in the vaginal pH and overgrowth of the vaginal anaerobes. These anaerobes produce proteolytic carboxylase enzymes that breakdown peptides into volatile malodorous amines, leading to increased vaginal transudation and exfoliation of the squamous epithelium.⁵⁷ Risk factors for bacterial vaginosis include sexual activity, concomitant STIs, vaginal douching and cigarette smoking.

Clinical features

The majority of women with bacterial vaginosis are asymptomatic. Those who are symptomatic typically present with vaginal discharge with or without an unpleasant odor (often described as a ‘fishy smell’). The odor tends to be more noticeable during or after sexual intercourse. The discharge is thin, homogeneous and off-white.³⁷ Bacterial vaginosis can lead to:

• endometrial bacterial colonization
• plasma cell endometritis
• postpartum fever
• post-hysterectomy vaginal cuff cellulitis
• postabortal infection
• HIV acquisition and transmission
• pelvic inflammatory disease

Bacterial vaginosis is also a risk factor for the acquisition of STIs.

Diagnosis

The Amsel criteria⁵⁸ for diagnosis of bacterial vaginosis are:

• a homogeneous, thin, grayish-white discharge that smoothly coats the vaginal walls
• a vaginal pH >4.5
• A positive whiff amine test, defined as the presence of a fishy odor when a drop of 10% potassium hydroxide (KOH) is added to a sample of vaginal discharge
• The presence of clue cells on saline wet mounts

At least three criteria must be present. However, the gold standard for diagnosing bacterial vaginosis is Gram staining of vaginal discharge.⁵⁹

Recurrent bacterial vaginosis is diagnosed when a patient has had three confirmed bacterial vaginosis episodes within a year. Approximately 30% of patients suffer from recurrence of bacterial vaginosis within 3 months and 50% within 1 year after initial treatment. Causes of recurrence include non-adherence to treatment, reinfection through sexual intercourse, and relapse due to failure to eradicate the infection and establish the normal vaginal flora.⁶⁰

Treatment

The aim of treatment is symptom relief and reducing the risk of acquiring an STI. For symptomatic non-pregnant patients, metronidazole for 7 days or clindamycin for 5 days is the treatment of choice, either vaginally or orally, depending on patient preference. Latex condoms should be avoided when using clindamycin cream. For those who are asymptomatic, observation rather than treatment is preferred to avoid the patient developing a symptomatic yeast infection after antimicrobial administration. Asymptomatic bacterial vaginosis tends to resolve after several months without treatment.

In patients undergoing gynecological surgery, treatment with the above regimen is recommended in symptomatic and asymptomatic patients with confirmed bacterial vaginosis to reduce the risk of postoperative infection. In pregnant or lactating women, it is best to avoid screening for and treatment of asymptomatic bacterial vaginosis. For pregnant women with symptoms, it is recommended that bacterial vaginosis be treated to reduce the risk of preterm labor. Oral metronidazole 500 mg twice a day for 7 days or oral clindamycin 300 mg twice a day for 7 days are appropriate regimens.

There is insufficient evidence to support the use of probiotics to treat bacterial vaginosis;¹ however, a randomized trial by Cohen et al. showed a lower incidence of recurrence with use of Lectin‑V (Lactobacillus crispate CTV‑05) after treatment with metronidazole.⁶¹

Recurrent bacterial vaginosis

Patients with confirmed recurrent bacterial vaginosis must undergo induction therapy followed by a long-term maintenance regimen, comprising 0.75% metronidazole gel (5 g dose) or oral nitroimidazole for 7 days, followed by 0.75% metronidazole gel (5-g dose) twice a week for 4–6 months.

Treatment with vaginal boric acid alone is another option for both induction and suppression therapy, but has not been well studied. Boric acid may cause death if consumed orally, and therefore should be stored safely away from children. A triple-phase regimen is used, comprising induction with oral nitroimidazole for 7 days in total, alongside vaginal boric acid 600 mg once at night for 21–30 days. Patients are reviewed after the completion of the vaginal boric acid regimen to confirm whether they are in remission. Once remission is confirmed, treatment with 0.75% metronidazole gel (5 g dose) vaginally twice weekly for 4–6 months should be started immediately. If remission is not confirmed, cultures and possible drug resistance should be reviewed, and maintenance on the induction regimen should be considered until remission is achieved.

