Genital Tract Infections Flashcards

1
Q

What is partner notification?

A

Process of providing access to specific forms of healthcare for sexual contacts who may be at risk from an individual (index patient) diagnosed with an STI

-Confidentiality: common law duty of confidentiality/ NHS venereal diseases regulations 1974/ NHS Directive 1991

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2
Q

Methods of partner notification

A

-Patient referral
=Chooses to inform their own partners, record details on electronic record
-Provider referral
=Health advisor contacts, what infection and need to get tested
-Conditional referral
=consents with conditions (wait on result if contact of STI/ diagnosed with HIV)
-No referral
=No details/ declines

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3
Q

When to do PN for chlamydia

A

-Look back period for men with urethral symptoms 4 weeks prior to onset/ 6 months if not
-NGU/LGV

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4
Q

When to do PN for gonorrhoea

A

-Everyone treated even if contact/ look back urethral symptoms 2 weeks to onset, everyone else 3 months, positive testing: TOC 3 weeks post treatment

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5
Q

When to do PN for syphilis

A

-Primary 3 months prior, secondary or early latent syphilis 2 years prior, late latent or late syphilis to last known syphilis test or far back as possible

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6
Q

When to do PN for Hepatitis B and C

A

-2 weeks prior to jaundice or last negative test/ far back as can go

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7
Q

When to do PN for HIV

A

-All contacts in 3 months, complete within 3 months

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8
Q

When to do PN for TV

A

-4 weeks prior to presentation or current partner, men not tested but treated as contact

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9
Q

When to do PN for Mycoplasma

A

-Current partner or most recent sexual contact

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10
Q

When to do PN for PID

A

-Current male partners offer testing for STI (Chlam, gon), treated empirically with Doxy 100mg twice daily for 7 days

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11
Q

When not to do PN

A

Herpes or genital warts

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12
Q

Definition of Non-gonococcal urethritis

A

-Male patients
-Urethritis = inflammation of the urethra
-Gonococcal urethritis: when Neisseria gonorrhoeae is detected
-Non-gonococcal urethritis (NGU): when Neisseria gonorrhoeae is not detected

-Non-specific urethritis (NSU) = non-gonococcal, non-chlamydial urethritis

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13
Q

Urethritis diagnosis

A

-Smear from anterior urethra
-Gram smear microscopy
-5 or more polymorphonuclear leucocytes per high powered field (average 5 fields)

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14
Q

Infectious causes of NGU

A

-C trachomatis (11-50% prevalence)
-M. genitalium (6-50%)
-Ureaplasmas (11-26%)
-T. vaginalis (1-20%)
-Adenoviruses (2-4%)
-Herpes simplex virus (2-3%)
-Rarely: bacterial UTI, EBV, CMV, N. meningitidis, Haemophilus sp, Candida sp, BV bacteria

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15
Q

Describe chlamydia NGU

A

-Obligate intracellular bacterium C. trachomatis
-Most common bacterial STI in UK: highest prevalence rates under 25s
-Asymptomatic (more common) or symptomatic: genital and extra genital sites
-Complications include pelvic inflammatory disease, tubal infertility, ectopic pregnancy, SARA, Reiter’s syndrome

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16
Q

Describe MG NGU

A

-Smallest known self-replicating bacterium
-Sexually transmitted: vast majority of individuals with MG are asymptomatic
-Major concern is increasing drug resistance (>40% cases in UK now macrolide resistant)
-Can cause NGU and may also cause PID
-Testing and treatment limited o known contacts or those with recurrent NGU and PID

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17
Q

Clinical features of NGU

A

-Urethral discharge
-Dysuria
-Urethral discomfort

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18
Q

Signs of NGU

A

-Nil
-Urethral discharge
-Blanoposthitis

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19
Q

Complications of NGU

A

-DVT
-Eyes
-Red swollen testes

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20
Q

Diagnosis and Investigation of NGU

A

-Only assess symptomatic patients for urethritis
-Microscopic diagnosis – operator dependent (both smear taking and slide reading)
-(Hold urine 2 hours)
-Other markers – obvious mucopurulent discharge, threads in urine (less specific)

-Urine chlamydia and gonorrhoea NAAT
=(NAAT from extra genital sites if indicated)
-HIV and syphilis
-Dipstick +/- MSSU if indicated (history, risk assessment)
-Mycoplasma genitalium test only if recurrent or persistent urethritis

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21
Q

Treatment of NGU

A

-1st line treatment for NGU is doxycycline100mg BD for 1 week
=95% effective in men who are chlamydia positive (so no further Rx if CT positive)
=70% Effective against Urea plasma
=(Only 30% effective against MG)

-If M.gen detected:
=Azithromycin 1g stat , then 500mg daily for 2days if macrolide sensitive
=Moxifloxacin 400mg OD for 10 days if macrolide resistant (significant SE profile)

