Mechanisms of Infection Flashcards

1
Q

What are common routes of entry?

A
  • mouth
  • conjunctiva
  • scratch, injury
  • arthropod
  • capillary
  • skin
  • anus
  • urogenital tract
  • alimentary tract
  • respiratory tract
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2
Q

Viruses that initiate infection of skin, oral mucosa, genital tract, or eye

A
  • poxviridae: minor abrasions or arthropod
  • rhabdoviridae: biological, bite of vertebrate
  • herpesviridae: genital tract
  • adenoviridae: conjunctiva
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3
Q

Viruses that initiate infection of respiratory tract

A
  • producing respiratory disease: adenoviridae, herpesviridae

- producing systemic disease, without initial respiratory signs: parvoviridae

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4
Q

Viruses that initiate infection of intestinal tract

A
  • producing diarrhea: coronaviridae, toroviridae

- producing systemic disease, without diarrhea: caliciviridae, picornaviridae

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5
Q

Mechanisms of spread in the body

A
  • local spread on epithelial surfaces
  • subepithelial invasion and lymphatic spread
  • spread by the bloodstream (viremia)
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6
Q

Pox virus

A
  • produce infection via the skin

- local subepithelial and lymphatic spread

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7
Q

Paramyxoviruses and influenza viruses

A

Do not invade subepithelial tissues!

- enter lymphatic and spread

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8
Q

Rotaviruses or coronaviruses

A

Do not invade subepithelial tissues

- enter lymphatic and spread

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9
Q

Skin

A

Not a very important route

- food and mouth disease, vesicular stomatitis, pox, herpes

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10
Q

Respiratory secretions

A

Most important route!

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11
Q

Saliva

A

Rabies and FIV

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12
Q

Feces

A

Poliovirus and rotaviruses

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13
Q

Genital secretions

A

Herpes and immunodeficiency viruses

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14
Q

Urine

A

Viruses that replicate in the kidney

- rinderpest, infectious canine hepatitis, food and mouth disease

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15
Q

Milk

A

Viruses replicate in the mammary gland (not important)

- caprine arthritis-encephalitis, tick borne flaviviruses

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16
Q

No shedding

A

Not all virus replication ends in shedding

- replicate in CNS

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17
Q

Persistent infections

A

Infections that persist for the life of the animal - episodes of clinical disease occur infrequently

  • herpesviruses
  • canine distemper virus
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18
Q

Why are persistent infections important?

A

Serve as source of infection for other animals (constant shedding)

  • can be reactivated and cause recurrent acute episodes of disease
  • lead to immunopathologic disease
  • associated with neoplasms
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19
Q

What are 3 categories of persistent infections?

A
  • latent
  • chronic
  • slow
20
Q

Latent infections

A

Virus is not demonstrable except when reactivation occurs

21
Q

Chronic infections

A

Virus always demonstrable and often shed

- disease may be absent, chronic, or develop late

22
Q

Slow infections

A

Virus gradually increases during a very long preclinical phase
- leads to a slowly progressive lethal disease

23
Q

Infectious bovine rhinotracheitis virus

A

Alphaherpesvirus

  • viral genome persists latently in neurons (episome)
  • when episome is reactivated, infectious virus is produced and moves down sensory nerves and reaches the nasal mucous membranes or the skin
  • proliferation occurs in epithelial cells, with virus shedding
24
Q

Episome

A

Similar to an extracellular plasmid

25
Q

Foot and mouth disease

A

Virus persists in the pharynx in cattle, sheep, goats and other ruminants

  • not all infected animals become carriers
  • no correlation between antibody levels and carrier
  • virus can be found in buffalo for up to 2 years after infection
26
Q

Lymphocytic choriomenigitis in mice

A

Caused by arenavirus, transmitted via horizontally and in utero (vertical)

27
Q

Vertical transmission

A

Offspring becomes infected

28
Q

Immunological trolerance

A

In presence of virus but in absence of antibody

29
Q

Immunological tolerance (incomplete)

A

The presence of virion IgG complement and the complex is infectious

30
Q

Offspring of infected females develop __________

A

Immuological tolerance

31
Q

Subacute spongiform viral encephalopathies

A
  • scrapie in sheep and goats (in the US)
  • Creutzfelt-Jakob Disease in humans
  • bovine spongiform encephalopathy (mad-cow)
  • chronic wasting disease in mule deer and elk
  • transmissible mink encephalopathy
32
Q

Prions

A

Proteinaceous infectious particles

  • concentrate in brain and spinal cord (not in muscle, milk, and blood)
  • resistant to steam sterilization and cooking
  • cannot grow prions, have to collect from infectious tissues
33
Q

Prions are _______ that concentrate in the tissues of CNS

A

Misfolded proteins

  • protein persuades other proteins to copy it
  • incubation time: 1.5-30 years
  • no immune responses, no interferon
34
Q

Canine distemper

A

Paramyxovirus

  • acute systemic infection, majority of dogs recover completely within 1 month
  • minority: recovered dogs harbor the virus in brain cells, where it replicates slowly and eventually produces old dog encephalitis
35
Q

Unique properties of persistent viruses

A
  • nonimmunogenic agents
  • integrated genomes
  • growth in protected sites
  • antigenic variation
36
Q

Noniummunogenic agents

A

Prions

  • do not induce interferon
  • no immune responses, so host can not restrict the replication and pathologic effects
  • ex: subactue spongiform encephalopathies
37
Q

Integrated genomes

A

Retroviruses whose proviral DNA is integrated are maintained indefinitely, from one generation to the next, as part of the genome of the host
- proviral DNA may be implicated in oncogenesis

38
Q

Alphaherpeviruses

A

Avoid immune elimination by remaining within cells of the nervous system

  • as episomal DNA in ganglion cells during the intervals between disease episodes
  • as viral DNA, subviral particles, or virions within axons prior to acute recurrent episodes
39
Q

Betaherpeviruses (cytomegalovirus) and gammaherperviruses

A

Avoid immune elimination by maintaining serial infection by cell to cell contact

40
Q

Antigenic variation

A

Visna/Maedi and equine infectious anemia viruses (lentiviruses, retroviridae)

  • avoid immune response of the host by antigenic drift (generate variants)
  • variants may become more virulent
41
Q

Modification of host defense mechanisms

A
  • defective antibody response
  • defective cell-mediated immunity
  • growth in macrophages
42
Q

Defective antibody response

A
  • viruses that replicate in lymphoid tissue and macrophages induce non-neutralizing antibodies
  • antibodies combine with viral antigens and virions in the serum to form immune complexes –> immune complex disease –> deposit complexes in renal glomeruli or other organs
43
Q

Growth in macrophages

A

In chronic infections, the virus appears to grow mainly in reticuloendothelial tissue (especially macrophages)
- viruses in macrophages avoid host immune resposne

44
Q

Defective cell mediated immunity

A
  • immunosuppression by the causative virus
  • immunological tolerance
  • presence of virus-antibody complexes
  • failure of immune lymphocytes to reach target cells
  • decrease in the numbers of Th lymphocytes
45
Q

Antiviral chemotherapy

A
  • attachment of virion to cell receptor - receptor analog
  • primary transcription - transcriptase inhibitor
  • reverse transcription - AZT
  • translation of viral mRNA into protein - interferons
  • posttranslational cleavage of proteins - protease inhibitors
  • replication of RNA viral genome - replicase inhibitors