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BDS4 BAMS Oral Disease, Medicine, Virology > Oral Viral Infections > Flashcards

Oral Viral Infections Flashcards

1
Q

Characteristics of a virus

A

small size
simple chemical composition - proteins, phospholipids, glycoproteins and possibly nucleic acids
no intracellular oraganelles
Genetic information as DNA or RNA

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2
Q

DNA virus example

A

herpes simplex

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3
Q

DNA virus replication steps

8

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

how to take a specimen

A

Viral swab
* Used flocked swab
* Place in molecular sample solution (MSS)
* After immersion remove swab
Blood sample
* EDTA (purple top)
* Use for serology and molecular

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5
Q

include of virology request form

A
  • Pt details & clinician details (inc phone no.)
  • Clinical details & ? diagnosis
  • Date of onset
  • Patient DOB or CHI number
  • Specify test (do not request “viral screen”)
    On trakcare or pdf

Specimen transport: Be aware of legislation and Health Safety Laws & ONL

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6
Q

common pathogens for maculo populat/erythematous lesions

A

Enterovirus, HHV6, HHV7, Measles, rubella

take mouth swab and send for DNA/RNA detection

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7
Q

common pathogens for vesicular lesions

A

HSV1, HSV2, VZV, Enterovirus

take mouth swab and send for DNA/RNA detection

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8
Q

common pathogens for ulcer lesions

A

HSV, enterovirus

take mouth swab and send for DNA/RNA detection

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9
Q

lab dx principles

A

Serology
Nucleic acid amplification or antibody levels
* Need knowledge to Interpret the significance of viral antibodies

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10
Q

primary immune antibody response by

A

IgM

CMV or EBV viruses

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11
Q

secondary immune antibody response

A

IgG

HSV or VZV viruses

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12
Q

clinical relevance of knowing appearance of common viral lesions

A

Linking clinical signs and symptoms to pathogenesis and dx

Selecting correct dx tests (do not use bacterial swabs)

Selecting appropriate antimicrobial chemotherapy
* Antibiotics will not tx viral infections

Laboratory stewardship – appropriate use of limited resources
* Most OVI can be diagnosed from history/clinical
* Lab tests supports clinical investigation does not replace

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13
Q

viruses in human herpes virus infection group

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

Fried egg appearance under SEM
Can’t tell type from electron micrograph

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14
Q

common features between human herpes viruses

A

primary infection
latency
recurrent infection

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15
Q

clincal features of herpes simples 1&2

A

Gingivo stomatitis
Herpes labialis
Keratoconjuctivitis
Herpetic whitlow
Bell’s palsy
Genital herpes

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16
Q

herpes tx key aspects

A

clinical features
pathogenesis
epidemiology
lab dx
prevention and tx

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17
Q

HSV 1&2 epidemiology

A

Very common infection >90% population
Reservoir: Saliva (note: 30% asymptomatic shedding)
Route of transmission: direct by close person to person contact
Occurrence: common in childhood
Think chain of infection

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17
Q

HSV 1&2 epidemiology

A

Very common infection >90% population
Reservoir: Saliva (note: 30% asymptomatic shedding)
Route of transmission: direct by close person to person contact
Occurrence: common in childhood
Think chain of infection

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18
Q

when to lab dx for HSV 1&2

A

Most dx can be made based on history and clinical appearance
Can be useful for atypical cases
* Vesicle/ulcer fluid – swab and molecular sample media for PCR

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19
Q

prevention and tx of HSV 1&2

A

Chemoprophylaxis
* ACV to prevent recurrent infection in difficult cases
(200mg x5 daily ACV)

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

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20
Q

complications of varcella virus

A

secondary bacterial infections
pneumonia
congenital, perinatal/neonatal

chicken pox

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20
Q

complications of varcella virus

A

secondary bacterial infections
pneumonia
congenital, perinatal/neonatal

chicken pox

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21
Q

clinical features of varicella virus

A

Vesicles appear in dermatome, representing cranial or spinal ganglia where the virus has been dormant.
* The affected area may be intensely painful with associated paraesthesia.

Complications
* Post herpetic neuralgia
* Secondary bacterial infections
* Ophthalmic zoster
* Ramsay Hunt syndrome can lead to paralysis of facial nerve

chicken pox

22
Q

clinical features of varicella virus

A

Vesicles appear in dermatome, representing cranial or spinal ganglia where the virus has been dormant.
* The affected area may be intensely painful with associated paraesthesia.

Complications
* Post herpetic neuralgia
* Secondary bacterial infections
* Ophthalmic zoster
* Ramsay Hunt syndrome can lead to paralysis of facial nerve

chicken pox

23
Q

pathogenesis of varicella zoster

A

Primary infection: infection with varicella zoster virus

Latency: sensory ganglion (Trigeminal)

Recurrent infection: Reactivation of latent virus from sensory ganglion

24
Q

how common is varicella (zoster) virus

A

v common - 90%

25
Q

source and route of transmission for varicella virus

not zoster

A

contact with varicella and zoster
highly infectious, esp resp secretions (48hrs pre-symptoms), vesicle fluid is infections

direct contact, droplet or airborne spread

26
Q

source for varicella-zoster

A

latent virus in sensory ganglion
low rate of transmission from vesicle fluid

27
Q

tx and prevention for varicella

chickenpox

A

not expected to have involvement in management of chicken pox

Chickenpox vaccine not part of the routine childhood vaccination schedule.
Currently only offered on the NHS to people who are in close contact with someone who’s particularly vulnerable to chickenpox or its complications

28
Q

tx for varicella-zoster

shingles

A

Important to diagnosis and treat early because ;
* Early treatment reduces severity & duration of pain & complications
* Pain may mimic toothache

Antiviral therapy
* Aciclovir: 800mg Oral x5 daily for 7 days

Refer all patients with herpes zoster to a specialist or their general medical practitioner.

