Viral Exanthemas + HSV1/2 + VZV Flashcards
Compare the structure of the Parovirus B19 and HHV6 and 7.
• what are do they have in commmon?
Parvovirus B19 (“Fifth Disease”)
Structure
Non-enveloped, ssDNA virus (simplest DNA virus)
Human Herpesvirus 6 and 7 (Roseola)
Structure
Enveloped large dsDNA virus
Compare and contrast the following Viruses with Respect to their structure.
What is the pathogenic mechanism of Parvo B19?
• what is the timing in the process?
• How does the mechanism correspond to symptoms?
Pathogenic Mechanism
Infection of RBC precursors and replication in these cells leads to progressive anemia throughout this disease. Infections of these cells is Bi-phasic:
1. Lytic Phase/Infectious phase – causes cytokine release and prodromal symptoms starting ~7days post-exposure
2. Non-infectious Immunologic phase – in this phase the immune response results in IgG production to neutralize the virus. It is in this phase that RASH and ARTHRALGIA presents from CELL-MEDIATED responses.
Who is at the highest risk of dying from Parvo B19?
• what symptoms present in these people?
Mortality
• This disease can have a profound impact on people with Heriditary Spherocytosis and Sickle Cell anemia leading to APLASTIC anemia in these people.
• Immunocompromised people may have persistent infection that leads to **Chronic Anemia
• Trasplacental Transmission**
is also risky with 5% of cases resulting in miscarriage/HYDROPS FETALIS.
How common is Parvo B19?
50% of adults are seropositive
How is Parvo B19 transmitted? Disease Caused?
• When does it replicate?
• What is the structure of Parvo B19?
Erythema Inectiosum - Parvovirus B19 (“Fifth Disease”)
Structure
Non-enveloped, ssDNA virus (simplest DNA virus)
Transmission
Respiratory Tract Secretions, Exposure to Blood products, Mother to Fetus
Replication Cycle
Depends on S-phase in RBC precursors (NOT mature RBCs) of host to replicate
What are the Key findings in Parvo B19 infections?
Key findings/Diagnosis
Slapped Face Rash on the cheeks and reticular body rash on children 1-2 wks after exposure. Arthralgias in adults.
Paramyxoviruses – Measles (Morbilivirus)
Structure?
How is it spread?
How contagious is it?
Paramyxoviruses – Measles (Morbilivirus)
Structure
Enveloped, Negative-sense, ssRNA
Transmission
EXTREMELY CONTAGIOUS spread via respiratory route
Requires a population size of more than 100,000 ppl. That is provided by undervaccination
Measles
• Structure
• Family
• What two factors make it different than other viruses in the family?
Paramyxoviruses – Measles (Morbilivirus)
Structure
Enveloped, Negative-sense, ssRNA
Replication Cycle
2 factors separate measles from the rest of the Paramyoviruses:
1. Receptor usage - MV receptors are CD46, SLAM and nectin-4 and separate H (hemagglutinin) and F (fusion) proteins. (H and F are important to establishing persistent infection in the CNS)
- Formation of intracellular inclusion bodies
How does measels present?
• Pathognomoic lesion?
• Structure?
Paramyxoviruses – Measles (Morbilivirus)
Structure
Enveloped, Negative-sense, ssRNA
Disease Presentation
Morbilivirus typically sits latent for 10-14 days after exposure then the patient get the 3C’s cough, coryza, and conjunctivitis along with high fever (101-105). Photophobia may result in this time due to conjunctivitis. Pathonognomic for measles are KOPLIK SPOTS (white spots on the inner cheek that occur before rash). About 2-3 days after symptoms onset a rash appears in accordance with the peak CD8+ T-cell proliferation (cell mediated response). So rash indicates that the virus is clearing.
Measles
• affect on immune function?
• Structure?
Paramyxoviruses – Measles (Morbilivirus)
Structure
Enveloped, Negative-sense, ssRNA
Pathogenic Mechanism
1. This virus has the ability to SUPPRESS immune function probably by infecting MONOCYTES specifically delayed-type hypersensitivity responses (false negative TB skin test). Suppression of immune function occurs just before the rash starts and persist for ~1 mo.
- Also antibody production and cellular immune responses to new antigens are also impaired
Measles
• Who gets them?
Paramyxoviruses – Measles (Morbilivirus)
Structure
Enveloped, Negative-sense, ssRNA
Epidemiology
Typically an infection of Children (kills 150K per year)
Measles
• Prophylaxis
• Structure
Paramyxoviruses – Measles (Morbilivirus)
Structure
Enveloped, Negative-sense, ssRNA
Treatment
If MMR vaccine is given within 6 days of exposure course of the disease may be improved
Vaccine is live attenuated and gives life-long immunity. Administration occurs 12-15 mo. (must be > 6 mo to avoid maternal ab interference) and at 4-6 year old. (note: kids would therefore be most susceptible btwn 6-12 mo w/o maternal abs or their own)
Measels
• why is the vaccine so effective?
