MANAGEMENT OF INFECTIVE AND NON-INFECTIVE GENITAL CONDITIONS
Genital ulceration
Joanna Rees
Raj Patel
Abstract
Genital ulceration can represent one of the more complex presenta-
tions encountered within genitourinary medicine. There are a wide
range of causes, which can make accurate diagnosis a challenge.
These include common and rare sexually transmitted infections
(STIs), dermatological conditions and trauma. This chapter aims to
provide an overview of genital ulceration secondary to STIs. The
most common causes of genital ulceration secondary to STI diagno-
ses in the developed world are genital herpes, primary syphilis and
lymphogranuloma venereum. Rarer STI presentations of donovanosis
and chancroid typically present in travellers returning from endemic
areas. We highlight the typical course and pattern of symptoms for
each diagnosis alongside relevant diagnostic tests and current recom-
mended treatment regimens. When not caused by an STI, genital ul-
ceration can occur following local trauma or as a manifestation of an
underlying dermatological condition.
Keywords Chancroid; donovanosis; genital herpes; genital ulcera-
tion; herpes simplex type 1; herpes simplex type 2; lymphogranuloma
venereum; MRCP; primary syphilis; tropical STIs
Genital ulceration
Genital ulceration can represent one of the more complex pre-
sentations encountered within genitourinary medicine. A wide
range of aetiologies are identified in the pathogenesis of the
presentation, which can make accurate diagnosis a challenge.
These include common and rare sexually transmitted infections
(STIs), dermatological conditions and trauma. This chapter aims
to provide an overview of genital ulceration secondary to STIs.
In assessing any patient presenting with genital ulceration, a
clinician should ensure that a comprehensive sexual history is
taken, including an up-to-date travel history. This should be
coupled with a thorough examination of both genital and extra-
genital skin.
The course and pattern of symptoms aid in diagnosis. Cat-
egorizing symptoms into painful or painless ulceration and
whether there is involvement at multiple or single sites can help
to narrow the possible causes. The most common causes of
genital ulceration secondary to STI diagnoses in the developed
world are genital herpes, primary syphilis and lymphogranu-
loma venereum (LGV). Rarer presentations of donovanosis and
Joanna C Rees MBBS MRCP is a Specialist Registrar at the Royal
South Hants Hospital, Southampton UK. Competing interests: none
declared.
Raj Patel MB ChB FRCP is a Consultant in Sexual Health and HIV
Medicine at Solent NHS Trust, Southampton UK and Senior Lecturer
in the Department of Medicine at the University of Southampton.
Competing interests: none declared.
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Key points
C The differential diagnosis of genital ulceration is wide; causes
include sexually transmitted infections, dermatological condi-
tions and trauma.
C The most common cause of ulceration is genital herpes sim-
plex infection. Syphilis and lymphogranuloma venerum are
other important infective causes.
C When individuals are diagnosed with herpes simplex virus it is
essential that they are counselled regarding natural history,
transmission and complications.
C An accurate travel history is essential for any individual pre-
senting with genital ulceration to consider investigation for
rarer tropical sexually transmitted infections (STIs), donova-
nosis and chancroid. A relapsing course, the involvement of
multiple mucosal and extragenital sites makes a non-STI cause
more likely.
chancroid typically present in travellers returning from endemic
areas.
It is recognized that the presence of genital ulcer disease in-
creases the risk of both acquisition and transmission of human
immunodeficiency virus (HIV). Therefore both initial exclusion
and appropriately timed follow-up to exclude HIV should be
performed in individuals identified as at risk.
Genital herpes
Genital herpes simplex virus (HSV) is the most common cause of
genital ulceration, with local, systemic and psychosexual com-
plications. It is caused by HSV type 1 (HSV-1) or type 2 (HSV-2).
Historically, most HSV-1 infections manifested as oropharyn-
geal infection in childhood, with a typical presentation of recur-
rent cold sores. Over time, oropharyngeal infection has become
less common, resulting in increased susceptibility to HSV-1 at
sexual debut. In the UK, HSV-1 is now the principal cause of first-
episode genital infection in most young men and women.
