Measles and Mumps Flashcards
describe the measles and mumps in terms of the structure of the virus and their nucleic acid content
paramyxoviruses
RNA single stranded negative sense enveloped helical
do paramyxoviruses have to carry RNA polymerase?
yes
are measles and mumps capable of radical antigenic shifts?
no- paramyxoviruses only contain one strand of RNA
how does the type of infection dictate the incubation period and subsequent immunity for measles and mumps?
they travel through the blood as viremia and cause systemic infections. thus:
1 incubation time is longer
2 IgG provides life long immunity
how many serotypes of mumps are there?
1
how many other animals act as resevoirs for mumps?
just humans
what is the normal incubation period for mumps?
3 weeks
what are the symptoms of mumps?
after 3 weeks, prodromal symptoms will develop
fever, malaise, anorexia
followed shortly by asymmetrical parotiditis and potentially orchitis post puberty. parotiditis is the presenting symptom.
aspetic meningitis is also common
describe transmission of mumps
occurs usually via respiratory exposure to saliva droplets containing virion
viremia spread from the parotids to the salivary glands, where virions produced there enter the mouth and spread via coughs and sneezes
describe antiviral therapy for mumps
none
describe the vaccine used for mumps
live-attenuated
parted of the MMR vaccine given twice
explain the occurrence of 3 year cycles of epidemics for measles
measles is the most contagious disease known. an outbreak would result in herd immunity, but as years go by and new people are born, the proportion of immune people decreases to a critical point where herd immunity is no longer effective, causing a new epidemic
describe measles transmissoin
transmitted through respiratory droplets (coughs/sneezes) and infects respiratory tract.
it multiplies in the lymph and respiratory epithelium
describe measles symptoms
prodromal symptoms occur first:
fever, cold-like symptoms, runny nose, red eyes, coughing, sneezing, photophobia
followed by Koplik spots (bright red lesions w white central spot inside mouth)- predicts measles rash
rash begins after 14 days. maculopapular erythematous rash generated at least partially by immune system
describe measles virus excretion
excreted from respiratory tract and in tears and urine in the days before and after rash
measles incubation period
14 days
measles complications
- pneumonia
- otitis media
- acute encephalitis
death in 1/1000
complications more common in kids under 5, people over 20, and immunocompromised
giant cell pneumonia- sometimes pneumonia results w/o measles rash d/t suppression of cell mediated immunity
measles treatment
none
treatment with vitamin A in developing countries has helped reduce mortality- death often occurs w/ measles and malnutrition
does mumps or measles cause syncitia
measles
describe what measles does to cell mediated immunity
suppresses it, causes anergy
how many serotypes of measles are there?
1
how many animals act as a resevoir for measles?
just humans
describe measles immunization
live attenuated
given twice in MMR
life long protection
“slow viruses”
- long incubation period (years)
- relentless course leading to death
- genetic predisposition
- re-emerge from latency b/c of immune suppression
examples: HIV, JC, BK neuropathy
JC virus
papovavirus
causes progressive multifocal leukoencephalopathy (PML)
PML is a progressive demyelinating disease of the brain (affects oligodendroglia) w/o inflammation
occurs w/ immunosuppression
progression includes blindness, dementia, and death
SSPE
subacute sclerosing panencephalitis
onset of intellectual deterioration, psychological disturbance, blindness and terminal paralysis
associated w/ measles-
- high Ab to measles
- CNS contains measle antigen
distinct inclusion bodies. relation to measles unclear. does occur after vaccination (one in a million)
prion characteristics
1 long incubation period 2. slow relentless course to death 3 confined to CNS 4 produce spongiform encephalopathy 5. genetic predisposition
what are prions?
theorized to be infectious proteins w/o nucleic acid
what are the 5 spongiform encephalopathies caused by prions?
KURU CDJ Cretzfeld-Jacob disease variant CDJ mad cow GSS- gerstmann straussler scheinker syndrome fatal familial insomnia
scarpie
chronic progressive CNS disorder in adult sheep
genetic predisposition indicated
incubation period of less than a year
prion disease- no nucleic acids
KURU
progressive degenerative disorder of the CNS, especially the cerebellum
limited to small tribe in new guniea
no environmental factors- partially genetic
could be transmitted to apes by eating the human brains
CDJ
most common human prion
most are the result of a mutation, w/ obvious cause. risk increases w/ age
some reported cases were iatrogenic- caused by physicians using contaminated surgical equipment
some variants are linked to families fCDJ
some are sporadic sCDJ
mad cow
variant CDJ
caused an epidemic in great britain as a result of using brains/bone marrow of cows to feed other cows, which became infected, and when consumed, infected other people
