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Repro > STIs and STI treatment > Flashcards

STIs and STI treatment Flashcards

1
Q

HPV structure, transmission, genome maintenance in host cell?

A
    • circular dsDN, icosahedral capsid composed of L1 and L2 “late” proteins that self assemble (Vaccine basis!)
    • Non enveloped = more stable, can survive on skin/fomites

– transmitted via skin-skin contact /fomites

    • Benign tumor cells (warts) –> extrachromosomal genome
    • Malignant tumor (cervical carcinomas) –> integrated into host genome (E6 and 7, with E2 disruption - loss of regulation)
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2
Q

how do papilloma viruses grow in permissive vs non - permissive cells? how does this effect tx?

A
  • initially infect germinal cells (non permissive = no viruses produced) and transform them
  • germinal cells mature/migrate to skin surface –> become permissive /produce virus progeny
    • tx: difficult to completely eradicate infection while virus remains in germinal cell layer
    • proliferating cells also shed virus ie spread via direct contact and tend to cluster
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3
Q

HPV Subtypes for:

    • common warts (verruca vulgaris or plana),
    • Anogenital (condyloma acuminata vs condyloma plana),
    • sub clinical papilloma infection (SPI) / cervical / penile / oral / neck cancers, laryngeal papilloma
A

– common warts - don’t know

– anogential:
acuminata = 6 and 11
plana = 16, 18

– SPI and carcinomas = 16, 11, 31, 33

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4
Q

Koilocyte

A

– squamous epithelial cells that are indicative of HPV infection

Histo: vacuolated cytoplasm

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5
Q

SPI

A

Sub Clinical Papilloma Infection: not readily detected, more of a concern than condyloma plana or acuminata bc of link to cervical cancer

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6
Q

Laryngeal Papilloma

A
    • chronic, benign warts in respiratory tract that generally appear < 5 yo (Genotypes 6 and 11)
    • due to maternal HPV infection intrapartum

**Associated with respiratory distress –> 3% = deaths

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7
Q

Epidermodysplasia

A

– inherited immune deficiency = can’t fight off HPV = numerous lesions throughout lifetime

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8
Q

co-factors for risk of cervical cancer development?

A

Smoking and concomitant HSV or HIV infection

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9
Q

HPV Dx? tx?

A

Dx: Routine Pap smears –> colposcopy for abnormal results to look for dyspolasia
**cannot be grown in culture! – use PCR to dx genotype?

Tx:

    • wart removal: Bi or trichloroacetic acid brushed on denatures proteins, cryotherapy, LEEP (loop electrosx excision), Podofilox (anti mitotic), Imiquimod (TLR 7 = inc T cell response),
    • Vaccine: gardasil (L1 capsid protein = 16, 18, 6, 11) and cervarix (16, 18 only)
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10
Q

Common urethritis/cervicitis (PID) agents?

A

Chlamydia trachomatis, Neisseria gonorrhoeae, ureaplasma urelyticum (mycoplasma)

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11
Q

Primary symptoms of Ct and GC? laboratory dx?

A

Presentation: dysuria, penile/vaginal exudation

DX: NAAT (nuc acid amp) on urine or exudate – bc they typically occur together!

  • -> GC = Oxidase+, G- stain + PMNs or Thayer Martin / chocolate agar medium (+ vanc/nystatin/colistin to xNormal flora)
  • -> Ct = no cocci on G stain, no polys
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12
Q

Can you use flouroquinolones for GC?

A

NO – no longer recommended due to resistance

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13
Q

How do you treat sexual contacts of GC/Ct infected pts?

A

??

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14
Q

Lymphogranuloma venereum (LGV) and Trachoma and C. Pneumoniae

A

LGV = more invasive strain of Ct –> invades inguinal LNs and causes ulceration at site of entry
— may have CHANCROID (painful, no hard rim)

Trachoma = Ct Strain that is potentially BLINDING chronic dz, prevelant in Asia, Middle East, Africa (do not cause urethritis)

Chlamydia Pneumoniae = Resp infections / PNA

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15
Q

High risk populations for GC, Ct (and ureaplasma)? are infections always clinically apparent?

A

Risk: sexually active, multiple partners, a partner w/ multiple partners, inner city, African American, 15-24 yo age groups

UNAPPARENT INFECTIONS ARE COMMON!!!

