Viruses Causing Exanthums Flashcards

1
Q

Measles

General Characteristics

A
  • Caused by Rubeola virus
  • Belongs to the family Paramyxovirus
  • Single-stranded ⊖ sense RNA virus
  • Enveloped
  • Only one antigenic type
  • Humans are the only reservoir
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2
Q

Rubeola Virus

Structural Proteins

A
  • Hemagglutinin (H) ⇒ important in viral attachment
  • Fusion factor (F) ⇒ fusion of cells and viral entry
  • Matrix protein (M) ⇒ located inside viral envelope, important in assembly of virion
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3
Q

Rubeola Virus

Transmission/Epidemiology

A
  • Respiratory droplet transmission
  • Highly contagious and very virulent
    • 90% attack rate
    • 100% symptomatic ⇒ everyone gets disease, no latent infections
  • Contagious from 1-2 days before onset of symptoms up to 4 days after onset of rash
  • Peak incidence: Winter & Spring
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4
Q

Rubeola Virus

Pathogenesis

A
  • Incubation period 7-21 days
  • Virus initially replicates locally in the respiratory epithelium
  • Spreads through the lymphaticsliver, spleen and lymph nodes
  • Period of replication there ⇒ primary viremiaconjunctiva, respiratory tract, urinary tract, secondary lymphoid organs, CNS
  • Second viremiaendothelial cells in vessels
  • Immune response to virus infected endothelial cells ⇒ maculopapular rash (DTH)
  • Virus induces syncytia formation and multinucleate giant cells
    • Causes pathology
    • Hides from the immune response
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5
Q

Measles

Histology

A

Virus induces syncytia formation and multinucleate giant cells.

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6
Q

Measles

Clinical Manifestations

A
  • Begins with cough, coryza, conjunctivitis, high fever
  • Koplik’s spots ⇒ characteristic spots on buccal mucosa
    • Appears first day or two of the infection
    • Frequently disappears when maculopapular rash develops
  • Characterized by maculopapular rash
    • Lasts ~ 5 days
    • Caused by T-cells targeted to infected endothelia cell lining vessels
  • Child is usually very sick
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7
Q

Measles

Complications

A
  • Bacterial superinfection (respiratory infections)
    • Measles infection is immunosuppressive
    • Allows fulminant superinfections
  • Post-infectious meningo-encephalitis
    • May occur 5-7 days after rash
    • Caused by the immune system reacting to virus in brain
    • Mortality 10-20%
    • Retardation 65%
  • Subacute sclerosing panencephalitis (SSPE)
    • Progressive degenerative disease of CNS
    • Caused by defective measles virus assembly during infection
    • Occurs 2-10 years after primary measles infection
    • Usually fatal
  • Progressive infectious encephalitis
    • Occurs in pts with defective CMI
    • Usually fatal
  • Immunocompromised (T-cell deficient)
  • Giant cell pneumonia with no rash
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8
Q

Measles

Immunity, Treatment, and Prevention

A
  • CMI in response to virus resolves disease
  • Responsible for life long immunity
  • Live attenuated measles vaccine (MMR)
    • Given at 12-15 mo
    • One boost given during elementary school
  • IGIV can provide transient protection for exposed immunocompromised children
  • No specific antiviral therapy
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9
Q

Roseola

Overview

A

“Exanthum subitem”

  • Caused by Human Herpesvirus-6
    • Herpesviridae family
    • Subtype: Beta-herpesviruses
    • Large dsDNA virus, enveloped
  • Transcription and translation coordinated and regulated:
    • Immediate early proteins ⇒ DNA binding proteins
    • Early proteins ⇒ DNA pol, transcription factors
    • Late proteins ⇒ structural proteins
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10
Q

Roseola

Transmission/Epidemiology

A
  • Spread via saliva and respiratory aerosols
  • Common in young children
  • Most are seropositive by age 4
  • Frequent cause of ER visits in young children d/t febrile seizures
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11
Q

Roseola

Pathogenesis/Clinical

A
  • 4-7 day incubation
  • High fever for 3-5 days
  • Rash for 1-2 days, due to T-cell response
    • Virus replicates in T-cells
    • Recovery with no complications
  • Virus remains latent (probably in T-cells)
  • Reactivation may occur with immunosuppression
    • Virus seen in AIDS pts
    • May contribute to pathogenesis of AIDS
    • Also contributes to transplant graft rejection
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12
Q

Roseola

Management

A

Dx: clinical

Treatment/Prevention: none

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13
Q

Erythema Infectiosum

Overview

A

“Fifth Disease”

  • Caused by Parvovirus B19
  • Small naked linear ssDNA virus
  • Icosahedral capsid
  • Extremely resistant to physical inactivation
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14
Q

Erythema Infectiosum

Transmission/Epidemiology

A
  • Respiratory secretions
  • Parenteral transmission
  • Age group 4-15 y/o
  • Late winter and spring
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15
Q

Erythema Infectiosum

Pathogenesis/Clinical

A
  • Initially replicates in nasopharynx or URT
  • 1st viremia to the bone marrow
  • Replicates in mitotically active cells of erythroid origin
  • 2nd viremia ⇒ viruses may cross placenta
  • Biphasic disease
    • 1st phase ⇒ flu-like symptoms
      • Infectious period
      • Stopped by antibody
    • 2nd phase (symptomatic) ⇒ “slapped cheek” rash and arthralgia
      • Caused by immune complexes
  • Individuals with chronic anemia (sickle cell) at risk for aplastic crisis
  • Seronegative pregnant women at risk for fetal loss
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16
Q

Erythema Infectiosum

Management

A
  • Clinical dx ⇒ slapped cheek rash, lacey rash on body
  • Parvo B19 IgM and IgG can be detected
  • Evaluation of exposed pregnant woman
  • Should be differentiated from rubella rash
  • Treatment/Prevention – none