GUM Flashcards
What is the 6 step plan for management of STIs?
1, Accurate diagnosis
- Look for and exclude other genital pathogens
- Effective (curative) Tx
- TOC
- Contact tracing, timely partner notification and Tx
- Education + appropriate counselling
GUM and confidentiality
VD acts - pts did not access care due to confidentiality concerns, additional pt rights beyond GMP, consequences of breach
New mandatory guidance issued by DH to all providers of sexual health services to NHS (includes proviate providers and GP)
Can not disclose to others unless:
- pt permission
- involved with care of that condition
- exceptional circumstances (court order) - major acts of criminality
Consequences - housing and access to GUM notes, communication with other clinicians, communicating results, contact tracing
2 situations where breach confidentiality in GUM?
Major acts of criminality
Blood borne STI and continues UPSI without disclosing status to partner
GP who wants to know results of STI screen - cannot disclose.
Casualty doctor looking after F1 needlestick from one of your patients - can tell the F1 but not the casualty doctor. Can disclose info in public interest but cannot perform HIV test without consent.
Pt attending as asymptomatic partner of pt who refuses to have presumptive Tx without knowing why - cannot disclose unless blood borne and having UPSI - must encourage pt to disclose first
Police investigating assault allegation asks if assailant is pt - cannot disclose.
General STI risk factors?
Young (esp <20), single, 2 or more partners in preceeding 6 months, non barrier contraception, inner city, current STI, Hx previous STI, ethnicity for some STIs
What causes infection patterns to change?
Pathogen - virulence, resistance to conventional therapy
Test - increased testing, better test
Population - susceptibility and sexual behaviour
Note: syphilis, GC and chlamydia increasing, most viral STIs increasing, new epidemics occurring particularly MSM - all despite intensive efforts to modify sexual behaviour and secondary prevention throughout contact tracing
What are differences between viral and bacterial STIs broadly speaking?
Bacterial - easy diagnosis, curable, limited period of infectivity, contact tracing
Viral - often subclinical so diagnosis difficult, often not curable, may be lifelong, limited role of contact tracing as often subclinical and long period of infectivity
Causes of viral STIs? Split into 2 main symptom categories?
Predominantly dermatological: HPV, molluscum contagiosum, HSV 1 + 2
Predominantly systemic: EBV, HHV 8, Hepatitis A-E, HIV
What might cause genital ulceration?
STIs (most common - least common): 1. HSV 2. Treponema pallidum 3. Chancroid 4. LGV 5. Donavanosis
Derm causes - Behcets disease, erythema multiforme, Steve-Johnson syndrome, acute reactive apthous ulceration
What is HSV?
DNA virus causing skin infections, latency in DRG - recurrent and infectious for life, diagnosis by nucleic acid identification, causes genital ulcer disease
What is HPV?
double stranded DNA - 120 types, 30 types infect ano-genital epithelium
oncogenic - 16 and 18 >95% SCC cervix
non-oncogenic 6 and 11 >90% external anogenital warts
What is MC?
Molluscum contagiosum - benign epidermal eruption of skin, large DNA pox virus
What are some bacterial STIs?
Neisseria gonorrhoea Chlamydia trachomatis Mycoplasma genitalium Ureaplasma urealyticum Treponema pallidum Haemophilus ducreyi Calymmatobacterium genulomatis Trichomonas vaginalis 'Gay bowel disease' - shigella, giardia, entamoeba, some chlamydial strains
What is N. gonorrhoea?
Gram negative intracellular diplococcus
Infects mucous membranes Can disseminate (not as serious as meningitis)
Dysuria Discharge (urethral, vaginal) Proctitis Cervicitis Pharyngitis Conjunctivitis Can ascend to cause PID / epididymitis
Diagnosis of gonorrhoea?
Nucleic acid tests - urine / swabs
Culture allows resistance testing (only 1/3 grow). Microscopy allows immediate diagnosis but needs lots of organism around (really only valuable in urethritis)
What is chlamydia trachomatis?