Although initial infections with HSV-1 and HSV-2 disease are
indistinguishable, HSV-2 disease is likely to recur most frequently.
Natural history
The herpesviruses cause latent and recurrent infections in
humans and animals.1,2 They comprise three subfamilies (a, b,
g). HSV is a human a-herpesvirus.
Following initial infection, replication of HSV at the portal of
entry results in infection of sensory nerve endings.2 The virus
enters into the distal axonal processes of the sensory neurone
and travels to the dorsal root ganglion, where it remains in a
latent state.2 The virus periodically reactivates, travelling down
the axon and into the basal skin layers.2 On virus reactivation,
some patients develop symptoms, whereas others remain
asymptomatic. In cells outside the sensory nervous system, a-
herpesvirus infection does not achieve latency, because viral
replication leads eventually to cell death through lysis.2
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 MANAGEMENT OF INFECTIVE AND NON-INFECTIVE GENITAL CONDITIONS
Transmission occurs through genital-to-genital and orogenital
contact.1e3 It is most likely when there are visible lesions, but
most transmissions occur in the absence of local symptoms in the
source partner. Infectivity is increased in the prodrome and
immediately after lesion healing. Viral shedding has been shown
to occur on an average of 2% of days in the absence of symptoms
or visible lesions.2 Several factors affect transmission:
 Infection is more easily passed from male to female than
from female to male individuals.2
 The impact of previous infection with the other viral type
on a partner’s susceptibility has not been clearly estab-
lished. However, subsequent infections tend to be milder.
The risk of infection remains high, and the overall average
annual risk of disease acquisition is about 10% per year of
exposure, regardless of previous HSV infection.2
 It is generally believed that there is little risk of reinfection
when the partner has already been infected with the same
viral type. Laboratory studies show that immunity to
subsequent reinfection is present at the site of initial
infection but can be overcome.2
The incubation period of HSV infection is 5e14 days and the
average untreated episode lasts 22e28 days.1e3 Fewer than 50%
of those infected with HSV develop signs or symptoms during
initial acquisition.1e3
The frequency and severity of recurrent episodes vary widely
between patients and also vary in an individual over time.3
Genital recurrences are the most common in individuals infec-
ted with HSV-2, particularly in the months immediately after the
initial infection. On average, patients experience 0.34 recurrences
per month, which is approximately four recurrences per year
with HSV-2.3 Recurrence is four times less frequent with HSV-1.3
A significant proportion of patients suffer 12 or more episodes
per year.3 Recurrence rates typically decline over time, but this is
variable.3
Transmission in pregnancy should be avoided where
possible.3 Transmission in the third trimester of pregnancy
carries a significant risk of transmitting HSV to the neonate if
vaginal delivery is attempted.3 Mother-to-baby transmissions are
rare, but because of the serious consequences of neonatal dis-
ease, expert advice should be sought in relation to all third-
trimester acquisitions to reduce risk at delivery (which in
these cases needs to be by caesarean section).2,3 The risk of
recurrent infections at term is small, and many guidelines now
emphasize the relative safety of a conservative approach to
delivery e even in the presence of a suspected genital HSV
recurrence.2,3
Strong epidemiological data implicate HSV infection in either
partner as facilitating both the transmission and acquisition of
HIV.1e3 The background prevalence of HIV worldwide varies
proportionately with HSV-2 prevalence. It is estimated that HSV
accounts for 30% of HIV, and that the presence of genital HSV
doubles the risk of HIV acquisition.2
Epidemiology
The prevalence of HSV infection worldwide is highly variable.
