This chapter should be cited as follows:
Selk A, Reardon J, et al, Glob. libr. women's med.,
ISSN: 1756-2228; DOI 10.3843/GLOWM.419993

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

Volume 12

Infections in gynecology

Volume Editors: Professor Francesco De Seta, Department of Medical, Surgical and Health Sciences, Institute for Maternal and Child Health, University of Trieste, IRCCS Burlo Garofolo, Trieste, Italy
Dr Pedro Vieira Baptista, Lower Genital Tract Unit, Centro Hospitalar de São João and Department of Gynecology-Obstetrics and Pediatrics, Faculdade de Medicina da Universidade do Porto, Portugal

Chapter

Other Sexually Transmitted Infections (Molluscum Contagiosum, Varicella Zoster, HIV, Mpox) and Ulcers

First published: July 2023

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INTRODUCTION

There are a number of infections that manifest with dermatologic findings on the genital skin. This chapter outlines the pathophysiology, epidemiology, clinical presentation, diagnosis and treatment of vulvar molluscum contagiosum, varicella zoster and infectious vulvar ulcers. Vulvar ulcers can be divided according to causative organisms: syphilis, human immunodeficiency virus (HIV), monkeypox, chancroid, granuloma inguinale and lymphogranuloma venereum. From this point forward, monkeypox will be referred to by the World Health Organization's (WHO) preferred term as of 2022, Mpox.¹

MOLLUSCUM CONTAGIOSUM

Pathophysiology

Molluscum contagiosum is caused by a DNA Poxvirus that is transmitted directly through skin-to-skin contact. Infections can manifest on the vulva, if spread through sexual activity, though inoculation can occur through shaving, scratching, and potentially fomite-based transmission like shared towels.² Cases of vertical transmission have also been reported.³ Infection mostly impacts skin, and rarely mucous membranes.⁴ The virus remains localized to the epidermis and does not appear to invade the basement membrane, thereby evading immune surveillance for much of the duration of infection. Long latencies between acquisition and symptoms have been reported at 2 months or longer.⁵ People with molluscum infections do develop antibodies but these titers do not relate to infection duration or severity.

Epidemiology

Viral infections occur most commonly in children with a range of incidence reported from 1.5–20%, and a worldwide prevalence of 3%.⁵ Adults represent a minor portion of infections. Other risk factors include immune-compromised status, those with atopic dermatitis, or individuals exposed to contaminated swimming pools.⁴

Clinical presentation

Symptoms of infection are minimal, though some endorse a mild pruritus. On exam, multiple skin-colored lesions are noted. Typically, they are small, 2–5 mm in size, well demarcated, smooth, dome-shaped lesions often. Lesions may have a central depression (“umbilicated” in appearance) especially larger, more mature ones. In children, these lesions are most commonly found on the trunk, whereas adults are more commonly affected in the genital region, buttocks, and medial thighs.

Diagnosis

Diagnosing molluscum is based on clinical history and examination. The differential diagnosis for small, raised, skin-colored lesions include human papillomavirus (HPV) infection, scabies, and lymphangiectasia. Clinical history and biopsy results can aid in differentiating these entities. Molluscum infection conveys characteristic histopathologic features² though biopsy is not usually necessary for diagnosis.

Treatment

In an immune-competent host, individual lesions resolve within 1–3 months. However, self-inoculation can occur with scratching or shaving so that apparent lesions are at different stages, and the total arc of infection can last up to 30 months. There is no evidence-based consensus on treatment⁴ and no intervention is necessarily recommended as lesions will resolve on their own in an immunocompetent person. However, for those who pursue therapy, there is a collection of proposed remedies. Below are some commonly accessed options, and a more exhaustive list of protocols can be found in this review.⁴

Curettage or surgical removal: this was found to be the most effective intervention compared to chemical or cryotherapy and should be considered if lesion number is small and/or confined to a small area.⁴

Cryotherapy: liquid nitrogen is suggested to be applied to each lesion and used as with the application to genital warts. Studied protocols involve a 10–20 second application to each lesion for up to two freeze–thaw cycles, repeated at 1-week intervals.