Use of vaginal acidifying agents has not shown any enhancement of cure rates in recurrent bacterial vaginosis, and vaginal douching should be avoided.^58,59

VULVOVAGINAL CANDIDIASIS

Introduction

Vulvovaginal candidiasis (VVC) is the second most common cause (after bacterial vaginosis) of vulvovaginal irritation, itching and vaginal discharge,⁶² and is characterized by inflammation in the presence of Candida species. Candida species are part of the normal vaginal flora in up to 25% of women; hence identifying Candida species on cultures alone is not indicative of pathology. VVC is not considered a sexually transmitted disease. Candida albicans is isolated in 80–92% of episodes of VVC in the USA, with Candida glabrata accounting for almost all of the remainder.⁶²

Risk factors

Risk factors for VVC include poor glycemic control in diabetic patients, use of broad-spectrum antibiotics, increased estrogen levels in pregnant women or patients on hormone replacement therapy, and immunosuppression. There is a genetic predisposition to recurrent VVC in patients with polymorphism in the SIGLEC15, mannose-binding lectin or TLR2 genes. The roles of sexual behavior, contraceptive devices and diet are less clear. VVC may be sexually transmitted to partners, but having multiple sexual partners does not increase the risk of acquiring VVC. The evidence supporting the risk of VVC after the use of tampons, menstrual pads or douching is weak and conflicting.

Clinical features

VVC predominantly presents as vulvar pruritus. Soreness, burning and irritation of the vulva are common, and may be accompanied by dysuria or dyspareunia. On physical examination, VVC manifests as erythema of the vulva and vaginal mucosa with vulvar edema.⁶³

Diagnosis

The diagnosis of VVC is based on the presence of Candida on wet-mount microscopy, Gram staining or culture of vaginal discharge in a woman with characteristic clinical findings.

Role of vaginal culture

There is no need for culture if microscopy shows yeast unless the patient has clinical features of VVC, normal vaginal pH, negative microscopy, or persistent or recurrent symptoms, as they may have a non-albicans infection that is resistant to azoles.⁵⁹ Self-diagnosis should not be encouraged, and patients are advised to seek medical advice.

Treatment

Topical and oral therapy for VVC have been shown to be effective treatment options with a cure rate of more than 90%.⁶⁴ In the absence of contraindications, oral therapy is the preferred option for many patients due to its convenience; however, topical treatment has been shown to have fewer systemic side-effects.⁶⁴

Uncomplicated infections

Uncomplicated infections⁶⁵ are best treated with a single dose of fluconazole 150 mg orally rather than multi-dose treatment and topical regimens. Criteria for an uncomplicated infection include all of the following:

• sporadic infection
• infrequent episodes (fewer than three episodes per year)
• mild to moderate symptoms
• probable Candida albicans infection
• healthy, immunocompetent and non-pregnant patients

Complicated infections

Individuals with complicated infections⁶⁵ tend to require treatment for more extended periods. The criteria for complicated infections are:

• severe signs and symptoms
• Any Candida species other than albicans
• pregnancy
• poorly controlled diabetes, immunosuppression (e.g. AIDS) or debilitation
• recurrent VVC (confirmed by culture three or more times within a year)

For those who are immunocompromised or suffering from severe symptoms, two doses of fluconazole 150 mg taken 3 days apart should suffice.⁶⁵

For Candida glabrata infection, intravaginal boric acid, nystatin pessary, amphotericin B or flucytosine cream should be considered as treatment options. For Candida krusei infection, treatment with a topical azole other than fluconazole should be considered, due to known resistance. For pregnant women, topical imidazole vaginally is the treatment of choice. Use of a nystatin pessary or an oral azole should be avoided.⁶⁵ A pattern of birth defects (abnormalities of the skull, bones, heart and face) has been reported after first-trimester exposure to high-dose oral azole therapy.⁶⁶ In addition, oral azole therapy in the first trimester should be avoided as extensive cohort studies showed a two- to threefold increased risk of miscarriage in those exposed to oral fluconazole in the first and second trimesters.⁶⁷

Patients on tamoxifen with recurrent VVC should be started on maintenance therapy as detailed below. Women who are breastfeeding can safely take fluconazole, as there is no evidence of an adverse effect on breastfed infants.