Reports from Public Health England indicate that the incidence of
genital herpes infection in the UK have been relatively stable in
men and women since 2013, following a period of increasing
incidence from 2007 to 2012.2 Rates of HSV-2 in both Germany
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and the USA are, however, declining. Because of the variability
of symptoms, a significant proportion of those affected remain
without a diagnosis, as only a minority present for clinical
evaluation. Studies have shown that <30% of HSV-2-
seropositive individuals are aware of their genital herpes, and
20% have no symptoms.1e3
Clinical features
Primary genital infection: the ‘first episode’ of HSV infection is
defined as the first presentation with symptoms and signs of
infection. This could be at initial acquisition of HSV or some time
after initial exposure.1e3
Initial erythematous papules form, followed by a character-
istic eruption of herpetic vesicles.1e3 At the time of clinical pre-
sentation, the vesicles have usually ruptured, and the resulting
ulceration is the dominant feature.2,3 (Figure 1) Herpetic ulcers
are intensely painful; the typical appearance is a superficial ulcer
with an erythematous outline and a greyish base.2,3 Lesions tend
to be bilateral and painful, with associated tender inguinal
lymphadenitis.1e3 Symptoms of primary genital herpes are usu-
ally severe; they are typically more severe in women and ho-
mosexual men, in whom larger areas of epithelium are often
involved.2 The most common systemic symptoms are headache,
malaise and photophobia, which are reported in up to 10% of
patients.2
Local complications, particularly candidal fungal infections
and streptococcal bacterial superinfection, are common, typically
presenting in the second week of lesion progression.2 Severe
external dysuria can lead to urinary retention in the absence of
neurological involvement.2 Extensive ulceration can occasionally
result in labial and vaginal adhesions. Uncircumcised men can
develop phimosis and paraphimosis. Up to 10% of patients
develop lesions in distant sites, particularly the pharynx. Up to
one-third of individuals with severe primary HSV have symp-
toms suggesting meningeal irritation, although few require hos-
pitalization.2 Autoinoculation to fingers and adjacent skin can
occur in primary infection. Autoinoculation to damaged or
inflamed skin is observed in both primary and recurrent disease.2
Rarer complications include autonomic nervous system
dysfunction, which can present with difficulties with urination,
constipation and altered sensation in the perineal, sacral and
lower back areas. Transverse myelitis is another rare complica-
tion; in this, the symptoms of autonomic dysfunction are coupled
with absent deep tendon reflexes and reduced strength in the
legs.2
Recurrent episode: recurrent episodes occur when latent virus is
reactivated, and are usually milder and of shorter duration (up to
8e12 days).1e3 Women are affected more severely than men.
Lesions appear in localized sites and are usually unilateral.
Lymphadenopathy occurs in only 25% of people and is usually
confined to the side affected by the lesions.1,2 Dysuria is un-
common in recurrent episodes.
Many patients link the development of recurrence to specific
triggers such as local trauma, menstruation or ultraviolet radia-
tion.1,2 About 50% of patients develop symptoms in the pro-
dromal phase of the illness. These vary from mild tingling
sensations in the areas affected by the eruption, to severe,
shooting pains in the thigh, buttocks or groin.1,2 Other prodromal
2 Ó 2018 Published by Elsevier Ltd.
 MANAGEMENT OF INFECTIVE AND NON-INFECTIVE GENITAL CONDITIONS
Figure 1 Vulval herpes.