Chemical: note that care should be taken when applying these remedies to the skin, with judicial use confined to the lesions themselves. These interventions can lead to skin blistering, erythema, and changes to pigmentation of the skin and patients should be advised of these effects prior to embarking on treatment.

• Cantharidin 0.9% applied only to the lesion itself to avoid surrounding skin, applied over 2–3 repeat office visits approximately 1 month apart. Subsequently a blister will develop within 24 hours, and each lesion will slough off as the blister peels. Application is not painful though mild irritation can develop alongside the blister formation and sloughing. Some clinicians recommend a loose bandage over the treated lesions to prevent exposure of surrounding skin.⁵
• Trichloroacetic acid 85–100% applied judiciously only to the lesion itself to avoid surrounding skin. Application is painful but the mechanism is similar to cantharidin. Repeat in-office application after a 2-week interval may be required.
• Imiquimod 5% applied at home overnight to the affected area three times weekly on alternating days for up to 16 weeks. Advise patients to wash off the affected area in the morning upon waking.
• KOH 10% applied at home with cotton swab to all lesions twice daily until lesions begin to show inflammation/ulcerations.

Special considerations

In immunocompromised patients, lesions can be larger, more disseminated, and less likely to resolve on their own. Molluscum infection can indicate progressive immune compromise in HIV patients. Consider testing for HIV in patients with extensive or unresolving infection.

VARICELLA ZOSTER

Pathophysiology

Herpes zoster, or shingles, is caused when the varicella zoster virus (VZV) is reactivated from its latent state in the posterior dorsal root ganglion. Affected individuals have previously acquired primary varicella, usually in childhood. Most cases of zoster impact T3–L3 nerve roots and associated dermatomes, with rare involvement reported in the sacral nerve roots.^6,7 Of those with sacral involvement, vulvar manifestations of zoster are rare, with a few case reports in the literature describing genital manifestations in up to 2% of cases. Infection can impact skin and mucous membranes. Of note, primary varicella can be transmitted to non-immune individuals through contact with droplets from zoster lesions, which contain live virus.

Epidemiology

The incidence of herpes zoster in the general population has been reported at 3.2–4.2/1,000 patients per year.⁸ Varicella zoster largely occurs in older, or other immune-compromised populations such as those with HIV, or those requiring immune modulation as part of the medical management of autoimmune conditions.

Clinical presentation

Symptoms typically include a prodrome of pain (itching, irritation, burning) localized to the affected nerve root and associated dermatome. Occasionally, there may be a mild systemic prodrome of malaise and low-grade fever, but often there is no systemic sign of infection that accompanies the local prodrome. The prodrome is usually followed within 1–3 days by an eruption of erythematous papules and plaques, as well as grouped vesicles that can coalesce into bullae overlying a red base. Throughout the subsequent 3 weeks, the blisters crust and heal over. The distribution of lesions is usually unilateral and does not cross the midline. In immune-competent hosts, varicella zoster usually does not recur.⁵

Diagnosis

Diagnosis is typically based on clinical presentation, as well as confirmatory viral polymerase chain reaction (PCR) testing for VZV deoxyribonucleic acid (DNA), which is favored over viral culture because it is a more sensitive, expedient test. Optimal swab technique involves unroofing a vesicular lesion or a crusted lesion. Interestingly, biopsy of a lesion demonstrates classic characteristics, but is not distinguishable from herpes simplex virus (HSV) on histopathology.

Treatment

Acute pain management should be considered for affected patients including the range of acetaminophen, non-steroidal anti-inflammatories and narcotic options.