Small intracellular (not seen on light microscope); strains A-K/L, D-F most prevalent genital. Some strains cause LGV (C. trachomatis L1/2/3) i.e. lymph swelling and proctitis – or urethritis if in penis
Same problems as gonorrhoea, acute illness often milder but lots of late complications. Some strains cause LGV
Discharge- urethritis, cervicitis, proctitis, conjunctivitis
Complications - SARA, spread to upper genital tract (PID), epididymitis
What is mycoplasma genitalium?
Low grade pathogen, very difficult to culture, causes similar problems to chlamydia
Dysuria, discharge, upper genital tract infection, proctitis
Diagnosed with NAATs on urine or swabs
What is treponema pallidum?
Causes syphilis - spirochaete bacteria
Seen on dark field microscopy
Diagnosis by PCR (early lesions) or serology
Risk populations - homosexual men especially HIV+, sexual contact with person from endemic area, pregnancy / tissue donation
ulcers rashes and all the problems of syphilis
What is trichomonas vaginalis?
STI: Flagellated protozoon parasite
Women: vagina / urethra, present in 90%, only site in 5% / paraurethral glands
Men: urethra (supreputial sac, lesions of penis)
Dysuria, discharge (males and females), problems in pregnancy and increase risk of HIV
What causes urethritis / urethral symptoms in males?
Worry
Physiological discharge
STIs: chlamydia, mycoplasma, gonorrhoea, ureaplasma, herpes, trichomonas, adenovirus
Very rarely UTI related / stricture
What is chemsex?
Methamphetamine, mephedrone, GHB/GBL, MDMA, ketamine
high risk STI transmission associated with unprotected sex and multiple partners, higher risk HIV due to not taking antiretrovirals and increased risk trauma
How is chlamydia diagnosed?
NAATs: first catch urine (15ml, hold >1 hour)
Self-taken vulvovaginal swab best in women
Cervical / rectal / pharyngeal / urethral swabs can also be taken
MUST BE >2 WEEKS AFTER SEX
How does chlamydia present?
complications?
Often asymptomatic (50% male 70-80% female) / acute illness milder than gonorrhoea
(Clear) discharge, dysuria, IMB, PCB, urethritis, cervicitis, proctitis, conjunctivitis
Complications
- Follicular conjunctivitis
- PID (acute or chronic)
- Endometritis, salpingitis
- Infertility (rare if one-off asymptomatic; massively increases if 2 episodes PID)
- Ectopic
- Fitz-Hugh Curtis
- Epididymitis
- SARA
Management of chlamydia?
Contact tracing really important for preventing repeat PID / infertility
DOXY 100mg BD 7 days: 100% cure: referred but not suitable for pregnancy or azithromycin 1g STAT (Preg/breast feeding: erythromycin 500mg BD 14 days or azithromycin – TOC 1 month)
TOC not needed but advised after 4-6 weeks, young retested 3/12 (30% reinfection rate)
How does chlamydia affect pregnancy?
50% vertical transmission if vaginal delivery, also possible in C-section: preterm birth, PPROM, LBW, chlamydia pneumonitis (staccato cough, failure to thrive, tachypnoea, 4-12 weeks after birth 10-20% infected)
How is gonorrhoea diagnosed?
NAT: urine / endocervical swab (also: pharynx, rectum)
Culture (only 1/3 grow) allows resistance testing
Microscopy allows immediate diagnosis but need lots of organism, only really valuable for urethritis – 70-95% sensitive
How does gonorrhoea present?
Complications?