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22
Q

Patient information on NGU

A

-Causes of NGU
-Possible short and long-term health implications
-Treatment, side-effects and adherence
-Partner notification and treatment
-Advice to abstain from sexual intercourse until he has completed therapy and his partner(s) have been treated
-Follow-up
-Advice on safer sex (see UK national guideline on safer sex

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23
Q

Partner notification and follow up in NGU

A

-‘Look back’ period 4 weeks:
=PN especially important if chlamydia detected
=Useful for partners of symptomatic MG
=May be helpful with some patients with UU
-Follow up generally not required unless symptoms persist
-(Recurrent and persistent NGU)

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24
Q

Management of recurrent and persistent NGU

A

-Confirm diagnosis (presence of urethritis)
-Confirm treatment adherence
-Confirm partner treatment
-Discuss that inflammation may not necessarily mean ongoing infection
-Test for MG (consider TV, HSV testing)
-Retreatment should usually include TV and BV related organisms

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25
Q

Routine sexual health screen

A

-Chlamydia
-Gonorrhoea
-HIV
-Syphilis
-Consider hepatitis B and C, depending on risk
-ALL patients being offered a routine sexual health screen should be offered testing for HIV and syphilis

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26
Q

How to discuss HIV testing with a patient

A

-It can be difficult to start the discussion about HIV/BBV testing.

-What would you say to a patient you were offering an HIV test to?
-What do you need to know about HIV before you can have this discussion with a patient?

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27
Q

Why do we need to test HIV?

A

-Reduce morbidity and mortality– Late diagnosis
=Poor morbidity and mortality outcomes
=43% of all new HIV diagnoses were at a late stage of HIV infection in 2018
=1 year mortality–Late diagnosis = 23.62 per 1000Vs–Early diagnosis = 2.01 per 1000

-Early initiation of antiretroviral (ARV) therapy
=Improves life expectancy and reduces complication associated with HI
= Undetectable viral load = untransmittable
-PUBLIC HEALTH BENEFITS: Reduce transmission

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28
Q

Offering an HIV test to a patient

A

-Risk assessment
=Especially if a patient is unaware of their risk of HIV it is useful to establish any risk factors for HIV
=Gather this information with a non-judgemental and empathic approach and use this information to direct further discussion about HIV testing
-Patient concerns/expectation
=Share the benefits of early testing and treatment with the patient

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29
Q

Key groups to offer HIV testing to

A

1) People belonging to groups at increased risk of testing HIV positive
2) People attending certain health services
3) People presenting with symptoms and/or signs consistent with an HIV indicator condition
4) People accessing primary and secondary healthcare in areas of high and extremely high HIV seroprevalence
5) Sexual partners of those with diagnosed HIV

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30
Q

Groups at increased risk of HIV

A

-Men who have sex with men (MSM)
-Female sexual contacts of MSM
-People reporting current or prior injecting drug use
-Sex workers
-Trans women
-People from a country with high diagnosed seroprevalence (>1%)
-People reporting sexual contact with anyone from a country with high diagnosed seroprevalence regardless of where contact occurs.

-HIV testing should be considered for the following individuals
=Trans men
=Heterosexuals who have changed sexual partner(s)

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31
Q

Specialist services offering opt-out HIV testing and when/where to offer

A

-Specialist sexual health services
-Addiction and substance misuse services
-Antenatal services
-Termination of pregnancy services
-Healthcare services for hepatitis B and C, TB and lymphoma

-Opt out testing for all patients attending A+E
-When registering with a new GP
-Annual testing at GP practices

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32
Q

Symptoms and signs consistent with HIV

A

-Seroconversion-type illness
=Fever, sore throat, rash (+ identified risk of HIV)

-Severe, or recurrent, common conditions
=Shingles, herpes zoster
=Community acquire pneumonia
=Severe/unresolving dermatitis (or psoriasis)

-Non-specific symptoms/signs
=Unexplained lymphadenopathy
=Unexplained weight loss
=Pyrexia of unknown origin
=Abacterial meningitis
=Unexplained oral candidiasis
=Unexplained leucopenia or thrombocytopenia

-Hepatitis B or C
-AIDS-defining condition

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33
Q

Epidemiology and prevalence of HIV

A

≥ 2 per 1000 HIV seroprevalence
-Geographical regions include:
=sub-Saharan Africa: nearly 1 in every 25 adults (4.4%) living with HIV
=Caribbean: HIV prevalence in the region is 1.1%
=Latin America
=Europe (Ukraine)
=Asia (Thailand)

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34
Q

Why do we test hep B

A

-Chronic hepatitis B infection
=257 million people worldwide
=30% will develop liver cirrhosis and/or hepato-cellular cancer (HCC)
-Aim is to reduce transmission
-Vaccine preventable infection– Since 2017 included in infant vaccination schedule