Recommended antiviral therapy

Therapy is recommended in elderly, or immunocompromised patients, and is considered optional in young healthy populations. Early diagnosis and treatment within 48–72 hours of lesion onset reduces the length of acute infection and potentially reduces the incidence of post herpetic neuralgia. After this window, it does not affect outcomes of duration or severity.⁵ Regimens are as follows:

• Acyclovir 800 mg PO 5 × daily for 7–10 days.
• Valacyclovir 1 g PO TID for 7–10 days.
• Famciclovir 500 mg PO TID for 7–10 days.

A vaccine exists to decrease the risk of reactivation of latent varicella zoster and is called the shingles vaccine. Where available, it recommended that adults over 50 are vaccinated and others over 18 who are immunocompromised.

Post-herpetic neuralgia

Pain localized to the area of infection can persist after the lesions are healed. This can affect up to 20% of patients and can last months to years. The approach to management should include the principles of managing chronic and neuropathic pain.

ULCERS

Sexually transmitted infections that are associated with genital ulcers include HSV, syphilis, HIV, chancroid, granuloma inguinale, lymphogranuloma venereum, and Mpox. HSV is covered in more detail in another chapter of this book and the rest will be reviewed below. In general, if any of these STIs are suspected or diagnosed, the person should be tested for other STIs (chlamydia,  gonorrhea, trichomoniasis, HIV, and syphilis) and sexual partners also need to be examined and tested/treated as appropriate.

Syphilis

Pathophysiology

Syphilis is caused by the spirochete Treponema pallidum. It is sexually acquired through breaks in the skin and quickly spreads distantly including the brain and can involve transplacental spread to a fetus in pregnant women.⁸ The average time between acquisition of syphilis and first symptoms is 21 days (range 10–90 days).⁹

Epidemiology

There has been a dramatic increase in rates of syphilis in the past 20 years. The highest rates are in men who have sex with men (MSM), however there are global increases in syphilis prevalence for MSM, heterosexual men and women, and in congenital syphilis.⁸ A recent global study of MSM looked at prevalence across 77 countries and found the global pooled prevalence between 2000–2020 was 7.5% (95% CI 7.0–8.0%) with ranges from 1.9% in Australia and New Zealand to 10.6% in the Caribbean and Latin America.¹⁰ Rates of syphilis have also increased in heterosexual men and women with rates in women in the United States doubling between 2014 and 2018.⁸ Worldwide at least 1% of pregnant women who attend care have syphilis, which is the second leading cause of stillbirth, and also leads to preterm birth, growth restriction, neonatal death, and significant morbidity in those that survive.¹¹ Other risks for syphilis are HIV infection and use of methamphetamines, intravenous drugs, and heroin.^8,12

Clinical presentation

Primary syphilis

Classically presents with a macule that becomes a papule and then ulcerates into a painless solitary chancre, which is firm and round. The lesion is ulcerated with a clean base and usually occurs on genital skin. It can also occur rectally, vaginally, peri-rectally, or orally and can sometimes be painful and may have multiple lesions. The lesion will usually heal over 3–6 weeks even if a person does not receive treatment. Local non-tender lymphadenopathy is common.¹³

Secondary syphilis

Can present with fever, lymphadenopathy, sore throat, hair loss, headaches, muscle aches, fatigue, a non-pruritic rash usually on the palms or soles (occurring 2–8 weeks after the initial chancre), condyloma lata (large raised gray or white lesions often in the mouth, underarm or groin, aphthae in the mouth, vagina or anus), and rarely, hepatitis or nephritis.^8,9

Latent stage

There can be no visible signs or symptoms of syphilis for years. This stage is broken down into early latent syphilis (initial infection occurred in the past 12 months), late latent syphilis (initial infection occurred more than 12 months ago), or latent syphilis of unknown duration.

