STIs 2 Flashcards

1
Q

ddx for genital ulcer disease

A

1. Herpes Simplex Virus (type 2 > type 1)
2. Syphilis (Treponema pallidum)

3. Chancroid (Haemophilus ducreyi)
4. Lymphogranuloma venerium (LGV), caused by C. trachomatis

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2
Q

Herpesviridae - species

A
  1. Human virus:
    -HSV1 (human herpesvirus 1)
    -HSV2 (human herpesvirus 2)
    -Varicella zoster virus (HHV-3)
    -Epstein Barr virus (HHV-4)
    -CMV (HHV-5)
    -HHV6
    -HHV7
    -HHV8 (Kaposi’s sarcoma herpesvirus)
  2. Simian virus:
    -Herpes B virus
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3
Q

human herpesviruses - overview

A

*establish latent infection in specific target cells
*infection persists despite the host immune response, often with recurrent disease
*HSV1, HSV2, VZV, EBV, CMV, etc

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4
Q

herpes simplex virus (HSV) - epidemiology

A

*most common cause of genital ulcer disease worldwide
*genital herpes most often due to HSV2, but HSV1 becoming more common
*most cases are asymptomatic
*risk related to lifetime number of sex partners, age of sexual debut, and history of other STIs

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5
Q

HSV - transmission

A

*close contact with person shedding virus:
-inoculation of HSV2 on susceptible mucosal surface or crack in skin
-vertical transmission from mother to fetus during pregnancy/birth
*majority of genital herpes infections are transmitted by persons who are unaware they are infected or aysmptomatic
*incubation period = 2 to 12 days
*drying and soap&water readily inactivate HSV; fomite transmission unlikely

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6
Q

HSV pathogenesis

A
  1. exposure to virus → viral replication in epidermis →
  2. infection of sensory/autonomic nerves →
  3. intra-axonal transport to nerve cell bodies →
  4. HSV1 (trigeminal), HSV2 (sacral ganglia)
  5. latent virus in sensory ganglion, which then reactivates (recurrent infection):
    -triggers: trauma, UV light, immunosuppression
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7
Q

HSV1 - latent cell

A

*latency in trigeminal nerve

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8
Q

HSV2 - latent cell

A

*latency in sacral ganglia

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9
Q

HSV clinical manifestations: primary episode

A

*characterized by multiple lesions that are more severe, last longer, and have higher titers of virus than recurrent infections
*typical lesion progression: papules → vesicles → pustules → ulcers → crusts → healed
*often associated with systemic sx including: fever, headache, malaise, myalgia
*cervicitis, urethritis, perianal infection, proctitis
*illness lasts 2-4 weeks

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10
Q

HSV clinical manifestations: recurrent disease

A

*usually localized to defined mucocutaneous site
*symptoms more mild, duration shorter
*frequency and number of recurrences decreases over time
*prodromal symptoms
*“atypical” syndromes common (fissures)

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11
Q

genital herpes - diagnosis

A

*patient history and clinical presentation
*laboratory tests:
-virus detection tests (culture, PCR of lesion)
-serology

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12
Q

HSV treatment

A

ACYCLOVIR
other options: valacyclovir, famciclovir
*generally treat for 7-10 days
*MOA: all phosphorylated by cellular and herpesvirus kinases that inhibit viral DNA synthesis (
requires the virus for the treatment to work
)

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13
Q

HSV prevention

A

*antivirals - decrease transmission by 55%
*condoms - decrease transmission by 30%

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14
Q

HSV - treatment approaches of recurrences

A
  1. episodic treatment
  2. suppressive treatment:
    -reduces frequency of recurrences
    -reduces but does not eliminate subclinical viral shedding
    -periodically, reassess need for continued suppressive therapy
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15
Q

HSV2 - complications

A

*urinary retention
*sacral radiculopathy

*aseptic meningitis
*pneumonia
*hepatitis
*transverse myelitis, autonomic sx, decreased reflexes/motor strength

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16
Q

syphilis - microbiology

A

*etiologic agent = Treponema pallidum
*corkscrew-shaped, motile microaerophilic bacterium

*cannot be cultured in vitro; cannot be viewed by normal light microscopy

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17
Q

syphilis - pathophysiology

A
  1. penetration: T. pallidum enters the body via skin and mucous membranes through abrasions during sexual contact
  2. dissemination: travels via the lymphatic system to regional lymph nodes and then throughout the body via the bloodstream

*vertical transmission: transplanted transplacentally from mother to fetus during pregnancy

18
Q

primary syphilis - clinical presentation

A

*primary lesion or “chancre” develops at the site of inoculation
*chancre: progresses from macule → papule → ulcer
-typically PAINLESS, indurated, and has a clean base
-highly infectious
-heals spontaneously in 1-6 weeks
-25% present with multiple lesions
*regional lymphadenopathy: classically rubbery, painless, bilateral
*note - serologic tests for syphilis may not be positive during early primary syphilis

19
Q

secondary syphilis - clinical presentation

A

*secondary lesions occur 3-6 weeks after the primary chancre appears; may persist for weeks to months
*primary and secondary stages may overlap
*manifestations: rash (maculopapular, can involves palms + soles), lymphadenopathy, malaise, MUCOUS PATCHES, CONDYLOMATA LATA, alopecia
*serologic tests are usually highest in titer during this stage