Dysuria, discharge, proctitis, pharyngitis, conjuctivitis
Men : 80% profuse purulent discharge, 50% dysuria, asymptomatic 5-10%
Women : 50-70% asymptomatic, mucopurulent discharge <50%, pelvic pain <5%
Pharynx: asymptomatic >90%, mild pharyngitis. Rectum ~90% asymptomatic, can cause purulent rectal discharge
Complications
- PID: infertility most common complication
- Dissemination: rare <1%, females, fever, rash, SEPTIC ARTHRITIS (aspirate), tendonitis
- Fetal loss
- Conjunctivitis
- Bartholin’s abscess
- Epididymo-orchitis
- Perihepatitis
- Appendicitis
- SARA (rarer compared to chlamydia)
Management of gonorrhoea?
Contact tracing really important for preventing repeat PID / infertility
Local sensitivities, travel & allergies– MDR becoming common, oral Tx no longer guarantee cure
CEFTRIAXONE 500mg IM (azithromycin recently dropped).
- TOC essential!
What is NSU?
Non-gonococcal non chlamydial urethritis
*Most common cause of infective urethral discharge is chlamydia (~50%; 10% mycoplasma (longer incubation), 5% gonorrhoea and few due to other organisms). Infective more likely if seen first thing in morning. Very very rarely UTI related or stricture related.
How is NSU diagnosed?
1) Microscopy of urethral specimen; evidence of polymorphs in discharge - if >5 PCs per HPF treat as GC but cover chlamydia as well. If <5 PCs / HPF: examine urine for pus.
2) Urine: If clear, repeat overnight samples / await lab tests > treat for GC/CT.
Urethritis: threads in urine (pus cells with mucus in 1st part, 2nd part clear)
Microscopy: evidence of polymorphs in urethral discharge
Complications and management of NSU?
Complications
- PID (acute or chronic)
- Epididymitis
Management
- High dose azithromycin (for mycoplasma) – saved for mycoplasma as dose of azithromycin used for chlamydia is enough to cause resistance!
Risk population for treponema pallidum?
Gay men, especially HIV+, sexual contact from endemic area.
Once exposed, antibody positive for life.
Acute (~6 weeks) = IgA. TPPA / TPHA positive for life. VDRL / RPR for Tx monitoring and disease activity. INFECTIOUS FOR UP TO 2 YEARS.
How is syphilis diagnosed?
Seen on dark field microscopy
Antigen based assays (EIAs)
Treponemal (specific): TPPA / TPHA – positive for life in 80%, do not correspond to disease activity.
o EIA: IgM usually detectable around end of week 2, IgG week 4-5
o TPPA / TPHA: positive in secondary and early latent syphilis
Non-treponemal/cardiolipin (non-specific): VDRL / RPR (staging and Tx monitoring)
o If negative: very early infection, treated old infection, not infectious
o Reinfection if becomes positive again
o Usually become positive in ~80% people, 7-10 days after chancre, serum regain levels typically low in primary syphillis and highest in secondary syphilis – Z 25% revert to negative serology if progress beyond secondary.
o May be positive in pregnancy, narcotics or HIV / chronic liver disease / EBV.
Virology swab from active lesions
How does syphilis present?
PRIMARY: chancre: painless ulcer (centre erodes to form ulcer), 9-90 days after exposure, lymphadenopathy – may have initial negative serology
SECONDARY: mucosal lesions, rash, arthralgia, lymphadenopathy, meningitis, CN palsies, iritis, uveitis (kidney and liver inflammation)
LATENT o Early (<2 years) or Late (>2 years): asymptomatic but abnormal serology
TERTIARY: ~40%
o CVS: aortic aneurysm, aortic regurgitation, CAD, gummatous syphillis
o Neurosyphilis: tabes dorsalis (demyelination: pre-ataxia, ataxia, paralysis) meningovascular, general paresis
o Gummatous: granulomas in liver/bone /skin
Management of syphilis?
- Early: benzathiane-penicillin 2.4 mu
- Late: benzathine penicillin 2.4 mu 3 doses
- If allergic: doxycycline
How is trichomonas v. diagnosed?
