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Herpesviridae - Objectives
1. To review the members of the Herpesviridae
family 2. To understand the concepts of primary infection, latent infection and reactivation disease 3. To recognize the common clinical syndromes associated with each virus and the principles of management
Herpesviridae Family
double stranded DNA viruses with envelope ubiquitous, world-wide distribution 8 human herpesviruses recognized; species specific Latency - once infected, always infected - site varies with virus type: - HSV 1 & 2, VZV - sensory nerve ganglia - CMV, EBV, HHV6, HHV7 lymphocytes Replication occurs in the nucleus of infected cell Viral DNA remains episomal (i.e. not integrated into host cell DNA)
Mode of Transmission
Herpesviridae
Transmission: do not survive for prolonged periods in the environment requires inoculation of fresh virus-containing body fluid of infected person into susceptible tissue of uninfected person may be transmitted during primary or reactivation infections; often the person shedding virus is asymptomatic
efficiency of transmission of HSV-2 is lower than HSV-1 Clinical Disease: Primary vs Recurrent
incubation period 2 to 12 days usually asymptomatic gingivostomatitis, pharyngitis multiple small vesicles in clusters or singly resolves in 10-14 days
Herpes, female
Herpes cervicitis
ii) Genital lesions pain, itching, burning for several hours before vesicles appear; healing within 6 - 10 days
HSV Complications
CNS infections Perinatal/Congenital
CT Scan
Autopsy
HSV Congenital/Perinatal
Intrauterine infection: rare; follows 10 infection Perinatal infection: 75% are due to HSV 2; acquired during delivery many women unaware they are infected; 60 - 80% have no signs or symptoms of genital herpes at time of labour (asymptomatic shedders) HSV-1 acquired from maternal genital, oral or breast lesions, paternal or other family member, or nosocomial infection from other infected babies
HSV Congenital/Perinatal
Perinatal Infections: pregnancy is associated with state of immunosuppression: shedding, reactivation, recurrences subclinical infection in neonates is uncommon not all infants of infected mothers will become infected; depends on 10 (30 50% risk) vs recurrent disease (1 3% risk)
HSV Congenital/Perinatal
Clinical manifestations of perinatal infection:
1. disseminated CNS disease (49%)
10 - 40% mortality
3. asymptomatic infection (1%)
HSV Congenital/Perinatal
Treatment: Mother - acyclovir relatively contraindicated during pregnancy Neonate - acyclovir if mother has active lesions or prolonged membrane rupture Prevention: maternal history, surveillance if active lesions at time of delivery then Csection indicated
Recurrences
IgM
Antibody
Detectable Level
IgG
7d
14d
21d
28d
2m
3m
6m
12m
2yr
3yr
Time
HSV Serology
Patients with Primary Infection
18% -30% with both IgG and IgM antibodies Patients with Recurrent HSV Infection 65% only IgG 35% both IgG and IgM
Type Specific Antibodies to HSV 1 and 2: Review of Methodology. Herpes 1998:5 33-38 Ashley R.L.
iii) No vaccine
Cytomegalovirus (CMV)
Transmission: 1) Sexual 2) Perinatal / Intrauterine 3) Blood / Blood product transfusion 4) Organ / tissue transplantation 5) Close contact most infections transmitted asymptomatically
Cytomegalovirus (CMV)
Intrauterine (Congenital) Infections: symptoms present in <25% of infected infants cytomegalic inclusion disease (CID) - jaundiced, hepatosplenomegaly, petechial rash, microcephaly, cerebral calcifications, chorioretinitis may develop symptoms (hearing loss, behavioral changes, mental retardation) years later
Cytomegalovirus (CMV)
Diagnosis: Culture - slow growing, may take weeks for virus to grow Electron microscopy - morphology of herpes viruses Immunofluoresence techniques Serology - IgM for acute infection - IgG for past infection PCR, DNA hybridization
Immunocompromised patients:
Ganciclovir Foscarnet
Prevention:
No vaccine