Genital Lesions

•  sores , ulcers
•  Warts, exophytic growths
•  Most are related to STDs or venereal
infections
•  In US, most common
•  HSV2
•  Treponema pallidum
•  Haemophilus ducreyi
•  Human papillomavirus
Infectious Causes - STDs
•  Syphilis •  Granuloma
•  Treponema pallidum inguinale
•  HSV 1 and 2 •  Calymmatobacterium
•  Chancroid granulomatis
•  H ducreyi •  Human
•  Lymphogranuloma papillomavirus
venereum
•  Sarcoptes scabiei
•  Chlamydia
trachomatis •  Molluscum
contagiosum
Non STD Infectious Causes
•  Folliculitis •  Histoplasmosis
•  Tuberculosis •  Candida
•  Tularemia •  Amebiasis
Nonvenereal Causes of
Lesions
•  Trauma •  Inflammatory Bowel
•  Malignancies Disease
•  Behcet s syndrome •  Dermatitis
•  Fixed drug eruption •  Lichen planus
•  Eczema •  Hidradenitis
•  Psoriasis suppurativa
•  Apthous ulcers
•  Postinflammatory
(assoc w/HIV)
hypopigmentation
•  Infectious lesions are generally
communicable
•  Individual health concern as well as a
public health concern
•  Morphology can vary from patient to
patient despite same cause
•  Morphology can vary in individuals
depending on location and pt s general
health
Presentation
•  Assume it s an infection if recent
sexual contact
•  Very proximate sexual exposure
(from hours to 1-2 days) suggest
trauma(mechanical/chemical),
allergic hypersensitivity, latex allergy
(esp if a recurrent lesion)
Presentation
•  Prodromal symptoms? If yes,
possible HSV
•  Hx of dermatologic diseases?
•  Any new/change in meds?
•  Any other sx?
Location of lesions
•  Mons pubis
•  Labia
•  Fourchette
•  Anywhere in the vagina
•  Cervix
•  Inner thighs
•  Perianal tissue
•  Oropharynx
•  Secondary syphilis
•  Site of rash has no connection to site of
inoculation
•  Disseminated gonorrhea
•  Arthritis/cutaneous manifestation has no
bearing on site of initial exposure
Pain, Dyasthesias and
Systemic Symptoms
•  Painless
• Primary syphilis
• LGV
• Scabies
• Molluscum
• Granuloma inguinale
•  Painful
• HSV
• Chancroid
• Immunologic causes- Behcets, Crohns, etc
•  Pruritis
• Scabies, lice
• Prodrome of HSV
•  Fever
• Secondary syphilis
• Primary HSV
Lymphadenopathy
•  Bilateral inguinal lymphadenopathy
•  Typical in syphilis
•  Can also be seen in HSV
•  Buboes
•  Expansive, tender lymph nodes, seen in
LGV and chancroid
•  Systemic infections
•  HIV
Lesions - Herpes
•  Vesicles - always in groups
•  Turn into pustules
•  Erupt into ulcers on erythemtous base
•  Crust over – non infectious
•  Painful!!
•  Primary HSV – lesions resolve in 2-3 weeks,
recurrence 5-12 days, little scarring
• 
Lesions – Primary Syphilis
•  Chancre – painless
•  Almost always solitary
•  Round, 1-2 cm in diameter
•  Clean margins, indurated border
•  Clean base, no exudate, but can become
superinfected with bacteria
•  Resolve on their own in 3-12 weeks
 • 

Figure 101-4 Chancre of primary

syphilis.

Figure 101-4 Chancre of primary syphilis.