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16
Q

GC and Ct treatment

A

Tx: Ceftriaxone + Azithromycin or Doxy
GC (beta lactam resistant) = Ceftriaxone (IM) +/-
Ct (intracellular) = Axithromycin / Doxycyclin

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17
Q

GC, Ct, ureaplasma virulence factors

A

GC: No capsule, LOS shedding (not classic LPS!) = inflammatory response, IgA1ase,
+ ANTIGENIC VARIATION (pilS –> pilE – silent inserts into expression locus) = no vaccine / reinfection common!
+ can DISSEMINATE = septicemia or rash

Ct: Obligate INTRACELLULAR parasite (G- Ish, deficient peptidoglycan), heat shock protein/low tox LPS –> inflammatory response!
+ distinct development cycle: Elementary Bodies (EB) = inert/ non infectious –> Reticulate bodies (RB) = grow in membrane vacuole

**Damage to human host = mainly result of inflammatory response

Ureaplasma: lack cell wall (not b-lactam susceptible),

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18
Q

Lower GU, upper GU, and other infections caused by GC and Ct?

A
    • Lower UG: cervicitis / urethritis
    • Upper UG: PID / salpingitis / epididymitis / prostatitis

– Other:
> Rectal infection (MSM),
> pharyngitis (Oral sex - GC only),
> Conjunctivitis in newborn “ophthalmia neonatorum” (Ct usually), Infant PNA (Ct only),
> Disseminated dz (GC only) = sepsis / rash / aseptic arthritis (Reiter’s syndrome) /endocarditis / meningitis

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19
Q

Urethritis discharge in GC vs Ct?

A

GC – “the clap” - thick, purulent

Ct – less purulent, milky

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20
Q

symptoms of infant Ct pneumonia?

A
    • Repetitive staccato cough w/ tychypnea (wheezing is rare!)
    • Afebrile, hyperinflation/bilateral infiltrates on CXR, preceding/concurrent conjunctivitis hx possible

– vertical transmission!
– raised IgM levels
Diff dx: RSV, ureaplasma, CMV, adenovirus, influenza, pertussis

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21
Q

Def, Symptoms, and consequences of PID?

A

PID: inflammatory process involving a variable combo of endometritis, salpingitis, tubo-ovarian abscess, and pelvic peritonitis

  • dull to severe lower abdominal pain (often starting w/ onset of menstrual cycle)
  • fever
  • Cervical motion tenderness + adnexal tenderness

Consequences: sterility, ectopic pregnancy, chronic pelvic pain, hospitalization, tubo-ovarian abscess,

**overt symptoms less common w/ Ct, but damage worse with Ct!

22
Q

HSV structure? Hallmark? replication cycle?

A

Structure:

  • large dsDNA virus w/ icosohedral capsid + lipid envelope
  • COMPLEX = 90+ Proteins = several anti herpetic Rx’s

Hallmark:
– LATENCY = quiescent virus genome in dorsal root ganglia = recurrent infections

Rep cycle:

  • fuses w/ plasma membrane in pH Independent manner
  • nucleocapsid released –> migrates to nucleus
  • immediate early expression (transcriptional regulator proteins / modify host RNA polymerase)
  • Replicate viral genome
  • “late” class proteins produced (structural)
  • viral assembly in nucleus
  • virus buds from plasma membrane
23
Q

Important “early” proteins in HSV replication? Why?

A

1) DNA polymerase = ultimate target of acyclovir and famciclovir
2) Thymidine kinase = required for phosphorylation / activation of acyclovir (increases cell specificity of ACV)

** Thymidine kinase mutations = resistance to ACV – particularly important w/ AIDS patients

24
Q

How does HSV form multinucleated giant cells? how is this diagnostically important?

A

– viral glycoproteins respsonsible for fusion (entry) = same as those present in plasma membrane of infected cell late in replication –> adjacent infected / uninfected cells can fuse and form giant cells

** Virus can spread cell to cell w/out progeny release!

** TZANCK SMEAR = diagnostic test taking cells from ulcerous lesion, looking for giant cells w/ nuclear inclusion bodies

25
Q

LAT

A

Latency Associated Transcript: HSV gene whose product is an RNA species that silences subset of cellular gene to prevent apoptosis in infected neuron – NO VIRUS PARTICLES PRODUCED during maintenence period

**Decline in cell mediated immunity (stress, etc) –> virus reactivation –> recurrent infection in epithelial cells innervated by latent infected neuron

26
Q

Diseases caused by HSV1 vs. HSV2

A

HSV1: herpes labialis/fever blister, gingivostomatitis, keratitis, ENCEPHALITIS (+ conjunctivitis, blepharitis, urogential lesions)

HSV2: Cervicitis, vulvular and penile vesicles, MENINGITIS, (SEM dz possible, urethritis - rare, perianal and vaginal vesicles, encephalitis)

  • *Generally self-limiting!
  • *Disseminated disease – immunocompromised and neonates! = can be severe/fatal!
27
Q

Primary vs. Recurrent HSV infection

A

**1o = generally worse symptoms/longer duration

Oral:

  • 1o = gingivostomatitis,
  • recur = fever blister(s), both +/- fever/HA

Ocular:

  • 1o = blepharitis/conjunctivitis, usually children
  • recur keratitis = corneal scarring if not treated

Genital:

  • 1o males = penile vesicles, 1o females = ext/int vesicles
  • recur = generally fewer lesions / heal more quickly, frequency diminishes w/ time
  • *both = +/- prodromal/flu-like symptoms = tip off to recurrence

CNS:

  • 1o HSV2 = Aseptic Meningitis / Encephalitis in neonates
  • recur HSV1 = Encephalitis in Adults (trigeminal N)
  • *70% mortality w/out treatment
28
Q

Neonatal HSV infections: symptoms/progression, chance of maternal transmission / delivery options

A

Symptoms:

  • -> develop 1-2 week postpartum,
  • -> can be limited to skin / eyes / mouth (SEM) w/ “zoster like” rash
  • -> or be more severe w/ CNS involvement (encephalitis: seizures, irritability, coma)
  • -> or disseminate to multiple organs

**75% severe infections = death, significant sequelae

  • *1o maternal infection = 30% chance transmission vs. recurrance = 2-3% chance – maternal Abs may be protective
    • DO A C-SECTION if mother presents with herpetic lesions!!
29
Q

HSV dx – genital, meningitis, encephalitis, neonatal

A

Genital:

    • Gold standard = PCR screening of vesicle swab (can distinguish serotypes!)
  • historically = virus was cultured or TZANCK SMEAR done

Meningitis:
– RULE OUT BACTERIAL SOURCE! = CSF used for PCR / culture

Encephalitis:
– CSF rarely positive, can do EEG followed by PCR amplification and southern blot confirmation

Neonatal/congenital:
– PCR / culture –> CHECK LFTs/Liver enzymes for disseminated disease!

30
Q

What Ag is used to serotype HSV?

A

Abs to Glycoprotein G – virus envelope component

**Only indicates PAST INFECTION unless you monitor for IgM vs. IgG

31
Q

HSV treatment

A

**NO CURE – infected? = infected for life due to latency

AntiHSV — lessens disease episode:

1) Acyclovir (dGuanine analog = xViral DNA polymerase)
2) Vidarabine and triflouridne (base analog, used in keratitis)
3) Foscarnet (pyrophosphate analog blocks pyrophosphate exchange)
4) Docosonal (Over the counter cold sore med, host membrane modifier =xFusion)

  • Neonatal/congenital herpes = IV, high dose ACV for 14 - 21 days
  • Herpes encephalitis = high dose IV ACV for 10 days - 3 wks
  • immunocompromised = aggressive ACV tx
32
Q

Most common agents causing BV/vaginitis? transmission/cause?

A

Candida albicans and C. glabrata – aka candidiasis

Gardnerella vaginalis, Mobiluncus spp. and other ANAEROBES

Trichomonas Vaginalis – single cell protozoan! = frank pathogen/sexually transmitted

  • *Candididasis and anaerobes = Opportunistic! – overgrowth of normal flora, not sexually transmitted due to disruption of other normal flora, especially G+ lactobacilli which maintain low pH by H2O2 production
    ex) sex, douching, IUDs, menstrual cycle, preg, antibiotics
33
Q

Is BV generally a single agent disease?

A

NO, usually a combination of various anearobes

34
Q

Vulvovaginal Discharge character in: normal vs. candidiasis, trichomonal, bacterial vaginitis

A

Normal: variable, clear/white, non-homogenous/patchy

Candidiasis: scant, white, clumped
“cottage cheese”, pH < 4.5

Bacterial: moderate, white/grey, adherent/coats vagina, homogenous, MALODOROUS (anaerobes), pH > 4.5

Trichomonas: PROFUSE, yellow/green, frothy, homogenous, pH > 4.5

35
Q

Microscopy of vaginal epithelial cell culture in: normal vs. candidiasis, trichomonal, bacterial vaginitis

A

normal: normal epithelial cells + G+ lactobacilli predominate

Candidiasis: leukocytes, epithelial cells, mycelia or pseudomycelia + yeast/branching hyphea on KOH wet mount

BV: CLUE CELLS (vaginal epithelial cells w/ adherent bacteria), a few leukocytes, lactobacilli outnumbered by mixed flora

Trich: leukocytes/PMNs, trichomonads (size of PMNs w/ TWITCHING MOTILITY!)