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35
Q

BBV risk assessment

A

-Sexual partners
=Of a person with hepatitis B
=Of a person who injects drugs
=Men who have sex with men
=Sex workers and their clients/partners
-People who inject drugs (PWID)
-Routine ante-natal screen
-People who sustain a needlestick injury or have shared razors or toothbrushes with an infected person
-Health care workers involved in exposure prone procedures

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36
Q

Why do we test Hep C

A

-70-75% infected with hepatitis C develop chronic infection
=34 500 living with chronic hepatitis C infection in Scotland in2016
-Up to 15% will develop cirrhosis and are at risk of HCC
-Effective treatment available- Direct acting antiviral (DAA) therapy leads to sustained viral clearance in over 90% of patients
-Early diagnosis and treatment
=Reduces transmission
=Reduces morbidity and mortality

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37
Q

How do we test for Hep C?

A

-People who inject drugs (accounts for over 90% of all infections in Scotland)
-Sexual partners of PWIDs or person infected with hepatitis C (rare but dependent on type of sex increasing risk of blood to blood transmission)
-Engaging in two or more types of high risk sexual behaviour significantly increases the risk of transmitting hepatitis C. This includes includes but is not limited to:
=Unprotected anal sex
=Sharing sex toys that have been used anally
=Unprotected fisting
=Sex involving more than two people
=Chemsex (using drugs during sex: commonly crystal meth, GHB/GBL). Sharing a straw to snort drugs while engaging in sexual activities increases the risk of transmitting HCV
=Vaginal sex during menstruation
=Having sex when infected with an STI that could lead to blood-to-blood contact
=Any sexual activities which have the potential for blood-to-blood contact inherently increase the risk of transmitting hepatitis C. This includes rough vaginal sex that could cause bleeding from the penis or vagina. There is also a risk of blood leaking from any lesions on the penis

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38
Q

HIV and BBV testing window

A

-HIV 45 days
-Hepatitis B 160
-Hepatitis C 160-180

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39
Q

Genital ulcers history taking

A

-Characteristics of the ulcers (duration, number, pain, tenderness)
-Other symptoms:
=Lymphadenopathy, viraemic illness, skin rashes (mouth ulcers, eye symptoms, joint symptoms)
-Previous episodes?
-Sexual history
-Travel history
-PMH
-Drug history

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40
Q

Genital ulcers examination

A

-Ulcer appearance (number, depth, induration, tenderness, contact bleeding)
-Regional/ generalised lymphadenopathy
-Other:
=Skin rashes
=Mouth examination

41
Q

Infective causes of genital ulceration

A

Sexually transmitted infections
=Herpes simplex virus
=Treponema pallidum
=Chlamydia trachomatis (LGVsubtype)
=Haemophilus ducreyi
=Klebsiella granulomatis
=Trichomonas vaginalis
=Sarcoptes scabiei

-Usually not-sexually transmitted
=Pyogenic ulceration
=Candidal infection
=Mycobacterium tuberculosis
=Entamoeba histolytica
=Epstein Barr virus

42
Q

Dermatological causes of genital ulceration

A

-Contact dermatitis(irritant/ allergic)
-Lichen sclerosus
-Lichen planus
-Lichen simplex
-Psoriasis
-Squamous intraepithelial
-neoplasia
-Vulval carcinoma
-Basal cell cancer
-Genital aphthous ulcers

43
Q

Systemic causes of genital ulceration

A

-Bechet’s syndrome
-Erythema multiforme/
-Steven Johnson Synd
-Crohn’s disease
-Pyoderma gangrenosum

44
Q

Miscellaneous causes of genital ulceration

A

-Trauma
-Fixed drug eruption
-Other drug reactions(e.g. to Foscarnet)

45
Q

Epidemiology of genital HSV

A

-Herpes simplex virus (HSV) is the commonest cause of genital ulceration in the UK
-There are two types of HSV: HSV-1 and HSV-2:
=>50% of genital HSV infection is due to HSV-1 infection
= >95% of orolabial HSV infection (cold sores) is due to HSV-1 infection
-HSV-1 prevalence very high and increases with age: 54% of 25-30 year old females, >70%of 80 year olds in UK
-HSV-2 antibodies in around 10% UK adults
-Transmission rates 8-10% per year between partners
=Transmission rates significantly higher male to female partners

46
Q

Life cycle of HSV

A

-Infection of mucosal cells or abraded skin at portal of entry
-Virus replication occurs and results in host cell death
-Virus enters the sensory neuron terminals and travels retrogradely (via axonal transportation) to the dorsal root ganglion supplying area of infection, where it establishes latency
-Episodic reactivation of virus, with synthesis of infectious virions and passage back to area of skin supplied by the nerve

