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Clinical Micro > Viral STIs > Flashcards

Viral STIs Flashcards

1
Q

What kind of virus is Molluscum contagiosum?

A

A large enveloped DNA poxvirus

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2
Q

What/who is the reservoir for M. contagiosum?

A

humans, no animal reservoir

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3
Q

What is the clinical presentation of Molluscum contagiosum? (2 symptoms)

A
  1. Flesh coloured lesions
    - Dome shaped and have a dimpled centre
    - 1-5 mm wide
  2. Itchiness but not usually painful
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4
Q

What is the usual method of diagnosis of M. contagiosum?

A

visual identification

- you could submit PCR or do EM but it’s unnecessary

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5
Q

What can happen if you scratch at the M. contagiosum lesions?

A

then you can spread them to other parts of the body

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6
Q

What tissues does M. contagiosum infect?

A

Skin and mucous membranes anywhere on the body

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7
Q

What 3 populations of people are at higher risk of contracting M. contagiosum?

A
  1. Children (ages 1-10)
  2. Immunocompromized people
  3. Sexually active adults*
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8
Q

What are 3 modes of transmission for M. contagiosum?

A
  1. Skin to skin contact
  2. Sexual contact
  3. Indirect via fomites (clothing or towels)
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9
Q

What is the incubation period for M. contagiosum?

A

2-7 weeks

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10
Q

How long is a person infectious with M. contagiosum?

A

until the lesions have cleared

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11
Q

How long does M. contagiosum take to resolve typically?

A

6-8 weeks

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12
Q

What should be avoided with M. contagiosum to let it clear? what can be the result?

A

Shaving should be avoided to prevent bleeding and autoinoculation/spread

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13
Q

What happens once the lesions clear? is there established immunity/latency?

A

No latency, MCV clears (unlike HSV) but there is also no permanent immunity so you can be infected again

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14
Q

What treatments are there for M. contagiosum?

A

no antivirals

you can burn off or surgically remove the lesions

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15
Q

What kind of morphology do the herpes viruses have?

A

enveloped icosahedral

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16
Q

What kind of genome do the herpes viruses have?

A

dsDNA

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17
Q

What are two enzymes that are unique to HSV?

A
  1. Thymidine kinase

2. viral DNA polymerase

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18
Q

What is HSV (HHV) 1 most often associated with?

A

oral/ocular infections

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19
Q

HSV(HHV)-2 is most commonly associated with?

A

Genital infections

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20
Q

What has changed recently in the epidemiology of HSV-1?

A

now is causing more genital infections

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21
Q

Which form of HSV can cause a self limiting type of meningitis? what is it called?

A

HSV-2 can cause Molleret’s meningitis

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22
Q

What are the 3 stages of a herpes virus infection?

A
  1. primary infection
  2. latency
  3. reactivation
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23
Q

What % of primary infections are asymptomatic?

A

80-90%

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24
Q

When do primary infections tend to occur? where?

A

Generally occur between the age of 6 months and 3 years of life

Infection via oral, genital, ocular epithelium or breaks in skin

25
Q

Where are the locations of latent infection for HSV-1 and HSV-2? what kind of migration occurs from the epidermis to the ganglia?

A 
HSV-1 = trigeminal ganglia 
HSV-2 = dorsal root ganglia

centipetal movement towards the ganglia along the axon

26
Q

what occurs during reactivation of an HSV infection? what kind of movement is this?

A

virus can reactivate, multiply in the nerve cell and be transported along the axon to the nerve terminals in the skin
- centrifugal movement to the epidermis

27
Q

What are two triggers for an HSV reactivation?

A

Immunosuppression and stress

28
Q

For people infected with HSV-1 how many recurrences are there in the 1st year? how common is asymptomatic shedding?

A

usually less than 1 in the first year

asymptomatic shedding is uncommon

29
Q

For HSV-2, how common is asymptomatic shedding? what % of people have a recurrence in the first year?

A

90% have 1 reoccurrence/year

Asymptomatic shedding has been shown to occur on 28% of days

30
Q

When would someone be given acyclovir? Does it prevent asymptomatic shedding?

