lecture 1 Flashcards
Pathogenesis
process by which infection leads to disease
tissue tropism
viral affinity for specific body tissue
incubation period
time between exposure to virus and onset of disease
congenital infections
infection of fetus as target organ
failed infections
virus can’t find material necessary for life cycle
acute infections
rapid onset, short duration (cold virus)
persistent or chronic infection
lasts many years and almost always detectable, latent infection (not detectable during dormancy), recurrent infection, transformation infection (virus permanently alters host genetic material-> cancer)
viral transmission
to host: shedding, respiratory-> enveloped viruses, saliva, blood, skin lesions, vectors
viral transmission
within host: viremia-spread via blood, via neurons
viral parthenogenesis
implantation of virus at portal of entry, local replication, spread within host to target organs, spread into the environment
laboratory diagnosis of viruses
description of virus-induced cytopathologic effects on cells-> changes in morphology, vacuolation, fusion, inclusion bodies. Electron microscope detection of viral particles
laboratory diagnosis of viruses
isolation and growth of virus in: tissue culture, embryonated eggs, expreimental animals, Detection of viral components: proteins, nucleic acid, hemagglutinatinins, evaluation of patients immune response-> serology tests
Prions
misfolded proteins with no nucleic acids
replication of prions
alteration of normal host protein into beta-sheets,beta-sheets are insoluble and resistance to proteases. resistance also to chemicals, UV radiation, heat up to 80 C.
Prions evade immune response how?
evade immune response because they are naturally occurring proteins
Prions and TSE’s
Prions cause transmissible spongiform encephalopathies due spongy nature of brain.
symptoms of TSE’s
progressive CNS degenerative disease, always fatal, dementia, ataxia, pyramidal signs, characteristic waves
Creutzfeld-Jazob disease (CJD)
individuals 50 years and older, rapid mental deterioration, spontaneous, by genetic mutation, contamination during medical procedure.
CJD symptoms
no fever or flu-like symptoms, impaired memory, coordination and judgment, insomnia. Late: myoclonus, blindness, comatose, ultimately death
Variant Creutzfeldt-Jakob disease (vCJD)
younger patients (28-29 years old). Linked with TSE’s of cattle.
Symptoms of vCJD
initially-> psychiatric symptoms (depression, schizophrenia-like psychoses), Late-> difficulty walking, become immobile, mute, ultimately death
Kuru
“trembling with fear”, outbreak in New Guinea, get from eating brains of those with Kuru, cannibalistic behaviors
Prion pathogenesis
oral ingestion, intestinal absorption, and transported to lymph tissue via blood, replication in lymph tissue, transport to brain via peripheral nerves, direct penetration across blood brain barrier