Sexual health Flashcards
Herpes simplex virus (HSV)
HSV-1 & HSV-2 infections generally manifest with oral, genital and ocular ulcers
seroprevalence for HSV is high with >90% of the population worldwide having detectable antibodies
NB HSV-1 usually oral, HSV-2 usually genital
transmission of Herpes simplex virus (HSV)
transmission via direct contact with mucosal tissue / secretions of infected individual or perinatal transmission (more common with HSV-2)
Presentation of Herpes labialis (cold sores)
prodrome (~24h) of tingling, burning or pain
recurring erythematous vesicles that turn into painful ulcerations on oral mucosa /lips
Presentation of genital herpes
painful genital ulceration ± dysuria & pruritis
usually presents as single/disseminated red bumps/white vesicles found around genitalia / anus
may have tender lymphadenopathy
NB primary infection is usually more severe and may present with systemic features such as fever, headache, malaise
Investigations for Herpes simplex virus (HSV) infection
cold sores are usually a clinical diagnosis
genital herpes usually requires nucleic acid amplification test (NAAT) or PCR
HSV serology may be used in asymptomatic pts, those with recurrent/atypical ulcers or to distinguish HSV types
Management of Cold sores
generally symptomatic management
consider topical choline salicylate gel or lidocaine or topical aciclovir (not recommended)
NB infection control is key e.g. don’t touch lesions, avoid kissing & oral sex
Management of genital herpes
Refer to GUM clinic
general:
saline bathing, analgesia, topical anaesthetics e.g. lidocaine
oral acyclovir/valaciclovir (within 5 days of symptom onset)
consider suppressive antiviral therapy with acyclovir daily if >6 attack per year)
Genital herpes in pregnancy
elective C-section if genital herpes at >28 weeks, & give suppressive therapy in the form of acyclovir if recurrent attacks
When to consider suppressive therapy for genital herpes
consider suppressive antiviral therapy with acyclovir daily if >6 attack per year)
Syphilis
A predominantly sexually transmitted infection caused by the spirochaete bacterium Treponema pallidum
more common in men especially those who have sex with men (MSM)
incubation period of 10-90 days
Window period for syphilis
12 weeks
Window period
the window period for a test designed to detect a specific disease (particularly infectious disease) is the time between first infection and when the test can reliably detect that infection. In antibody-based testing, the window period is dependent on the time taken for seroconversion.
Presentation of primary syphilis
local lesion at site of infection (NB often not seen in women as it may be on cervix)
small painless papule rapidly forms under and ulcer (the chancre), usually single, round/oval PAINLESS surrounded by bright red margins
resolves spontaneously within 3-6 weeks
may have regional (usually inguinal) non tender lymphadenopathy
Presentation of secondary syphilis
~6-10 weeks after primary infection
systemic symptoms of fever, malaise, lymphadenopathy, hight time headaches, aches
Rash: generalised polymorphic rash on palms/soles/trunk, reddish brown or copper colour, non pruritic
Buccal snail track ulcers
condylomata lata (board based, wart like smooth white papular erosions usually found in moist & warm areas e.g. genitalia)
NB rash on soles/palms = pathomemonic
Presentation of tertiary syphilis
3 distinct clinical syndromes that may co-exist
Cardiovascular syphilis:
characterised by aortitis (usually of aortic root), ascending aortic aneurysm
manifests with aortic regurgitation, angina & aortic aneurysms
Gummata:
chronic destructive granulomatous lesions with necrotic centres that tend to ulcerate, can occur in any organ
usually seen in skin/bones
Neurosyphilis:
dorsal column loss (tabes dorsalis = impaired proprioception, broad based gait, ataxia, absent reflexes), dementia (general paralysis of the insane), Argyll Robertson pupil (bilateral miosis, pupils accommodate but pupillary light reflex is absent)
Cardiovascular syphilis
characterised by aortitis (usually of aortic root), ascending aortic aneurysm
manifests with aortic regurgitation, angina & aortic aneurysms
Gummata
chronic destructive granulomatous lesions with necrotic centres that tend to ulcerate, can occur in any organ
usually seen in skin/bones
Tertiary syphilis
Neurosyphilis
CNS invasion causing inflammatory reaction of the meninges/cerebral parenchyma
dorsal column loss (tabes dorsalis = impaired proprioception, broad based gait, ataxia, absent reflexes)
dementia (general paralysis of the insane)
Argyll Robertson pupil (bilateral miosis, pupils accommodate but pupillary light reflex is absent)
managed with IM/IV benzathine pencillin for 10-14 days
Congenital syphilis presentation
blunted upper incisors (hutchinson's teeth) mulberry molars linear scars at angle of mouth keratitis saber shins saddle nose deafness hepatomegaly jaundice sensorineural hearing loss
Effects of in utero syphilis
miscarriage
stillbirth
hydrops fetalis
Investigating syphilis
Treponemal specific antibody tests:
e.g. treponema enzyme immune assay (EIA), T.pallidum particle agglutination test (TPPA), T.pallidum hem agglutination test (TPHA) etc
stay +ve after treatment
Non treponema specific:
anticardiolipin antibodies
-ve after treatment, insensitive for advanced syphilis
screen for other STIs
dark field microscopy (for T. pallidum)
Management of syphilis
1st line: single dose IM bezathine penicillin (alternatives = azithromycin / doxycycline)
Neurosyphilis = IM/IV benzathine pencillin for 10-14 days
Jarisch-Herxheimer reaction
ruction to treatment, after 1st dose
acute febrile illness with headache, myalgia, riggers, tachycardia
generally self resolved in 24h
Syphilis causative organism
spirochaete bacterium Treponema pallidum