47
Q

Types of genital HSV infection and episodes

A

-Primary infection: first infection with either HSV-1 or HSV-2 in an individual with no pre-existing antibodies to either type
-Non-primary infection: first infection with either HSV-1 or HSV-2 in an individual with pre-existing antibodies to the other type

-Initial episode: first symptomatic episode with either HSV-1 or HSV-2
-Recurrent episode: recurrence of clinical symptoms due to reactivation of pre-existent HSV-1 or HSV-2 infection after a period of latency

48
Q

HSV 1 vs 2

A

-On average, symptomatic primary genital HSV-2 infection tends to be more severe than primary genital HSV-1 infection
-On average, symptomatic genital HSV-2 infection tends to have more recurrences than symptomatic genital HSV-1 infection:
=90% chance of HSV-2 recurrence in first year, 40-50% chance of HSV-1 recurrence
=HSV-2 four-five recurrences per year on average, HSV-1 zero-one recurrence per year
-Also higher rates of asymptomatic viral shedding with HSV-2 versus HSV-1 infection
-HOWEVER, 63% HSV-2 first infections are asymptomatic versus 37% of HSV-1 first infections. WHY?
=Prior HSV1 infection does not reduce the chance of getting HSV2, but does increase the chance of asymptomatic seroconversion

49
Q

Presentation of genital HSV

A

-Only about 1/3 of individuals develop symptoms around the time of infection acquisition (usually within 12-days of sexual contact)
-Prior infection with one type of HSV usually makes symptoms less severe during first infection with the other type of HSV (or results in asymptomatic infection)
-Severity usually worse in first episode versus recurrent disease

-Commonest symptoms and signs: multiple, painful blisters and ulcers (may be fissures)affecting external genitalia (also sometimes urethra, vagina, cervix, rectum, etc)
-Dysuria and penile discharge* Vaginal discharge
-Proctitis (HSV is a common cause of proctitis in MSM)
-Painful regional lymphadenopathy
-Systemic ‘flu-like’ symptoms – fever, malaise, myalgia, headache (usually in first episode)
-May have prodrome in recurrent disease (e.g. tingling neuralgia)

50
Q

Complications of genital HSV

A

-Bacterial superinfection of skin lesions
-Labial adhesions, phimosis, paraphimosis
-Urinary retention (result of severe pain or autonomic neuropathy)
-Autoinoculation to fingers and other skin (e.g. thighs, whitlow, keratitis)
-Eczema herpeticum
-Neurological complications - aseptic meningitis, encephalitis, etc
-Disseminated HSV disease (in immunosuppression, pregnancy, etc)
-Vertical transmission
-Increases both HIV transmission and acquisition risks

51
Q

Diagnosis of genital HSV

A

-Main investigation is HSV PCR
-ALL patients with genital ulceration should have syphilis serology performed
-MSM patients and those with atypical ulcers should also have syphilis PCR undertaken
-Offer full STI screen (NAATs can be deferred till review if patient in discomfort)
-Consider MCS test if suspicion of pyogenic ulceration or secondary bacterial superinfection

52
Q

HSV serological testing

A

-Type-specific testing for HSV antibodies: distinguishes between HSV 1 and HSV 2
-Can look for both IgG and IgM antibodies (established versus recent infection)
-May be useful in certain specific clinical scenarios. E.g:
=First HSV episode in 3rd trimester pregnancy
=Planning pregnancy, male partner has known HSV disease (but not female partner)
=Recurrent genital ulceration, proctitis, neurological symptoms, etc with no definite dx
-Careful discussion with patient/ partner required

53
Q

Treatment of genital HSV

A

-More important for first episodes
-Symptomatic management includes:
=Salt bathing (reduce bacterial superinfection and adhesions)
=Instillagel or lidocaine ointment
=Oral analgesia
=(Pee in shower if significant dysuria)
- Admit to hospital if there is of urinary retention, intractable pain, encephalitis/meningitis or if a female patient in the second or third trimester of pregnancy
-Treatment for first episode genital HSV: Aciclovir 400mg three times per day, for five days

54
Q

Follow up in genital HSV

A

-Not always necessary
-Review at 5-days if severe episode:– may require further course of treatment if still new lesions or continuing systemic symptoms
-For patients with milder symptoms, consider review at 2 weeks when results available
-Patients should be offered NAAT tests at review, if deferred at first visit

55
Q

Treatment for recurrent genital HSV

A

-Patient initiated episodic antiviral therapy (started within 6-12 hours of symptom onset, may abort 20-30% episodes, reduces the duration of an episode by a median of 1-2 days, Regimens: Aciclovir 400mg three times daily for 3 to 5 days OR Aciclovir 800mg three times daily for 2 days )
-Suppressive antiviral therapy (virologically confirmed genital HSV, recurrence rate of more than 6 episodes of genital herpes in the last 12 months, can reduce virus transmission to negative partners, has not been demonstrated to affect HIV transmission or acquisition risks in HSV seropositive individuals, aciclovir 400mg twice daily)
-The majority of patients with recurrent HSV will require only supportive measures