Tertiary syphilis

While this is rare and can occur 10–30 years after acquiring syphilis, tertiary syphilis is very serious and can be fatal. It is characterized by end organ complications often affecting the cardiovascular or nervous system or the development of gummatous lesions, which are locally destructive granulomatous lesions most commonly in bones or skin.¹³

Diagnosis

The tradition sequence testing for syphilis is as follows. The first step in diagnosing syphilis is usually a blood test for non-treponemal antibodies. These are screening tests because they are not specific to Treponema pallidum (the cause of syphilis) and, therefore, a positive test needs to be confirmed with a secondary test. The most common non-treponemal screening tests are called either the rapid plasma reagin test and venereal disease research laboratory (VDRL) test. If one of these screening tests is positive, treponemal antibody tests are then used to confirm infection, but treponemal antibodies stay positive forever even after treatment and thus cannot distinguish new from old infection. In a patient with treated syphilis, history, physical examination, and the use of non-treponemal testing helps distinguish a new infection. Dark field microscopy uses a sample from a skin sore or lymph node looking for the treponemal organism with a special microscope, but this is difficult for many in the world to access. PCR testing of lesions, fluid or affected tissue is available in some places.⁹
An alternative way of testing for syphilis is called the reverse screening algorithm. This involves starting with a treponemal test such as an antibody test (IgG by ELISA) and, if negative, then retesting in 3–12 months if the patient has risk factors for syphilis, versus if the ELISA is positive, then go on to non-treponemal testing such as rapid plasma reagin (RPR) with a reflex titer. If the RPR test is positive, syphilis is likely; while, if it is negative, then Treponema pallidum antibodies are ordered and, if those are reactive, then syphilis is likely and, if they are negative, then syphilis is unlikely and the IgG is thought to have been a false positive.

Treatment

The goal of treatment is to prevent disease progression but it does not repair damage that has already occurred. From the Center for Disease Control (for adults and adolescents):⁹

Primary, secondary, or early latent syphilis

• Benzathine penicillin G 2.4 million units administered intramuscularly in a single dose

Late latent syphilis or latent syphilis of unknown duration

• Benzathine penicillin G 7.2 million units total, administered as three doses of 2.4 million units administered intramuscularly each at weekly intervals

Neurosyphilis, ocular syphilis, or otosyphilis

• Aqueous crystalline penicillin G 18–24 million units per day, administered as 3–4 million units intravenously every 4 hours or continuous infusion, for 10–14 days

There are no good data regarding response to alternative treatments and in the case of severe penicillin allergy consultation with local infectious disease experts is important. It is important that those receiving treatment abstain from sex until lesions have healed and all sexual partners should be notified for testing and treatment if required.

Human immunodeficiency virus

Pathophysiology

Human immunodeficiency virus is a ribonucleic acid (RNA) retrovirus that attacks the immune system and impairs immune cells, specifically CD4+ T lymphocytes.¹⁴ If not treated, it develops into acquired immunodeficiency syndrome (AIDS), which is life-threatening. Transmission of HIV is by exposure to bodily fluids including blood, breast milk, semen and vaginal secretions, as well as vertical transmission during pregnancy.¹⁵ It is considered a STI.

Epidemiology

There is a global epidemic of HIV and the incidence in women in particular is increasing. In 2021, 38.4 million people worldwide were living with HIV.¹⁵ That same year, 650 000 people died from HIV-related causes.¹⁵ Africa is disproportionately affected compared to the rest of the world, with two thirds of those living with the virus worldwide living there.¹⁶ Risk factors for contracting HIV include high-risk sexual behaviors including sex work, having other STIs, injectable drug use, undergoing unsterile medical procedures that involve exposure to blood, living in prison and other closed settings, men who have sex with men, and being trans and gender diverse.^15,17 HIV transmission can be prevented by antiretroviral treatment for those living with HIV. When viral load is suppressed to less than or equal to 1,000 copies/ml (or undetectable), transmission of the virus does not occur.¹⁷ Other methods to reduce transmission include proper use of condoms or dental dams, pharmacologic pre-exposure prophylaxis and post-exposure prophylaxis, voluntary male medical circumcision (recommended in areas of active epidemic), and use of sterile needles and syringes.^14,17

