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Virology > Host-pathogen interactions > Flashcards

Host-pathogen interactions Flashcards

1
Q

pathogenicity

A

ability of a virus to cause disease in a host

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2
Q

pathogen

A

virus which causes disease

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3
Q

pathogenesis

A

mechanism of development of a disease

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4
Q

virulence

A

measure of degree of pathogenicity of the infecting virus

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5
Q

avirulent

A

not harmful to the host

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6
Q

is virulence an absolute property?

A

no, depends on many variables

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7
Q

lethal dose 50 (LD 50 )

A

dose of virus required to cause death in 50% of animals

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8
Q

infectious dose 50 (ID 50)

A

dose of virus to infect 50% of an experimental group of hosts/animals

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9
Q

lower LD and ID = ???

A

more virulent the organism!!!!

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10
Q

routes of entry (4)

A

skin, mucous membranes, GI tract, respiratory tract

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11
Q

skin defenses (6)

A

dense outer layer of keratin, low pH, prescence of fatty acids, bacterial flora, dryness, components of innate and adaptive immunity

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12
Q

transcutaneous injection (3)

A

bite of arthropods, bite of infected animal, contaminated objects

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13
Q

GI defenses (9)

A

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

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14
Q

respiratory tract defenses (5)

A

mucociliary blanket, alveolar macrophages, NALT, BALT, temperature gradient

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15
Q

disseminated infection

A

infection spreads beyond the primary site of infection

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16
Q

systemic infection

A

if many organs and tissues are infected

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17
Q

apical release facilitates ??
basolateral release provides access to ??

A

apical = virus dispersal
basolat. = access to underlying tissues, facilitating systemic spread

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18
Q

viremia

A

presence of a virus in the blood, virus may be free in blood or in a cell, such a lymphocytes

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19
Q

primary viremia

A

initial entry of virus into the blood after injection

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20
Q

secondary viremia

A

virus has replicated in major organs and once more entered the circulation

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21
Q

passive viremia

A

direct inoculation of virus into the blood
EX: bite of arthropods or contaminated syringe

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22
Q

active viremia

A

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

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23
Q

neurotropic virus

A

virus infects neural cells
infection can occur by neural or hematogenous spread

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24
Q

neuroinvasive virus

A

viruses that enter the CNS (spinal cord and brain) after infection of a peripheral site

25
Q

neurovirulent virus

A

viruses that cause disease of nervous tissue, manifested by neurological symptoms and often death

26
Q

Herpes simplex virus exhibits…

A

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

27
Q

mumps virus exhibits…

A

neuroinvasiveness but low neurovirulence. most infections lead to invasion of CNS but neurologic disease is mild

28
Q

rabies virus exhibits…

A

high neuroinvasiveness and high neurovirulence. it readily infects PNS and spreads to CNS with 100% lethality unless antiviral therapy is administered shortly after infection

29
Q

retrograde spread

A

travel opposite direction of nerve impulse flow. invades axon terminals, dendrite, cross synapse to reach next axon terminal

30
Q

anterograde spread

A

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

31
Q

can viruses spread through olfactory route?

A

YES

32
Q

can viruses spread through BBB?

A

YES

33
Q

features of localized vs systemic viral infection
-site of pathology
-incubation period
-viremia
-duration of immunity
-secretory IgA

A

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

34
Q

acute infection

A

intensive shedding over short time period

35
Q

persistent infection

A

shed at lower titers for months to years

36
Q

viral tropism

A

specificity/affinity of a virus for a particular host tissue

37
Q

pantropic viruses:

A

can replicate in more than one host organ/tissue

38
Q

Viral injury to skin (6)

A
  1. vesicles: small distinct elevation with fluid
  2. ulcer: opening in the skin caused by sloughing of necrotic tissue, extending past epidermis
  3. nodule/tumor: solid, elevated mass, nodules have distinct borders, tumors extend deep into the dermis
  4. warts: benign skin growth that infects top layer of the skin
  5. papule: solid elevation without fluid with sharp borders
  6. erythema: reddening of the skin, consequence of systemic viral infection
39
Q

GI tract injury via two ways:
and pathway

A
  1. ingestion
  2. 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

40
Q

respiratory tract injury (9)

A

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

41
Q

viral-bacterial synergism

A

infects respiratory tract and infection is much worse in both bacT and virus are together

42
Q

CNS injury

A

neuronal necrosis, phagocytosis of neurons (neuronophagia) and infiltrations of inflammatory cells (perivascular cuffing) – characteristic of encephalitits

43
Q

CNS injury
-progressive demyelination
-neuronal vacuolation

A

-EX: canine distemper, nerve impulse cant travel properly

-in prions !!

44
Q

damage to endothelium (4)

A

hemorrhages, disseminated intravascular coagulation, edema, infarction (ischemic necrosis)

45
Q

petechial vs. ecchymotic hemorrhage

A

petechial: pin point hemorrage
ecchymotic: diffuse hemorrhage

46
Q

Disseminated intravascular coagulation

A

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

47
Q

Teratogenesis

A

abnormal development or arrests in development of the embryo or fetus – may result in death or malformations during the antenatal period

48
Q

Arthrogryposis

A

stiff and tight joints

49
Q

viral infection of the fetus example

A

bovine viral diarrhea BVD -porencephaly, depression, dome shaped skull

50
Q

virus induced immunopathology

A

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

51
Q

immunopathology

A

tissue damage mediated by hypersensitivity reactions
-autoimmune diseases EX: moon blindness in a horse
-inflammation mediated tissue damage EX: fibrosis
immunodeficiency disorders

52
Q

viral injury to organs — what immune cell is responsible

A

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

53
Q

toll like receptors

can free radicals cause injury?

A

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

54
Q

toxicity from AB response

A

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

55
Q

vasculitis mediated by virus - induced immunopathology

A

binding causes inflammation in blood vessels and edema

56
Q

immunosuppression EX

A

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

57
Q

inapparent infections

A

clinical signs and symptoms are not evident, too few cells may be infected, stimulate host immune response, possible source of virus spread

58
Q

acute infection

A

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

59
Q

persistent infection (3 types)

A
  1. latent infection: virus is not demonstratable except when reactivation occurs due to stress
  2. chronic infection: acute infection followed by chronic infection in which the virus is continuously shed from or is present in infected tissue
  3. slow infection: prolonged incubation period, lasting months or years, slow progressive lethal disease

Virology (29 decks)

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