-Discuss oral antiviral therapy – most people will feel a benefit within 48-hours,though they should continue the full course of Rx. The ulcers may take up to 7-10days to completely heal however
-Discuss symptomatic relief measures

56
Q

General genital HSV patient information

A

-Genital HSV is a STI, acquired via SI (including oral SI). It is caused by the herpes virus, either HSV-1 (also causes cold sores) or HSV-2.
-HSV infection is common (can be either oral or genital carriage)
-Infection is life-long
-Many carriers are asymptomatic – up to 50% of those with HSV antibodies area symptomatic (or have not recognised symptoms), so do not know they have the virus and can pass on infection
-Only a minority of symptomatic carriers have their first episode around the time of infection acquisition. So first symptomatic episode does NOT necessarily mean recent infection acquisition
-HSV infection has no impact on fertility
-HSV infection is not usually an issue in pregnancy, unless first acquisition is in the 3rdtrimester (woman should be encouraged to tell their midwives in future pregnancies after a HSV diagnosis)
-Males should discuss diagnosis with their female partners, especially if considering pregnancy

57
Q

Natural history and Rx in genital HSV

A

-In symptomatic patients, first episode usually more severe than recurrences:
=at first infection there is a systemic immune response, causing the ‘flu-like’ symp
=local genital symptoms also tend to be more severe
-After the first episode, the virus then ‘goes to sleep’ in the local nerve root
-Every so often, there is virus activation, with virus coming to the surface of the skin again – patients are infectious when this happens
-Patients may experience symptoms (recurrent episodes) on SOME of these occasions
-Recurrent episodes are usually mild, local symptoms only and self-limiting (‘a cold sore at the genitals’)
-Recurrences tend to reduce in frequency over time (the first year is usually the worst)
=HSV-2 tends to recur more frequently than HSV-1, though everyone’s response to the virus is individual
-Treatment is only required for recurrences if significant symptoms
-If taking episodic treatment, it should be started early in recurrences (within 6-12 hours of symptom onset) to be effective
-Suppressive therapy may be appropriate for a small number of individuals, with frequent and severe recurrences

58
Q

Patient information for partners

A

-Partners, including future partners, should be informed of diagnosis
-Transmission probability is highest during symptomatic episodes and prodrome (so abstain from SI during these periods)
-Transmission between symptomatic episodes is possible, due to asymptomatic viral shedding
-Consistent and correct use of condoms, can reduce transmission of virus (though not definitely prevent it)
-Remember however that partners (including future partners), may be silent carriers of the virus themselves!

59
Q

Pathophysiology of syphilis

A

-Spirochete bacterium: Treponema pallidum subspecies pallidum
-Spirochetes: distinctive corkscrew like organisms that move with a spiralling motion (seen on DGM)
-Pathogenic and non-pathogenic treponemal types:– Pathogenic treponemes also cause the diseases Yaws, Pinta and Bejel

60
Q

Transmission of syphilis

A

-Primarily via SI – penetration of mucous membranes(easily transmitted via OI) or via abrasions on epithelial surfaces
-Around 45-60% of sexual contacts of infectious syphilis will be infected (10-60%)
-Placental transmission can occur at any stage of syphilis, commoner in early disease
-Very rarely (case reports): IVDU, blood transfusions(screening), kissing

61
Q

Epidemiology of syphilis

A

-Epidemic Ongoing since early 2000
-Initially in urban centres – London, Brighton, Manchester, Edinburgh
-Significant majority of those infected MSM (>70-80%)
-HIV co-infection common ( up to 25%)
-Slow drift in to the general population
-Some antenatal diagnoses of infectious syphilis now seen – threat of congenital infection (opt-out antenatal screening)

62
Q

Classification of syphilis

A

-Congenital infection (at birth)
=Early congenital
=Late congenital
-Acquired infection
=Acquired in adulthood

63
Q

Staging of acquired syphilis

A

-Early syphilis (infectious) within 2 years of acquisition
=Primary secondary early latent infection
-Late syphilis (after 2 years)
=Tertiary: gummatous/benign (15%), cardiovascular (10%), neurological (7%)
=Late latent

64
Q

Describe primary syphilis (chancre)

A

-Early localised infection
-Lesion at site of innoculation (commonly ano-genital region or oropharynx): initially papule, then ulcer
-Associated regional lymphadenopathy
-Incubation period 10-90 days (median 21)
-Spontaneous healing usually over 3-8 weeks
-May be unrecognised by patients
-Take PCR test from suspected chancres

65
Q

What is chancre?