Diagnosis

The American Centers for Disease Control and Prevention recommends that all individuals seeking STI screening be tested for HIV, regardless of behavioral risk factors.¹⁴ For those at higher risk, annual testing should be considered. The WHO recommends screening for HIV, syphilis and hepatitis B surface antigen, chlamydia and gonorrhea at least once per pregnancy.¹⁷ A variety of types of HIV tests are acceptable including lab-based antigen/antibody assays, self-tests and rapid diagnostic tests. The chosen test should be used as part of a testing algorithm with appropriate confirmatory testing.¹⁷ HIV tests can be negative in the early acute phase of infection, so if negative, it may need to be repeated.¹⁴ At time of diagnosis, referral should be made immediately to a healthcare provider specializing in HIV care.¹⁴

Presentation

In the weeks after infection with HIV, non-specific flu-like symptoms may develop including fever, malaise, lymphadenopathy, arthritis, rash, or sore throat.¹⁴ Infection can be asymptomatic. As HIV progresses, opportunistic infections with characteristic presentations, including vulvar ulcers, can occur (see Special Considerations, below).

Treatment

HIV can be managed but not cured. Lifelong antiretroviral therapy should be initiated at the time of diagnosis with HIV for all, including pregnant or breastfeeding individuals and regardless of CD4 cell count.¹⁷ On appropriate treatment, lifespan is nearly normal and sexual transmission is prevented.¹⁶ From a gynecologic perspective, people with HIV are eligible to use all categories of contraception including hormonal and intrauterine devices.¹⁶ For patients living with HIV, screening should be done at least annually or more frequently based on risk factors for syphilis, chlamydia, gonorrhea, and trichomonas infections,¹⁸ and be screened for cervical cancer according to local guidelines (typically more frequently than baseline screening).

Special considerations

The following conditions relevant to gynecologic practice are important to recognize in patients living with HIV so they can be managed appropriately, and also to consider testing for HIV when the clinical situation dictates. Importantly, the presence of STIs in a person with HIV can increase viral concentration in the genital tract and increase risk of transmission, while the presence of untreated STIs including syphilis or HSV approximately triple the risk of acquisition of HIV for someone without the infection.¹⁷

Herpes simplex virus

HSV is a common co-infection with HIV, ranging from 52–95% prevalence.¹⁶ Compared to the typical lesions of HSV, these patients may develop chronic ulcers¹⁹ or disseminated infection.¹⁶ Any ulcer persisting longer than 1 month in a patient with HIV should be tested for HSV,¹⁵ ideally by PCR test taken from the base of a lesion.¹⁹ Cytomegalovirus can also cause large, chronic ulcers in immunosuppressed people but this is rare.¹⁹ Lesions may begin as vesicles that coalesce and deepen into large, well-demarcated ulcers on the anogenital skin.¹⁹ Pain may be less severe than in immunocompetent patients.¹⁹ Lesions can also be exophytic nodules or papules and may be confused for malignancy.¹⁹ Treatment with oral antivirals, such as acyclovir, valacyclovir, or famciclovir (taken until fully healed) can lead to complete resolution and can be started prior to results of diagnostic testing.¹⁹ Treating HSV co-infection is important and can delay progression to AIDS.¹⁶

Human papillomavirus

Genital warts are usually caused by low-risk HPV genotypes. High-risk genotypes can cause high-grade lesions that may progress to cancer. Both high- and low-risk genotypes can be present together.¹⁹ In patients living with HIV, genital warts may be larger, more widespread and keratotic.¹⁹ The lesions can coalesce to form plaques.¹⁹ Diagnosis of genital warts is usually clinical, but if there is concern for dysplasia there should be a low threshold to biopsy.¹⁹ Treating genital warts does not eradicate HPV, but it may be necessary if lesions are becoming infected or obstructing.¹⁹