29
Q

prevention for varicella-zoster

A

Vaccine: Protection from Zoster
* Zostavax

Live attenuated virus

Schedule: All people aged 70 + years

30
Q

enterovirus is

A

hand, foot and mouth disease

31
Q

clinical features of enterovirus

A

Fever, runny nose, sneezing, cough

With skin rash, mouth blisters and body/muscle aches (last longer on skin, oral mucosa thinner so join together to form sore ulcers)

hand, foot and mouth disease

32
Q

transmission of enterovirus

A

nose and throat secretions
fluid from blisters or scabs
faeces

infectivity esp in 1st week

33
Q

epidemiology of enterovirus

A

Common in children under 5 years old, but anyone can get infected.
Very contagious.
Outbreaks in nurseries & schools

34
Q

prevention and tx for enterovirus

A

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

35
Q

clincal features of measles

A

14 days after exposure
* High fever, cough, runny nose, conjunctivitis

2-3days later
* Tiny white spots inside mouth (Koplik spots)

3-5 days later
* Rash begins on the face and spreads downwards

36
Q

possible complications from measles

A

Pneumonia
Diarrhoea
Hearing loss
Brain swelling
Death

3/10 people will develop

37
Q

possible complications from measles

A

Pneumonia
Diarrhoea
Hearing loss
Brain swelling
Death

3/10 people will develop

38
Q

pathogenesis of measles

A

RNA virus spreads through airborne transmission or direct contact with infected respiratory secretions
* Virus can live on surfaces for 2 hours
* 1 person can infect 18 others

39
Q

tx and prevention of measles

A

No specific tx
Vaccine preventable

40
Q

epidemic parotitis a.k.a

A

mumps

41
Q

clincal featurs of mumps

A

IP = 12 to 24 days
(can get asymptomatic carriage)

Symptoms= headache and fever, swelling of the parotid glands (uni or bilateral)

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

42
Q

pathogenesis of mumps

A

Paramyxovirus family - RNA
Transmission is by direct contact with saliva/fomites or aerosol
Highly transmissible

43
Q

lab dx for mumps

A

Oral swab for RNA detection

UKHSA (England) offer diagnosis from oral fluid samples for oral fluid IgM antibody tests or PCR

44
Q

prevention and tx of mumps

A

Treatment is aimed at relieving symptoms.

Routine vaccination can prevent the infection

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

45
Q

HPV vaccine impact on oral HPV infections

A

Oral HPV infections were 88% lower among young adults who received at least one HPV vaccine dose

HPV-16 risk factor for head and neck squamous cell carcinoma

papilloma virus

46
Q

moneky pox clinical features

A

Usually a self-limited disease

Symptoms begin 5 to 21 days after exposure

Rash 1 to 5 days post fever.
* Blistering rash or skin lesions, on the face and genital area.

Clinical diagnosis of monkeypox can be difficult,
* May be confused with herpes simplex virus, chickenpox or syphilis.

47
Q

pathogenesis of monkey pox

A

An enveloped DNA virus

A viral zoonotic disease primarily in tropical rainforest areas of central/west Africa.

Transmitted through close contact with an infected person or animal, or with material contaminated with the virus.

Zoonotic sources include rope squirrels, tree squirrels, Gambian pouched rats, dormice, & non-human primates

48
Q

lab dx of monkey px

A

PCR for viral DNA from swabs

49
Q

prevention and tx of monkey pox

A

Vaccine = Modified Vaccinia Ankara (MVA)
* Attenuated (weakened) strain of the vaccinia virus.
* Does not contain smallpox virus and cannot spread or cause smallpox.

Highest risk transmission routes are direct contact, droplet or fomite.
* Transmission seen so far in this outbreak is consistent with close direct contact

Minimum PPE for staff working with possible or probably cases inc fluid repellent surgical facemasks (FRSM), gowns, gloves and eye protection

50
Q

acyclvir is an

A

acyclic purine nucleoside

Looks like Deoxyguanine (DOG)
* Tricks the replicating virus to incorporate the defective molecule into its growing DNA chain, so blocks the synthesis of the growing DNA (inhibits DNA polymerase)

51
Q

acycolvir is an

A

acyclic purine nucleoside

Looks like Deoxyguanine (DOG)
* Tricks the replicating virus to incorporate the defective molecule into its growing DNA chain, so blocks the synthesis of the growing DNA (inhibits DNA polymerase)

52
Q

how does acyclovir work

A

Viral enzyme =thymidine kinase
Viral thymidine kinase = higher affinity for acyclovir

Active only in infected cells (selective action of acyclovir)

Acyclovir triphosphate = better substrate for viral than for host cell DNA polymerase and thereby causes preferential termination of viral DNA synthesis

SDCEP for guidance on doses

53
Q

uses of acyclovir

A

From dental perspective used for managing Herpes simples (cold sores) and Zoster (shingles) infections
* Latency stage of the viral infection is not affected

Resistance to acyclovir can occur due to mutations in viral thymidine kinase

SDCEP for doses

used topically or systemically, orally, or intravenously.

BDS4 BAMS Oral Disease, Medicine, Virology (23 decks)

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