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Microbiology > Exam #6: Viral STIs II > Flashcards

Exam #6: Viral STIs II Flashcards

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1
Q

What is the difference between initial genital infection & primary infection?

A

Primary= first time that the person has EVER had HSV infection, regardless of the location of infection

Initial Genital Infection= when primary infection is of the genitals (vs. mouth)

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2
Q

What are the symptoms of HSV genital infection?

A

Genital lesion
Fever
Inguinal adenopathy
Malaise

Symptoms more severe in women

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3
Q

Describe the lesion seen in HSV.

A

Progression from macules, papules, vesicles, pustules, to ulcers

Last 3 weeks

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4
Q

What is a recurrent lesion?

A

Lesion that re-appears after first infection

  • 3-5 lesions on the shaft of the penis in males
  • Vulvar irritation or lesions in females
  • Prodrome of tingling & pain where the lesions will form
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5
Q

List the characteristics of HSV.

A

Herpesvirus family
Enveloped
dsDNA genome
HSV-2 is most common (HSV-1 causes outbreaks but no recurrence)

Encodes own enzymes for genome replication that is the target of antivirals

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6
Q

What else can HSV cause?

A
  • Herpetic Whitlow
  • Herpes labialis (cold sore)
  • Herpes simplex keratits
  • Herpes simplex encephalitis
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7
Q

What is Neonatal Herpes Infection? What is it important to remember regarding Neonatal Herpes Infection?

A
  • Baby comes into contact with Herpes Simplex Virus during birthing process & develops Herpes
  • Process is almost always symptomatic, & can be fatal
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8
Q

What are the three presentations of Neonatal Herpes Infection?

A

1) Disease localized to skin, eyes & mouth
~30% –if untreated–will develop blindness, microcephaly, & spastic quadriplegia
2) Encephalitis
~ 1/3 infants with Herpes infection will develop encephalitis; of these, 1/2 will die
3) Disseminated Infection that involves the skin & visceral organs; 8/10 will die

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9
Q

What are the symptoms of encephalitis?

A 
Seizures 
Lethargy 
Irritability 
Tremors 
Poor feeding 
Temp instability 
Bulging fontanel
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10
Q

What are the characteristics of Neonatal Disseminated HSV?

A

Lesions in visceral organs & skin

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11
Q

How is Neonatal HSV infection prevented?

A

1) Examine mother with known HSV history for lesions & perform & c-section if suspicious
2) Remove healthcare workers with Herpetic Whitlow from NICU & mask those with orolabial lesions

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12
Q

How is Neonatal HSV infection treated?

A

IV administration of antivirals (for all three presentations)

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13
Q

Describe the mechanism of HSV infection.

A

1) HSV attack
2) Virus replication in peripheral epithelial tissues
3) Retrograde transmission via sensory neurons
4) Latency in cell body

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14
Q

Describe the mechanism of HSV infection that occurs with spontaneous reactivation.

A

1) Reactivation
2) Anterograde transmission via neuron
3) Replication in peripheral tissue
4) HSV shedding with new lesions

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15
Q

What is the difference between HSV-1 & HSV-2?

A

HSV-1= oral
- Peak primary infection is before age 4

HSV-2= genital
- associated with sexual activity

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16
Q

How is HSV transmitted?

A
  • Direct contact with lesion
  • Saliva
  • Sexual
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17
Q

How is HSV diagnosed?

A

Clinically by the appearance of lesions

  • Tzanck smear
  • PCR
  • Immunohistochemistry to detect antigens
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18
Q

How is HSV treated?

A

Oral lesion= NOT treated

Genital=
- Primary= oral antiviral
- Recurrent= long-term
oral antiviral

Neonatal=
- IV antiviral

Ocular=
- topical antiviral

*Note that these drugs do NOT act on the latent stage; goal is to shorten time to lesion healing & increase time between outbreaks

19
Q

What are the two classes of HSV antivirals?

A

Nucleoside analog

Nonnucleoside inhibitor

20
Q

Describe the mechanism of action of the nucleoside analogs.

