Viral maculopapular rashes
Measles, rubella, echovirus, coxsackievirus, adenovirus, parvovirus B19.
Vesicular/papular viral rashes
Varicella, smallpox, molluscum contagiosum, herpes simplex virus, Coxsackievirus group A
Viral petechial/purpuric rashes
Coxsackievirus group A and echovirus
Where does influenza replicate?
Orthomyxoviruses replicate in the nucleus, despite being an RNA virus
Virus with a large, enveloped, -ssRNA with a non-segmented genome that replicates in the cytoplasm.
Paramyxoviruses: parainfluenza (PIV types 1 & 3), measles virus, mumps virus, human PIV types 2, 4a and 4b, RSV and hMPV.
How does infection by paramyxovirus occur?
Capsule glycoproteins bind target cell -> -ssRNA genome transcribed by viral RNA-dependent RNA polymerase to form +ssRNA (then goes to more -ssRNA) and mRNA -> Protein translation from mRNA -> Formation of new viral particles -> Budding out of cell membrane
What makes up the different glycoproteins on the outside of a cell infected by measles virus?
Fusion protein and hemagglutinin protein. These glycoproteins are what are responsible for formation of the syncytium.
How does the lab detect infection by paramyxovirus?
Isolation from body secretions -> inoculation of human cells in culture -> viral replication detected by hemadsorption cell fusion (forms giant cells or syncytia), immunofluorescence or reverse transcriptase PCR.
How do we detect the immune response status of a patient infected by paramyxovirus?
Complement Fixation. Hemagglutination Inhibition. Hemadsorption Inhibition. Virus Neutralization.
Types of glycoproteins present on paramyxoviruses that will react with neutralizing antibodies.
F (fusion protein that fuses the virus membrane to the cell membrane), H (hemagglutinin), HN (hemagglutinin and neuraminidase, which cleaves sialic acid) and G (glycoproteins).
Syndromes associated with parainfluenza virus
All symptoms are confined to the respiratory tract: minor respiratory infection -> Croup (laryngo-tracheitis) -> Bronchitis -> Bronchiolitis -> Bronchopneumonia
Why do kids repeatedly get parainfluenza virus?
Secretory IgA is what develops against parainfluenza viruses because you do not get viremia. This type of immunity is not long-lived.
A bunch of kids 6 months old to 5 years old present to the hospital with croup in the fall months. What is the most likely paramyxovirus?
Parainfluenza virus types 1 and 2
A bunch of kids present within the 1st 6 months of life with bronchiolitis and pneumonia during all months of the year. What is the most likely paramyxovirus?
Parainfluenza virus 3
A bunch of kids present with upper respiratory infections during all months of the year. What is the most likely paramyxovirus?
Parainfluenza virus 4.
A bunch of kids present in the first six months of life with bronchiolitis and pneumonia as a part of an ongoing winter epidemic. What is the mod likely paramyxovirus?
What is the target for the only antibody therapy approved by the FDA for prophylactic use against RSV?
F (fusion) glycoprotein is the target of palivizumab (Synagis). Since it is a pneumovirus, it does not have hemagglutinin or neuraminidase activity.
What is the course of mumps infection?
Initial respiratory tract infection -> Viremia -> Epithelial cells infected in the parotid, tests, ovaries, pancreas, meninges, thyroid, bladder and kidney -> Orchitis, aseptic meningitis or post-infectious encephalitis.
Why does infection confer lifelong immunity in people affected by mumps and measles?
There is only one serotype worldwide and viremia develops IgG response.
What type of vaccine is MMR?
What are the major sequelae associate with mumps infection?
Aseptic meningitis, encephalitis, deafness, orchitis and parotitis.
What is the course of measles infection?
Initial respiratory tract infection -> Viremia -> Target organs -> Fever + Koplik spots -> Maculopapular rash (skin is last to be infected and rash is caused by CD8 T-cell response to infected epithelial cells)
When will a patient not get the maculopapular rash associated with measles?
If they are immunocompromised, particularly in their ability to have a CD8+ T-cell response because these are what cause the rash.
Sequelae from measles infection
2-4 weeks = Acute Disseminated Encephalomyelitis (ADEM). 1-12 months = Measles Inclusion Body Encephalitis (MIBE, typically in immunocompromised). 1-12 years = Subacute Sclerosing Panecephalopathy (SSPE, chronic demyelinating syndrome)
Lab diagnosis of someone with measles who was immunocompromised? How do you protect these people from infection?
Measles giant cell pneumonia w/syncytia. You can give passive IgG to protect these people.
This virus is a small, enveloped, +ssRNA virus with a non-segmented genome that is a very serious gestation infection with dire consequences for the fetus.
Rubella virus (German measles), which is a Togavirus
How does infection by rubella virus occur?
Respiratory epithelium -> Glycoproteins attach to host cell -> Enveloped virus endocytosis -> low pH of endosome releases +ssRNA -> translation begins -> Viremia w/lymph node spread -> skin and fetal spread across placenta (Congenital Rubella Syndrome)
In many cases, infection with rubella is mild and asymptomatic. How does clinically apparent rubella present?
Maculopapular (rubelliform) rash forms in 95% of cases, lymphadenopathy, fever, conjunctivitis, sore throat and arthralgia.
Why do you need to be extra careful when you have a baby that was born with Congenital Rubella Syndrome?
They can shed the virus for months to years and infect other mothers
Major sequelae of Congenital Rubella Syndrome?
Deafness, blindness, cataracts, heart and brain defects.