Karteikarten
CSIM1.20
Karten in diesem Stapel (34)
- 1List the members of the herpes familyHerpes Simplex Virus (HSV) 1 and 2
Varicella Zoster Virus (VZV)
Cytomegalovirus (CMV)
Epstein Barr Virus (EBV)
Human Herpes Virus 6 (HHV6)
Human Herpes Virus 7 (HHV7)
Human Herpes Virus 8 (HHV8) (Kaposi’s sarcoma associated herpes virus) - 2Describe the virology of the herpesviridae virusFamily Herpesviridae
Double-stranded DNA
Envelope
(derived from cell nuclear membrane) - 3Describe the life cycle of the herpesviridae virusPrimary Infection
Latency: Viral DNA persists in specific cell types lifelong.
No replication. No intact virus.
Reactivation: Viruses reactivates intermittently.
May be symptomatic or asymptomatic. - 4What species are in the herpesviridae family?HSV-1 and HSV-2 (both of which can cause orolabial herpes and genital herpes), Varicella zoster virus (which causes chicken-pox and shingles), Epstein-Barr virus (which causes mononucleosis), and Cytomegalovirus
- 5What is the difference between HSV1 and HSV2?Most people get HSV-1 (herpes simplex type 1) as an infant or child. This virus can be spread by skin-to-skin contact with an adult who carries the virus. An adult does not have to have sores to spread the virus. A person usually gets HSV-2 (herpes simplex type 2) through sexual contact. About 20% of sexually active adults in the United States carry HSV-2.
- 6Define a HSV primary infectionfirst infection with either HSV 1 or HSV 2
- 7Define an initial infection of HSVUsually first HSV 2 infection in a patient who has already been infected with HSV 1 (or vice versa)
- 8What causes HSV reactivation?Stress
Fever and other infections
Menstruation
Cold
Sunlight - 9Describe transmission of HSVOral - close social contact – kissing, nurseries
Genital – sexual contact - 10Describe HSV – Primary Oral herpesPrimary infection with HSV 1 or HSV 2
Usually asymptomatic
Can be severe Gingivostomatitis - 11What is Gingivostomatitis?a combination of gingivitis and stomatitis, or an inflammation of the oral mucosa and gingiva.[1] Herpetic gingivostomatitis is often the initial presentation during the first ("primary") herpes simplex infection
- 12Describe oral reactivation of HSV?Reactivation usually HSV 1
Usually asymptomatic
Can cause cold sores - 13Describe HSV genetic diseasePrimary infection with HSV 1 or HSV 2
Reactivation usually HSV 2
Primary more severe than reactivation
Reactivation can be asymptomatic - 14What are the main complications of HSV?Secondary bacterial infection
Corneal Ulcers, risk of scarring, loss of vision
Meningitis, self limited, usually HSV 2, can be recurrent (Mollaret’s meningitis)
Herpes Simplex Encephalitis, life-threatening, usually HSV 1 - 15What are the risk groups for HSV infection?Neonates
Untreated high mortality and risk of poor neurodevelopmental outcome
Main risk is maternal primary genital HSV at the time of delivery.
Immunocompromised
Reactivations more frequent and severe - 16What is herpetic whitlow?HSV-1 or HSV-2 infection on the fingers or thumbs, thumb sucking, dental workers etc. Symptoms of herpetic whitlow include swelling, reddening and tenderness of the skin of infected finger.
- 17Describe ocular infection in HSV?Dendritic corneal ulcer
Risk of scarring and loss of vision - 18What is the cause of neonatal HSV infection?Highest risk is maternal primary or initial genital herpes.
Usually infected at the time of birth via the birth canal
Range of severity: mild disease to life-threatening disseminated disease - 19What is HSV encephaliltis?Commonest cause of viral encephalitis
70% mortality untreated
High rate of poor neurological outcome - 20What is Aciclovir?Inactive in unmodified form.
Activated by a viral enzyme – thymidine kinase.
So only active in infected cells.
Fewer side effects
Activated drug inhibits Viral Polymerase - 21How is Aciclovir administered?Most effective if started within 24-48 hours of rash onset
Poor oral bioavailability, 5 x per day dosing
Alternative Valaciclovir – prodrug of aciclovir –better oral bioavailability – converted to aciclovir after absorption. More expensive.
