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PT > STD: Syphilis, Herpes > Flashcards

STD: Syphilis, Herpes Flashcards

1
Q

what is syphilis caused by?

A

Treponema pallidum (bacteria)

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2
Q

what are the transmission routes of syphilis?

A
  1. sexual contact

2. mother-to-child (transplacental during pregnancy)

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3
Q

how do we diagnose syphilis?

A
  1. Darkfield microscopy of exudates from lesions
  2. TWO serological tests needs to be conducted:
    a. Treponemal test (for confirmatory)
    b. non-treponemal test (for monitoring)
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4
Q

what is presentation for primary syphilis?

A
  • heals spontaneously in 1-8 weeks
  • site of infection: external genitalia, perianal region, mouth, throat

Signs and sx:
- single painless ulcer or chancre at the site of infection but can also present with multiple, atypical or painful lesions

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5
Q

what is the presentation for secondary syphilis?

A
  • develops 2-8 weeks after the initial infection in untreated or inadequately treated individual
  • disappears in 4-10 weeks if untreated
  • Site of infection: multisystem due to hematogenous and lymphatic spread
    • Signs and sx:
  • includes skin rash, mucocutaneous lesions, and lymphadenopathy (swollen and painful lymph node)
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6
Q

what is presentation for latent syphilis?

A

definition:
~ early <1yr
~ late >1yr

  • develops 4-10 weeks after secondary stage in untreated or inadequately treated individual

site of infection: possible multisystem involvement

    • signs and symptoms:
  • asymptomatic but picked up by serology testing
  • internal organs continue to be affected by infection

note: as asymptomatic –> untreated can go to tertiary wo the person knowing

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7
Q

what is the presentation for tertiary syphilis

A
  • develops in ~30% of untreated or inadequately treated individual 10-30yrs after initial infection

site of infection: possible multisystem heart, eyes, bones, joint

signs and symptoms:

  • gummatous lesions in joints leading to impaired movement
  • cardiac involvement leading to heart-aortic insufficiency
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8
Q

what is the presentation for neurosyphilis

A
  • CNS involvement occurring at ANY stage of syphilis
  • site of infection: CNS
  • signs and symptoms:
  • -> cognitive dysfunction, motor or sensory deficits, –> ophthalmic or auditory symptoms,
  • -> signs and sx of meningitis, stroke
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9
Q

what is the purpose of treponemal serology test for diagnosing syphilis?

A
  • uses treponemal antigen to detect treponemal antibody

1st type of test: T. pallidum Hemagglutination test (TPHA)

2nd type of test: T. pallidum passive particle agglutination assay (TPPA)

  • these treponemal tests are more sensitive and specific than non-treponemal test, thus used as CONFIRMATORY tests
  • may remain reactive for life, thus NOT for monitoring response to treatment
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10
Q

what is the purpose of non-treponemal serology test for diagnosing syphilis?

A
  • uses nontreponemal antigen (cardiolipin) to detect treponemal antibodies

1st type of test: venereal disease research laboratory (VDRL) slide test

2nd type of test: rapid plasma reagin (RPR) card test

results: a positive test can indicate presence of ANY stage of syphilis

results reported in quantitative manner = the most dilute serum conc with a positive reaction

e. g.
1: 16 positive means at 1:32 no reaction is seen
(note: 1:16 means that easier to clear the bacteria out of the body compared to 1:32)

  • used as a tool to monitor response to treatment
    (note VDRL/RPR are NOT interchangeable)
  • titres usually declines after treatment and can become non-reactive with time
  • less specific, thus if positive is seen in this nontreponemal test, it needs to be confirmed with a treponemal test
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11
Q

syphilis treatment for primary, secondary, or early latent (<1yr)

A
  1. IM benzathine penicillin G 2.4 million units x 1 dose

for pencillin-allergic:
2. PO doxycycline 100mg BID x 14 days
(counselling: take w food to reduce GI upset.
take with water and remain upright for at least 30min to prevent heartburn.
don’t take with milk, Ca, Fe, take 2 hours apart.