Regarding high-risk HPV infections, people living with HIV have a six-fold increased risk of developing cervical cancer,²⁰ a 20-fold increased risk of developing an anal cancer¹⁷ and also have an increased risk of vulvar cancer.²¹ In general, cervical cancer screening should occur earlier in life and more frequently than in immunocompetent individuals because precancerous lesions develop at a younger age and progress to being cancerous more quickly.²¹ High-grade squamous epithelial lesions and anogenital squamous cell carcinomas may initially appear like genital warts but be larger, grow faster, and not respond to wart treatments,¹⁹ and there should be low threshold to biopsy. Lesions that are hyperkeratotic, ulcerated, or large lesions should be biopsied in multiple locations or excised to rule out cancer.¹⁹

Syphilis 

Presence of syphilis infection increases the chance of acquiring HIV by 2.5-fold and is present in 12.4–15.7% of patients with HIV.¹⁶ Clinical presentation is typical of patients without HIV and treatment is also the same. Providers should be aware there is an increased risk of false positives of non-treponemal tests for syphilis.^15,18 Patients with HIV are at risk of faster progression to more advanced stages of syphilis.¹⁶

Other genital infections

A number of other genital infections are more common or more severe in patients living with HIV and in general require more intense or prolonged treatment. Presence of bacterial vaginosis (BV) increases risk of both spreading and contracting HIV and infection tends to be more persistent.¹⁶ BV treatment is the same regardless of HIV status. In patients living with HIV, pelvic inflammatory disease (PID) is more likely to occur and may present with a more severe course with tubo-ovarian abscesses being more common.¹⁶ Trichomonas infection is also more common in patients with HIV and associated with developing PID.¹⁸ Molluscum contagiosum is more severe in patients living with HIV.¹⁹ Lesions may persist, be larger, coalesce into plaques and be more widespread on the body and biopsy may be needed for diagnosis.¹⁹ 

Mpox (formerly Monkeypox)

Pathophysiology

The mpox virus is a DNA orthopoxvirus with symptoms similar to smallpox. Zoonotic transmission (mammal to human) can occur via contact with blood, bodily fluids, or lesions.²³ Human-to-human transmission can occur by exposure to respiratory droplets, short-range aerosols or contact with lesions and via fomites.^23,24 The first documented sexual transmission occurred in 2022 and was due to a new viral lineage, clade IIb.²⁴ Vertical transfer can occur across the placenta and congenital mpox can be fatal.²⁵ For sexually transmitted mpox, incubation is about 6–9 days, with significant transmission occurring prior to onset of symptoms.²⁶ The infectious period ends when all skin lesions are scabbed over and re-epithelialized.²⁴

Epidemiology

The first documented mpox infection in humans was in 1970.²³ It is endemic to some African countries and many previous outbreaks were in Africa, related to zoonotic spread. The first outbreak outside of Africa was in 2003.²³ A worldwide outbreak in over 100 non-endemic countries began in May 2022, mainly in clusters of MSM.^23,24 The WHO declared the outbreak a Public Health Emergency of Concern in July 2022.²⁷ 97% of mpox infections have been in men,²⁴ but infections have also been documented in cis women, non-binary individuals, and transwomen.²⁸

Primary prevention of mpox involves avoiding close contact (sexual or otherwise) with individuals who are infected, and vaccination with the smallpox vaccine. Three smallpox vaccines have been used since the 2022 monkeypox outbreak: ACAM2000, MVA-BN, and LC16.²⁹ The WHO recommends primary preventive vaccination for men who have sex with men with multiple sexual partners, sex workers, and other healthcare workers or lab personnel at risk of exposure.²⁹

