HSVInfections Flashcards Preview

Micro Exam VI > HSVInfections > Flashcards

Flashcards in HSVInfections Deck (33):
1

Initial HSV Genital Infection:

Had been exposed to HSV somewhere OUTSIDE of genital tract originally (cold sore > genital)

2

Primary HSV Genital Infection:

First contact with HSV (more severe response)

3

**Symptoms of HSV Genital Infection (Primary + Initial):

Progress from macules > papules > vesicles > pustules > ulcer **(PAINFUL)**, fever, lymphadenopathy

4

Recurrent Genital Lesions with HSV:

Will have less lesions (3-5) with a prodrome of tingling and pain.

5

Herpetic Whitlow:

Infection of digits leading to an ulcer (commonly seen in fingers of healthcare field workers) Caused by HSV infection

6

Herpes Labialis:

Cold Sore - caused by HSV

7

Herpes Simplex Keratitis:

Initial outbreak: conjunctivitis. Recurrent outbreak can build scar tissue > blindness.

8

Highest risk for Neonatal Herpes Infection:

When mother has a primary infection at the time of delivery.

9

Most Neonatal Herpes Infections acquired when?

At birth. HSV not thought to be able to cause infection PRIOR to birth.

10

Least severe presentation of Neonatal Herpes Infection and its possible complication:

Disease localized to skin, eyes and mouth. Have recurrences in first 6 months and UNTREATED can lead to encephalitis.

11

Symptoms of Neonatal Herpes Infection: Encephalitis:

This can present WITH or WITHOUT skin lesions. Seizures, lethargy, tremors, bulging fontanel.

12

Most severe form of Neonatal Herpes Infection:

Disseminated Infection. Will have presence of lesions in wherever it has disseminated to.

13

Treatment for Neonatal Herpes Infection:

IV administration of antivirals.

14

HSV Virus Family:

Herpesvirus

15

**Genome (?) + Envelope (?) of HSV:

dsDNA Enveloped

16

HSV Genome Replication:

Encodes for many of its own enzymes for genome replication. HSV polymerase= target for antivirals.

17

Life Cycle of HSV Infection:

Attacks epithelium where it can replicate > retrograde transport of HSV in SENSORY NEURON > nucleus > latent infection established.

18

Life Cycle of HSV Spontaneous Reactivation:

HSV reactivates (due to stress,UV light, trauma, hormones) > anterograde to epithelium > virus replication and shedding in epithelial tissue

19

HSV-1 Commonly associated with:

oral lesions

20

HSV-2 commonly associated with:

genital lesions

21

Over what % of adults are seropositive for HSV-1 or HSV-2?

90%

22

Primary infection by HSV-1 usually occurs before:

Age 4

23

**Diagnosis of HSV:

clinical appearance of lesions: **1-2mm diameter in groups**, Tzanck Smear (cells fused > large multinucleated cell)

24

Tzanck Smear Appearance and Use:

used for HSV-1 or 2 and Varicella diagnosis

25

**Differentiating Diagnostically between HSV-1 and 2:

PCR to detect genome or Immunocytochemistry to detect Antigens

26

What is the treatment of HSV dependent on?

What TYPE of lesions are present.

27

Treatment of HSV: Oral Lesions:

Generally not treated.

28

Treatment of HSV: Genital Herpes- Primary and Recurrent:

Primary: oral antivirals Recurrent: long term oral antivirals

29

Goals of Anti-herpetic Drugs:

To shorten time to lesion healing and increase time between outbreaks

30

Anti-herpetic drugs do not target what stage:

THEY DO NOT ACT ON LATENT STAGE INFECTION

31

HSV Antivirals: Nucleoside Analogues MOA:

Viral Thymidine Kinase MUST phosphorylate the drug into monophosphate form= CRITICAL FOR DRUG TO BE ACTIVE. Drug continues to be phosphorylated and looks like nucleotide > chain termination + binds to DNA polymerase. ONLY ACTIVE WITHIN INFECTED CELLS BECAUSE OF NECESSITY FOR VIRAL THYMIDINE KINASE.

32

**Three types of Nucleoside Analogues for HSV treatment:

Famciclovir, Valacyclovir (ideal for ORAL administration) Acyclovir

33

HSV Antivirals: Nonnucleoside Inhibitors MOA + Use:

HSV Thymidine Kinase NOT NEEDED. IMMEDIATELY ACTIVE. Used in RESISTANT HSV infection.