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--HERPES VIRUSES—

HERPES SIMPLEX VIRUSES VARICELLA-ZOSTER VIRUS


PROPERTIES ~ belong to alphaherpesvirus subfamily ~ belong to alphaherpesvirus subfamily
~ genomes HSV-1 & HSV-2 share 50-70% homology ~ one antigenic serotype only, although there is some
~ share several cross-reactive epitopes w each other cross reaction w HSV
~ some antigenic cross-rxn w VZV
~ man is only natural host for HSV
EPIDEMIOLOGY ~ spread by contact, virus shed in saliva, tears, ~ primary infection is Varicella- endemic, one of
genital & other secretion, kiss given to child classical papulo-vesicular exanthematous disease of
~ primary infxn maybe subclinical in most pt, childhood, prevalence occur in 4-10 yrs old
disease mainly of below 5 yrs. ~ varicella; highly communicable, 90% in close cntct
~ 2 peaks of incidence, 1st at 0-5 yrs and 2nd in late ~most infected b4 adulthood but 10% young adult
teens; when sexual activity commences remain susceptible
~ generally, HSV-1- infxn above the belt ~ herpes zoster, in contrast, occur sporadically, and
HSV-2- elow the belt evenly throughout the year
~ 40% fr genital sores are HSV-1, 5% fr facial sores
are HSV-2 (d2 oral sexual practice)
~ actual recurrence frequency varies. Mean number
of episodes per year is 1.6
PATHOGENESIS during primary infxn, HSV spread locally and a ~ virus is thought to gain entry via the respi. Tract
short-lived viraemia occur. Spead to sensory and spread shortly after to the regional lymphoid
craniospinal ganglia system and blood causing viraemia
~ after incubation period 14 days, 2ndary viremia the
virus established latency in craniospinal ganglia virus arrives main target organ, the skin.
~ remain latent in cerebral or posterior root ganglia,
~ exact mechanism of latency is unknown in 10-20% pt, single recurrent infection occur after
~ reactivation : triggered by physical/psychological several decades
stress, pneumococcal and meningococcal infxn, ~ reactivates in sensory ganglion and track down
fever, irradiation like sunlight and menstruation sensory nerve to area of skin innervated by
~ infect & replicate in mucoepithelial cell--- disease nerve,producingvaricelliform rash in distribution of
at siteof infection dermatome
~ immunity following infection is lifelong (>20)
CLINICAL ~ acute gingivostomatitis ~ varicella
MANIFESTATION ~ herpes labialis ( clod sore ) ~rash of chicken pox
~ ocular herpes ~ herpes zoster (shingle)
~ herpes genitalis ~congenital VZV infection
~ other form of cut, herpes ~ neonatal varicella
~ meningitis
~ encephalitis
~ neonatal herpes
LAB DX ~ direct detection ~ virus isolaton- fr ulcer fluid, 1 week for result
– EM of vesicle fluid, rapid result but cant ~ direct detection- EM of vesicle fluid, rapid result
distinguish btwn HSV-VZV but cant distinguish btwn HSV-VZV
- imunoflrescence of skin crapping – distinguish - imunoflrescence of skin crapping – distinguish
btwn HSV-VZV btwn HSV-VZV
~ virus isolation – rapid growth in 1-3 days - Tzanck Smear – stained ulcer swab / giant cell
~ serology- not that useful bcoz takes 1-2 wks b4 Ab ~ serology- VZV IgG indicate past infection &
appear, used to document recent infection immunity , IgM indicate recent primary infection
~ PCR

MANAGEMENT ~ Acyclovir- drug choice, available in : ~ self-limited, so no specific tx