SEL GI, photosensitivity)

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12
Q

syphilis treatment for late latent (>1yr) or unknown duration or tertiary

A
  1. IM benzathine penicillin G 2.4 million units once a week x 3 doses

for penicillin-allergic:
2. PO doxycyline 100mg BID x 28 days

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13
Q

syphilis treatment for neurosyphilis

A
  1. IV crystalline penicillin G 3-4 million units q4h OR 18-24 million units/day as continuous infusion x 10-14 days

OR

  1. IM procaine penicillin G 2.4 million units daily + PO probenecid 500mg QID x 10-14 days

for penicillin allergic:
3. IV/IM ceftriaxone 2g daily x 10-14 days (note: cross-reactivity of penicillin with cephalosporins v low)

(if concern for cross-sensitivity - skin test to confirm pencillin allergy, desensitize if necessary)

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14
Q

what are the monitoring parameters for syphilis?

A
  1. Jarisch-Herxheimer rxn: acute febrile rxn accompanied w headache, myalgia, and other symptoms
    - appears within the first 24 hours after any therapy for syphilis
    - note: antipyretics will help but NOT prevent
  2. for primary/secondary syphilis:
    - VDRL or RPR at 6 and 12 months
    - treatment success = decrease of VDRL or RPR titre by at least fourfold (e.g. 1:64 to 1:16)
  3. for latent/tertiary syphilis: VDRL or RPR at 6, 12 and 24 months
  4. for neurosyphilis: CSF examination every 6 month until CSF normal
  5. Treatment failure at 6 months:
    a. shows signs and symptoms of disease OR
    b. fail to decrease VDRL or RPR titre by fourfold OR increases (1:16 to 1:64)
    c. retreat and re-evaluate for unrecognized neurosyphilis
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15
Q

what are some management protocols of the sexual partners for syphilis?

A
  • sexual partners should be evaluated for STIs and treated if tested positive
  • abstinence for 7 days after single-dose regimen OR
  • abstinence during the 10-14/28-day regimen and resolution of symptoms, if present
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16
Q

what is the herpes virus

A
  • is an enveloped virus with double-stranded DNA
  • lacks a cell wall, cell membrane, and ribosomal structures
  • replicate in host cell nucleus
  • persist indefinitely (life-long) in infected host (latent infection)
  • periodic reactivations, esp in immunocompromised hosts
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17
Q

how is herpes virus replication inhibited

A
  • acyclovir/ valacyclovir inhibits viral DNA polymerase –> inhibits DNA synthesis and replication
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18
Q

3 common types of herpes viruses and what are their common names?

A
  • Human herpesvirus 1 = Herpes simplex virus 1
  • Human herpesvirus 2 = Herpes simplex virus 2
  • human herpesvirus 3 = varicella-zoster virus
19
Q

difference between HSV-1 and HSV-2

A

HSV-1:

  • young children
  • contact (often saliva) transmission
  • diseases: herpes gingivostomatitis, herpes labialis (cold sore)
  • management = self-limiting usually; PO acyclovir or valacyclovir; topical acyclovir (modest benefit)

HSV-2:

  • young adults
  • sexual*
  • disease = genital herpes

management = usually self limiting; PO acyclovir or valacyclovir

For BOTH HSV-1 and HSV-2:
reactivation (relapse/ recurrence/flares) =
- stimuli e.g. fever, menstruation, sunlight, stress etc can reactivate the virus

  • reactivation may be clinically asymptomatic, or it may produce life-threatening disease
20
Q

varicella zoster virus; what two form of diseases it can cause?

A
  1. primary VZV = diffuse vesicular rash of varicella, or chicken pox
  2. reactivation of latent VZV = herpes zoster, or shingles
    - virus persisting in the nerve ganglia reactivated
21
Q

what are the characteristics of varicella (chickenpox)?

