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My BDS4 > Oral Viral Infections > Flashcards

Oral Viral Infections Flashcards

1
Q

List characteristics of a viral cell. (4)

A
  • Small size
  • Simple chemical composition – proteins, phospholipids, glycoproteins and nucleic acids
  • No intracellular organelles therefore these are obligate intracellular parasites
  • Genetic information is stored as DNA or RNA
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2
Q

What makes a virus an obligate intracellular parasite?

A

No intracellular organelles

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3
Q

Name an example of a virus which contains genetic info as DNA.

A

Human herpes

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4
Q

Name an example of a virus which contains genetic info as RNA.

A

Mumps

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5
Q

In herpes simples (DNA virus) where does the primary infection occur?

A

Epithelial cells

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6
Q

In herpes simples (DNA virus) where does the secondary infection occur?

A

neurons of ganglia near the OG infection site

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7
Q

List the 8 stages of virus replication (herpes simplex)

A
  1. Binding
  2. Entry
  3. Release and nuclear transport
  4. Nuclear entry
  5. Gene expression
  6. DNA replication
  7. Packaging
  8. Egress
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8
Q

Describe what occurs in stage 1 of herpes simplex replication.

A

Viral cell binds (can bind to several) to receptor molecules on the hosts cell membrane

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9
Q

Describe what occurs in stage 2 of herpes simplex replication.

A

Once bound the viral cell’s envelope (capsule) fuses with the membrane and the cell contents (capsid) are released into the cytoplasm of host.

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10
Q

Describe what occurs in stage 3 of herpes simplex replication.

A

The released capsid then moves down a scaffold of microtubules and reaches the nuclear membrane

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11
Q

Describe what occurs in stage 4 of herpes simplex replication.

A
  • Herpes chromosome enters the nucleus via a nuclear pore on the nuclear membrane
  • DNA circularises
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12
Q

Describe what occurs in stage 5 of herpes simplex replication.

A

The DNA can either cause;
- A lytic expression via immediate early mRNA
Or
- A latent infection via LAT mRNA (where the DNA circle can persist within the cell for decades before switching to a lytic infection)
Commonly occurs in nerve cells

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13
Q

Describe what occurs in stage 6 of herpes simplex replication (5)

A
  • The immediate early mRNA genes from a lytic infection leaves the nucleus and are transcribed into viral proteins by ribosomes. These translated proteins then renter the nucleus and cause the expression of another set of genes called early mRNA.
  • The early genes then leave the nucleus and are translated into proteins.
  • The early proteins re-enter the cell and because they contain viral DNA polymerase they replicate the circular viral DNA (rolling-circle method)
  • The newly formed DNA then expresses late mRNA which leaves the nucleu for translation to create late-stage proteins.
  • Late stage proteins re-enter the nucleus and form capsids which capture DNA genomes
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14
Q

What can trigger latent herpes simplex infection? (3)

A
  • Stress (menstruation)
  • Sunlight exposure
  • Immunosuppression
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15
Q

What type of swab is required for a viral sample? Describe how this sample is taken.

A

flocked swab - Placed in molecular sample solution (extracts the viral DNA/RNA) for a period of time and then removed from the solution

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16
Q

What does 2x triangle symbol mean?

A

Provisional diagnosis

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17
Q

What does 1x triangle symbol mean?

A

Diagnosis

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18
Q

What details are required for a virology request? (5)

A
  • Patient & clinician details (including phone no.)
  • Clinical details & provisional diagnosis
  • Date of onset
  • Patient DOB or CHI number
  • Specify which test you require (do not request “viral screen”)
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19
Q

List the common pathogens associated, the specimens and the tests required for a macula papular/erythematous lesion.

A

pathogen - enterovirus, HHV6, HHV7 Measles, rubella

specimen - mouth swab

test - DNA/RNA detection

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20
Q

List the common pathogens associated, the specimens and the tests required for a nucleic acid amplification of a vesicular lesion.

A

Pathogen - HSV1, HSV2, VZV, enterovirus

Specimen - Mouth swab

Test - DNA/RNA detection

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21
Q

List the common pathogens associated, the specimens and the tests required for serology testing of a maculo papular/erythematous lesion.