NAAT Gold standard, can also use in men
POCT – 80-94% sensitivity, 15-30 mins, risk false positive
Culture can also be used in men
Wet film microscopy 40-60% sensitivity
Cervical cytology if need to confirm diagnosis
How does TV present?
Complications?
Women: vagina / urethra / paraurethral glands: discharge, itching, offensive odour, vulval itching (ocassional abdo pain, ulceration). Men: urethra and lesions of penis; discharge and dysuria common. OFTEN ASYMPTOMATIC in both.
Complications
- Preterm, LBW, postpartum sepsis – screening not recommended, vertical transmission in 5% infected women, usually clearly 3-6 weeks
- Increased risk of HIV transmission
Tx of TV?
Metronidazole 400mg BD 5 days or 2g stat
Contact trace back 4 months and treat regardless of test results
Tx of BV?
Also: BV (Gardenella): not an STI but…
- Oral metronidazole 400mg BD 5 days
- Intravaginal metronidazole gel
- Intravaginal clindamycin cream
- Soap substitute
If recurrent (>2 proven episodes in 6m): intravaginal metronidazole 2x weekly, probiotic lactobacilli / lactic acid gel OTC.
How does HIV present?
Seroconversion typically 2-6 (3-12 weeks) post-infection, symptomatic in 60-80% of patients, similar to EBV. Sore throat, lymphadenopathy, malaise, myalgia, arthralgia, diarrhoea, maculopapular rash, mouth ulcers, rarely meningoencephalitis. Triad of fever, pharyngitis and rash should increase suspicion.
How is HIV diagnosed?
Raised inflammatory markers, low lymphocytes. antibodies may not be present
HIV PCR and p24 antigen tests can confirm: p24 usually positive between 1-4 weeks after infection (sometimes used as additional screening in blood banks)
Antibody test: most common and accurate, usually both ELISA and confirmatory Western Blot – most develop at 4-6 weeks, but 99% do by 3 months
Complications HIV?
Early (CD4 <500): usually asymptomatic, generalised lymphadenopathy, skin disorders (seborrhoeic dermatitis, eosinophilic folliculitis, psoriasis)
CD4 200-500: worsening skin disorders, recurrent HSV, herpes-zoster multi-dermatomal, weight loss, diarrhoea, CAP
CD4 50-200: oral / oesophageal candidiasis, cervical dysplasia, PCP pneumonia, Kaposi sarcoma, lymphoma, mycobacteria avium intracellulare, histoplasmosis
Late (CD4 <50): cervical cancer, CMV retinitis, disseminated mycobacterium avium intracellulare, cerebral toxoplasmosis, primary brain lymphoma, multifocal leuko-encephalopathy and dementia
What is ART? When is it given?
Offered for chronic infection regardless of CD4 count, when presenting with AIDS-defining illness/bacterial infection or CD4 <200, offered immediately for primary infection
- also recommended in neurological involvement, AIDS-illness, CD4 <350, negative HIV test 12 weeks before diagnosis of primary infection
Triple therapy (HAART) = 2 NTRIs + either NNRTI / PI / II
- Entry inhibitors: Enfuvirtide, Maraviroc
- NRTIs: zidovudine, tenofovir, didanosine, TAF, lamivudine, abacavir, emtricitabine, stavudine
- NNRTIs: nevirapine, efavirenz, etravirine, rilpivirine
- Protease inhibitor (navir): darunavir, tripanavir, lopinavir, ritonavir, saquinavir, indinavir, fosamprenavir, nelifinavir, atazanavir
- Integrase inhibitors (gravir): raltegravir, dolutegravir, elevitegravir
Adherence critical, may need tailoring according to: baseline resistance profile, co-infection e.g. Hep B, TB, intolerable side effects, interactions e.g. CYP450.
HIV prevention measures?