Clinical presentation

Mpox symptoms last 2–4 weeks.²⁴ The sexually transmitted form of mpox may present with painful lesions as the first symptom.²⁶ There can be a prodromal phase, lasting 1–5 days, with symptoms including fever, headache, sore throat, myalgia, fatigue, and prominent lymphadenopathy.^23,24,28 Lesions progress from macules to papules, vesicles and then pustules and ulcers prior to crusting over and falling off.²⁴ Infection without rash can also occur.²⁸ Lesions range from less than 10 to more than 100 and can leave scars.^28,30,31 They are firm or rubbery, with well-circumscribed edges and can be umbilicated.³¹ They can be single or coalesce and may appear in various stages at the same time.³¹ In its sexually transmitted form, lesions are commonly genital (55–61%) or on the extremities (50–60%), and can be perianal, oropharyngeal, and on the face or trunk.²⁴ Notably, lesions can appear on the palms or soles.²⁴ Location may reflect type of sexual activity during exposure and could be vaginal, vulvar, anal, rectal, or oral.²⁸

Diagnosis

In the presence of symptoms as described above, mpox should be considered.²³ Women or non-binary individuals may be more likely to be misdiagnosed or experience delayed diagnosis,²⁸ emphasizing the importance of considering mpox as a diagnosis. Conditions with overlapping features include varicella zoster, measles, hand, foot, and mouth disease, herpes simplex virus, bacterial skin infections, disseminated gonococcal infection, chancroid, lymphogranuloma venereum, granuloma inguinale, molluscum contagiosum, and syphilis.^23,28 Suspected cases should be examined in a well-ventilated area with appropriate personal protective equipment.^23,30 Examination should include a full-body skin exam including looking at the genital and perianal skin, oral mucosa, and a lymph node exam. Preferred diagnostic test is a PCR sample from skin or mucosal lesions.²³ If skin lesions are not present, PCR swabs can be done of the oropharynx, anus, or rectum.²³ PCR blood-testing is not recommended because of low circulating viral loads. One case of mpox is considered an outbreak and the WHO recommends reporting suspected cases immediately to public health authorities.²³

Treatment

Post-exposure preventive vaccination is recommended for all contacts of cases.²⁹ Most cases of mpox are mild and managed supportively.³² The disease is self-limited. Risk factors for severe infection for mpox are young age, living with untreated HIV or being pregnant, breastfeeding or being immunocompromised.^23,29,30 1–13% of cases require hospital admission for management.^24,28 Antivirals and immune globulin have been used experimentally for treatment and prevention of severe disease,^30,32,33 but studies are ongoing and this is an area of active research. Testing for other STIs should be considered at time of testing for mpox, including HIV because of high rates of co-infection.³¹

Complications of mpox include severe anorectal pain or proctitis, sore throat, difficulty swallowing or breathing, genital edema, skin necrosis, secondary bacterial infection, and conjunctivitis.^24,33 Meningitis, encephalitis, and seizure are possible.²⁸ Scarring and strictures can cause difficulty swallowing, urinating, or passing bowel movements.³³ Fatality rate is less than 1% for the clade IIb outbreak.²⁴

Chancroid

Pathophysiology

Chancroid is a sexually transmitted genital infection caused by the Gram-negative bacteria Hemophilus ducreyi. It infects humans through disrupted skin or mucosa.³⁴

Epidemiology

Chancroid has been dramatically decreasing in the world since the WHO recommended treatment of all genital ulcer disease in the year 2000 and is extremely rare in high-income countries.³⁵

Clinical presentation

Painful red papules develop in the genital areas 3–7 days after infection. The papules become pustules and then rupture leaving painful ulcers that may have irregular edges. The ulcers can bleed if scraped and often have purulent discharge.³⁴ Painful inguinal lymphadenitis may also be present and is more common in men than women and is usually unilateral.³⁴ Self-inoculation can lead to more lesions and gangrene can occur.³⁵

Diagnosis

The most accurate test (most sensitive and specific) is PCR of exudate from the lesion but this is not available in most places.³⁵ Often treatment is empiric if clinical presentation is suggestive of chancroid.

Treatment

Recommended regimens according to the American Centers for Disease Control and Prevention:³⁶

• Azithromycin 1 g orally in a single dose.
• Ceftriaxone 250 mg IM in a single dose.
• Ciprofloxacin 500 mg orally twice a day for 3 days.
• Erythromycin base 500 mg orally three times a day for 7 days in a single dose.