A

E.g. acyclovir, valacyclovir, & pencyclovir

  • Administered drug is a “prodrug”
  • Viral enzyme “Thymidine kinase” cleaves into active drug
  • Active form inhibits viral DNA polymerase & can incorporate into DNA chains & terminate them

*Low cytotoxicity because of dependence on thymidine kinase

21
Q

Describe the mechanism of action of Non-nucleoside inhibitors.

A

E.g. Foscarnet

  • Administered IV
  • Binds pyrophosphate binding site of viral DNA polymerase, preventing DNA replication
  • DOES NOT rely on viral thymidine kinase & is associated with higher levels of toxicity

*Used in HSV infections that are resistant to the nucleoside analogs

22
Q

List the characteristics of HPV.

A

Popovaviridae family
Nonenveloped
dsDNA

Replication tied to the differentiation status of the tissue it infects

23
Q

What does HPV cause?

A
  • Genital warts
    Condyloma acuminatum
  • Respiratory Papillomatosis
24
Q

List the characteristics of genital warts.

A

Hyperkerototic
Firm
Exophilic papules

25
Q

How can you tell the difference between wart & normal tissue?

A

3-5% acetic acid solution will turn warts white

26
Q

What is Respiratory Papillomatosis?

A
  • Nodules on ciliated & squamous epithelial junction of larynx
  • Caused by HPV-6 & HPV-11 passed from mother to child

*Note that c-section has NOT been proven to reduce risk

27
Q

What are the symptoms of Respiratory Papillomatosis ?

A

Altered cry
Hoarseness
Stridor
Respiratory distress

28
Q

How is Respiratory Papillomatosis treated?

A

Surgical removal

29
Q

What serotypes of HPV effect cause Laryngeal Papillomas?

A

6

11

30
Q

What serotypes of HPV effect cause Anogenital Warts?

A

Noncancerous:

  • 6
  • 11

Cancerous

  • 16
  • 18
  • 31
  • 33
31
Q

What serotypes of HPV effect cause Common Warts?

A

2
3
10

32
Q

What serotypes of HPV effect cause Plantar Warts?

A

1

4

33
Q

What is the connection between HPV and cervical cancer?

A

Certain types of HPV infection are associated with increased risk for developing cervical cancer
- Specifically, HPV-16 & 18

34
Q

How does HPV cause cancer?

A
  • E6 & E7 are two early genes expressed by HPV
  • These proteins are normally blocked by the transcriptional repressor, E2
  • In cancer causing strains, HPV DNA is linearized & integrated into host DNA without functional E2
  • E6 inhibits p53 & E7 inhibits normal Rb function
  • These proteins that normally prevent transcription and progression through G1-S phase of the cell cycle are inhibited
  • Thus, these two gene products promote aberrant growth of infected cells
35
Q

When is peak HPV infection?

A

15-25

36
Q

When are most precancerous lesions seen?

A

28-30 years

37
Q

When is HPV cancer most prevalent?

A

40

38
Q

How is HPV transmitted?

A

Sexual transmission

39
Q

How is HPV diagnosed?

A

Clinically–hyperkeratosis & koilocytes (Pap Smear)

PCR , 12, 16, & 18 (high risk)

40
Q

What is a Koilocyte?

A
  • Enlarged keratinocyte
  • Irregular hyperchromatic nuclei
  • Halo
41
Q

How is HPV treated?

A

Genital warts

  • Cryotherapy
  • CO2 laser

Pre-malignant & malignant

42
Q

How is HPV prevented?

A

Pap smears
Reduce risk behavior
HPV vaccine

43
Q

What is the HPV vaccine

A

Capsid proteins L1 that form the natural shape of the HPV capsid

44
Q

What are the vaccination recommendations for males & females.

A

It is recommended that BOTH sexes be vaccinated between 11 & 12 years.

  • Females= bivalent or quadrivalent vaccine
  • Males= quadrivalent
Bivalent= HPV-16 & 18 ONLY (most common cancer) 
Quadrivalent= same as bivalent + 6 & 11, causes of genital warts

Microbiology (49 decks)

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