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Clinical Micro > Viral STIs > Flashcards

Viral STIs Flashcards

(59 cards)

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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?

Study These Flashcards
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
Where are the locations of latent infection for HSV-1 and HSV-2? what kind of migration occurs from the epidermis to the ganglia?
``` HSV-1 = trigeminal ganglia HSV-2 = dorsal root ganglia ``` centipetal movement towards the ganglia along the axon
26
what occurs during reactivation of an HSV infection? what kind of movement is this?
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
What are two triggers for an HSV reactivation?
Immunosuppression and stress
28
For people infected with HSV-1 how many recurrences are there in the 1st year? how common is asymptomatic shedding?
usually less than 1 in the first year asymptomatic shedding is uncommon
29
For HSV-2, how common is asymptomatic shedding? what % of people have a recurrence in the first year?
90% have 1 reoccurrence/year Asymptomatic shedding has been shown to occur on 28% of days
30
When would someone be given acyclovir? Does it prevent asymptomatic shedding?
If someone presents with lots of recurrences a year No acyclovir doesnt
31
What is the lab diagnostic method of choice for diagnosing HSV?
RT-PCR with melt curve analysis
32
How does melt curve analysis work?
The temp at which the primer will melt off of the sequence (and expose fluorochorme?) will tell you what virus you have
33
Review: what accomplishes the first step of acyclovir activation?
Viral thymidine kinase (phosphorylation)
34
What are the rates of acyclovir resistance in competent vs. immunocompromised people?
0.1 in competent | 4-7 in immunocompromised
35
What is the more common source of acyclovir resistance?
``` Thymidine kinase (TK) mutants (95%) Viral DNA polymerase (5%) ```
36
What are two alternate drugs to acyclovir? How do they work?
Cidofivir = phosphorylated nucleotide analog (doesn’t need TK) Foscarnet = pyrophosphate analog (blocks viral DNA polymerase)
37
What family of viruses does human papilloma virus belong to?
Papillomaviridae
38
What kind of genome/structure does HPV have?
dsDNA virus | non-enveloped
39
What % of adults are infected with HPV?
80%
40
Can HPV be grown in culture?
no
41
What are two methods of testing for HPV?
1. Molecular detection possible | 2. Papanicolaou test (Pap test or Pap smear)
42
What are the two types of HPV? How are they contracted?
High (through sexual contact) and low (dermal type) risk
43
What 3 things are high risk HPV associated with?
Cervical cancer, Head and neck cancer, other anogenital cancers
44
What 2 things are low risk HPV associated with?
1. recurrent respiratory papillomatosis | 2. anogenital warts
45
What are the two important serotypes of high risk HPV?
16 and 18
46
What are the two important serogroups for low risk HPV?
6, and 11
47
What types of symptoms are congruent with a skin to skin (contact) transmission of HPV?
plantar, common and flat warts
48
What is respiratory papillomatosis?
Benign warts in the upper airway that can cause airway obstruction
49
What can be done to treat respiratory papillomatosis?
surgical removal
50
What serotypes cause respiratory papillomatosis? When is it acquired?
6 and 11 Childhood - usually acquired at birth Adult acquisition - usually related to oral intercourse
51
What are 3 treatments for genital warts?
1. Podophyllin resin 2. Trichloroacitic acid 3. Cryotherapy
52
When does infection with HPV normally occur? Can multiple co-infections occur?
Typically very shortly after onset of sexual activity Co-infections can occur, pretty common
53
How long do individual episodes of infection with HPV last? What occurs in the majority of people?
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
HPV 16 and 18 are associated with what % of cervical cancer?
75%
55
In women, infection with HPV 16 or 17 will lead to formation of first...
precancer or high grade precursors and then full blown cervical cancer
56
What is detected on a PAP test?
Detection of patients with cervical cells abnormalities | - Atypical squamous cells of unknown significance (ASCUS)
57
What results in some HPV strains being oncogenic while others are not? What is increased in expression?
Disruption/deletion E2 transcriptional repressor leads to them having a selective growth advantage and later cancer Increased expression of E6 and E7
58
What is the role of E6? how is this different in the low risk types?
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
What are the two HPV vaccines and how are they different?
1. Gardasil - quadrivalent (against 6, 11, 16 and 18) | 2. Cervarix (16 and 18 only)

Clinical Micro (28 decks)

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