- I.V ( in normal & immunosupprssed pt) ~ Acyclovir : to immunocompromised pt and normal
- Oral (tx & long term suppression of mucocut, ppl w serious complication(pneumonia &
herpes & prophylaxis in immunosuppressed encephalitis
pt) ~ ~ famciclovir and valacyclovir
- Cream ( skin & mucous membrane) ~ passive immunization ( Zoster Ig)
- Ophthalmic ointment ~ live attenuated vaccine is available
~ famciclovir and valacyclovir- oral only, costly
CYTOMEGALOVIRUS EPSTEIN-BARR VIRUS
PROPERTIES ~ belong to Betaherpesvirus subfamily ~ belong to Gammaherpesvirus subfamily
EPIDEMIOLOGY ~ transmission occur in uterus, perinatal or postnatal ~ in dvloped cntries:
~ latency: once infectedm carries for life - 2 peaks infection; 1st- 1-6 yrs old, 2nd: 14-20 yrs
~ maybe reactivated fr time to time, during which old
virions appear in saliva and urine ~ in dvlping cntries:
~ reinfection may occur, do not differ fr reactivation - occur much earlier at 2 yrs old, 90% kids
~ in dvloped countries w high hygiene, 40-70% sero+ve
inected ~ virus transmitted thru saliva, in kissing
~ in dvlping countries, 90% infected
PATHOGENESIS Once infected, virus remain for life and may ~ once infected, a lifelong carrier state dvlop low
reactivated, esp in immunocompromised person grade infection, kept in check by immune defenses
~ perinatal infection- thru genital secretion, breast ~ low grade replication & shedding in epi. Cell of
milk, 10 times common than congenital infection pharynx of all sero+ve person
~ 2-10% infants infected at 6 months worldwide ~EBV can immortalize B-lymphocyte in vitro&vivo
~ postnatal infection- thru saliva, sexual tansmission ~assoc w several diff diseases act directly or one of
may occur as well as blood & transplanted organs several cofactors
CLINICAL ~ congenital infection- ~ infectious mononucleosis
MANIFESTATION - 2nd most cause of mental retard, 40% chance ~ Burkitts lymphoma
follow primary infection ~ nasopharyngeal carcinoma
- Maybe transmitted to fetus in all stages ~ lymphoproliferative disease & lymphoma
- No evidence of teratogenicity, damage of fetus ~ X-linked lymphoproliferative syndrome
result fr destruction of target cell once ther are ~ chronic infectious mononucleosis
formed ~ oral leukoplakia in AIDS pt
cytomegalic inclusion disease: ~ chronic interstitial pneumonitis in AIDS
- CNS abnormalities( microcephaly, retardation,
spastic, epilepsy)
- Eye- optic atrophy & choroidoretinitis
- Ear – sensorineural deafness
- Liver- hepatosplenomegaly, jaundice
- Lung(pneumonia), heart(myocarditis)
- Late sequela- sensorineural deafness & low IQ
~ perinatal infection- asymptomatic
~ postnatal infection- asymptomatic
~ immunocopromised : retinitis, colitis, encephalpthy
~ reactivation or reinfection is asymptomatic except
in immunocompromised pt
LAB DX ~ direct detection ~ acute EBV usually made by heterophil Ab test
-pp65 CMV antigaenaemia test for rapid dx and/or detection of anti-EBV VCA IgM
-biopsy specimen for CMV inclusion Abs ~ cases of Burkitts Lymphoma diagnosed by hstology
~ virus isolation-4 weeks for result. DEAFF test give The tumor can be stained w AB to lambda light chains
result in 24-48 hours which reveal monoclonal tumor of B-cell
~ serology: IgG (past infection) IgM (primary infxn) ~caes of NPC diagnosed by Histology. Determination
~ PCR assays of titre of anti-EBV VCA IgA is screening for lesion
MANAGEMENT Tx : Vaccination :
~ congenital infection : choice of abortion - vaccine that prevent primary EBV infection
~ peri and postnatal infection: no need to treat should be able to control both BL & NPC
~ immuncompromised : antiviral therapy, - given in early life. Useful in sero-ve transplant
ganciclovir, foscarnet, cidofovir recipient and those w severe IM, eg male
Prevention: offspring of Xlinked proliferative syndrome
~no vaccine available, a candidate live-attenuated carrier
vaccine, recombinant vaccine also being developed - not preferably be a subunit vaccine since there
~ prevention in transplant recipient is complicated. It is a danger that live vaccine still tumoregenic
needs measure : - Ag chosen is the MA Ag gp 340/220
- screen & match CMV status, use CMV –ve - Still try in Africa
blood transfusion, administer CMV Ig to sero-
ve recipient, give antiviral agent eg ganciclovir
HUMAN HERPESVIRUS 6 AND 7 HUMAN HERPESVIRUS 8
PROPERTIES ~belong to Betaherpesvirus subfamily ~ belong to Gammaherpesvirus subfamily
~dsDNA genome of 170 kb ~ originally isolated fr Kaposi’s Sarcoma (KS)
~ main target cell is T-lymphocyte, B-lymphocyte too ~ to be firmly assoc. w KS
~ HHV-6 & 7 share limited nucleotide homology and
antigenic cross-reactivity
~ both related to each other in similar manner HSV-1
and HSV-2
EPIDEMIOLOGY ~ both ubiquitous and found worldwide
~ both infection are requied rapidly after age 4 month
when the effect of maternal AB wears off
~ by the time adulthood, 90-99% infected by both
PATHOGENESIS ~ transmitted thru contact w saliva & breastfeeding
~ remain latent in body after primary infection and
reactivate time to time
CLINICAL ~ primary HHV-6 : Roseala Infantum (in child)
MANIFESTATION ~most cases occur in infant btwn 4m-2 yrs old
~ spiking fever dvlop over period 2 days followed by
mild rash. Fever high enough to cause febrile
convulsion
~ if primary infction is delayed to adult, there is small
chance an infectious mononucleosis-like disease.
~ no firm evidence linking HHV-6 to lymphoma or
lymphoproliferative disease
~ no firm disease assoc. w HHV-7 at present
LAB DX ~ Roseala Infantum: diagnosed on clinical grounds ~ HHV-8 DNA is found in almost 100% of KS
~serology: IgM and IgG detected ~ most pt w KS have Ab against HHV-8
~ seroprevalence of HHV-8 is low among the general
population but high in person susceptible to KS, such
as homosexual
MANAGEMENT ~ no specific antiviral tx for HHV-6 infection
HERPES GENITALIS
HERPES GENITALIS DISSEMINATED HERPES SIMPLEX
~ genital lesion maybe primary, recurrent, initial
~ genital lesion maybe primary, recurrent, initial ~ in immunocompromised person, widespread vesicular like
~site: penis, vagina, cervix, anu, vulva, bladder, sacral
~site: penis, vagina, cervix, anu, vulva, bladder, sacral chickenpox, involve lung, liver, spleen, CNS
nerve route, spinal & meninges.
nerve route, spinal & meninges.
~ dysuria, severe cases : urinary retention ~ encephalitis is severe, brain is liquefied
~ dysuria, severe cases : urinary retention
~mild meningitis can present OTHER CUTANEOUS MANIFESTATION :
~mild meningitis can present
~ 60% will have recurrence, in perianal area tend to be ~ Eczema herpaticum
~ 60% will have recurrence, in perianal area tend to be
more numerous & longer than oral HSV-1 ~ herpetic whitlow = arise fr implantation of virus into skin &
more numerous & longer than oral HSV-1
typically affect the finger