symptoms include malaise, fever and hyperaesthesia at the site
where the lesions subsequently occur.1,2 Many patients suffer
‘atypical’ recurrent episodes in which vesicles and ulcers do not
occur and various epithelial abnormalities can be seen, including
fissuring, furuncles, excoriations and non-specific erythema.1,2
Diagnosis
The diagnosis of genital herpes is mainly clinical, but should be
confirmed by a laboratory method. Real-time polymerase chain
reaction (PCR) testing is widely available and has become the
diagnostic method of choice.1,2 PCR has been shown to be more
sensitive than culture for all stages of HSV infection, for early and
late presentations, and provides a rapid turn-around of speci-
mens, often within hours. PCR also allows for viral typing. The
British Association for Sexual Health and HIV recommends
nucleic acid amplification testing as the preferred diagnostic
method for genital herpes.3
Viral culture is occasionally still required. It is particularly
valuable when looking at persistent or atypical lesions in
immunocompromised patients when viral types resistant to some
antiviral agents may be present. The best results are obtained
with vesicle fluid, but about 25% of swabs taken from healing
scabbed lesions are culture-positive.2
Type-specific serology can be used to identify serologically
discordant couples in high-risk situations (e.g. late pregnancy); it
can also be helpful to exclude HSV in patients with atypical
genital symptoms.1,2 However, serology often detects isolated
HSV-1 antibodies (present in >50% of the older population), in
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which case it is of little help in excluding or establishing a genital
infection. Serology can fail to detect established infections with
either viral type.1,2
Mixed infections with other genital pathogens are common,
and screening for other STIs is essential in primary cases.1e3
Management
Primary (first-episode) genital herpes: nucleoside analogues
(aciclovir, valaciclovir, famciclovir) are effective in the treatment
of primary genital herpes. Oral antiviral treatment should be
initiated on clinical suspicion.1,2 Aciclovir 200 mg five times a
day or aciclovir 400 mg three times a day for 5 days is usually
adequate. The dosing frequency can be reduced if valaciclovir
500 mg twice daily or famciclovir 250 mg three times daily for
five days is used. The cost of the three agents varies
considerably.3
Antiviral medication is worthwhile when initiated up to 6
days into an episode or when the vesicles are still present.
Treatment should be offered even if disease appears relatively
mild as progression can be rapid. If new lesions continue to
develop, or if complications or severe systemic symptoms are
present, treatment should be continued beyond 5 days.3
Symptomatic treatment with analgesics, saline bathing (1
teaspoon of salt per mug of water) and ice packs is usually
helpful.3 Patients should be warned that they will feel ill for a few
days, and are advised to rest and take time off work.3 Compli-
cations, particularly urinary retention associated with severe
dysuria, should be anticipated; patients can manage these
symptoms by applying topical anaesthetic gels and passing urine
in the bath.3 Counselling over an extended period of time may be
required. Patients must be aware of the likelihood of recurrence,
the possibility of disease transmission and disclosure to new
sexual partners.3
Recurrent genital herpes: most patients report that recurrences
are mild and short lived. These mild or infrequent episodes
require only symptomatic therapy. Severe, complicated or
frequent recurrences, defined as six or more per year, can be
managed with antiviral treatment.1,2
Episodic therapy with short courses of antiviral treatment
initiated early in a recurrence may reduce the duration and
severity of symptoms. Studies have shown that there are benefits
of episodic therapy if treatment is taken within the first 24e48
hours of the evolution of an episode, and that there is little
benefit in extending therapy beyond 3 days.3 The patient should
be given a small supply of the drug to initiate at the first sign of
symptom recurrence, and if possible during the prodrome.2,3
For patients with severe, frequent or complicated disease,
continuous daily suppressive therapy is likely to be beneficial.3
Suppressive therapy can be used to manage many of the com-
plications of genital infection, including psychosexual problems,
transmission risk and anxiety, and medical problems such as
recurrent meningitis and erythema multiforme.1e3 Daily aciclo-
vir is effective in controlling recurrent disease, but many pa-
tients experience occasional breakthrough episodes while taking
treatment. If suppression is initiated, special monitoring is not
required, except in individuals with advanced renal disease.2
The need for continuing suppression should be regularly
reassessed.2
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 MANAGEMENT OF INFECTIVE AND NON-INFECTIVE GENITAL CONDITIONS
Counselling
Accurate counselling for HSV infection and psychosexual support
is essential when providing patients with a diagnosis. There are
many lay misconceptions regarding HSV infection, leading to
increased patient anxiety. Counselling over an extended period of
time can be required.2
Patients must be aware of the likelihood of recurrence, the
possibility of disease transmission and the requirement to
disclose status to new sexual partners. Transmission of infection
remains a major source of anxiety in many with HSV infection.
