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Stage 3 Human Diseases > HD5 Herpes Virus > Flashcards

HD5 Herpes Virus Flashcards

1
Q

What is this:

Herpes Simplex Virus 2

A

you know herpes, but if recurrent probs this one

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2
Q

What is this:

Herpes Simplex Virus 1

A

you know herpes, if not recurrent probs this one

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3
Q

What is this:

Varicella Zoster Virus

A

this is the chicken pox virus, reactivation causes shingles

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4
Q

What is this:

Cytomegalovirus

A

usaully assymptomatic, can occasionally cause glandular fever in adolescents when contracted, greatest concern is congenital infection and solid organ donners.

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5
Q

What is this:

Epstein Barr Virus

A
  • young children ( asymptomatic or sore throat) and adolescents (glandular fever/ infectious mononucleosis)
  • the one that causes oral hairy leukoplakia (white patches that cannot be rubbed off, sign pt is immunocompromised)
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6
Q

What is this:

Human Herpes Virus 6

A 
Roseola Infantum (rash illness in infants)
Common in infants aged 2 and younger
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7
Q

What is this:

Human Herpes Virus 7

A 
Roseola Infantum (rash illness in infants)
Common in infants aged 2 and younger
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8
Q

What is this:

Human Herpes Virus 8 (associated with Kaposi’s sarcoma)

A

Kaposi’s sarcoma associated virus
a type of cancer that can form masses in the skin, lymph nodes, or other organs. The skin lesions are usually purple in color. They can occur singularly, in a limited area, or be widespread.

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9
Q

1) How long do cold sores last?
2) (typically where are the lesions, and where can they be rarely?)
3) what is the treatment for cold sores?
4) what are the triggers of cold sores?

A

1) 5-12 days
2) typically at vermillion border of lips, rarely intra-oral (but still can be)
3) 5% Aciclovir (most effective during active replicaiton, usually can feel tingling or itching before vesicles
4) many: including UV radiation, cold, menstruation, fever, stress

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10
Q

1) How long do cold sores last?
2) (typically where are the lesions, and where can they be rarely?)
3) what is the treatment for cold sores?
4) what are the triggers of cold sores?

A

1) 5-12 days
2) typically at vermillion border of lips, rarely intra-oral (but still can be)
3) 5% Aciclovir (most effective during active replicaiton, usually can feel tingling or itching before vesicles
4) many: including UV radiation, cold, menstruation, fever, stress

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11
Q

Which HSV 1 or 2, usually causes meningitis?

A

HSV2

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12
Q

what is meningitis known as if it is recurrent ?

A

mollaret’s meningitis

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13
Q

What are the main complications of HSV 1 or 2?

6

A
  1. secondary bacterial infections
  2. corneal ulcers
  3. meningitis
  4. herpes simplex encephalitis
  5. neonatal herpes simplex (life threatening (mother gives birth to baby before she has time to develop immunity)
  6. death (in immunocomprimised)
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14
Q

HSV in genitals, reactivation is usually HSV __a__.

the pimmary infection is b

A

a) 2

b) either

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15
Q

in genital HSV, what is worse primary or reactivation infection, which can be asymptomatic?

A

primmary is worse, secondary can be assymptomatic

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16
Q

What type of infections can HSV cause?

A

1) oral manifestation
2) genitals
3) hands = herpetic whitlow (most common amongest dentists, lesions on hands)
4) eyes= ocular infection
5) in babies= neonatal infections
6) brain =encephalitis

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17
Q

What does a HSV occular infection look like?

A

a little crack in the jelly of the eye

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18
Q

how does HSV infection affect delivery of babies?

A

if mother has active primary or initial genital HSV at time of delivery then will have a C section, unless recurrent as doesn’t out weigh the risks of the C sections

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19
Q

describe the mortality of HSV if untreated in babies?

A

high

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20
Q

what 3 parts of the body can neonatal HSV affect?

A 
mucocutaneous only (mildest), primarily
Central Nervous System or Disseminated.
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21
Q

What ways can a baby get HSV?

A

contact during delivery adn post-delivery

cold sores, asymptomatic shedding in close contacts

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22
Q

What is the most common virus cause of encephalitis?

2) neurological outcome?

A

HSV

2) poor (high rate of poor neurological outcome)

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23
Q

what is the mortality of untreated encephalitis?

2) what is the treatment?

A

70%
2) Mimimum of 10 days treatment with intravenous aciclovir is needed
(most would give 21 days).

24
Q

What are the methods of detecting HSV?

A

Direct Viral Detection (PCR = polymerase chain reaction)
 Lesion swab
 Cerebrospinal fluid

25
Q

What is the action of aciclovir, valaciclovir and zovirax?

A

inhibit viral polymerase

26
Q

what is zovirax?

2) when is it most effective?

A

1) topical form of aciclovir

2) before lesion has fully formed

27
Q

What is valaciclovir?

2) what are the benefits and draw backs?

A

prodrug of acyclovir, metabolised into aciclovir

2) good oral bioavailability, but more expensive

28
Q

What is valaciclovir?

