Viral Exanthems: Cutaneous Manifestations of Viral Infection

Skin Lesions:
Macules Macules and Papules Vesicles
Papules
Rubella Measles Papilloma HSV-1, HSV-2
viruses
EBV Echovirus Molluscum VZV
Contagiosum
HHV-6 Parvovirus B19 Poxviruses
Coxsackie Coxsackie
Echovirus

Direct effects
- viral replication in the epidermis
- Direct inoculation of the epidermis: Papilloma viruses, Poxviruses, Primary HSV
- Local spread from an internal source: Recurrent VZV, HSV
- Spread from a systemic infection: Primary VZV

Secondary effects
- viral replication elsewhere in the body
- Skin lesions resulting from a systemic infection
- Measles: rubeola
- Parvovirus B19: (fifth disease)
- Rubella
- Human herpes viruses types 6 & 7: roseola infantum

Herpes simplex viruses 1 & 2

a- Ubiquitous and cause a variety of illnesses
b- Most commonly known for:
- cold sores (HSV-1)
- genital lesions (HSV-2)
c- Transmission of HSV
- Virus - shed in fluid from lesions
- Route of transmission:
 HSV-1 infections transmitted through saliva: usually acquired as a child
 HSV-2 Infections are a acquired prenatally or onset of sexual activity
- Shed in body fluids, i.e. saliva
- Close contact
  Cracks in the skin
 Mucosal surfaces
d- Diagnosis based:
- Clinical presentation- lesions
- Laboratory analysis
i. Viral culture:
o gold standard for definitive diagnosis
o Results available in 48 hrs (challenge)

ii. Histology: Tzanck Smear- HSV is an enveloped virus, causes cells to fuse (syncytium
formation) = multinucleated giant cells

o Multinucleated giant cells (non specific)

dark purple= nucleus surrounded by large cytoplasm surrounding the nucleus

o Eosinopilic intranuclear Cowdry A inclusion bodies (non specific)
o Results available within 1 hr

iii. Rapid detection of HSV DNA- PCR (specific)

iv. Direct Fluorescent Antibody test

green cells: interacts with fluroscence antibody that is specific for HSV antigen, green staining indicates that the protein
was present
v. Serology for primary seroconversion : looking for IgM bodies to herpes simplex virus,
helps distinguish between HSV-1 and HSV-2
e- Treatment of HSV infections
i. decrease in duration and severity of infection (most effective if initiated within 72 hrs of
onset of infection
ii. Reduction of viral shedding
iii. Recurrence cannot be prevented
iv. Medications:
o Acyclovir (zovirax): synthetic purine nucleoside as analogue
o Famciclovir (Famvir): prodrug that is converted to penciclovir
o Valacyclovir (Valtrex): prodrug rapidly converted to acyclovir
v. Symptomatic treatment
 o IV Fluids
o Barrier creams to avoid lip adhesion
o Pain relief (oral or IV)
o Antipyretics
o Antibiotics for bacterial superinfection
f- Avoidance
- Barrier protection: gloves, condoms
- Isolate of hospitalized patients with shedding lesions

g- 1st Primary mucutaneous infection

i. Course of disease:
o Acute Disease last 5-7 days
o Symptoms subside in 2 weeks
o Viral shedding may continue for 3 weeks or more
ii. Acute Herpetic Gingivostomatitis

o abrupt onset
o High fever,
o Anorexia, Listlessness
o Vesicular lesions
o Regional lymphadenopathy
iii. Acute Herpetic Pharyngotonsillitis

o Acute HSV-1 infection in adults

o Fever
o Malaise
o Sore throat
o Ulcerative lesions on tonsils and posterior pharynx
iv. Orolabial HSV infections

o >90% are HSV-1

o Usually acquired early in life
o Primary occurrences
o Recurrent episodes
 h- 2nd Latent HSV infection in the neuronal ganglia
i. Recurrent Disease:
 viral reactivation
o Prodrome: Burning, tingling, itching sensation
o Clinical: Small reddened areas develop in site of primary lesion
o Followed by vesicle formation
 subsequent mucocutaneous infections
ii. Latency
 HSV-1, trigeminal ganglia
 HSV-2, sacral nerve root ganglia
i- HSV complications
- Bacterial and fungal superinfections
- Skin infections
o Eczema Herpeticum:

 Seen in pts with underlying inflammatory skin conditions where the herpes virus
infections spreads quite extensively on surface of epidermis
 Underlying genetic condition that HSV takes advantage of
o Herpetic Whitlow:

 On fingers
 m/c in dentists: cracks in dentist skin who work on pts with HSV shedding in oral
cavity
o Herpes Gladiatorium

 m/c in athletes
 seen in pediatric pts who wrestle (gyms should contaminate their mats after use)
- Ocular infections
o Herpes keratitis:
  Pain and light sensitivity
 Discharge, gritty feeling, scarring
 #1 cause of blindness caused by infection (and with transplantation)
 m/c common cause of corneal infections in US
 Fluorescein put in eye  tracing, branching, dendritic lesion in eye
- Perinatal infections
 Transmission to newborn infant
 High frequency of visceral and CNS infection
 Neurological sequelae (rare)
- Immunosuppressed
 Life threatening disease
 Disseminated infection
- Encephalitis

Papilloma Viruses:

- Small, naked viral particle

- dsDNA, circular genome
- Hardy, resistant to inactivation
- Can remain infectious on fomites
- Shed from skin to mucous membranes
- Warty lesions: acquired thru skin breaks or inoculation thru mucous surfaces
- Multiple genotypes
- Clinical presentations:
 Common warts (verrucae vulgaris)
 Palmo-plantar Warts
 Flat warts (verrucae plana)
 epidermodysplasia verruciformis (EDV): rare, heridarty genetic disorder that leads to
widespread papilloma virus infection if the person gets inoculated
 genital warts (condyloma acuminatum)
- HPV genome organization
 Early genes:
o E1- Replication
o E2- Replication and transcription
 o E4- Viral release
o E5- immune evasion
o E6- binds p53
o E7- binds pRB
 Late genes
o L1- Major capsid protein
o L2- Minor capsid protein
- Host cells and Papilloma virus
-