20
Q

latent syphilis - overview

A

*host suppresses infection (no lesions are clinically apparent)
*only evidence is positive serologic test
*may occur between primary and secondary stages, between secondary relapses, and after secondary stage
*categories:
-early latent = < 1 year duration
-late latent = 1+ year duration

21
Q

tertiary (late) syphilis - clinical manifestations

A

*approx 30% of untreated pts progress to tertiary stage within 1-20 years
*rare d/t widespread availability and use of antibiotics
*manifestations:
1. gummatous lesions
2. CARDIOVASCULAR SYPHILIS (ascending thoracic aortic aneurysm)

22
Q

neurosyphilis - overview

A

*occurs when T. pallidum invades the CNS
*may occur at any stage of syphilis
*clinical manifestations:
-asymptomatic; psychiatric changes
-acute syphilitic meningitis
-meningovascular (strokes classically in middle cerebral artery distribution)
-ocular syphilis (uveitis)
-general paresis (progressive dementia & generalized paralysis)
-TABES DORSALIS

23
Q

neurosyphilis: tabes dorsalis

A

*demyelination of sensory neurons in posterior columns:
-paresthesias
-locomotor ataxia (high-stepping gait with foot slap due to lack of proprioception)

24
Q

syphilis - diagnosis

A
  1. primary: clinical + serology
  2. secondary: serology
  3. tertiary: clinical + serology
  4. neurosyphilis: serology on serum + CSF
25
Q

syphilis serology - nontreponemal

A

*traditional screening
*not specific for T. pallidum (can be positive with other syndromes)
*purified cardiolipin with TITER
*tests:
-RPR (rapid plasma reagin) = most common
-VDRL (venereal disease research laboratory) = on CSF

26
Q

syphilis serology - treponemal

A

*cannot distinguish active vs past infection
*performed when nontreponemal test (RPR, VDRL) is positive
*automated screening and confirmation
*tests:
-FTA-ABS
-MHA-TP

27
Q

syphilis - treatment

A

TREATMENT OF CHOICE IS ALWAYS PENICILLIN
*primary, secondary, and early latent: benzathine PENICILLIN G injection
*late latent and tertiary: 3 injections (1 per week) if benzathine PENICILLIN G
*neurosyphilis: aqueous crystalline penicillin G IV for 10-14 days (DOES NOT MATTER IF ALLERGIC TO PENICILLIN)

28
Q

syphilis treatment - penicillin allergy

A

*must DESENSITIZE pt to penicillin (give small doses in escalating levels)
*this is required if pt is pregnant or has neurosyphilis

29
Q

Jarish-Herxheimer reaction

A

*acute febrile reaction with headache, myalgia, fever within 24 hours of syphilis therapy
*transient, cytokine-mediated reaction to rapid killing of circulating spirochetes

30
Q

chancroid (Haemophilus ducreyi)

A

*declining prevalence in US and worldwide (sporadic outbreaks)
*clinical dx: painful ulcer, regional LAD
*treatment: azithromycin or ceftriaxone

31
Q

Lymphogranuloma venereum (LGV) - overview

A

*classic Chlamydia trachomatis genital ulcer disease
*self-limited, tender papule → ulcer; LAD
*serovars L1, L2, and L3
*most frequently in tropical and subtropical areas
*more common in men than women

32
Q

Lymphogranuloma venereum (LGV) - diagnosis

A

clinical dx:
*genital ulcer disease with lymphadenopathy (groove sign)
*proctitis (in MSM)

dx = SEROLOGY

33
Q

Lymphogranuloma venereum (LGV) - treatment

A

doxycycline

34
Q

condyloma acuminata - overview

A

*human papillomavirus (HPV types 6 or 11)

contrast to condyloma lata associated with syphilis; syphilitic lesions are broader, flatter, and paler than HPV lesions

35
Q

human papillomavirus (HPV) - epidemiology

A

*90% of adults in the US will become infection with HPV
*after exposure, infection with HPV often clears spontaneously

36
Q

human papillomavirus (HPV) - microbiology

A

*nonenveloped double-stranded DNA virus
*more than 400 types identified

*ONCOGENIC strains = 16 and 18
*NONONCOGENIC strains = 6 and 11

37
Q

HPV-related squamous cell dysplasias

A

*cervical
*vulvar/vaginal
*penile
*anal
*oropharyngeal

38
Q

HPV - diagnosis

A

*clinical
*pap smear (cervical, anal in high-risk pts)
*culture (not reliable)
*molecular techniques = nucleic acid probe tests, amplification

39
Q

HPV vaccines

A

*Gardasil 9 (9vHPV) vaccine: protection against HPV types: 6, 11, 16, 18, 31, 33, 45, 52, 58
*noninfectious core proteins
*3 doses or 2 doses if < age 15

40
Q

HPV vaccine - considerations

A

*vaccine is still recommended if:
-history of genital warts
-abnormal pap test
-positive HPV DNA test
*routine pap smears should still be performed after vaccination

41
Q

prevention of STIs - overview

A

*limit sexual partners
*condom use (correct & consistent)
*screening of asymptomatic populations
*pt counseling: abstain from sexual intercourse until partners are treated and for 7 days after tx
*partner treatment: most recent partner & all partners in past 90 days