Lesions – Secondary Syphilis
•  Can start anywhere
•  Macular lesionsàpigmented papules
•  Fine circumferential scale
•  Condyloma lata – meatier than HPV
condyloma, in moist areas only
•  VERY infectious – loads of treponemes in
these lesions
•  Resolve on their own in 3-12 weeks, no
scarring
Generalized pustular rash of secondary syphilis
 • 

Figure 101-5 Condylomata lata of

secondary syphilis

Figure 101-5 Condylomata lata of secondary syphilis

Lesions - Chancroid
•  Similar in size to syphilitic chancres, but
edges are ragged
•  Ulcer base is necrotic with purulent exudate
•  Induration is less prominent than a
chancre, soft chancre
•  Occasional multiple lesions
•  W/out therapy, lesions are slowly
destructive and are scarring
• 
Lesions – Granuloma
Inguinale
•  Start as firm SQ nodules or papules that
eventually ulcerate
•  Lesions become hypertrophic and beefy
and bleed easily
•  Lots of local tissue destruction
•  Swelling of vulva common
•  Can be confused with squamous cell ca
•  W/out therapy, slowly destructive, scarring
Lesions - LGV
•  Also called Nicholas-Durand-Favre
disease
•  Caused by C trachomatis serovars L1,
L2 and L3
•  Starts as small papule or HSV like
ulcer à asymptomatic, resolves
•  Progresses to tender
lymphadenopathy
Lesions - HPV
•  Clinically visible lesions are caused by
HPV types of low oncogenic potential –
types 6 and 11
•  Can vary in size and number from
relatively inconspiculous to large
cauliflower like lesions
•  Grow in pregnancy, regress postpartum
• 
•  Types 16, 18, 31, 33 – oncogenic
potential
•  Mostly affect moist mucous surface,
but can affect keratinized epithelium
•  HPV associated ca in situ on
keratinized epithelium – Bowenoid
paupulosis or Bowen s disease
Lesions - Molluscum
•  Benign, wart like lesions
•  Poxvirus
•  Spread is sexual or non sexual – seen in
kids
•  Small, 3-5 mm
•  Pearly, w/central umbilication
•  Destruction is cure, but lesions rarely
progress
• 
Epidemiology
•  In US – most of genital lesions are
HSV and HPV
•  Worldwide, HSV2 is most common
•  In tropical areas, H ducreyi is
common
•  LGV – in tropics and subtropics
Immunosuppressed Patients
•  Severity and extent of lesions can be
very different than non
immunosuppressed pts
•  Lesions can be much larger than
expected (molluscum, HSV)
•  Pain may also be much more severe
(HSV)
•  Alteration in the normal mucosal
barriers of genital region allows
easier entry of HIV into system
•  Physical barriers
•  Immumologic barriers
Lab Testing
•  H ducreyi
•  Gram neg slender rod
•  school of fish pattern
•  Mueller-Hinton chocolate agar

•  Syphilis
•  Darkfield exam – spirochetes
•  Tightly coiled white oragnisms
•  RPR or VDRL
 • 

Figure 101-11 Gram stain of

Haemophilus ducreyi.

Figure 101-11 Gram stain of Haemophilus ducreyi.

•  HSV
•  Light microscopy Tzanck smear
•  Cell culture – pathognomonic cyptopathic effect
in 48 hrsàmonoclonal Ab confirms dx
•  No use in typing HSV 1-2
•  C granulomatis
•  Wright s or Giemsa stain, may need bx of deep
tissue
•  Clusters of blue rods w/prominent polar granules,
surrounded by pink capsules (Donovan bodies)
 • 