Treatment as prevention: undetectable viral load = untransmittable
Antenatal screening introduced 2000, women with VL <40 can deliver vaginally
Infants born to mums with undetectable VL: 1 month Zidovudine (PEP) and tested until 18 months age
Indications chart
- Recommended if risk >1:1000 (risk source has HIV x risk of exposure)
- Consider if risk >1:10,000 + aggravating factor (risk source has HIV x risk of exposure)
- If it says ‘consider’ PEP as opposed to ‘recommend’: start PEP, test source next day, if negative, stop, if positive, continue PEP
What is PEP?
Truvada and raltegravir
- 48-72 hour window before HIV detected in regional lymph nodes
- Give PEP within 72 hours (but earlier better; 1-2 hours) and continue for 4 weeks
- Consists of combination of oral antiretrovirals (e.g. Tenofovir, emtricitabine, lopinavir and ritonavir)
- Testing at 12 weeks following completion of PEP, reduces transmission risk by 80%
Actions after pt presents with high risk of HIV exposure?
- Immediate test and start treatment if positive (with contact tracing); and arrange additional blood tests to later confirm diagnosis
- If negative: PEPSE if within 72 hours + advise about PREP (start after 28 days)
- Offer HPV and HEP A + B vaccination (long incubation periods)
- Full STI screening (return to clinic for full screen as chlamydia has 7-21 day incubation period and gonorrhoea has 5-8 day incubation period) – chlamydia and gonorrhoea screening after 2 weeks, HIV blood test after 6 weeks, syphilis testing after 12 weeks.
- Start 3 monthly testing program and arrange TOC.
What is PreP? When is it used?
PreP = Truvada (emtricitabine + tenofovir disoproxil fumarate)
- Event based dosing or daily dosing
- EBD: double dose (2 tablets) 2-24 hours before and 1 dose 24 & 48 hours after
- EBD only protects for anal sex, daily dosing also protects for vaginal sex
PreP given if: MSM likely to have unprotected anal sex in next 3 months, sex workers or paying for sex in countries with high prevalence, partners of HIV positive with detectable viral load (if undetectable for 6 months can stop PreP).
What is herpes simplex?
Neurotrophic DNA virus; HSV-1 usual cause of oro-labial cold sores; if new symptoms 80% chance it is HSV1; HSV2 is more likely to cause recurrent anogenital symptoms (cannot re-emerge from cervical spine but will re-emerge from lumbosacral spine).
At infection acquisition, 2/3rd establish latency in DRG, remaining 1/3rd have symptomatic first episode for 2-14 days; can cause potential transmission. If latency, can reactivate in form of asymptomatic shedding (transmissible) or symptomatic recurrent disease (also transmissible).
How is HSV diagnosed?
PCR (NAAT): HSV type-specific DNA detection, swab taken from base of lesion
Serology: HSV specific antibody detection – IgM unreliable, IgG indicates infection at some point, poor predictive value and takes several weeks to develop after primary infection
How does HSV present?
- Often asymptomatic
- Local: painful ulceration, dysuria, vaginal/urethral discharge
Progression of lesions: erythema / possible swelling of skin, may be painful/itchy> thin walled vesicles (blisters) on erythematous base > ulcers > scabbing > healed skin
Fever, myalgia, more common in primary infection
Recurrences are self-limiting and generally have minor symptoms only
Complications of HSV?
Super-infections with candida / strep
Autonomic neuropathy – urinary retention due to pain (peak pain day 11)
Autoinoculation to fingers and adjacent skin (stop wearing contacts)
Aseptic meningitis
Herpes proctitis (16% of proctitis in men) – only 1/3rd have visible external anal ulcers
Management of HSV?
1st episode: saline bathing, analgesia, topical anaesthesia e.g. 5% lidocaine ointment. Immediate oral acyclovir TDS 5 days or valaciclovir TDS 5 days (within 5 days of start of episode, while new lesions forming or persistence of systemic symptoms)
Recurrent: episodic antivirals (2 days acyclovir TDS, famaciclovir BD 1 day, valaciclovir BD 3 days) reduce duration by 1-2 days and severity, early (prior to papules) is most effective; short-course more convenient and cost-effective
Suppressive antivirals are given for 6 or more recurrences year, severe psychological morbidity, severe recurrences not controlled with episodic – reduces transmission; acyclovir BD.