A

Pathogen - B19, CMV, EBV

Specimen - EDTA blood

Test - DNA/RNA detection or serology

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22
Q

What does the serological marker IgM detect? (3)

A

IgM = detects primary immune response
- Used to detect (herpes) cytomegalo virus or Epstein barr virus

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23
Q

What does the serological marker IgG detect? (3)

A

IgG = Secondary immunological response
- Used to detect (human herpes) herpes simplex virus or varicella zoster virus

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24
Q

List the 8 human herpes viral infections.

A

Ÿ Herpes simplex type 1
Ÿ Herpes simplex type 2
Ÿ Varicella zoster
Ÿ Epstein Barr
Ÿ Cytomegalovirus
Ÿ HHV-6
Ÿ HHV-7
Ÿ HHV-8 (Kaposi’s Sarcoma Associated virus)

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25
Q

What are features common to all hrepes viral infections? (3)

A
  • Primary/acute Infection
  • Latency
  • Recurrent Infection
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26
Q

What are the clinical features of herpes simplex 1&2. (6)

A
  • Gingivo stomatitis
  • Herpes labialis
  • Keratoconjuctivitis
  • Herpetic whitlow
  • Bell’s palsy
  • Genital herpes
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27
Q

Where does type 1 herpes simplex commonly cause recurrent infection?

A

Occurs in oral sites since the HSV1 is good at establishing latent infection in the trigeminal ganglia

28
Q

Where does type 2 herpes simplex commonly cause recurrent infection?

A

Occurs in genital sites since the HSV2 is good at establishing latent infection in the sacral ganglia

29
Q

Describe the pathological process of a herpes simplex primary and secondary infection. (5)

A
  • Virus enters the body via a mucosal surface or abraded epithelium
  • Virus replicates in epithelial cells
  • The virus is Neurotrophic (has an affinity to sensory neurons) so virus travels to neurons
  • Undergoes retrograde transport along the neurons and back to sensory ganglions (where latent infection establishes)
  • latent infection can reactivate in the ganglia (unsure why) and it travels back along the sensory neurons to the mucosa and lesions occur again on mouth etc = reactivated/recurrent infection
    since the recurrent leisons occur via neurons you can feel tingling in the site before lesions appear
30
Q

What is the reservoir for herpes simples 1&2?

A

Saliva

31
Q

What is the route of transmission of herpes simples 1&2?

A

direct by close person to person contact

32
Q

How do we diagnose herpes simplex 1&2?

A

Most diagnoses do not require lab samples however can be useful for atypical cases;
- Vesicle/ulcer fluid swap and placed in the appropriate molecular sample media for PCR

33
Q

How do we prevent herpes simplex 1&2?

A

Ÿ Chemoprophylaxis - only for recurrence
- Acyclovir to prevent recurrent infection in difficult cases (200mg x5 daily ACV)

34
Q

How do we treat herpes simplex 1&2? (2)

A

Ÿ Antiviral therapy;
- topical therapy with ACV (aciclovir cream 5%)
- IV therapy for severe & immunosuppressed

35
Q

What is the primary infection of varicalla?

A

chickenpox

36
Q

What are the complications of varicella - chickenpox? (3)

A

Ÿ Secondary bacterial infections e.g. group A strep
Ÿ Pneumonia
Ÿ Congenital, perinatal/neonatal

37
Q

What are the clinical features of varicella zoster - shingles? (3)

A

Vesicles appear in dermatome, representing cranial or spinal ganglia where the virus has been dormant

  • Vesicles/ulcers don’t cross the midline
    Ÿ- The affected area may be intensely painful with associated paraesthesia.
38
Q

what are the complications of varicella zoster - shingles? (4)

A

Post herpetic neuralgia
ŸSecondary bacterial infections
Ophthalmic zoster
ŸRamsay Hunt syndrome (paralysis of the facial nerve and hearing loss)

39
Q

Describe the primary infection, latency and recurrent infection of varicella.