2) what are the benefits and draw backs?

A

prodrug of acyclovir, metabolised into aciclovir

2) good oral bioavailability, but more expensive

29
Q

What is the viral enzyme that activates aciclovir?

2) what is the benefit of this?
3) what are the disadvantages of aciclovir compared to valaciclovir?

A

thymidine kinase

2) specific to infected cells
3) poor oral bioavailability, 5 times per day dosing

30
Q

What is the viral enzyme that activates aciclovir?

2) what is the benefit of this?
3) what are the disadvantages of aciclovir compared to valaciclovir?

A

thymidine kinase

2) specific to infected cells
3) poor oral bioavailability, 5 times per day dosing

31
Q

What happens in the lead up to developing chicken pox?

A
  1. infection via respiratory mucosa/conjunctive
  2. replication in regional lymph nodes
  3. primmary viraemia
  4. replication in liver and spleen
  5. seconday viraemia
  6. dissemination to skin = chickenpox
32
Q

What is the difference between primmary viraemia and secondary viraemia when infected with varicella-zoster virus?

A

secondary has a larger load in blood so causes lesions

33
Q

what are the lesions you get with varicella zoster virus :

A

Macules (Red spot)
Papules (raised spot)
Vesicles
Pustules (pus filled vesicle)

34
Q

what is the prodromo of the rash when infected with VZV in primmary infection?

A

fever

35
Q

what is the distribution pattern of lesions in primmary infection by VZV (chikcen pox)?

A

centripedal (concentrated at trunk)

36
Q

if the hypoglossal nerve ganglion is infected with varicella zoster virus, what would be the clinical presentations of a secondary infections:

A

white lesions on tongue only (shouldn’t cross midline)

37
Q

what determines dermatome affected by secondary infection by VZV?

A

which nerve it is latent in

38
Q

what nerve ganglion is VZV latent in in ophthalmic zoster?

2) what would increase the risk of ocular complications

A

trigeminal

2) if nasociliary branch is affected i.e. there are lesions on the nose

39
Q

Diagnosis of virus infections involves:

A

clinical evaluation adn direct viral detection e.g. lesion swab or cerebrospinal fluid followed by detection of viral DNA by PCR

40
Q

Diagnosis of virus infections involves:

A

clinical evaluation adn direct viral detection e.g. lesion swab or cerebrospinal fluid followed by detection of viral DNA by PCR

41
Q

when would post-exposure prophylaxis be carried out for VZV?

A

Give if significant contact:

Varicella: Face to face contact or >15 mins in same room
- Zoster: Exposure to uncovered rash
 And not immune to varicella

42
Q

whats the maximum number of days that can pass before VZV post-exposure prophylaxis is no longer effective?

A

10 days

43
Q

who is post-exposure to VZV prophylaxis for ?

A

pregnant women and immunocompromised

44
Q

what is the procedure for post-exposure to VZV prophylaxis?

A

Zoster Immunoglobin (VZIG - IM injection)

45
Q

the varicella vaccine.

1) how is it used in the UK?
2) how is it used in the US?
3) who is it not given to and why?

A

1) despite indication, only given to healthcare workers
2) Used as part of childhood vaccine schedule for 12 years in USA (2 doses with MMR (USA Varicella vaccine is formulated with MMR (MMRV).)
3) Live attenuated vaccine (can’t be given to immunocompromised individuals)

46
Q

What is the aim of the shingles vaccine?

2) who is it given to?

A

1) Aim to boost immunity and prevent reactivation

2) All 70 year olds form September 2013

47
Q

affect of epstein-barr virus on young children:

A

asymptomatic or sore throat

48
Q

affect of epstein-barr virus on adolescents:

A

glandular fever/infectious mononucleosis

 Also associated with variety of lymphomas and cancer

49
Q

What cell type does epstein barr lye latent in?

A

B lymphocytes

50
Q

What does reactivation of epstein barr virus result in?

A

shedding in saliva

51
Q

Epstein – Barr Virus (EBV) mode of transmission:

A

saliva or sexual contact

52
Q

how is Cytomegalovirus (CMV) transmitted?

A

via direct contact with infected secretions (saliva, sexual..)

53
Q

what is the seroprevalence of Cytomegalovirus (CMV) in the UK?

A

~40% for young adults, increases ~1% per year.

54
Q

what does primmary infection of Cytomegalovirus (CMV) present as most commonly?
2) and occasionally?

A

Usually asymptomatic

 Occasionally glandular fever-like picture (Lymphadenopathy/ hepatitis)

55
Q

Cytomegalovirus (CMV)can reactivate intermittently, how does this present?

A

Asymptomatic in the immunocompetent

56
Q

What are the concerns with cytomegalo virus?

A

congenital infection ( standard precautions mean however, pregnant healthcare workers are no more likely to contract than other pregnant women

57
Q

In what situation what an organ recipient be at increased likely hood of contracting Cytomegalovirus?

A

D+R- = donor seropositive, recipient seronegative: At increased risk of CMV disease after
solid organ transplant.

Stage 3 Human Diseases (10 decks)

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