Figure 101-12 Biopsy of granuloma

inguinale lesion revealing Donovan
bodies consistent with
Calymmatobacterium granulomatis.
Figure 101-12 Biopsy of granuloma inguinale lesion revealing Donovan bodies consistent with Calymmatobacterium granulomatis.
•  LGV
•  Dx based on clinical criteria
•  PCR of bubo drainage, typing of serovar
•  HPV
•  Clinical appearance
•  Bx can be done to confirm – AWE lesions
•  No cell culture system to confirm
•  Cytologic change c/w HPV – koilocyte w or w/o
nuclear atypia
Treatment
•  Syphilis
•  Primary
• Pcn G – 2.4 million units IM à healing w/in
24-48 hrs, conversion to darkfield neg lesions
• Alternative tx – doxycycline x 7days,
ceftriaxone 8-10 days, azithromycin 2 g po x
1
• Repeat serologic testing q 6 mos, fourfold
decrease indicates response
•  HSV
•  Nucleoside analogues
• Goal to resolve lesions and reduce infectivity
• Acyclovir/valacyclovir/famcyclovir
• Treatment/suppression
• In immunocopmpromised pts, thymidine
kinase deficient strains seen – need to use
alternate med – foscarnet (IV or topical –
renal dysfunction and hypophosphatemia)
•  Chancroid
•  Lesions are slow to heal, even w/tx
•  Eryhtromycin and azithromycin
•  Ceftriaxone
•  HPV
•  Ablative treatment, but can cause tissue
damage and possible scarring
•  Laser, TCA, excision, cautery, cryotherapy
•  Imiquimod
•  Podophyllin
•  Interferon
•  LGV
•  Tetracycline/doxycycline, erythromucin
•  14-21 days
•  Donovanosis
•  Doxycycline, bactrim, fluoroquinolones
•  3 weeks
Nonvenereal Lesions
•  Candida
•  Fixed drug eruptions
•  Antibiotics, NSAIDs,
•  Eryhtematous, violaceous sharply demarcated
macules
•  Aphthous ulcers
•  Behcet s syndrome, HIV
•  Small, 1-2 mm, surrounding erythema, tx w/
topical steroids
HSV
•  HSV 1 and 2
•  Mucocutaneous infections
•  Infections of the CNS
•  Occasional infection of visceral organs
Herpes viruses
•  8 types of herpes viruses
•  Alpha–herpesviruses – HSV1, HSV2 and
VZV
•  Beta-herpesviruses – CMV, HHV6, HHV7
•  Gamma-herpesviruses – EBV, KSHV or
HHV8
•  Linear, DS DNA virus
•  Overall sequence homology between
HSV1 and HSV2 is about 50%
•  Transcription/replication and
assembly takes place in the host
nucleus
•  Replication cycle can take from 4-12
hrs
•  HSV is cytopathic to any cell that
harbors the entire replication process
•  Latency – in neuronal cells
•  Reactivation – release of virus from
neuron and entry into epithelial cells
Epidemiology
• No animal vectors
• HSV1 is acquired more frequently and earlier in life
than HSV2
•  Up to 80% of adults will have Ab to HSV1
• Abto HSV2 appear in individuals related to sexual
activity
Transmission
•  Close contact w/person who is
shedding virus
•  Mucosal surface
•  Genital/oral secretion
•  Via lesions or small cracks in surface
•  Inactivated by drying or at room
temperature
•  Aerosol/fomitic spread highly unlikely
Pathogenesis
•  Initial infection often subclinical
•  Can have primary infection w/
systemic sx
•  Infection involves sensory or
autonomic nerve endings
•  HSV1 – trigeminal ganglia
•  HSV2 – sacral root ganglia (S2 to S5)
•  Virus can spread to other mucosal
surfaces via migration of infectious
virions thru peripheral sensory
nerves
•  After primary infection, infectious
HSV can no longer be recovered in
the ganglia
•  Latent HSV live there
•  In immunocompetent pts who acquire
both HSV1 orally and genitally
•  HSV1 is reactivated more often in the oral
than genital region
•  Similarly in HSV2
•  Reactivation in the genital region is 8-10
times more frequent than oral-labial
reactivation of HSV2
Spectrum of Diseases caused
by HSV1-2
•  Genital infection
• Primary – systemic sx, cervix and urethra
involved in nearly 80% of primary infxn
• Recurrence – in 1st 12 mos – 90-95%, decrease
in recurrence rates over 10 yrs
•  Complications
• Meningitis
• Extragenital lesions
• Disseminated infxn
Neonatal HSV
•  90% perinatally acquired, 5-8%
congenital, few cases acquired
postnatally
•  Risk of transmission w/a primary
infxn momà baby 40-50%
•  If not treated, neonatal HSV
disseminates in more than 70% of
cases
•  Overall rate of death from
disseminated neonatal HSV is 65%
•  Less than 20% of neonates w/CNS
HSV infxn develop normally