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Infection & Immunity Block > Viral Exanthems > Flashcards

Flashcards in Viral Exanthems Deck (27):

Direct Effects

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

Secondary effects
Skin lesions resulting from a systemic infection
Measles (rubeola)
Parvovirus B19 (fifth disease)
Human herpes viruses types 6 & 7 (roseola infantum)


Dx of Viruses

1. Clinical Presentation and History

2. Lesions: culture, microscopic examination, detection of viral antigens and viral nucleic acid (only use if direct effect)

3. Serology: good for systemic effects


Viruses that cause Macules

Macule = red lesions

Echo viruses
Parvovirus B19


Viruses that cause Macules and Papules

Maculopapular: red raised lesions

Measles virus
Parvovirus B19


Viruses that cause Papules

Papules: raised lesions

Papilloma viruses
Molluscum contagiosum


Vesicle Forming Viruses

HSV-1, HSV-2
Coxsackie viruses

Vesicles are fluid filled spots like blisters because virus replication causes lysis of cells causing the fluid and debris
Some viruses can present with macules first and then progression to vesicles in VZV for example


HSV: Transmission

Virus is shed in fluid from lesions
Route of transmission: close contact, mucosal surfaces, cracks in the skin
Shed in body fluids, i.e. saliva


HSV: Symptoms

1st - Primary mucocutaneous infection
2nd - Latent infection in the neuronal ganglia

Recurrent disease: viral reactivation and subsequent mucocutaneous infections

Course of disease:
Acute disease lasts 5-7 days
Symptoms subside in 2 weeks
Viral shedding may continue for 3 weeks or more


Acute Herpetic Gingivostomatitis

Abrupt onset
High fever
Anorexia, listlessness
Vesicular lesions
Regional lymphadenopathy

Parent to child transmission
Systemic symptoms
90% are due to HSV 1


Primary HSV-1 Infection in Adults

Acute herpetic pharyngotonsillitis
Fever, malaise, sore throat
Ulcerative lesions on the tonsils and posterior pharynx


HSV Pathophysiology

Neurovirulence: infect neuronal tissue

HSV-1, trigeminal ganglia
HSV-2, sacral nerve root ganglia

Reactivation: where initial infection was, and then under stress the virus can be reactivated and replicate again


Recurrences of HSV

Prodrome: burning, tingling or itching sensations

Clinical disease:
Small reddened areas develop in site of primary lesion
Followed by formation of blisters


Dx of HSV

Clinical presentation

Laboratory analysis
Isolation of virus in tissue culture
Histological appearance of lesion
Rapid detection of HSV DNA – PCR
Serology for primary sero-conversion


Tx of HSV

Acyclovir (ZoviraxR)
Synthetic purine nucleoside analogue

Famciclovir (FamvirR)
Prodrug that is converted to penciclovir

Valacyclovir (ValtrexR)
Prodrug rapidly converted to acyclovir

Treat the infection where all drugs target DNA polymerase that replicate viral DNA
Compounds: nucleoside analogs; these drugs can be typical nucleosides (left) or modified (right)
Must be phosphorylated by thymidine kinase, which can develop resistant to the drugs to allow virus to replicate


HSV Complications

1. Bacterial and fungal super-infections

2. Skin infections:
Eczema herpeticum
Herpetic whitlow
Herpes gladiatorium

3. Ocular infections
Herpes keratitis: pain and light sensitivity, discharge, gritty feeling, scarring

4. Perinatal infections
Transmission to newborn infant
High frequency of visceral and CNS infections
Neurological sequelae

5. Immunosuppressed: life-threatening disease, disseminated infection

6. Encephalitis


Papilloma Viruses: Transmission and Clinical Presentation

Shed from skin, mucous membranes
Acquired through skin breaks

Clinical presentations:
common warts (verrucae vulgaris)
palmo-plantar warts
flat warts (verrucae plana)
epidermodysplasia verruciformis (EDV)
genital warts (condyloma acuminate)


Common, Plantar, Mosaic, Flat, and Butcher Warts

Common wart: mostly hands, genotype 2,4
Plantar wart: bottom of feet, genotype 1
Mosaic wart: hands and feet, genotype 2
Flat wart: arms, face, and knees, genotype 3, 10, 28, 41
Butcher wart: hand, genotype 7


HPV: Route of Infection

HPV: gains access through break in the skin and affects basal cells in epidermis, and these infected cells express limited amount of viral Ag, but as the cells differentiate the viral genes that are expressed will change because the virus is taking advantage of differentiation and the cells replicate abnormally and eventually release virus into the environment
Late genes (L) are expressed on apical cells
Basal cells will continue to be infected; must eliminate basal cells to get rid of viral genome


HPV: E6 and E7

E6 and E7 early genes: proteins inactivate cellular proteins; E6 blocks p53, and E7 interacts with pRB to disrupt cell cycle regulation
HPV will cause cells to make E7 and cause inactivation of retinoblastoma protein, which normally keeps the cells from replicating
P53: important for cell death when infected, but E6 causes prevention of cell death (HPV makes E6)


Papilloma Virus Dx, Tx, and Prevention

Diagnosis: clinical presentation, histology

Topical application of caustic agents
Cryotherapy - liquid N

Prevention: vaccination


Molluscum contagiosum: Transmission, Pathophysiology, and Differentiation

Transmission: skin to skin contact or fomites to skin
Shed from skin lesions
Self-limiting disease
Cluster of lesions

Targets epidermal keratinocytes
Typical inclusion bodies

How to differentiate between this and warts: contagiosum are smooth and have “belly button”
Present with cluster of 6-8 lesions; hyperplastic response


Molluscum contagiosum: Tx and Complications

Treatment: curretage, cryosurgery, topical agents
Complications: none


Rubella Virus: Transmission, Clinical Presentation, Congenital Infections, Prevention, and Complications

Transmission: respiratory droplets, from mother to fetus
Initial infection in upper respiratory tract then systemic spread and replication in lymph nodes

Clinical presentation:
Mild, exanthematous disease
Low grade fever
Short-lived maculopapular rash

Congenital Infection: cataracts, cardiac abnormalities

Prevention – vaccination (MMR)

Complications: athralgia, encephalopathy, birth defects


HHV-6: Transmission, Symptoms, Dx, Tx, and Complications

Route of transmission: respiratory tract, shed in saliva; enveloped virus
Symptoms – elevated temperature, rash
Diagnosis – clinical presentation, roseola infantum, 6th disease
Treatment – symptomatic
Complications in immunologically suppressed patients

Usually seen in infants 9-12 months of age
Abrupt onset of fever (40 C)
Lasts 3 days, development of rash: maculopapular exanthem


Measles Virus Characteristics, Dx, and Prevention

Cough, coryza, conjunctivitis
Koplik’s spots: in oral cavity; gray-white spots on soft palate
Maculopapular rash

Diagnosis: clinical presentation, Ab titers, virus isolation and tissue culture, RT-PCR

Prevention: vaccination (MMR - attenuated aka makes it less virulent/harmless)


Measles: Spread, Growth, Fever, Rash, and Transmission

Spread: breathing in virus containing droplets or touching contaminated surfaces
Virus grows in cells in back of throat and lungs
Fever lasts 2-4 days followed by a cough, runny nose, and red, watery eyes
Rash lasting 5-6 days appears on the face, head, torso, hands, and feet (spreads this way)
Transmission: 4 days prior to and after appearance of rash
**Reportable virus