polio, rabies, viruses, prions, Flashcards
Compare and contrast Salk and Sabin vaccines. Diagnose diseases caused by Coxsackie A and B viruses and enteroviruses. Diagnose rabies from clinical presentation and lab findings. Recommend treatment for rabies. Identify neurological syndromes caused by JC, measles, and rubella viruses. Compare and contrast viruses and prions.
morphology of rabies virus
rod shaped enveloped RNA virus
type of virus causing rabies
rhabdovirus
route of rabies transmission from wound to brain
nerve endings –> dorsal root ganglia –> Spinal cord –> brain
parts of the brain infected by rabies
brain stem, hippocampus, cerbellum
how virus moves up neurons
axonal transport
rabies virus spreads from CNS to:
salivary glands, kidneys, cornea (highly innervated areas)
factors associated with rabies incubation period
distance of wound to brain
concentration of virus in inolculum
severity of wound
host age and immune status
immune response to rabies infection
neutralizing antibody is protective
cell mediated responses not effective
inflammation response to infected (non-nervous) tissue
none
major resirvoirs of rabies
domestic animals, cattle, small carnivorous mammals
non-animal bite possible rabies tranmission mode
cornea/organ transplants
lab diagnosis of rabies
cytoplasmic negri bodies in neurons
viral RNA in skin or CNS by PCR
viral antigen in skin or CNS by IF
treatment of rabies exposure
killed virus vacciene before sx occur
diseases caused by slow viruses (5)
progressive mutifocal leukoencephalopathy subacute panencephalitis subacute measles encephalitis progressive rubella panencephalitis AIDS
prion diseases
Kuru CJD gertsmann-straussler syndrome scrapie BSE
virus causing PML
papovavirus (JC virus)
clinical signs of PML
cerebral sx (confusion, dementia, aphasia, visual field defects)
SSPE virus
defective measles virus
sx of SSPE
children: withdrawal, intellectual decline, mycoclonic jerks, visual decline. progresses to vegetative state and death
pathologic features of PML
infection of oligodendrocytes
• multifocal areas of demyelination
• lesions only in white matter of brain
• little or no inflammatory response
risk for PML
immunocompromised pts