A

-Classically a single, painless, indurated ulcer
-Clean base and a sharply defined border
-Serous exudate
-May be atypical however, especially if peri-anal ororo-pharyngeal sites (MSM) or in HIV positive patients

-Primary chancre of the penis (not classical, consider STS PCR/ serology on all patients with genital ulcers not typical of herpes- esp MSM or HIV positive)

66
Q

Describe secondary syphilis

A

-Affects >25% of infected patients
-Presents within 6 months of infection (average3 months)
-Systemic disease, thus varied presentations
=Rash (generalised, reddish and maculopapular. Usually non-pruritic, non-sparing of palms and soles)
=Generalised painless lymphadenopathy
=Constitutional symptoms (e.g. fever, myalgia, malaise, sore throat)
-Secondary syphilis symptoms will settle within3-12 weeks even if untreated
-Symptoms can relapse within first two years

67
Q

Less common symptoms of secondary syphilis

A

-Muco-cutaneous lesions: mucous membrane ulcers, condylomata lata, ‘moth-eaten’ alopecia
-Neurological: aseptic meningitis, cranial nerve palsies, nerve deafness/tinnitus, (syphilitic stroke)
-Ophthalmological: uveitis, keratitis, optic neuritis, retinitis
-Hepatitis
-Splenomegaly
-Glomerulonephritis (nephrotic syndrome)
-Periostitis
-Pneumonitis

68
Q

Describe condylomata lata

A

-Raised papules/nodules on moist areas of skin(perineum, peri-anally)
-May be mistaken for common warts
-Extremely contagious
-Do PCR testing

69
Q

Describe early syphilis in general

A

-Symptoms of both primary and secondary syphilis will resolve spontaneously even if untreated
-Disease moves to latent stage (early vs late)
-Untreated, a significant proportion (1/3) will progress to late stage symptomatic disease

70
Q

Describe latent syphilis

A

-Diagnosed on serology
-Arbitrary cut off of early vs late infection (2 years from acquisition)
-Early latent: infectious to sexual partners
-Late latent: non-infectious to sexual partners (but occasional MTC transmission)
=Serology cannot differentiate between syphilis and other pathogenic endemic treponemal infections
=Serology cannot differentiate late latent and treated infection

71
Q

Describe tertiary syphilis

A

-Late stage symptomatic disease
-Rare in the developed world (infection controlled by antibiotics given for other reasons)
-Affects 30-40% of untreated pts (average 10-40 years from initial infection)

72
Q

Describe gummatous tertiary syphilis

A

-Granulomatous lesions, with central necrosis
-Most frequently affects skin, bone
-Typically 15 years after infection acquisition
-Lesions resolve with treatment but scarring may remain

73
Q

Describe cardiovascular tertiary syphilis

A

-Possible manifestations:
=Aortitis (substernal pain)
=Aortic aneurysm(ascending aorta)
=AR (cardiac failure)
=Angina (coronary ostia involvement)

74
Q

Describe neurological involvement in syphilis

A

-Divided into 5 groups, which may overlap:
=Asymptomatic neurosyphilis
=Syphilitic meningitis
=Meningovascular syphilis
=General paresis
=Tabes dorsalis

75
Q

Describe syphilis in pregnancy

A

-60-70 percent pregnancies will be affected if mother has infectious syphilis
-Risk falls over time but pregnancies may rarely be affected up to 10 years from maternal infection acquisition (if woman remains untreated)
- >99% pregnant mothers in the UK currently receive antenatal STS screening

-Adverse pregnancy outcomes include:
=Miscarriage
=Stillbirth
=Preterm delivery
=LBW
=Perinatal death
=Congenital syphilis

76
Q

History taking in syphilis

A

-Previous syphilis testing:
=STI screening, blood donation, antenatal screening
-Previous diagnosis:
=When, where, treatment regimen, serology results
-Possibility of endemic treponemal infection:
=Residency in an endemic country, past skin infections, signs of Yaws, etc
-Previous/ current symptoms:
=Primary and secondary symptoms, neurological, ophthalmic or auditory symptoms, adverse pregnancy outcomes, tertiary symptoms
-Sexual history, partner notification details (including details about children, if relevant)

77
Q

Examination in syphilis

A

-Depending on symptoms, contact history, etc
-Early disease:
=Genitals, lymph nodes, skin (also mouth, scalp, palms and soles), neurological (ophthalmoscopy)
-Late disease:
=Skin, cardiovascular (AR), neurological
=Musculoskeletal system (if congenital syphilis suspected)

78
Q

Diagnosis of syphilis

A

-Clinical features
-Investigations:
=DGM: mainly for penile lesions (less suitable for other ano-genital lesions and unsuitable for oral lesions)
=PCR: both oral and genital lesions
=Serology: request extended panel testing if syphilis suspected or known positive contact
=(Full STI screening should be performed in any patient with suspected syphilis or attending as a contact)

79
Q

Types of serology testing in syphilis

A

-Treponemal: EIA IgG/IgM, TPPA (TPHA), FTA-Abs, T pallidum immunoblot
=Used in routine screening
=Treponemal antibody titers become positive soon after infection and usually remain positive for life, even with adequate therapy
=Positive in other pathogenic treponemal infections
=Antibody titers do not correlate with disease activity

-Nontreponemal: VDRL, RPR
=Tests are not specific for Treponemal infection
=Used for follow up
=Quantitative results correlate with disease activity: titers rise when disease is active, fall when treated(latent infection)

80
Q

Examples of serology

A

?