36
Q

Symptoms of cystitis, pylonephritis, cervicitis

A

cystitis: dysuria, suprapubic pain, leukocytes/polys in urine, ^bacteria in urine

Pylonephritis: cystitis signs/symp + Significant fever, flank pain, WBC and RBC casts in urine

Cervicitis: dysruia, mucopurulent discharge (from cervix), +/- fever/abdominal pain/pruritis

37
Q

TX: candidiasis, BV, trich

A

Candidiasis: intravaginal Imidazole, oral fluconazole
– partner = nothing if asymptomatic / tx for contact dermatitis

BV: Metronidazole or Clindamycine (intravagnially)
– partner: none

Trich: Metronidazole
– partner = metronidazole

38
Q

DM /immunodeficient and Vaginitis?

A

Can suffer from CHRONIC CANDIDIASIS (genital and oral)

39
Q

Syphilis/Treponema pallidum: structure? Hallmark? dev/proliferation?

A

Structure: spirochete (spiral bacterium) = inner periplasm w/ peptidoglycan + outer sheath (no LPS), axial filaments = motile
**too thin to see on G stain/direct light transmission microscopy

Hallmarks:
1o = non painful chancre/ulcer @ site of entry,
2o = systemic infection w/ snail track lesions +/- palmar and sole rash/condylomata lata

Proliferation: distinct sequential phases, including latent phase that can last for years (continue for life/3o dz)

40
Q

Syphilis Immune Response

A
  • Rigorous humoral / cellular response that DOES NOT eliminate infection
  • *host cellular immune response controls infection but ALSO PATHOLOGY (esp tertiary syphilis)
41
Q

1o, 2o, 3o syphilis

A

1o = 2-3 wk incubation, painless chancre/non tender inguinal lymphadenopathy, resolves in 3-6 wks

2o = 1-2 months following infections, disseminated infection (blood and lymph):

  • hyperpigmented/maculopapular rash +/- palms and soles
  • SNAIL TRACK LESIONS on mucous membranes
  • Condylomata lata (wart like lesions @ moist skin folds)

3o = almost any organ can be affected (heart, CNS, skin, bone)

42
Q

Congenital syphilis: symptoms at birth? transmission? early/late symptoms? tx?

A
  • may or may not have symptoms at birth
  • disseminated infection transmitted transplacentally after 1st trimester via blood
  • early = snuffles, bullous rash, snail track lesions, condylomata lata, enlarged liver/spleen
  • late (~2 years) = stigmata may develop, bone abnormalities (saber shins / frontal bossing), vision defects, Hutchinson’s triad

Tx: 10 day course crystalline Pen G or Procaine Pen G

43
Q

Hutchinson’s triad?

A

CONGENITAL SYPHILIS - late symptom possibility

  1. notched incisors/screwdriver teeth
  2. Keratitis
  3. deafness
44
Q

Syphilis dx

A

1st: NON TREPONEMAL SEROLOGIC TEST – RPR (rapid plasma reagin) or VDRL (venereal disease research lab test)
* sensitive, but not specific

Next: Treponemal test – FTA-ABS (flourescent treponemal Ag absorbed…have to remove cross reacting Abs against normal spirochetal flora)
* specific

**non treponemal = Ag is NOT T. PALLIDUM – beef heart cardiolipin instead = cheaper, relatively sensitive, good to monitor antibiotic efficacy!

45
Q

How long will T pallidum titers remain high?

A

Can remain high for months after patient is cured of syphilis!

46
Q

Darkfield Microscopy

A

Historical method of diagnosing T. pallidum/syphilis
(or useful early on – titers are not high enough)

– light projected at oblique angle –> light refracted through objective lens if spirochete is present

47
Q

Treatment for syphilis/T pallidum?

A

Large, single dose of Pen G

Macrolides, azithromycin as alternatives

48
Q

Which STIs are reportable to health department?

A
    • Syphilis
    • GC
    • Ct
49
Q

E6, E7, E2

A 
E6 = binds/inactivates p53
E7 = binds/inactivates RB

E2 = regulates E6 and E7 expression – get’s disrupted when viral DNA is inserted into host DNA

50
Q

Do acyclovir/valacyclovir and famciclovir cause DNA chain termination? how are they metabolized/prodruging? toxicity?

A

NO - competitively inhibit viral DNA polymerase by competing w/ dGTP for incorporation into viral DNA

Valacyclovir –> acyclovir (better bioavailability)
Famciclovir – deacetylated–> Penciclovir

Toxicity:
acyclovir /valACV = neurotoxicity/seizures
Famaciclovir = n/a

51
Q

Benzathine Pen G: uses, special?, limitations

A

Uses: syphilis, latent syphilis

Special bc: IM administration = drug depot that liberates drug for 2 weeks – good for non compliant pts

Limitations: poor penetration of CSF, not good for neurosyphilis

52
Q

Jarisch Herxheimer Reaction

A

– chills, fever, HA, myalgias, arthralgias +/- cutaneous lesions may become more prominent

  • common w/ secondary syphilis after Pen G administration -DO NOT STOP DRUG!

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