Oral Viral Infections Flashcards
Characteristics of a virus
small size
simple chemical composition - proteins, phospholipids, glycoproteins and possibly nucleic acids
no intracellular oraganelles
Genetic information as DNA or RNA
DNA virus example
herpes simplex
DNA virus replication steps
8
- Binding
- a/b Entry
- Release and nuclear transport
- Nuclear entry
- Gene expression
- DNA replication
- Packaging
- Egress
how to take a specimen
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
include of virology request form
- 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
common pathogens for maculo populat/erythematous lesions
Enterovirus, HHV6, HHV7, Measles, rubella
take mouth swab and send for DNA/RNA detection
common pathogens for vesicular lesions
HSV1, HSV2, VZV, Enterovirus
take mouth swab and send for DNA/RNA detection
common pathogens for ulcer lesions
HSV, enterovirus
take mouth swab and send for DNA/RNA detection
lab dx principles
Serology
Nucleic acid amplification or antibody levels
* Need knowledge to Interpret the significance of viral antibodies
primary immune antibody response by
IgM
CMV or EBV viruses
secondary immune antibody response
IgG
HSV or VZV viruses
clinical relevance of knowing appearance of common viral lesions
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
viruses in human herpes virus infection group
- 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
common features between human herpes viruses
primary infection
latency
recurrent infection
clincal features of herpes simples 1&2
Gingivo stomatitis
Herpes labialis
Keratoconjuctivitis
Herpetic whitlow
Bell’s palsy
Genital herpes
herpes tx key aspects
clinical features
pathogenesis
epidemiology
lab dx
prevention and tx
HSV 1&2 epidemiology
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
HSV 1&2 epidemiology
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
when to lab dx for HSV 1&2
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
prevention and tx of HSV 1&2
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
complications of varcella virus
secondary bacterial infections
pneumonia
congenital, perinatal/neonatal
chicken pox
complications of varcella virus
secondary bacterial infections
pneumonia
congenital, perinatal/neonatal
chicken pox
clinical features of varicella virus
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
clinical features of varicella virus
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
pathogenesis of varicella zoster
Primary infection: infection with varicella zoster virus
Latency: sensory ganglion (Trigeminal)
Recurrent infection: Reactivation of latent virus from sensory ganglion
how common is varicella (zoster) virus
v common - 90%
source and route of transmission for varicella virus
not zoster
contact with varicella and zoster
highly infectious, esp resp secretions (48hrs pre-symptoms), vesicle fluid is infections
direct contact, droplet or airborne spread
source for varicella-zoster
latent virus in sensory ganglion
low rate of transmission from vesicle fluid
tx and prevention for varicella
chickenpox
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
tx for varicella-zoster
shingles
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.
prevention for varicella-zoster
Vaccine: Protection from Zoster
* Zostavax
Live attenuated virus
Schedule: All people aged 70 + years
enterovirus is
hand, foot and mouth disease
clinical features of enterovirus
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
transmission of enterovirus
nose and throat secretions
fluid from blisters or scabs
faeces
infectivity esp in 1st week
epidemiology of enterovirus
Common in children under 5 years old, but anyone can get infected.
Very contagious.
Outbreaks in nurseries & schools
prevention and tx for enterovirus
No specific medical treatment for hand, foot, and mouth disease.
Relieve symptoms and prevent dehydration
Role of hand hygiene important in limiting spread
clincal features of measles
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
possible complications from measles
Pneumonia
Diarrhoea
Hearing loss
Brain swelling
Death
3/10 people will develop
possible complications from measles
Pneumonia
Diarrhoea
Hearing loss
Brain swelling
Death
3/10 people will develop
pathogenesis of measles
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
tx and prevention of measles
No specific tx
Vaccine preventable
epidemic parotitis a.k.a
mumps
clincal featurs of mumps
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
pathogenesis of mumps
Paramyxovirus family - RNA
Transmission is by direct contact with saliva/fomites or aerosol
Highly transmissible
lab dx for mumps
Oral swab for RNA detection
UKHSA (England) offer diagnosis from oral fluid samples for oral fluid IgM antibody tests or PCR
prevention and tx of mumps
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
HPV vaccine impact on oral HPV infections
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
moneky pox clinical features
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.
pathogenesis of monkey pox
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
lab dx of monkey px
PCR for viral DNA from swabs
prevention and tx of monkey pox
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
acyclvir is an
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)
acycolvir is an
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)
how does acyclovir work
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
uses of acyclovir
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.