A
  • benign self-limiting
  • but can be severe disease in immunocompromised individuals
  • fever starts 1-2 days before rash appears and lasts for 4-5 days;
  • fever is gone once the rash has completely appeared
  • groups of new lesions appear over 4-7 days
  • pox/rash on most parts of the body
  • -> got papules (no pus), vesicles (clear fluid), pustules (pus), scabs
22
Q

what are the characteristics of herpes zoster (shingles)

A
  • increase risk: increasing age and immunosuppression
  • rash begins as papules, evolves into vesicles, and onto pustules
  • new lesions appear for 3-5 days, usually dries with crusting in 7-10 days
  • rash usually precedes by tingling, itching, or pain (or combination of these) for 2-3 days, and these symptoms can be continuous or episodic
  • post-herpetic neuralgia occurs in 10-50% of patients
  • pain that persist after the rash has resolved
  • pain may persist for many months
23
Q

treatment for varicella/shingles (human herpesvirus 3)

A

Acyclovir and valacyclovir (to start within 24-48 hours of rash) to reduce duration and severity of symptoms

  1. Acyclovir dose: PO 800mg 5 times daily x 7 days
  2. Valacyclovir dose: PO 1g 3 times daily x 7 days (vala preferred over acyclovir)
  3. vaccines available to PREVENT chicken pox and shingles
24
Q

which herpes virus causes genital herpes?

A

HSV-2

HSV-1 causes cold sore, not a STI

HSV-3 causes (varicella) chickenpox/ (herpes zoster) shingles not a STI

25
Q

characteristics of genital herpes

A
  • HSV-1 & HSV-2 but
  • HSV-2: most recurrent genital herpes
  • 5 stages of a HSV infection:
    a. primary mucocutaneous infection
    b. infection of the nerve ganglia
    c. establish latency
    d. reactivation
    e. recurrent outbreaks/flairs
  • vesicles develop over 7-10 days, heal in 2-4 weeks
  • intermittent viral shedding from epithelial cells –> person can be asymptomatically transferring herpes to their sexual partners
  • chronic and life-long viral infection
  • may not be symptomatic while shedding and transmission occurs
26
Q

how is genital herpes transmitted?

A

transfer of body fluids and intimate skin-to-skin contact

27
Q

how is HSV-3 transmitted (chickenpox and shingles)

A

virus can be inhaled

28
Q

how do we diagnose genital herpes?

A
  1. patient history: previous lesion/ sexual contact with similar lesions
  2. Presentation/symptoms:
    - classical painful multiple vesicular or ulcerative lesions
    - local itching, pain, tender inguinal lymphadenopathy
  • flu-like symptoms (e.g. fever, headache, malaise) during the first few days after appearance of lesions
  • prodromal symptoms (before the lesions): mild burning, itching, tingling seen in ~50% of patients prior to appearance of recurrent lesions (seen in the recurrent disease)
  • symptoms are less severe in recurrent disease (less lesions, heal faster, milder symptoms)
    (as ab from the first infection)
29
Q

what are 2 test can be done to diagnose genital herpes

A
  1. Virologic test
    - viral cell culture and NAAT/PCR for HSV DNA from genital lesions
  2. Type-specific serologic tests (send blood to look for ab)
    - Ab to HSV develop during the first several weeks after infection and persist indefinitely
    - serology is NOT useful for first episode infection as it takes bet 6-8 weeks for serological detection after the first episode
    - presence of HSV-2 Ab implies anogenital infection
30
Q

what is the goal for the treatment of genital herpes?

A
  • relieve symptoms, shorten clinical course, prevent complications and recurrences, decreases transmission
31
Q

what are the supportive care (non-pharmacological) for genital herpes?

A
  • warm saline bath relieves discomfort
  • good genital hygiene to prevent superinfection
  • counselling regarding natural history
32
Q

what are the antiviral treatment for FIRST episode of genital herpes?

A
  1. Acyclovir
    - 400mg TDS x 7-10days
    OR
    - IV 5-10mg/kg q8h x 2-7 days, complete with PO for total 10 days (for severe disease or complications that requires hospitalisation)
  2. Valacyclovir 1g BD for 7-10 days

Treatment can be extended if healing is incomplete after 10 days of therapy

33
Q

why use acyclovir and valacyclovir as the anti-viral treatment for genital herpes?