81
Q

Serology difficulties

A

-Cannot differentiate between pathogenic treponemal infections (Syphilis, Yaws, Pinta, Bejel)
-Not reliable alone for identifying disease stage or whether previous adequate treatment
-False positives with both treponemal and non-treponemal antibody tests
-Negative non-treponemal tests may occur early in primary or late in tertiary disease
-HIV patients can often have unusual serology:– prozone, false negative, delayed seroreactivity, etc

-Remember up to 3-months window period with screening tests
-Undertake full panel of serological tests in contacts and offer epidemiological treatment (as early syphilis)
-Repeat serology on day starting treatment: provides baseline for monitoring response to treatment
-General rule – treat if positive serology and no satisfactory history of adequate past syphilis Rx

82
Q

Treatment of syphilis

A

-Length of treatment regimen dependent on disease stage
-First line: penicillin based regimens (especially for HIV positive patients and in pregnancy)
=Benzathine penicillin (Procaine penicillin)
-Alternatives: Doxycycline, Ceftriaxone, Amoxy + Probenecid
-If cardiovascular or neurological involvement (including ophthalmic/ auditory complications) – oral steroid cover required

-Possible Rx complications include allergy (anaphylaxis),Jarisch-Herxheimer reaction and procaine mania
-Rx success decided by resolution of symptoms and change in serology:
=Serology must be repeated on first day of treatment to document baseline level (for peak VDRL/ RPR)

83
Q

Jarisch- Herxheimer reaction

A

-Acute inflammatory response to sudden release of dead treponemes into blood stream following treatment
-Manifestations: fever, chills and rigors, headache, general malaise or temporary exacerbation of the syphilitic lesions
-Usually with early infection, esp secondary syphilis
-Occurs within 6-12 hours of initial Rx (usually within 4-6hours), resolves within 24 hours
-May be confused with antibiotic allergy
-Steroid cover required if clinical symptoms of neurological, ophthalmic or cardiovascular disease

84
Q

Early (infectious) syphilis treatment

A

-First line:
=Single dose of Benzathine2.4 MU IM
-Alternative treatments:
=Doxycycline 100mg BD daily for 14 days

85
Q

Late syphilis (latent, cardiovascular or gummatous) treatment

A

-First line:
=Benzathine 2.4 MU IM weekly for 3 weeks
-Alternative treatments:
=Doxycycline 100mg BD daily for 28 days
-Steroids are required for cardiovascular syphilis treatment;40–60 mg prednisolone OD for three days, starting 24 h before antibiotics

-Neurosyphilis:
=Steroid cover and different penicillin regimen
-Treatment in pregnancy:
=Depends on stage of syphilis and pregnancy trimester

86
Q

Partner notification in syphilis

A

-Look-back periods:
=Primary syphilis: 3 months
=Secondary/ early latent syphilis: look-back period up to 2 yrs
=Late latent disease: patients do not usually transmit disease to partners. MTC transmission can happen for years after infection, but risk falls with time.
==If timing of late infection cant be determined, as minimum, current partners (and children of women diagnosed with late syphilis) should be tested

-Patients receiving treatment for syphilis should be seen by a health advisor for partner notification purposes
-Epidemiological Rx should be offered to contacts of infectious syphilis still within the window period
-Patients with infectious syphilis should be advised not to have sexual intercourse till 2-weeks after Rx completion and resolution of any syphilis lesions

87
Q

Follow up in syphilis

A

-Follow-up required to decide Rx success and detect reinfection
-Baseline serology should be undertaken on the first day of treatment, for follow-up comparison
-Serology repeat frequency:
=Usually at 1, 3, 6 and 12 months post Rx completion
=Then 6-monthly until VDRL/RPR negative or serofast – careful documentation to prevent unnecessary retreatment

88
Q

Aetiology and natural history of genital warts

A

-Anogenital warts are benign lesions caused by the human papillomavirus (HPV)
-90% are caused by HPV types 6 or 11
-Warts may also contain oncogenic HPV types (16 and 18)
-HPV infection is very common and most infections do not result invisible genital tract lesions
-Most infections resolve spontaneously within a year
-Incubation is variable, but generally between 3 weeks to 8 months