Recurrent VVC

For patients with recurrent VVC (three or more episodes/year), it is recommended that they be started on induction therapy with fluconazole 150 mg every 72 h for three doses, then maintenance fluconazole 150 mg once per week for 6 months. Attempts should be made to eliminate or reduce risk factors for infection. Assessing the drug minimum inhibitory concentration to adjust the dose of azole may be necessary for patients with refractory VVC with positive cultures for C. albicans. Sexual dysfunction and marital discord tend to accompany recurrent VVC, and such issues should be addressed.⁶⁵

Prevention

There is no role for oral nystatin in preventing VVC. Use of Lactobacillus has also not been found to help prevent post-antibiotic vulvovaginitis. For women susceptible to VVC after antibiotic therapy, fluconazole 150 mg orally at the start and end of antibiotic treatment is recommended for prevention.⁶⁸

TRICHOMONIASIS 

Introduction

Trichomoniasis, caused by the protozoan Trichomonas vaginalis, is a genitourinary infection and is the most common non-viral STI worldwide, affecting female patients more often than male patients. Trichomoniasis, alongside bacterial vaginosis and VVC, is one of the commonest infectious causes of vaginal symptoms among women of reproductive age. However, the infection may be asymptomatic.⁶⁹

The peak rate of detection is in women aged between 47 and 53 years of age. Trichomoniasis is predominantly sexually transmitted, and is identified in 70% of the sexual partners of infected female patients.⁶⁹ It is commonly found in conjunction with other STIs and bacterial vaginosis; therefore, screening for trichomoniasis should be offered to those with diagnosed HIV or risk factors for STIs.¹

Microbiology

The flagellated protozoa T. vaginalis commonly infects the squamous epithelial lining of the urogenital tract, but may also be found in the Bartholin glands, bladder and cervix. On a wet-mount slide, T. vaginalis appears as a pear-shaped or round organism with an undulating membrane and four anterior flagella that aid in its motility.⁷⁰

Clinical sequelae of infection

Untreated trichomonal vaginitis may lead to urethritis or cervicitis. Infection with T. vaginalis has been linked to a range of adverse outcomes, including post-hysterectomy cuff cellulitis or abscess, increased cervical neoplasia risk in the presence of high-risk HPV infection,⁷¹ infertility, atypical pelvic inflammatory disease and preterm birth, and may also increase susceptibility to HIV‑1 infection.⁷²

Clinical features

The clinical presentation ranges from severe inflammatory disease to an asymptomatic carrier state. Female patients tend to present with thin, malodorous, purulent discharge accompanied by pruritus, dysuria, burning, increased urinary frequency and dyspareunia. Male patients are often asymptomatic but may present with urethritis. The patient may be asymptomatic for up to 3 months after infection with T. vaginalis, making it challenging to identify the source of infection.^73,74,75,76 

Diagnosis

Evaluation of female patients with suspected trichomoniasis starts with wet-mount microscopy, as it is convenient and cost-effective, although less accurate than other methods. If wet-mount microscopy confirms the presence of motile trichomonads, no further testing is indicated. If the wet-mount microscopy is not diagnostic, nucleic acid amplification tests or cultures should be performed instead; the choice is based on cost and availability within local facilities. When considering a diagnosis of trichomoniasis, patients should also be tested for gonorrhea and chlamydia.