A

If someone presents with lots of recurrences a year

No acyclovir doesnt

31
Q

What is the lab diagnostic method of choice for diagnosing HSV?

A

RT-PCR with melt curve analysis

32
Q

How does melt curve analysis work?

A

The temp at which the primer will melt off of the sequence (and expose fluorochorme?) will tell you what virus you have

33
Q

Review: what accomplishes the first step of acyclovir activation?

A

Viral thymidine kinase (phosphorylation)

34
Q

What are the rates of acyclovir resistance in competent vs. immunocompromised people?

A

0.1 in competent

4-7 in immunocompromised

35
Q

What is the more common source of acyclovir resistance?

A 
Thymidine kinase (TK) mutants (95%)
Viral DNA polymerase (5%)
36
Q

What are two alternate drugs to acyclovir? How do they work?

A

Cidofivir = phosphorylated nucleotide analog (doesn’t need TK)

Foscarnet = pyrophosphate analog (blocks viral DNA polymerase)

37
Q

What family of viruses does human papilloma virus belong to?

A

Papillomaviridae

38
Q

What kind of genome/structure does HPV have?

A

dsDNA virus

non-enveloped

39
Q

What % of adults are infected with HPV?

A

80%

40
Q

Can HPV be grown in culture?

A

no

41
Q

What are two methods of testing for HPV?

A
  1. Molecular detection possible

2. Papanicolaou test (Pap test or Pap smear)

42
Q

What are the two types of HPV? How are they contracted?

A

High (through sexual contact) and low (dermal type) risk

43
Q

What 3 things are high risk HPV associated with?

A

Cervical cancer, Head and neck cancer, other anogenital cancers

44
Q

What 2 things are low risk HPV associated with?

A
  1. recurrent respiratory papillomatosis

2. anogenital warts

45
Q

What are the two important serotypes of high risk HPV?

A

16 and 18

46
Q

What are the two important serogroups for low risk HPV?

A

6, and 11

47
Q

What types of symptoms are congruent with a skin to skin (contact) transmission of HPV?

A

plantar, common and flat warts

48
Q

What is respiratory papillomatosis?

A

Benign warts in the upper airway that can cause airway obstruction

49
Q

What can be done to treat respiratory papillomatosis?

A

surgical removal

50
Q

What serotypes cause respiratory papillomatosis? When is it acquired?

A

6 and 11

Childhood - usually acquired at birth
Adult acquisition - usually related to oral intercourse

51
Q

What are 3 treatments for genital warts?

A
  1. Podophyllin resin
  2. Trichloroacitic acid
  3. Cryotherapy
52
Q

When does infection with HPV normally occur? Can multiple co-infections occur?

A

Typically very shortly after onset of sexual activity

Co-infections can occur, pretty common

53
Q

How long do individual episodes of infection with HPV last? What occurs in the majority of people?

A

4-20 months

Most often it is a transient infection that the immune system clears. Reappearance of the same type is uncommon
- only a small subset of people continuously shed the virus

54
Q

HPV 16 and 18 are associated with what % of cervical cancer?

A

75%

55
Q

In women, infection with HPV 16 or 17 will lead to formation of first…

A

precancer or high grade precursors and then full blown cervical cancer

56
Q

What is detected on a PAP test?

A

Detection of patients with cervical cells abnormalities

- Atypical squamous cells of unknown significance (ASCUS)

57
Q

What results in some HPV strains being oncogenic while others are not? What is increased in expression?

A

Disruption/deletion E2 transcriptional repressor leads to them having a selective growth advantage and later cancer

Increased expression of E6 and E7

58
Q

What is the role of E6? how is this different in the low risk types?

A

Binds and leads to degradation of p53 (tumor suppressor)

HPV E6 from low risk types do not bind p53 or don’t result in degradation

59
Q

What are the two HPV vaccines and how are they different?

A
  1. Gardasil - quadrivalent (against 6, 11, 16 and 18)

2. Cervarix (16 and 18 only)

Clinical Micro (28 decks)

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