Host-pathogen interactions Flashcards
pathogenicity
ability of a virus to cause disease in a host
pathogen
virus which causes disease
pathogenesis
mechanism of development of a disease
virulence
measure of degree of pathogenicity of the infecting virus
avirulent
not harmful to the host
is virulence an absolute property?
no, depends on many variables
lethal dose 50 (LD 50 )
dose of virus required to cause death in 50% of animals
infectious dose 50 (ID 50)
dose of virus to infect 50% of an experimental group of hosts/animals
lower LD and ID = ???
more virulent the organism!!!!
routes of entry (4)
skin, mucous membranes, GI tract, respiratory tract
skin defenses (6)
dense outer layer of keratin, low pH, prescence of fatty acids, bacterial flora, dryness, components of innate and adaptive immunity
transcutaneous injection (3)
bite of arthropods, bite of infected animal, contaminated objects
GI defenses (9)
mucous membrane of oral cavity, acidity of stomach, alkalinity of the intestine, layer of mucus covering the gut, lipolytic activity of bile (not good for enveloped viruses!!), proteolytic activity of pancreatic enzymes, defensins, igA, scavenging macrophages
respiratory tract defenses (5)
mucociliary blanket, alveolar macrophages, NALT, BALT, temperature gradient
disseminated infection
infection spreads beyond the primary site of infection
systemic infection
if many organs and tissues are infected
apical release facilitates ??
basolateral release provides access to ??
apical = virus dispersal
basolat. = access to underlying tissues, facilitating systemic spread
viremia
presence of a virus in the blood, virus may be free in blood or in a cell, such a lymphocytes
primary viremia
initial entry of virus into the blood after injection
secondary viremia
virus has replicated in major organs and once more entered the circulation
passive viremia
direct inoculation of virus into the blood
EX: bite of arthropods or contaminated syringe
active viremia
viremia following initial virus replication in host
-release of virions from initial site of replication, such as lymphatics or epithetlium of intestine to the blood stream
neurotropic virus
virus infects neural cells
infection can occur by neural or hematogenous spread
neuroinvasive virus
viruses that enter the CNS (spinal cord and brain) after infection of a peripheral site
neurovirulent virus
viruses that cause disease of nervous tissue, manifested by neurological symptoms and often death
Herpes simplex virus exhibits…
low neuroinvasiveness of CNS but high neurovirulence
- always enters peripheral nervous sytem but rarely enters CNS. when it does, consequences are always severe, if not fatal
mumps virus exhibits…
neuroinvasiveness but low neurovirulence. most infections lead to invasion of CNS but neurologic disease is mild
rabies virus exhibits…
high neuroinvasiveness and high neurovirulence. it readily infects PNS and spreads to CNS with 100% lethality unless antiviral therapy is administered shortly after infection
retrograde spread
travel opposite direction of nerve impulse flow. invades axon terminals, dendrite, cross synapse to reach next axon terminal
anterograde spread
travel in direction of nerve impulse flow. invades dendrites or cell bodies, then spread to axon terminals, then cross synaptic contacts to invade dendrite of next neuron
can viruses spread through olfactory route?
YES
can viruses spread through BBB?
