viral STIs 2 Flashcards

(31 cards)

1
Q

symptoms associated with herpes simplex virus/genital herpes

A
  • fever, inguinal adenopathy, malaise

- painful lesion lasting 3 wks- on butt, thighs, penis, peritoneum, cervix and vulva

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2
Q

initial genital infection vs primary infection

A

initial- patient has been exposed to herpes simplex but on mouth or elsewhere besides genitals

primary infection- first time pt has ever seen virus

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3
Q

after initial infection, what can a patient expect

A

recurrent lesions that are less painful and may even show up as vulvar irritation in women

preceding outbreak- tingling and pain

heal within 7-10 days

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4
Q

what other conditions can herpes simplex virus cause

A
  • herpetic whitlow- infection of digits
  • herpes simplex keratitis- can lead to blindness
  • herpes labialis
  • herpes simplex encephalitis
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5
Q

when is the risk for neonates contracting herpes from mom the highest

A

when mom is experiencing primary infection

can be lethal to baby

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6
Q

what are the three types of neonatal herpes infections

A

1) localized in skin, eyes and mouth
2) skin lesions and encephalitis
3) disseminated

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7
Q

characteristics of neonatal herpes of the skin, eyes and mouth

A
  • not lethal
  • 10 days post birth
  • recurrences in first 6 mo
  • 30% untreated lead to blindess, microcephaly and spastic quadraplegia
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8
Q

characteristics of encephalitis/skin lesion neonatal herpes

A

1/3 of infections
seizures, lethargy, tremors, poor feeding, temp instability, BULGING FONTANEL
50% mortality if untreated
survivors often have neuro probs

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9
Q

disseminated neonatal herpes

A

-lesions in visceral organs and skin- liver, cns, lungs, eyes, adrenals
-symptoms- seizures, respiratory distress, jaundice, bleeding, shock
-80% mortality untreated- antiviral reduce by 23%
complications- pneumonia and DIC

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10
Q

prevention of neonatal herpes

A
  • c section

- healthcare worker precautions for herpetic whitlow and orolabial lesions

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11
Q

treatment of neonatal herpes

A

IV admin of antivirals for all neonates with herpes

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12
Q

herpes simplex virus characteristics

A
  • dsDNA
  • enveloped
  • encodes many of its own enzymes including DNA polymerase that is often targeted by ANTIVIRALS
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13
Q

pathogenesis of herpes simplex virus

A

1) infiltrates epithelial cells - replicates
2) taken up by a host neuron via retrograde transportation
3) stays latent in ganglia of neuron-either sacral ganglia = genital herpes or trigeminal ganglia = cold sores
4) recurrence -herpes sim comes back down the neuron and out to epithelial cells
- triggers: stress, UV light, trauma, hormone change

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14
Q

what are the types of herpes viruses and what are they associated with? when are you expected to get them?

A
  • HSV1 and 2
  • HSV1 = oral, HSV2 = genital
  • HSV1- before age 4, HSV2- sexual activity
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15
Q

how is HSV transmitted

A

sexually, direct contact with lesions, saliva

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16
Q

diagnosis of herpes simplex virus

A
  • clinical appearance of lesions that are 1-2 mm in GROUPS
  • PCR to detect genome
  • immunocytochem to detect antigens
  • microscope- do TZANCK SMEAR- where you scrape a part of lesion and look for nucleated cells
  • for dendritic lesion in eye- can see with fluorescent dye
17
Q

treatment of herpes simplex virus

A

oral- nothing
genital- oral antiviral, recurrent- long term antiviral
neonatal herpes-IV and antiviral treatment
ocular-topical antiviral

18
Q

treatment goals for hsv

A
  • not to cure
  • decrease time to heal
  • increase time between outbreaks
19
Q

treatment for HSV

A

acyclovir- (mnemonic- cycle like herpes)

1) nucleoside inhibitor: enters the system and is immediately phosphorylated by VIRAL thymidine kinase
2) further phosphorylated and pretends it’s a nucleotide analog
3) binds polymerase chain and terminates viral dna replication

foscarnet
1) nonnucleoside inhibitor- no HSV phosphorylation needed, active right away stops viral DNA polymerase -used in immunosuppressed pt

20
Q

why is acyclovir such a successful drug

A

because it is phosphorylated and able to infiltrate viral genome by the cells that have the virus.. of no virus, no phosphorylation and thus those cells that are not infected are unharmed

21
Q

Genital warts- condyloma acuminatum

what do they look like? how do you see them better

A
  • hyperkeratotic, firm, exophilic papules
  • 1mm-2 cm
  • causes itching, pain, burning
  • cervical warts- exophilic, endophilic, flat
  • see them better with 3-5% acetic acid spray
22
Q

what is respiratory papillomatosis/laryngeal papillomas

A
  • nodules on ciliated and squamous epithelial jxn of larynx
  • usually found in babies
  • HPV infection
  • causes altered cry, horseness, stridor, respiratory distress
23
Q

treatment for respiratory paillomatosis/laryngeal paillomas

A
  • surgical removal of growth but they often come back

- c section rarely prevents

24
Q

HPV charcteristics

A
  • non-enveloped

- dsDNA

25
pathogenesis of HPV
- can't replicate without certain layers of skin at certain stages in development- replication is closely tied to differentiation status of tissue it infects - 1) infection starts at basal layer 2) viral gene expression occurs in basal layer 3) suprabasal layer you get viruses assembled 4) virus sheading at external environ
26
what are the top HPV strains that cause cervical cancer?
1- HPV 16 | 2- HPV 18
27
pathogenesis of cervical cancer
- instead of HPV developing in the different layers of the epithelium, it stops producing viruses and instead ramps up genes E6 and E7 - how? normally E2 limits the activity (negative inhibitor) of E6 and E7 that promote cell proliferation - however, in cancer- there is an integration/straightening out of the cell and you get a cutting off of the E2 gene and over ramping of E6 and E7 - E7- inhibits activity of Rb which limits cells from going from G1 phase of the cell cycle to S phase- this causes excessive cell prolif - E6- inhibits p53 with same effect
28
how is HPV transmitted? incubation? Diagnosis
- sexually - cuts and abrasions - incubation 3-4 mo - diagnosis- clinical appearance-lesions, hyperkeratosis and koilocytes via pap smear, PCR for DNA
29
Koilocytes
-enlarged keratinocytes that contain irregular hyperchromatic nuclei surrounded by halo
30
treatment for HPV
warts -cryo, CO2 laser pre-malignant and malignant cervical neoplasm-cauterize, loop excision, co2 laser, loop excise hi grade lesions/cancer treatment may include -hysterectomy, radiation, chemo
31
hpv vaccine
-made in yeast and self assemble in virus-like particles but orient the capsid protein to look like wild type infection -comes in bivalent (18, 16) and tetravalent (HPV 18, 16 (c. cancer), 6,11 (warts)) -suggestion: boys 11-12 y.o to get tetravalent girls 11-12 to get either