There is strong evidence to show that condoms used consistently
protect both men and women from infection.2,3 Patients should
be advised to reduce risk of transmission by avoiding sex during
symptomatic episodes and during prodromal illness.2,3 As viral
shedding can occur in the absence of symptoms or signs, patients
with HSV should be aware that there is a small but significant
risk of passing HSV infection to a sexual partner even in the
absence of symptoms.
Syphilis
Syphilis is caused by the spirochaete bacterium Treponema pal-
lidum. Syphilis is a progressive multisystem bacterial infection. It
can be staged as primary, secondary, tertiary and latent.
The primary stage of syphilis infection is characterized by
genital ulceration at the site of primary inoculation. Trans-
mission typically arises from oro-genital or genital-to-genital
contact. Most individuals develop ulceration 14e21 days after
inoculation, but primary symptoms can arise at any time from 9
to 90 days after exposure.1,4
Initial symptoms are the development of a papule that then
ulcerates to form a syphilitic chancre.1,4 Ulcers are usually soli-
tary and round with an indurated base and well-defined edges.
Syphilitic chancres are typically painless with associated painless
inguinal lymphadenopathy. However, they can present atypically
as painful ulcers in multiple sites.1,4 Chancres are usually found
in the genital or perianal areas but can be extragenital. The
mouth is the most common extragenital site of infection. Without
treatment, the syphilitic chancre typically heals within 3e4
weeks.1,4
Following this, 3e6 weeks later, generalized symptoms and
signs of secondary syphilis can arise. Secondary syphilis is
characterized by a rash and constitutional symptoms such as
fever and malaise. This can be accompanied by generalized
anogenital ulceration. These ulcers also heal spontaneously
without treatment but can be accompanied by relapsing symp-
toms of secondary syphilis over the following months.1,4
The diagnosis of primary syphilis in specialist services relies
on careful clinical assessment and diagnostic tests. Diagnostic
tests include use of PCR to identify T. pallidum material in the
ulcer. In addition, serological testing for T. pallidum enzyme
immunoassay immunoglobulin M or G should be conducted.
This test can be negative in early primary syphilis, and may
therefore need to be repeated after 2e3 weeks.1,4
Penicillin is the treatment of choice for syphilis. A single dose
of benzathine penicillin can be administered intramuscularly to
all individuals presenting with uncomplicated primary, second-
ary and early latent syphilis (asymptomatic syphilis without
signs in the first 2 years after acquisition).4 Patients who have a
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penicillin allergy or decline parenteral treatment can be pre-
scribed a course of doxycycline.4 Patients should be warned of
the potential for a JarischeHerxheimer reaction after injection
with penicillin.4 This reaction is common in primary and sec-
ondary syphilis and is characterized by flu-like symptoms 3e12
hours after penicillin administration. Transient worsening of skin
lesions is occasionally observed.4
Auditory and optic symptoms can occur in early syphilis. Such
cases require specialist assessment and treatment as for
neurosyphilis.
Lymphogranuloma venereum
LGV is also known as tropical or climatic bubo and lympho-
granuloma inguinale. It is an STI caused by the invasive L
serovars (L1, L2, L3) of Chlamydia trachomatis.1,5 These invade
and destroy lymphatic tissue. In recent years, LGV has emerged
as an important cause of proctitis among men who have sex with
men in the developed world.5
LGV can be divided into three stages of infection: primary,
secondary and tertiary. The primary stage occurs 3e30 days after
exposure and is characterized by papules or ulcers at the site of
inoculation.1,5 Ulcers are typically solitary and non-indurated,
and heal quickly without scarring. The secondary stage occurs
2e6 weeks after the primary stage.5 The typical presentation is of
an inguinal syndrome with unilateral inguinal or femoral
lymphadenopathy and bubo formation. Around 30% of patients
display the groove sign, with lymphadenopathy above and below
the inguinal ligament.1,5 Inguinal buboes can suppurate and
rupture. The tertiary stage follows chronic untreated infection
and can occur any number of years after initial infection. Patients
typically develop genital lymphoedema as a result of lymphatic
obstruction from fibrosis and scarring.1,5
Diagnosis is obtained by testing lesional samples for the L
serovar of C. trachomatis.5 Treatment is with doxycycline 100 mg
twice daily or erythromycin 500 mg four times daily for 3 weeks.5
Buboes may need aspiration even after adequate antibiotic
therapy.5 Patients should be advised to abstain from sex until
they and their partner(s) have completed treatment.5
Chancroid
Haemophilus ducreyi, a Gram-negative coccobacillus, is the
causative pathogen of the tropical STI chancroid (see Further
reading).1 Historically, chancroid has been a common cause of
genital ulceration in tropical regions of Africa, Asia, South
America and the Caribbean. The global incidence of chancroid
has decreased in recent years; this is thought to be the result of
appropriate antibiotic use and increased condom use. The ma-
jority of cases seen are either acquired abroad or from a partner
who has been abroad.