YES
features of localized vs systemic viral infection
-site of pathology
-incubation period
-viremia
-duration of immunity
-secretory IgA
localized: portal of entry, short, no because virus doesnt infect blood, variable/short, very important
systemic: distant sites, relatively long because it takes time to see clinical signs, yes, mostly lifelong, not important
acute infection
intensive shedding over short time period
persistent infection
shed at lower titers for months to years
viral tropism
specificity/affinity of a virus for a particular host tissue
pantropic viruses:
can replicate in more than one host organ/tissue
Viral injury to skin (6)
- vesicles: small distinct elevation with fluid
- ulcer: opening in the skin caused by sloughing of necrotic tissue, extending past epidermis
- nodule/tumor: solid, elevated mass, nodules have distinct borders, tumors extend deep into the dermis
- warts: benign skin growth that infects top layer of the skin
- papule: solid elevation without fluid with sharp borders
- erythema: reddening of the skin, consequence of systemic viral infection
GI tract injury via two ways:
and pathway
- ingestion
- hematogenous spread (from the blood) leading to systemic infection
both lead to destruction of enterocytes due to viral replication –> GI disease, malabsorption, diarrhea –> pronounced dehydration, acidosis and hemoconcentration
respiratory tract injury (9)
loss of ciliary activity, loss of integrity of the lining of mucus layer, destruction of epithelium, inflammation, exudation, influx of inflammatory cells, obstruction of air passages, hypoxia and respiratory distress, secondary bacT infection
viral-bacterial synergism
infects respiratory tract and infection is much worse in both bacT and virus are together
CNS injury
neuronal necrosis, phagocytosis of neurons (neuronophagia) and infiltrations of inflammatory cells (perivascular cuffing) – characteristic of encephalitits
CNS injury
-progressive demyelination
-neuronal vacuolation
-EX: canine distemper, nerve impulse cant travel properly
-in prions !!
damage to endothelium (4)
hemorrhages, disseminated intravascular coagulation, edema, infarction (ischemic necrosis)
petechial vs. ecchymotic hemorrhage
petechial: pin point hemorrage
ecchymotic: diffuse hemorrhage
Disseminated intravascular coagulation
clots form in small blood vessels throughout the body due to viral replication –> organs do not get blood –> organ failure. later, raw material for clot exhausted due to over use –> no clot formation in later stages –> hemorrhages throughout the body
Teratogenesis
abnormal development or arrests in development of the embryo or fetus – may result in death or malformations during the antenatal period
Arthrogryposis
stiff and tight joints
viral infection of the fetus example
bovine viral diarrhea BVD -porencephaly, depression, dome shaped skull
virus induced immunopathology
tissue injury mediated by host immune response to viral infection, depends on balance between protective and destructive effects of host immune response to viruses
-common w viruses that are non cytolytic and persistent
immunopathology
tissue damage mediated by hypersensitivity reactions
-autoimmune diseases EX: moon blindness in a horse
-inflammation mediated tissue damage EX: fibrosis
immunodeficiency disorders
viral injury to organs — what immune cell is responsible
T Cells
-cytotoxic cell mediated lysis/killing of infected host cell
-release of cytokines that cause inflammation and tissue damage becomes chronic against persistent viral infections
toll like receptors
can free radicals cause injury?
persistent activation of these causes production of pro-inflammatory cytokines and interferons, as well as signals that recruit and activate cells involved in inflammation
YES
toxicity from AB response
AB response to virus may contribute to tissue damage
-occurs when AB binds to an infected cell, activates complement and causes an inflammatory reaction
-AB mediated inflammatory reactions involve toxicity following: engagement of IgG with Fc receptors on inflammatory cells, which causes inflammatory mediator release, following deposition of viral antigen - antibody complexes in capillary beds, leading to activation of the complement cascade —-BINDING releases inflammatory mediators
vasculitis mediated by virus - induced immunopathology
binding causes inflammation in blood vessels and edema
immunosuppression EX
infectious bursal disease: virus replication causes atrophy of the bursa and a severe deficiency of B ymphocytes, resulting in immuno suppression – infected birds are suspectible to other pathogens
inapparent infections
clinical signs and symptoms are not evident, too few cells may be infected, stimulate host immune response, possible source of virus spread
acute infection
short clinical course and rapid clearance from host immune response
-shed large number of virus over a short period of time with very severe clinical signs
persistent infection (3 types)
- latent infection: virus is not demonstratable except when reactivation occurs due to stress
- chronic infection: acute infection followed by chronic infection in which the virus is continuously shed from or is present in infected tissue
- slow infection: prolonged incubation period, lasting months or years, slow progressive lethal disease