A

proven to:

  • reduce viral shedding by 7 days
  • reduce duration of symptoms by 2 days
  • reduce time to healing of FIRST episode by 4 days
  • both drugs have comparable efficacy and tolerability; thus the choice of drug is dependent on patient compliance and cost (valacyclovir BD vs acyclovir TDS)
  • maximum benefit when initiated at the earliest stage of disease (within 72hours)
  • DOES NOT prevent latency or affect frequency and severity of recurrent disease after drug is discontinued
  • topical antiviral offers minimal clinical benefit, also can cause local irritation; thus use of it is discouraged
34
Q

acyclovir and valacyclovir; their route of inhibition (MOA)

A
  • acyclovir inhibits viral DNA polymerase –> inhibits DNA synthesis and replication
  • valacyclovir is a L-valine ester of acyclovir
    valacyclovir –> acyclovir + valine

acyclovir’s F: 10-20%, t1/2 = ~3hrs

valacyclovir’s F: 55%, t1/2 = ~3hrs

35
Q

counselling when administering acyclovir and valacyclovir

A

acyclovir: take wo regards to food, after food is possible if GI upset is present

SE: Malaise, headache, N/V/D
- maintain adequate hydration to prevent crystallisation in renal tubules (more common in IV)

valacyclovir:
as per acyclovir hydration
- main SE: headache

36
Q

definition of recurrent genital herpes

A

median of 4 recurrence the year after their first symptomatic episode

  • recurrent flares are common
37
Q

what are the pharmacological management for recurrent genital herpes

A

Chronic suppressive or episodic therapy

- choice based on patient’s preference

38
Q

what are the advantages and disadvantages of chronic suppressive therapy

A

advantages:
- reduces freq of recurrence by 70-80% in patient who have freq recurrence (i.e. >6 recurrences per year)

  • many pts report no symptomatic outbreaks
  • improved QOL
  • established long term safety and efficacy
    • decrease risk of transmission (in combi with consistent condom use and abstinence during recurrence)
  • -> reduces viral shedding, including asymptomatic shedding

disadvantages:

  • cost and
  • compliance
39
Q

the treatment regimen for chronic suppressive therapy

A
  1. *acyclovir 400mg PO BD

OR
2. valacyclovir 500mg PO OD (this many not effective for those that have >=10 episodes/year)

  1. *valacyclovir 1g PO OD
  2. famciclovir (not found in SG): 250mg PO BD

duration: dependent on patient and disease
- patient with complicated disease e.g disseminated disease (encephalitis, meningitis, keratitis), usually in immunocompromised host, may need indefinite suppression

40
Q

advantages and disadvantages of episodic therapy

A

advantages:
- shorten duration and severity of symptoms

  • less costly vs chronic suppression therapy
  • patients more likely to be compliant

disadvantages:

  • requires initiation of therapy WITHIN 1 day of lesion onset or during prodrome that precedes some outbreaks
  • does not reduce the risk of transmission (doesnt reduce viral shedding)
41
Q

the treatment regimen for episodic therapy

A
  1. acyclovir 800mg PO BD x 5 days
    (400mg TDS x 5 days also can but not recommended bcos of freq of dosing)

or

  1. acyclovir 800mg PO TDS x 2 days

or

  1. valacyclovir 500mg PO BD x 3 days

or

  1. valacyclovir 1g OD x 5 days

or

5. Famciclovir 1g PO BD X 1 day
or
6. Famciclovir 500mg PO once, followed by 250mg BD x 2days
or
7. Famciclovir 125mg PO BD x 5 days
42
Q

counselling of persons with HSV infection

A
  • educate concerning the natural hx of the disease
  • encourage to inform their current and future sex partners
  • sexual transmission of HSV can occur during asymptomatic periods
  • those w genital herpes should remain abstinent from sexual activity with uninfected partner when lesions or prodromal symptoms are present
  • risk of HSV sexual transmission can be decreased by daily use of acyclovir/valacyclovir by the infected person
  • latex condoms when used consistently and correctly, might reduce risk of genital herpes transmission
  • risk of neonatal HSV infection (during labour process)
  • increase risk for HIV acquisition (2x more likely)
43
Q

management of sex partners for genital herpes

A
  • symptomatic sex partners should be evaluated and treated in the same manner as pts who have genital lesions
  • asymptomatic sex partners of patients who have genital herpes should be questioned concerning hx of genital lesions and offered type-specific serologic testing for HSV-2 (as HSV-2 causes genital herpes)

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