Lecture 26 Flashcards
Parvovirus
smallest DNA virus
only human pathogen is B19
Also canine, feline, goose, porcine parvoviruses
Parvovirus structure
non-enveloped
single-stranded DNA
Three structural proteins and two non-structured proteins
Parvovirus
B19 is widespread
Infections occur throughout the year in all age groups
Common outbreaks in schools and in childhood
Mode of transission - person to person, direct, respiratory droplets, indirect fomites
Viruses are stable in environment so contaminated surfaces involve transmission
Sibling transfer is important
Parvovirus replication
The virus is trophic for erythroid cells (bone marrow or fetal liver also prefers mitotically active cells)
Attachs to RBC blood group P antigen to enter cell
Uncoding takes place in the nucleus
Host cell polymerase produces a complimentary negative strand of DNA
Parvovirus replication
mRNA is translated in cytoplasm on ribosomes
Virus is released by lysis
Parvo patho
Virus first replicated in the upper respiratory tract, next virus enters blood - viremia, next virus is spread to bone marrow and other erythroid precursor cells
B19 disease is determined by direct killing of these cells and the immune response is rash and arthralgia
Parvo clinical disease
Erythema infectiosum AKA fifth disease Rash (slapped cheek appearance) Incubation period virus shed into blood Pt is infectious Prodromal period - once virus enters blood, rash on face in children - Flu-like symptoms - pt infectious for up to fourteen days
Symptomatic stage - get IgM Ab (immune complexes)
- rash appears on face spreads to extremities in children
- adults: rash may or may not occur but has polyarthritis of hands, wrists, knees and ankles
Parvo clinical disease
Aplastic crisis - RBC and platelet levels drop - in pt's with sickle cell Hydrops fetalis - aplastic crisis of pregnant females - B19 infection of seronegative mother increases risk of fetus
Paramyxovirus
measles (morbillivirus)
mumps and parainfluenza (paramyxovirus)
respiratory syncytial (pneumovirus)
All have similar structures and cause formation of syncytia (cell to cell fusion resulting in multi-nucleated giant cells
paramyxovirus structure
single stranded RNA negative sense helical capside enveloped -two glycoproteins F-fusion factor -H, HN, or G - viral attachment proteins ----H-measles ----HN-mumps and parainfluenza ----G-respiratory synctial virus
Measles patho
acquired by inhalation of infectious droplets
highly contagious
replication followed by spread to local lymph nodes and then to lymphatics and blood
about 6 days after infection, virus spreads systemically resulting in infection of all epithelial surfaces (conjunctiva, skin, respiratory tract, bladder)
Measles patho 2
Mucosal lesions in mouth may be observed these lesions are pathognomonic of measles and are called kopliks spots
symptoms become worse until rash appears at day 10-14
rash is caused by T lymphocytes targeting infected endothelial cells lining the small blood vessels
starts on forehead and moves down
lifelong immunity after recovery
Measles patho 3
complications - otitus media, diarrhea and pneumonia
Vaccination MMR
Rubella
Actually a togavirus virus: rubivirus prodrome -mild catarrhal -tender lymph nodes
Exanthem -starts on face spreads down - Day 1 - 1-4mm macules Day 2 - pinpoint papules Day 3 - Clears
Rubella
fetuses of non-immune women infected with Rubella have many complications
- hearing loss
- heart defects
- neurological
- opthalmic
First trimester - 65-85% of neonates have sequelae
Prevention - MMR