Chancroid typically presents with anogenital ulceration with
lymphadenitis progressing to bubo (inguinal abscess) forma-
tion.1 A break in the skin is usually required for sexual trans-
mission to occur, and the incubation period is 4e7 days. Lesions
start as tender papules that progress to form pustules; these then
rupture to form an ulcer. Classically, ulcers are painful, have a
ragged edge and bleed on contact. Usual sites of infection are the
coronal sulcus, frenulum and glans in men, and the labia minora
or forchette in women.1 Painful lymphadenopathy can lead to
4 Ó 2018 Published by Elsevier Ltd.
 MANAGEMENT OF INFECTIVE AND NON-INFECTIVE GENITAL CONDITIONS
bubo formation; buboes should be aspirated rather than incised
and drained.1
The diagnosis is made using culture and microscopy, but
sensitivity is poor. Some specialist laboratories have developed
in-house PCR methods, but no commercial assays are available.
Recommended treatment regimens are either: azithromycin 1
g in a single dose; ceftriaxone 250 mg intramuscularly in a single
dose; ciprofloxacin 500 mg orally twice daily for 3 days; or
erythromycin 500 mg orally four times a day for 7 days. Suc-
cessful treatment of chancroid should cure the infection, resolve
the symptoms and prevent transmission. Partners who have had
sexual contact with the patient within 10 days before the onset of
symptoms should attend for assessment and initiate treatment
even if asymptomatic. Patients should be advised to avoid sexual
intercourse until both they and their partner have completed
treatment and are asymptomatic.
Donovanosis (granuloma inguinale)
The causative organism of donovanosis is Klebsiella (formerly
Calymmatobacterium) granulomatis (see Further reading).1
Donovanosis is a tropical STI that has been reported in local-
ized areas of India, Papua New Guinea, the Caribbean, Brazil, the
Guyanas, South Africa, Zambia, Vietnam and Aboriginal
Australia.1
Papules develop at the site of primary inoculation, progressing
to become slow-growing painless friable ulcers or hypertrophic
lesions.1 Lesions are typically found in the genital and inguinal
regions, and are described as granulomatous, beefy red and
haemorrhagic.1 Complications include haemorrhage, genital
lymphoedema, genital mutilation and cicatrization, development
of squamous cell carcinoma and, rarely, haematogenous
dissemination to bone and viscera.
Diagnosis is made by identifying intracellular Donovan bodies
in cellular fluid or tissue biopsy. All patients with active lesions
TEST YOURSELF
To test your knowledge based on the article you have just read, please complete the questions below. The answers can be found at the
end of the issue or online here.
Question 1
A 16-year-old woman presents with a 24-hour history of painful
bilateral labial ulceration and difficulty voiding urine. She reports
associated symptoms of lethargy, fever and headache. On clinical
examination, there are multiple erythematous shallow labial ul-
cers present that are exquisitely painful. She reports recent sex-
ual debut with a regular male partner 7 days ago but no other
sexual history. She is unaware of a personal or partner history of
cold sores.
What is the likely diagnosis?
