Structure

Transmission

Pathogenesis

Clinical findings

Laboratory diagnosis

Treatment

Family: herpevirus

Genome: linear double-strand DNA.

Size: 100m

Icosahedral nucleoapsid

Lipoprotein envelope

HSV-1 and HSV-2 are structurally and morphologically indistinguishable.

Transmitted by sexual contact.

Sources: generally people with herpetic lesion.

Carriers of latent virus shed virus in saliva without symptoms – source of infection.

Infection is most common in childhood and is usually symptomless.

There is another peak in incident during adolescence.

Infection is universal in virtually all human populations.

Replicates in the skin or mucous membrane at initial site of infection.

Migrates up neuron and becomes latent in lumbar and sacral ganglia.

Reactivated by sunlight, hormonal changes, trauma, stress & fever.

Reactivation does not stimulate a rise in titre of herpes antibody.

Skin lesion is a vesicle containing serous fluid filled with virus particles.

Multinucleated giant cells found at base of lesions.

Immunity is type-specific but some cross-protection exists.

Immunity is incomplete and both reinfection and reactivation occur in presence of IgG.

Cell-mediate immunity is important –its suppression results in reactivation, spread and severe disease.

HISV-2 causes several diseases, both primary and recurrent.

Many infections are asymptomatic.

Genital herpes:

- painful vesicular lesions of the male and female genitalia and anal area.

- lesions are more severe and protracted in primary disease than in recurrences.

- primary infections are associated with fever and inguinal adenopathy.

Neonatal herpes:

- due to contact with vesicular lesions within birth canal.

- shedding of HSV-2 from mother can infect child during birth.

- varies from a sever generalized disease or encephalitis to mild local lesions to asymptomatic infection.

- neither HSV-1 or HSV-2 causes congenital abnormalities.

Aseptic meninigits: usually a mild, self-limited disease with few sequelae.

Infection in pregnancy:

- primary infection in 1st trimester is associated with higher risk of fetal loss.

- infection of fetus in utero is associated with keratoconjunctivitis.

- primary maternal infection at birth is 5 times more likely to result in neonatal infection than recurrent maternal infection.

Associated with cervical cancer but with no strong correlation.

Type 1 and 2 share group-specific antigens, but can be differentiated by type-specific antigens and by DNA restriction enzyme analysis.

Isolation:

- swab or fluid from vesicles, skin, saliva, conjunctiva.

- corneal scrapings.

- brain biospy.

Diagnosis:

- isolate virus, grow in cell culture.

- produce CPE with ballooning and rounding of cells.

- identified by fluorescence-antibody staining of infected cells.

- detect virus-specific glycoproteins by ELISAs.

Tzanck smear:

- rapid diagnosis from skin lesions.

- cells from base of vesicles stained with Giemsa’s stain.

- presence of multinucleated giant cells suggest infection.

Serology:

- complement fixation test useful for diagnosing primary infections.

- of little use in recurrent infections as many adults already have antibodies.

Direct demonstration of virus or viral antigen in vesicles by EM or immunofluorescence.

PCR is now used to detect herpes-specific DNA in CSF in cases of suspected encephalitis.

Acyclovir:

- treatment for encephalitis, systemic disease, primary and recurrent genital herpes.

- shortens duration of lesions.

- reduces extent of viral shedding.

- no effect on latent state, but long-term use can suppress clinical occurrences.

- administered intravenously, orally or topically.

Also used:

- valaciclovir

- famciclovir

Prevention:

- avoid contact with vesicular lesion or ulcers.

- cesarean section is recommended for women who are at term with genital lesions.