Laboratory testing for trichomoniasis is essential as the signs and symptoms of trichomoniasis are not specific or sensitive enough to make a clinical diagnosis.⁵⁹ Use of a nucleic acid amplification test is suggested, where available, in patients with clinical findings of elevated vaginal pH and an increased number of polymorphonuclear leukocytes in the absence of motile trichomonads and clue cells on wet-mount microscopy. Alternatively, antigen tests or DNA hybridization probes for diagnosing T. vaginalis may be used in the absence of nucleic acid amplification tests.

Treatment

Treatment aims to relieve symptoms, reduce the prevalence of T. vaginalis in the population and reduce the risk of sequelae. Therefore, treatment is indicated in both symptomatic and asymptomatic patients. For non-pregnant female patients and their sex partners, or in HIV-infected female patients, the treatment of choice is metronidazole, 500 mg twice daily, for 7 days. It is recommended that pregnant women who are symptomatic or have confirmed T. vaginalis infection be treated with a similar regimen. Oral administration has shown to be significantly more effective than topical administration.

Male patients with urethritis can use the same treatment regimen as non-pregnant women. A single-dose treatment with either oral metronidazole or tinidazole 2 g is preferred to improve compliance in both sexes.^1,77 For patients with refractory trichomoniasis, the dose and duration of metronidazole or tinidazole should be increased.

Sexual intercourse is best avoided until the patient and their partner complete treatment and their symptoms resolve; this generally takes about 1 week. Female patients should be retested 3 months later to confirm a cure.^1,77

Prevention

Reduction of the risk of acquiring T. vaginalis infection may be achieved by consistently using condoms and limiting the number of sexual partners. The rate of transmission has been found to be reduced with the use of spermicidal agents such as nonoxynol‑9.⁷⁸

BARTHOLIN GLAND ABSCESS

Anatomy

The Bartholin glands, also known as the greater vestibular glands, are located deep in the posterior aspects of the labia majora, and are the female homologs of the male bulbourethral glands. Their primary function is to secrete mucus, providing lubrication to the vagina and vulva. Each Bartholin gland is approximately 0.5 cm across, with a 2.5-cm duct that drains the mucus, and the glands are located at the 4 o’clock and 8 o’clock positions on the vulvar vestibule on each side of the vaginal orifice, just below the hymenal ring.⁷⁹ The Bartholin gland comprises multiple epithelial types. The body comprises mucinous acini, the duct is mainly transitional epithelium, and the orifice is squamous epithelium.⁸⁰ A Bartholin cyst forms when the duct becomes obstructed, and the mucus produced accumulates. This leads to cystic dilatation, which is usually sterile. A Bartholin cyst may become infected and form a Bartholin abscess.⁸¹ Polymicrobial infections and sexually transmitted infections (Chlamydia trachomatis and Neisseria gonorrhea) have been found to contribute to infections of the Bartholin glands, but Escherichia coli is the commonest pathogen isolated.^82,83

Cysts and abscesses are the commonest types of Bartholin gland masses, with abscesses being three times more common than cysts.⁸⁴ It has been estimated that 2% of patient visits to the gynecology clinic were due to a Bartholin cyst or abscess,⁸⁵ with a peak incidence around the time of the menopause.⁸⁶ There are no well-established risk factors for developing a Bartholin cyst or abscess, but a previous Bartholin cyst or abscess has been found to be a risk factor for recurrence of either.

Clinical presentation

Most Bartholin cysts are asymptomatic and painless and tend to be found on routine examination or by the patient. Larger cysts may cause discomfort during sexual intercourse or sitting. Some patients find cysts to be disfiguring, which may disrupt sexual function even when asymptomatic. Patients with a Bartholin abscess may present with severe pain, and complain of difficulty walking, sitting and having sexual intercourse.

Diagnosis

Diagnosis of a Bartholin cyst or abscess is based on the clinical findings at the time of examination.

A Bartholin cyst is a soft, non-tender, 1–3 cm-mass at the posterior aspect of the vaginal introitus, lower medial labia majora or lower vestibular area. Bartholin cysts are commonly unilateral and may drain clear or white fluid.