A

Primary infection = varicella virus (chickenpox)

Latency = lays dormant in the trigeminal sensory ganglion

Recurrent infection = reactivation of latent virus from sensory ganglion when px immunosuppressed

40
Q

What is the source of infection for varicella - chickenpox? (3)

A

contact with varicella & zoster
- highly infectious esp from respiratory secretions (spread 48 hrs pre-symptoms)
- Vesicle fluid infectious

41
Q

What is the source of infection for varicella zoster-shingles? (2)

A

latent virus in sensory trigeminal ganglion
- low rate of transmission (compared to chickenpox) from vesicle fluid

42
Q

What is the route of infection for varicella? (2)

A

Direct contact, droplet or airborne spread

43
Q

What population group is most commonly affected by varicella - chickenpox?

A

children

44
Q

What population group is most commonly affected by varicella zoster - shingles? (2)

A

highest in elderly & immunocompromised

45
Q

How do we prevent shingles?

A

Protection from Zoster (Zostavax) - offered to those 70 and above

46
Q

How do we treat shingles?

A

Antiviral therapy:
Aciclovir: 800mg Oral x5 daily for 7 days
- Refer all patients with herpes zoster to a specialist or their general medical practitioner.

47
Q

List other viral infections. (6)

A
  • Enteroviruses: Group A
  • Cocksackie virus
  • Measles
  • Mumps
  • Papilloma virus
  • Monkeypox
48
Q

What are the clinical features of hand, foot and mouth virus? (5)

A
  • Fever
  • runny nose
  • sneezing
  • cough
  • alongside macular skin rash, mouth blisters, and body and muscle aches.
    Blisters last longer on the skin (oral mucosa thinner – ulcers instead)
49
Q

How is H,F&M spread? (3)

A
  • nose and throat secretions
  • fluid from blisters or scabs
  • Faeces
50
Q

When is H,F&M most infectious?

A

week 1

51
Q

What population group is most commonly affected by H,F&M disease?

A

children under 5 - anyone at risk

52
Q

How is H,F&M disease diagnosed?

A

Not usually required (diagnosis based on clinical history & appearance)
- An oral swab for detection of enterovirus RNA can be used if uncertain diagnosis

53
Q

How do we treat HFM disease?

A

No specific medical treatment for hand, foot, and mouth disease.
- Relieve symptoms and prevent dehydration
(Role of hand hygiene important in limiting spread)

54
Q

What are the dental relevant signs of measles?

A

Koplik spots on oral mucosa

55
Q

What are the complications of measles? (5)

A
  • Pneumonia
  • Diahorrea
  • Hearing loss
  • Brain swelling
  • Death
56
Q

How is measles spread? (2)

A

The RNA virus spread through airborne transmission or direct contact with infected respiratory secretions.

57
Q

What is the incubation period of mumps?

A

12-24 days (can get symptomatic carriage of infection)

58
Q

What are the symptoms of mumps? (4)

A
  • Headache
  • Fever
  • Swollen parotid glands (uni or bilateral)

Other organs can also be affected causing;
pancreatitis, neuritis, arthritis, mastitis, nephritis, thyroiditis, ovaries (oophoritis), swelling of the testes (orchitis) and pericarditis.

59
Q

What is mumps also known as?

A

epidemic parotitis

60
Q

How is mumps spread? (2)

A

direct contact with saliva/fomites (objects or materials which are likely to carry infection, such as clothes, utensils, and furniture)

aerosol

61
Q

How is mumps diagnosed in Scotland?

A
  • Oral swab for RNA detection
62
Q

How do we prevent mumps?

A

routine vaccination
- UK children measles mumps rubella (MMR) vaccine as part of the routine childhood immunisation schedule.

63
Q

What is acyclovir?

A

An acyclic purine nucleoside (has a similar structure to deoxyguanine)

64
Q

What is the action of acyclovir? (3)

A

Similar structure to deoxyguanine in DNA so tricks the replicating herpes virus into incorporating the defective molecule into the growing viral DNA chain = Inhibits DNA polymerase

  1. viral enzymes add a phosphate group to ACV
  2. human enzymes add 2 more phosphate groups = ACV triphosphate
  3. during viral DNA replication, ACV added to the growing viral strands rather than GTP
    = haunts further elongation of the DNA replication and therefore viral replication
65
Q

Why is the latency stage of viral infection not affected by ACV?

A

due to the fact that when the virus is latent its not actively replication (replication is where acyclovir targets)

66
Q

What causes ACV resistance?

A

mutations in viral thymidine kinase

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