Abstinence during recurrences / prodromes; condoms reduce transmission 50%, disclosure delays transmission
How does HSV affect pregnancy?
Management?
30% localised to skin / eye / mouth, causes <2% neuro/ocular morbidity if treatment given.
- Encephalitis carries 6% mortality and 70% neurological morbidity
- Disseminated infection has 30% mortality and 17% neurological morbidity with Tx
Management: If 1st episode in 3rd trimester: oral acyclovir 400mg TDS until delivery, elective C-section, 41% risk of neonatal herpes with vaginal delivery!
If acquired before pregnancy or in 1st-2nd trimester: vaginal delivery and consider antiviral prophylaxis from 36 weeks > 400mg TDS.
What is HPV
Double stranded DNA virus, 120 types, 30 infect ano-genital epihtlium: 16 & 18 are oncogenic (95% SCC of cervix) 6 & 11 are low risk (>90% of external ano-genital warts). 80% exposed to virus and 50% within 3 years of first sex; DNA found in 10-20% of those <50; <10% go on to develop warts (1% population), most common in 16-24 females and 20-24 males. Transient infection in most (HPV 6 lasting 6 months on average). Transmission ~65% in susceptible partners, majority develop warts at 2-3 months, condoms limited role, infectivity duration after treatment of warts is unknown.
How does HPV present?
Management?
Warts: usually little discomfort but irritation and soreness can occur especially around anus. If internal warts: distortion of urine flow, bleeding from urethra/anus.
All have significant failure+ relapse rate, doesn’t eradicate virus, may cause discomfort/local skin reactions, guided by site / extent / keratinisation / number / pregnancy.
- Podophyllotoxin: local tissue necrosis, for non-keratinised only, not safe for pregnancy
- Imiquimod: stimulates immune response, for keratinised warts, not for pregnancy, expensive
- Physical ablation (cryotherapy, hyfrecation, excision) – safe in pregnancy but painful, needs LA – for any site and any type.
Prophylaxis: bivalent 16+18 vaccine plus quadrivalent (6, 11, 16, 18)
- Over 90% effective in preventing new infections and cervical precancerous lesions
- Length of protection unknown
What is molluscum contagium?
Who does it affect?
Benign epidermal eruption of skin, large DNA pox virus (poxviridae). Routine physical contact (fomites) commonest presentation (over 90% to GPs) – children <15 on face neck trunk limbs. Max incidence 1-4 years, often children with eczema. STI: young adults, genitals, pubic region, lower abdomen, upper thighs, buttocks. Severe infection in context of immunocompromise especially late stage HIV.
How is molluscum diagnosed?
Presentation?
Clinical appearance (biopsy rarely needed)
Pinkish or pearly white papules with central umbilication, up to 5cm diameter
1-30 lesions at a time in clusters, can become koebnerised and affect almost any part of the body, often asymptomatic, occasionally: itch / discomfort / secondary bacterial infection, does not affect palms/soles. Very rarely oral mucosa / eyelids
Usually regress spontaneously within months
Complications of molluscum?
Mangement?
- Referral may be needed if HIV positive with extensive lesions, if eyelid/ocular lesions associated with red eye, anogenital lesions need GUM referral for screening for STIs
Management
- Self-limiting, spontaneous resolution within months
- Avoid sharing towels/clothing/baths
- Encourage not scratch, consider Tx for itch if problematic
o Squeezing or piercing following bath, few lesions at a time
o Cryotherapy in older children
o If eczema /inflammation – emollient, mild corticosteroids, topical Abx if infected
Exclusion from school/gym/swimming not needed
