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virology > lecture 8 > Flashcards

lecture 8 Flashcards

1
Q

pathogenicity

A

-refers to ability of virus to cause disease in host

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2
Q

pathogen

A

virus which causes disease

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3
Q

pathogenesis

A

manner/mechanism of development of diseases

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4
Q

virulence

A
  • quantitative or relative measure of the degree of pathogenicity of the infecting virus
  • not absolute property of virus, depends on many variables
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5
Q

avirulent

A

not virulent

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6
Q

lethal dose 50 (LD50)

A

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

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7
Q

infectious dose 50 (ID50)

A

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

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8
Q

with a lower ID50 and LD50 will the virus be more/less virulent?

A

more

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9
Q

routes of entry of viruses into host

A
  1. skin
  2. mucous membrane
  3. GI tract
  4. respiratory tract
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10
Q

defenses of the skin against viruses

A
  • dense outer layer of keratin
  • low pH
  • presence of fatty acids
  • bacterial flora
  • dryness
  • innate and adaptive immunity (migratory dendritic cells: Langerhans cells)
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11
Q

routes of transcutaneous injection of virus

A
  1. bite of arthopods
  2. bite of infected animal
  3. contaminated objects
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12
Q

defenses of the GI tract against virus

A
  • mucous membrane of oral cavity & esophagus
  • acidity of stomach
  • alkalinity of intestine
  • layer of mucous covering gut
  • lipolytic activity of bile
  • proteolytic activity of pancreatic enzymes
  • defensins (host defense peptides)
  • IgA
  • scavenging macrophages
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13
Q

defenses of the respiratory tract against virus

A
  • mucociliary blanket
  • alveolar macrophages
  • NALT (nasal associated lymphoid tissue)
  • BALT (bronchus- associated lymphoid tissue)
  • temperature gradient
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14
Q

disseminated infection

A

-infection spreads beyond primary site of infection

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15
Q

systemic infection

A

if a number of tissues or organs are infected

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16
Q

apical release of viruses causes…

A

virus dispersal

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17
Q

basolateral release of virus causes…

A

spread to underlying tissues (systemic spread)

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18
Q

Directional shedding of viruses from the infected epithelium is critical to what type of viral spread?

A

-subepithelial spread

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19
Q

viremia

A
  • presence of virus in the blood

- virus may be free in blood or in a cell, such as lymphocytes

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20
Q

primary viremia

A

initial entry of virus into blood after infection

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21
Q

secondary viremia

A

virus replicates in major organs and enters the circulation again

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22
Q

active viremia

A
  • viremia following initial virus replication in host

- release of virions from the initial site of replication, such as lymphatics or epithelium of intestine to blood stream

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23
Q

passive viremia

A
  • direct inoculation of virus in host, such as contaminated syringe or bite of arthopods
  • no initial replication elsewhere in host before
24
Q

true/false: mosquito bites are an example of active virema

A

false, passive viremia

25
Q

neurotropic virus

A
  • viruses that can infect neural cells

- infection may occur by neural or hematogenous spread

26
Q

neuroinvasive virus

A

-viruses that enter the CNS after infection of a peripheral site

27
Q

neurovirulent virus

A

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

28
Q

virus with low neuroinvasiveness, high neurovirulence

A
  • always enters the PNS, rarely enters CNS

- if enters CNS then consequences almost always severe, potentially fatal

29
Q

virus with neuroinvasivenesss, low neurovirulence

A

-most infections lead to invasion of CNS, neurological disease is mild

30
Q

virus with high neuroinvasiveness, high neurovirulence

A

-readily infects the PNS, spreads to CNS with 100% lethality unless antiviral therapy is administered shortly after infection

31
Q

retrograde spread of viruses

A

travel opposite direction of nerve impulse flow, invades axon terminals, then spreads to dendrite or cell body and cross synapse to reach next axon terminal

32
Q

anterograde spread

A

travel in direction of nerve impulse flow, virus invades dendrites or cell bodies and then spreads to axon terminals, then cross synaptic contacts to invade dendrite of next neuron