A Bartholin abscess tends to be 3–6 cm in diameter, soft, tender and warm. They are also commonly unilateral, and may present with cellulitis or lymphangitis. Where the abscess is large, expansion into the upper labia may occur. If the abscess is very close to the skin, ‘pointing’ may occur, followed by drainage of a yellow or green purulent discharge.

Cultures for aerobic bacteria and nucleic acid amplification tests for patients at risk of STIs are commonly performed to aid in antimicrobial management. This has also become important following the increase in methicillin-resistant S. aureus (MRSA) infections.⁸¹

A biopsy should be performed on any patient with suspected Bartholin gland malignancy. This biopsy may be obtained from the inner wall of the Bartholin gland at the time of incision and drainage, marsupialization or gland excision. Indications for biopsy include being postmenopausal, a mass with a solid component, a mass wall fixed to surrounding tissue, or a mass that is persistent despite treatment.

Treatment

Various treatment options exist for managing a Bartholin gland cyst or abscess. Incision and drainage, in conjunction with any other method that keeps the tract open, permit continued drainage of the mass contents and help reduce the risk of recurrence. In a meta-analysis that included approximately 700 patients with symptomatic Bartholin abscess or cyst, no surgical intervention was found to be more effective than others in preventing recurrence.⁸⁷ In many cases, patients present after spontaneous rupture and drainage of the cyst or abscess. These patients should be offered analgesia and advised to use warm compresses or sitz baths.

The size of the Bartholin mass and whether it is a cyst or a mass determines the initial management. A Bartholin cyst less than 3 cm in diameter is best managed expectantly. Patients are advised to use sitz baths or warm compresses to help resolve the cyst and aid drainage. A Bartholin abscess greater than 3 cm in diameter should be treated with incision and drainage alone, followed by sitz baths. A Word catheter cannot be inserted in many cases due to the size of the abscess.^87,88

Patients with a Bartholin cyst or abscess greater than 3 cm in diameter are best managed with incision and drainage, obtaining cultures, and placement of a Word catheter or marsupialization to aid with content drainage. Marsupialization should be considered for those with a latex allergy (which contraindicates use of the Word catheter). The efficacy of both methods is similar. However, marsupialization requires an operative setting for effective anesthesia, and is more invasive compared with use of local anesthetics in the office/clinic setting.⁸⁹

Antibiotic treatment is best avoided when possible in the initial management of a Bartholin cyst or abscess. However, patients with recurrence, large masses, risk factors for complicated infections or signs of systemic infection should be treated with the appropriate antibiotics.⁵⁵ Fasciitis and sepsis have been reported after drainage of a Bartholin abscess.^90,91 The choice of antibiotics should aim to treat staphylococcal and streptococcal species, enteric gram-negative aerobes and specific antibiotics in cases of chlamydia or gonorrhea.^90,91

Management of recurrent masses

Recurrence may occur immediately after treatment or after complete resolution of the first episode. Recurrences present with signs and symptoms similar to those of the initial occurrence. Bartholin cysts that recur without infection are managed expectantly or with incision and drainage. For patients with a recurrence of a Bartholin cyst that has become infected, management depends on patient preference and the number of recurrences. Those who present with a second episode and the presence of infection are best treated with adjunctive antibiotics, incision and drainage, and Word catheter placement or marsupialization based on patient preference. Those who present with a third episode are best treated with adjunctive antibiotics followed by marsupialization. If recurrence occurs after marsupialization, patients are best offered gland excision as a last resort, as it comes with the risk of bleeding, hematoma formation, dyspareunia, fibrosis and disfigurement.^92,93

Based on the results of a single study, pregnant patients have a low incidence of Bartholin gland abscesses (0.13%).⁹⁴ The microbiological characteristics are similar to those in patients who are non-pregnant, and the management is the same. Cyst excision is best avoided during pregnancy and in the immediate postpartum period due to the risk of excessive bleeding. Patients who are immunocompromised are also treated in the same way as fit and well non-pregnant patients.

PRACTICE RECOMMENDATIONS

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