• Structure?
Paramyxoviruses – Measles (Morbilivirus)
Structure
Enveloped, Negative-sense, ssRNA
Vaccine efficacy is related to viruses being ANTIGENICALLY STABLE and MONOTYPIC (aka abs produced against 1 virus are protective against all)
Disease could be eradicated because: only 1 serotype, clinically identifiable, no animal reservoirs.
Measels
• What typically kills people?
• What other complications could occur?
• When do they occur?
Paramyxoviruses – Measles (Morbilivirus)
Structure
Enveloped, Negative-sense, ssRNA
Mortality
Death by this virus is typically due to superimposed Bacterial Pneumonia
Autoimmune demyelination is not uncommon (1/1000) may also occur Acute disseminated encephalomyelitis (ADEM) or postinfectious encelphalomyelitis (PIE) may also occur in 3 wks following infection leading to CONVULSIONS, DEAFNESS, and RETARDATION
Persistent infection in the brain (from H and F mutations) may lead to:
Encephalitis (inclusion body (5 mo later) and subacute sclerosing (7 years later)) may also occur.
Measels
• What are some key things you’re looking for?
• Structure?
Paramyxoviruses – Measles (Morbilivirus)
Structure
Enveloped, Negative-sense, ssRNA
Key findings/Diagnosis
Defined Clinically as a generalized rash lasting more than 3 days, with a temperature above 101 F and the 3 C’s cough, coryza, and conjunctivitis + KOPLIK’s SPOTS on bucal mucosa
Rubella
• Transmission: how and when can it occur?
• Structure
Rubella - Togavirus
Structure
Enveloped positive-sense ssRNA
Transmission
Primarily Aerosols
Viral Shedding of particles lasts for 1 month after initial exposure (~week after the rash is gone)
Rubella (Togavirus)
• How does it present?
• Structure?
Rubella - Togavirus
Structure
Enveloped positive-sense ssRNA
Disease Presentation
Rubella (togavirus) typically incubates for ~1 week. Mild disease characterized by low-grade fever, occasional conjunctivitis, LAD. A little over 2 weeks later (16-21 days) a Morbilliform Rash that starts on the face and spreads.
Rubella (Togavirus)
• Who suffers the most severe consequences of this infection?
• Structure?
Rubella - Togavirus
Structure
Enveloped positive-sense ssRNA
Mortality
THE MOST SERIOUS CONSEQUENCE OF RUBELLA IS FOR THE FETUS IN 1st and 2nd Trimesters of Pregnancy. Virus crosses the placenta and replicates in all tissues and organs. Result is severe neurological deficits and cataracts.
Rubella
• Where can you isolate virus from?
• Structure?
Rubella - Togavirus
Structure
Enveloped positive-sense ssRNA
Key findings/Diagnosis
Virus can be isolate from Stool (make sense b/c its enveloped) and nasopharynx
Picornavirus (family)
• what groups are in this family?
• what makes them distinct from rhinovirus?
- *Picornavirus**
- *General: 4 groups Poliovirus, Coxsackievirus, Echovirus, Enterovirus.** These are differentiated from rhinovirus by 2 main factors: Acid Stability and Less Stringent Growth Requirement (both human and primate at 37 C).
Picronavirus
• what makes enterovirus different from the others in this family?
Enterovirus humans are the ONLY known reservoir.
Picornavirus
• Structure?
• Transmission?
Picornavirus
Structure
Non-enveloped positive sense ssRNA
Transmission
- *Oral-Fecal** route (enterovirus and Coxsackie)
- *Aerosol** contamination of Fomites (Coxsackie)
Picornavirus
• In what two ways can it present?
• How does presentation depend on serotype?
- *Picornavirus**
- *General: 4 groups Poliovirus, Coxsackievirus, Echovirus, Enterovirus**
Disease Presentation
***DISEASE OCCURS PRIMARILY IN THE SUMMER AND FALL (MAY-NOV)**
Incubation typically occurs for 2-10 days followed by a somewhat bisphasic illness that consists first of flu-like symptoms then stiff neck and headache about 1 week later (~18 days post infection).
Hand, Foot, and Mouth Disease:
• Caused by Coxsackievirus A16, A6 and enterovirus 71; presents as ulceration of tonsils and uvula (herpangia) along with abdominal pain and flu-like symptoms. Disease gets its name from vesicular lesions on the hands and feet.