-Transmission is most often via sexual contact
-HPV may be transmitted perinatally
-Genital lesions resulting from transfer of infection from hand warts have been reported in children
-HPV preventative vaccination: bivalent (16,18) vaccine 2008for girls aged 12-13, quadrivalent vaccine (HPV 6/11/16/18)2012 (introduced for boys 2020)
-In Scotland quadrivalent vaccine introduced in MSM patientsup to the age of 45 in 2017

89
Q

Prevalence of genital HPV infection

A

-255 no prior or current genital papillomavirus infection
-60% prior infection probable antibodies to genital papillomavirus
-10% subclinical papillomavirus infection detected by DNA or RNA probes with amplification
-4% subclinical papillomavirus infection detected by colposcopy or cytology
-1% genital warts

90
Q

Symptoms of genital warts

A

-Asymptomatic
-Single or multiple lumps
-Typical lesions are condylomata acuminata
-Irritation or discomfort
-Bleeding
-Rarely, secondary infection or maceration

91
Q

Signs of genital warts

A

-Hyperplasic warts: commonly on non-keratinised stratified squamous epithelium (pink genital skin!)
-Women:
=posterior part of the vaginal introitus and on the adjacent labia majora and minora.
=clustered at the orifices of the greater vestibular glands(Bartholin’s glands).
-Men: glans penis and foreskin

92
Q

Other sites of HPV warts

A

-Other sites with similar epithelium:
=In both sexes, condylomata may be found in the anal canal, and can cause bleeding during defaecation
=Distal part of the urethra (uncommon proximal to this)
=Peri-genital keratinised stratified squamous epithelium:
==Perineum, pubis, inner thighs, buttocks
==‘Sessile’ flat warts more like typical non-genital warts

93
Q

Differential diagnosis of candylomata acumina

A

-Penile papillae (pearly)
-Vestibular papillae
-Pilosebaceous and Tyson’s glands/ Fordyce spots
-Molluscum contagiosum (pathological)
-Skin tags
-Condylomata lata (a feature of secondary syphilis): pathological

94
Q

Diagnosis of genital warts

A

-Usually a clinical diagnosis
-Occasionally biopsy may be required
-Examination should include the external anogenital and surrounding skin under good illumination
-Some patients present with intraepithelial neoplastic lesions
-Diagnosis of this is through biopsy
-Features which may raise suspicion include: Pigmentation/Depigmentation, Pruritus, Immune-deficiency, Prior history of intraepithelial neoplasia

95
Q

Management of genital warts: patient information

A

-Caused by human papillomavirus
-Very common
-Latent period is months or years
-Asymptomatic carriage is common
-No implication of infidelity in regular relationship
-Spread almost always sexual
-Notification of previous sexual partner(s) is not recommended

-New warts may appear even during treatment
-About 70% of people are clear of warts after 5 weeks of therapy
-Recurrence is very common
-Damaged skin may make them worse; make sure you look after your skin
-Smoking delays resolution of warts

96
Q

Treatment of genital warts

A

-No treatment is an option for small warts
-Cryotherapy is effective but takes up clinic time
-For very small warts a single treatment of cryotherapy may be appropriate. Give return appointments at 2 week intervals for cryotherapy only if other treatment options are contraindicated
-Do not continue with ineffective wart treatments – change to a different therapy
-Have a low threshold for the use of Imiquimod in extensive genital warts and in intra-anal warts (used if external genital warts extensive >10/ >5cm area, perianal)

-Fleshy external genital warts (<10/5cm^2):
1. Cataphen 3xD, men: podophyllotoxin 0.5% solution/ 0.15% cream, women: 0.15% cream 2xD for 3 days weekly for 5 weeks (contraindicated in pregnancy
2. Cryotherapy (2 weekly intervals for 5 cycles)

97
Q

Condom use in genital warts

A

-With any new partner, or a partner with whom sex has previously been protected, use condoms while warts are being treated and for six months after clearance although this does not guarantee prevention of transmission
-With a partner with whom sex regularly took place without a condom before warts appeared, there is little evidence of benefit in starting to use condoms. There is some evidence that the rate of clearance of warts is improved in those using condoms
-Condom use cannot be guaranteed to prevent transmission. Condoms do protect against the acquisition of HPV – young people without warts can be advised that condoms will provide some protection

98
Q

Treatment of anogenital warts in pregnancy

A

-Treatment not always warranted but aims to minimise the number of lesions present at delivery to reduce neonatal exposure to HPV
-Caesarean section is not indicated to prevent vertical transmission
-Podophyllotoxin is teratogenic, Imiquimod is not approved for use in pregnancy (no data available).
-Cryotherapy is the safer option in pregnancy
-Breastfeeding: Imiquimod: no specific advice in SPC. Podophyllotoxin: not recommended