A. Primary syphilis
B. Genital herpes simplex type 2
C. Chancroid
D. Genital apthosis
E. Genital herpes simplex type 1
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shown to contain Donovan bodies should be given antimicrobial
treatment. Treatment is for a minimum of 3 weeks or until the
lesions are healing. Common recommended treatment options
include: azithromycin 1 g weekly or 500 mg daily; ceftriaxone 1 g
intramuscularly, daily; co-trimoxazole 960 mg orally twice daily;
or erythromycin 500 mg orally four times daily. Any person with
a history of unprotected sexual contact with a patient with active
donovanosis or within 40 days of the onset of lesions should
have a clinical assessment and be offered treatment. A
KEY REFERENCES
1 Rogstad KE, Patel R, Gupta N. Genital ulcer disease. In: ABC of
sexually transmitted infections. 6th edn. BMJ Books, 2011
[Chapter 12].
2 Patel R. Genital herpes. Medicine 38: 276e280.
3 Patel R, Green J, Clarke E, et al. 2014 UK national guideline for the
management of anogenital herpes. Int J STD AIDS 2015; 26: 763e76.
4 Kingston M, French P, Higgins S, et al. UK national guideline on the
management of syphilis 2015. Int J STD AIDS 2016; 27: 421e46.
5 White J, O’Farrell N, Daniels D, British Association for Sexual
Health and HIV. 2013 UK national guideline for the management of
lymphogranuloma venereum: clinical effectiveness group of the
British association for sexual Health and HIV (CEG/BASHH)
guideline development group. Int J STD AIDS 2013; 24: 593e601.
FURTHER READING
O’Farrell N, Lazaro N. UK National Guideline for the management of
chancroid 2014. Int J STD AIDS 2014; 25: 975e83.
Richens J. United Kingdom national guideline for the management of
Donovanosis (Granuloma inguinale) 2011. Clinical Effectiveness
Group, British Association for Sexual Health and HIV. https://www.
bashhguidelines.org/media/1061/3194.pdf (accessed 15 Dec
2017).
Question 2
A 28-year-old man presented with a 2-day history of painless
ulceration of the glans of his penis and lumps in his groin. He had
had unprotected penetrative anal intercourse with three casual
male sexual partners 3 weeks ago at a party. He was otherwise
well. He had no known allergies.
On clinical examination, there was an indurated, well-
demarcated solitary ulcer and bilateral inguinal lymphadenopa-
thy. He is otherwise systemically well with no other extragenital
signs.
What is the initial treatment of choice for the most likely
diagnosis?
A) Benzathine penicillin 2.4 megaunits intramuscularly once
weekly for three doses
B) Erythromycin 500 mg orally 6-hourly for 2 weeks
5 Ó 2018 Published by Elsevier Ltd.
 MANAGEMENT OF INFECTIVE AND NON-INFECTIVE GENITAL CONDITIONS

C) Doxycycline 100 mg orally 12-hourly for 2 weeks
D) Benzathine penicillin 2.4 megaunits intramuscularly stat
E) Ceftriaxone 500 mg intramuscularly daily for 10 days
Question 3
A 26-year-old woman presented for advice regarding sexual
activity with her partner who was known to have herpes sim-
plex virus type 2. She was 24 weeks’ pregnant. She had no
previous history of symptoms of genital ulceration or cold sores.
She was having regular unprotected vaginal intercourse. She
had read that herpes infection could be harmful to the baby and
wanted to reduce the risk of transmission of herpes during
pregnancy.
What is the most appropriate advice?
A. She should have a caesarean section to prevent neonatal
acquisition of infection regardless of whether or not she
has symptoms
B. The man should start suppressive therapy with aciclovir
400 mg 12-hourly for the remainder of the pregnancy, and
she should present urgently for treatment should she
develop symptoms
C. No action is required
D. Sexual contact should be avoided for the third trimester of
pregnancy, and she should present urgently should she
develop symptoms during this time
E. She should commence suppressive therapy from 36 weeks
to avoid neonatal transmission of infection

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