ORAL-FACIAL HERPES HERPES SIMPLEX ENCEPHALITIS


ORAL-FACIAL HERPES HERPES SIMPLEX ENCEPHALITIS
Acute Gingivostomatitis ~ most serious complication of herpes simplex disease.
Acute Gingivostomatitis ~ most serious complication of herpes simplex disease.
~ commonest on primary infection, neonatal- globally & brain is liquefied.mortality 100%
~ commonest on primary infection,
~ pain and gum bleeding, 1-8 mm ulcer,
~ pain and gum bleeding, 1-8 mm ulcer, CLINICAL
CLINICAL
neonatal- globally & brain is liquefied.mortality 100%
focal disease- common affect temporal lobe.appear in chilfren
focal disease- common affect temporal lobe.appear in chilfren
With necrotic bases, cervical lymp gland enlarged & adult.possible that it arises fr reactivation. Mortality 70%
With necrotic bases, cervical lymp gland enlarged
~ self-limiting, last around 13 days
~ self-limiting, last around 13 days
MANIFESTATI
MANIFESTATI & adult.possible that it arises fr reactivation. Mortality 70%
without tx
Herpes Labialis without tx
Herpes Labialis
Recurrence of oral HSV, prodrome og tingling, warmt, ON
ONOF
OFHERPES
HERPES
~important to dx HSE early,IV acyclovir given to all suspected
~important to dx HSE early,IV acyclovir given to all suspected
HSE before lab result available
Recurrence of oral HSV, prodrome og tingling, warmt, HSE before lab result available
itching at site
itching at site
12 hrs later, redness—papule--vesicles
SIMPLEX
SIMPLEX
12 hrs later, redness—papule--vesicles
VIRUSES
VIRUSES

NEONATAL
NEONATAL HERPES
HERPES SIMPLEX
SIMPLEX (1)(1)
~ babyusually infected primarily during passage thru birth canal
~ babyusually infected primarily during passage thru birth canal
~ premature membrane rupturing is risk factor
~ premature membrane rupturing is risk factor
~risk of perintl transmision high if florid primary infection in mom
~risk of perintl transmision high if florid primary infection in mom
~ smaller risk fr recurrent maternal lesion bcoz lower viral load and presence of specific Abs.
~ smaller risk fr recurrent maternal lesion bcoz lower viral load and presence of specific Abs.
~ baby can be infected fr other sources like oral lesion fr mother or hepatic whillow in nurse
~ baby can be infected fr other sources like oral lesion fr mother or hepatic whillow in nurse
~ spectrum of neonatal HSV varies fr mild disease localized to skin to fatal disseminated infection
~ spectrum of neonatal HSV varies fr mild disease localized to skin to fatal disseminated infection
~ when
~ whenbrain is involved, prognosis is poor. If survived, they have residual disabilities
brain is involved, prognosis is poor. If survived, they have residual disabilities
~ give acyclovir and prevent by caeserian section
~ give acyclovir and prevent by caeserian section

CLINICAL MANIFESTATION OF VARICELLA ZOSTER VIRUS