Patients with coexisting HIV infection and uncircumcised men may require longer courses of therapy.³⁶

Granuloma inguinale (Donovanosis)

Pathophysiology

Granuloma inguinale is an ulcerative disease caused by the intracellular Gram-negative bacterium Klebsiella granulomatis (formerly known as Calymmatobacterium granulomatis). It is generally spread through sexual contact and through feces (either from direct contact or anal sex).

Epidemiology

It is rare with most cases occurring in tropical and subtropical areas. It is more common in women than men.

Clinical presentation

Granuloma inguinale usually presents a papule or subcutaneous nodule in the genital area that develops into painless ulcers with the median incubation time of 50 days. The ulcers will continue to enlarge without treatment. There are four different presentations (ulcerogranulomatous, hypertrophic, necrotic, and sclerotic). The most common presentation (ulcerogranulomatous) involves beefy red ulcers that bleed. In the hypertrophic subtype, the ulcers have irregular raised edges or large vegetating masses. The necrotic subtype has a deep and foul-smelling ulcer. With the sclerotic (cicatrical) type significant scarring develops.³⁴ Granuloma inguinale ulcers appear on the genitals in most cases while a minority of cases have inguinal ulcers.³⁷ Complications include bleeding, secondary infection, swelling, and destruction of architecture.³⁴

Diagnosis

Generally, diagnosis is made by direct microscopy of Giemsa-stained crushed tissue smear looking for characteristics Donovan bodies or by histological examination of a tissue biopsy.

Treatment

Azithromycin 1 g orally once a week for three weeks or 500 mg daily for greater than 3 weeks until all lesions are cleared is the recommended treatment.³⁸ Relapses can occur 6–18 months after treatment.³⁸ Alternative regimens involve doxycycline, erythromycin base, and trimethoprim-sulfamethoxazole.

Lymphogranuloma venereum (LGV)

Pathophysiology

LGV is caused by Chlamydia trachomatis serotypes L1, L2 or L3. It is acquired through sexually activity and enters the host through breaks in the skin or mucous membranes. It then spreads through the lymphatic system to regional lymph nodes.³⁴

Epidemiology

LGV is endemic in parts of Africa, Asia, South America, and the Caribbean but has been increasing in industrialized countries in MSM.³⁹

Clinical presentation

The clinical course of LGV is divided into three stages. In the first stage (incubation period of 3–6 days) papules, pustules or shallow ulcers develop that heal quickly without scarring. The secondary stage appears 2–6 weeks after the primary infection with painful and swollen lymph nodes in the groin, which can be unilateral or bilateral. Systemic flu-like illness can develop. Painful buboes, which are inflammatory swelling of the glands around the groin, can develop and rupture.³⁴ Those with anal acquisition can develop rectal discharge, pain, bleeding, constipation, and symptoms of proctocolitis.³⁴ Tertiary infection results from prolonged untreated infection and leads to strictures, fibrosis, abscess, fistulas, infertility, and other complications.³⁴

Diagnosis

When LGV is suspected a C. trachomatis nucleic acid amplification test should be taken from the affected site (genital or oral lesions, rectal specimens, and lymph node specimens-swab or bubo aspirate).⁴⁰

Treatment

When LGV is suspected it should be treated presumptively, i.e., before confirmatory testing is available.⁴⁰ This includes those with symptoms or signs of proctocolitis, severe inguinal lymphadenopathy with buboe formation especially if recent history of genital ulcer or if genital ulcer is present and other causes have been ruled out.⁴⁰ The goal of treatment is to cure the infection and prevent further tissue damage. Buboes may need to be aspirated or undergo incision and drainage to prevent formation of large ulcers.⁴⁰ The recommended treatment is doxycycline 100 mg orally twice a day for 21 days.⁴⁰ Alternative regimens include azithromycin or erythromycin base.

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