B3: Herpes

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Herpes

General

Sensitivity

Organic solvent

Thermolabile

Replication

Where does replication occur?

Nucleus

Structure

Lipid envelope

Icosahedral

Linear dsDNA

Others

HH8

Kaposi's Sarcoma

HH7

May cause mononucleosis-like syndrome

Almost all children infected by age 2

Resembles HH6

HH6

VZV

VZV Ig

Live, attenuated vaccine

Immunological test

For Ag detection

Chickenpox

Shingles

CMV

Transplacental transmission

Most common transplacentally transmitted infection in the U.S.

Resembles infectious mononucleosis

No heterophile Ab

Owl's eyes

Enlargement of infected cells with pronuclear inclusions

EBV

Supportive

No specific AV

Early infection

leads to..

Benign disease

Subtopic

Monospot

Heterophile antibodies

Cross-react w/ sheep, goat RBCs

Heterophile Ab

All of these may serve as buzzwords

Immunosuppressed

Oral Hairy leukoplakia

B cell lymphoma

African Burkitt's lymphoma

Where would you find a high incidence of African Burkitt's lymphoma?

Regions w/ high incidence of malaria

Non-Hodgkin's lymphoma

Nasopharyngeal carcinoma

Where is it endemic?

China

Hodgkin's Disease

Infectious mononucleosis

Downey cells

Atypical lymphocytes

HSV

Treatment

Requires activation by viral thymidine kinase

Foscarnet

When resistant to acyclovir

Valacyclovir

Valacyclovir or "Valtrex" is a prodrug of...

Acyclovir

Prevention

Experimental vaccines

C-section

Avoid contact esp. sexual

Epidemiology

Predisposing factors

SES

Immuno. status

Place

Humans only reservoir

Transmission

Asymptomatic shedding

Direct contact w/ infected secretions

Diagnosis

Serology

Only for primary infection

EIA

Antigen detection

Tzanck smear

Scrape the lesion

Isolation in cell culture

Most definitive

Clinical

HSV-2

Clinical manifestations of HSV-2 infection

1. Primary infection presents as papules progressing to vesicles and pustules,

lymphadenopathy and tenderness, 3-4 weeks duration

2. Recurrent infection characterized by prodrome followed by groups of vesicles on external genitalia, 1-2 weeks duration

3. Neonatal herpes usually due to HSV-2 acquired by passage through infected birth

canal; 60% mortality with survivors suffering neurologic sequelae; disseminated vesicular lesions with internal organ involvement

Neonatal herpes

HSV-1

Clinical manifestations of HSV-1 infection

1. Primary infection often asymptomatic; 50-90% of population is seropositive

2. Primary gingivostomatitis—fever, irritability, painful vesicular lesions on buccal

mucosa, tongue, gums, throat, 1-2 weeks duration

3. Recurrent infection characterized by prodrome, followed by unilateral vesicles of 1

week duration

4. Ocular lesions can lead to permanent corneal scarring

5. Causes 10% of viral encephalitis with 70% mortality if untreated

Genital herpes

Encephalitis

Ocular herpes

Herpetic whitlow

Fever blisters

Gingivostomatitis

Characteristics

Pathophysiology

Pathophysiology of infection

1. Acute infection results in multinucleated cells (syncytia), ballooning degeneration of epithelial cells, necrosis, inclusion bodies, inflammatory response, cell to cell spread, latent infection of ganglia

2. Latent infection does not destroy ganglia; viral genome persists as circular DNA; reactivation of virus replication leads to recurrent disease

3. Recurrence triggered by stress, ultraviolet light, hormonal flux

4. Spreads from cell to cell in presence of antibody

5. Cell-mediated immunity contributes to symptoms and resolution

Triggers for recurrence

Hormonal flux

UV light

Stress

Syncytia