33
Q

Ways that virus can get into the CNS

A
  • olfactory routes

- through blood-brain-barrier

34
Q

acute infection

A

intensive shedding over a short period of time

35
Q

persistant infection

A

can be shed at lower titers for months to years

36
Q

tropism

A

specificity/affinity of virus for particular host tissue

37
Q

pantropic viruses

A

can replicate in more than one host organ/tissue

38
Q

Virus injury to skin

A
  • vesicles: fluid filled sacs
  • ulcers: opening in the skin caused by sloughing of necrotic tissue, extending past the epidermis
  • nodule: palpable, solid, elevated mass
  • warts: benign skin growths that appear when virus infects top layer of skin
  • papule: solid elevations without fluid with sharp borders
  • erythema: reddening of skin, from systemic viral infection
39
Q

virus injury to GI tract

A
  • ingestion
  • hematogenouos spread, systemic infection
  • causes: destruction of enterocytes due to viral replication, hypersecretion
  • GI disease, malabsorption, D+
  • pronounced dehydration, acidosis, hemoconcentration
40
Q

virus damage to respiratory tract

A
  • loss of ciliary activity
  • loss of integrity of the lining mucous layer
  • multifocal destruction of epithelium
  • inflammation
  • exudation
  • influx of inflammatory cells
  • obstruction of air passages
  • hypoxia and respiratory distress
  • secondary bacterial infection
41
Q

virus damage to central nervous system

A
  • encephalitis, or encephalomyelitis
  • neuronal necrosis
  • phagocytosis of neuronss (neurophagia)
  • perivascular infiltrations of inflammatory cells (perivascular cuffing)
  • progressive demyelination (canine distemper)
  • neuronal vacuolation in prion disease
42
Q

virus damage to endothelium

A
  • hemorrhages- petechiae hemorrhage (pin-point/small spots)

- ecchymoses hemorrhage (larger areas of hemorrhage, ill-defined margins)

43
Q

disseminated intravascular coagulation (DIC)

A
  • clot forms in small blood vessels throughout the body, organs do not get blood, organ failure
  • later stages, raw material for clot exhausted due to over use
  • no clot formation in later stages, hemorrhages throughout body
44
Q

teratogenesis

A
  • abnormal development or arrests in development of the embryo or fetus
  • may result in death or malformations during the antenatal period
45
Q

virus-induced immunopathy

A
  • tissue injury mediated by host immune response to virus infection
  • price paid by the host to clear viral infection
  • depends on balance between protective and destructive effects of host immune response to viruses
46
Q

immunopathy

A
  • tissue damage mediated by hypersensitivity reactions
  • autoimmune diseases (moon blindness in horse)
  • inflammation-mediated tissue damage (fibrosis)
  • immunodeficiency disorders
47
Q

virus injury to organs/tissues (role of T cells)

A
  • cytotoxic cell mediated lysis/killing of infected host cells
  • may be release of cytokines from T cells (CD4+ and CD8+) and other cells that cause inflammation and tissue damage that becomes chronic against persistent virus infection
48
Q

Toll like receptors

A

-persistent activation of TLRS of innate host cell by viruses cause production of pro-inflammatory cytokines and interferons, as well as signals that recruit and activate cells involved in inflammation

49
Q

nitric oxide and superoxide

A

-free radicals that also mediate injury

50
Q

toxicity from antibody responses

A

-antibody responses to viruses also may contribute to tissue damage

51
Q

virus induced immunopathy- immunosupression

A
  • infecious bursal disease: virus replication causes atrophy of bursa and severe deficiency of B lymphocytes resulting in immunosupression
  • result: infected birds become susceptible to other pathogens
52
Q

inapparent infections

A
  • clinical signs and symptoms not evident
  • too few cells may be infected
  • stimulate host immune response
  • possible source of virus spread
53
Q

acute infection (short term infection)

A
  • short clinical course

- rapid clearance from host immune response

54
Q

latent infection (persistent infection)

A
  • virus is not demonstrable except when reactivation occurs

- reactivation often stimulated by immunosupression and/or by the action of a cytokine or hormone

55
Q

chronic infection

A

-acute infection followed by chronic infection in which the virus is continuously shed from or is present in infected tissue

56
Q

slow infection (persistent infection)

A
  • prolonged incubation period, lasts months or years

- slow, progressive, lethal disease

virology (12 decks)

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