Aciclovir must must be given IV in severe disease (encephalitis / neonates)
(Topical aciclovir cream available across the counter for cold sores. Must be started very early and efficacy is limited) - 22Describe the parthenogenesis of varizella zozsterInfection via respiratory mucosa/conjunctiva
Replication in regional lymph nodes
Primary Viraemia
Replication in liver and spleen
Secondary Viraemia
Dissemination to skin
Varicella = Chickenpox
Latency in dorsal route ganglion
Reactivation
Zoster = Shingles - 23Describe the symptoms of a primary infection ChickenpoxProdrome of fever before rash is common
Centipetal distrubution
Macules -> Papules-> Vesicles -> Pustules
Crops of lesions at different stages
More severe in adults - 24Describe the epidemiology of chickenpoxUK > 90% seroprevelance (naturally immune)
Outbreaks mainly in winter/spring
Attack rate for household contacts is >90%
Peak age is now <5 years in UK
Respiratory transmission or direct contact
Incubation period 8-21 days (average 14 days)
Infectious from 2 days before rash to full crusting of vesicles - 25What are the complications of chickenpox?Bacterial Sepsis
Varicella Pneumonia (especially smokers)
Varicella Encephalitis (rare, cerebellar ataxia in children) - 26What are the risk groups for chickenpox?Pregnancy
Possibly increased severity - pneumonitis
Congenital varicella syndrome (1-2% before 20 wks gestation)
Neonatal Chickenpox - Can be life-threatening
Immunocompromised - Can be life-threatening - 27Describe the epidemiology of shingles25% of individuals experience an attack of zoster (shingles)
Most cases occur in those >50 years with numbers increasing with age.
Infectious from day of rash until vesicles fully crusted.
Transmission via direct contact (not respiratory) - 28What are the complications of zoster?Post herpetic neuralgia - Pain lasting >4 weeks
15% of zoster
40% of zoster >60 years - 29What is Ophthalmic Zoster?Affecting trigeminal nerve.
Ocular complications particularly likely if nasociliary branch is involved (lesions on side of nose). - 30How is zoster diagnosed?Detection of viral DNA by PCR (PCR = polymerase chain reaction)
Lesion swab
Cerebrospinal fluid
Serology (antibody testing) has no role. (but VZV IgG denotes immunity) - 31How is zoster treated?Children not normally treated
Adults tend to have more severe disease and varicella or zoster should be treated if within 24 hours of rash
Aciclovir (or Valaciclovir)
As for HSV, needs activated by a viral enzyme – thymidine kinase
Less active against VZV than HSV (need 4x oral HSV dose). So valaciclovir may be better choice
IV for severe infection in the immunocompromised
Not licensed in pregnancy but has been frequently used. (Aciclovir in pregnancy register – no adverse effects so far) - 32Describe the varicella vassineLive attenuated vaccine
Used as part of childhood vaccine schedule for 12 years in USA (2 doses with MMR)
Indications in UK
Healthcare workers with no CP history, or no VZV IgG
VZV IgG negative contacts of immunosuppressed children (live vaccines contraindicated in the immunosuppressed) - 33What is post exposure propholaxis is available for zoster infection?Zoster Immunoglobin (VZIG - IM injection)
Aciclovir also used occasionally
Give if significant contact:
Varicella: Face to face contact or >15 mins in same room
Zoster: Exposure to uncovered rash
And not immune to varicella (VZV IgG negative)
And at increased risk:
Pregnant women / neonates
Immunocompromised
VZIG will prevent 25% of infections completely, 25% will be asymptomatic and 50% will be symptomatic (but normally less severe) - 34What is the zoster vaccine?Live attenuated vaccine
Identical to varicella vaccine but over 10x the dose
Acts by boosting immunity and preventing reactivation.
UK implemented zoster vaccination for 70 year olds in August 2013
Informationen
- Beschreibung
- Karteikarten am CSIM1.20, erstellt von victoriascudamore am 03/05/2015.
- Erstellt von
- victoriascudamore
- Aufrufe
- 1
- Bewertung