Immunity to Microbes Flashcards

1
Q

What must the pathogen do to establish an infection?

A

Enter and invade host tissues
Evade host immunity
Replicate

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2
Q

What are the 5 major types of pathogens?

A

Extracellular bacteria, intracellular bacteria, viruses, parasites, fungi

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3
Q

Innate Immunity to Microorgs

A

Mucosal immunity first line of defense (physical, mechanical and chemical barrier, anti- microbial peptides)
Complement Activation
Phagocytosis
Inflammatory response

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4
Q

Antimicrobial immunity

A

Early innate response followed by a sustained adaptive response

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5
Q

4 families of PRRs

A

Toll-like receptors (TLR)
Nucleotide-binding oligomerization domain-like receptors (NLR)
C-type lectin receptors (CLR)
RIG-1 like receptors (RLR)

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6
Q

How is complement activated?

A

Peptidoglycans in the cell walls of Gram-positive bacteria
LPS in Gram-negative bacteria
Mannose on bacterial surface

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7
Q

What does the complement system activate?

A

Opsonization
Membrane attack complex (MAC)
Expansion of inflammation

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8
Q

What is the response to bacterial infections?

A
  1. Neutralization of toxins or enzymes by antibody
  2. Killing bacteria by classical complement pathway
  3. Opsonization of bacteria by antibodies and complement –> destruction or phagocytosis
  4. Destruction of intracellular bacteria by activated macrophages (cell mediated)
  5. Direct killing of bacteria by cytotoxic T cells
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9
Q

Whats responsible for phagocytosis and activation of phagocytes

A

Neutrophils and macrophages on:
Mannose receptors
Scavenger receptors
Fc receptors
Complement receptors

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10
Q

What happens once phagocytosis is activated?

A

Cytokines are secreted to induce leukocyte infiltration into the sites of infection
Destruction of bacteria

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11
Q

Extracellular bacteria

A

Don’t have to enter host to replicate
Occupy interstitial regions in CT, blood circulation, lumens of respiratory, urogenital and Gi tracts

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12
Q

Humoral Immunity

A

Block infection, eliminate microbes, neutralize their toxin
Involves IgA, opsonization and phagocytosis IgG, CCP with IgM and IgG

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13
Q

Intracellular bacteria

A

Cannot be detected by complement or Ab
Eliminated using cell-mediated response
Infected macrophages present bacterial peptides on their cell surface using MHC class II molecules
Antigen presentation

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14
Q

IFN-g cytokine

A

Released by Th1 if bacterial peptide presented
Stimulates killing mechanisms (production of lysozyme)
Increases antigen presentation by cells

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15
Q

Virus-host interactions

A

Viruses are not obligate intracellular organisms
Death of host due to infection is not beneficial to virus
Evolution of viruses that evade host- immunity and evolution of hosts that resist viruses

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16
Q

Innate Immunity to viruses

A

Inhibition of infection by type 1 interferons (IFNs) and NK cell-mediated killing of infected cells

17
Q

Type 1 IFNs

A

Induced by pathogen-associated molecular patterns (PAMPs)- dsRNA, aaRNA, cytosolic DNA –> the transcription of IFN
Inhibit viral replication

18
Q

What are the effects of interferon?

A

Signals neighboring uninfected cells to destroy RNA and reduce protein synthesis
Signals neighboring infected cells to undergo apoptosis
Activated immune cells

19
Q

______________ is shut off in virally infected cells

A

MHC 1 expression

20
Q

Where is cytotoxicity increased?

A

In NK and CD8+ cells

21
Q

What happens when cytotoxity is increased?

A

Promotes differentiation of naive T cells to the TH1
Enhance innate and adaptive immunity
Activation of intrinsic apoptotic death pathways in infected cells
Enhanced sensitivity to extrinsic inducer apoptosis

22
Q

Immunity to Parasites

A

Parasitic infections from protozoa, helminths, ectoparasites
Most resistant to phagocytic killing and can replicate within macrophages

23
Q

Eosinophils

A

Major basic protein in cytoplasmic granules released onto parasites kills them
IgE or IgG enhances the release of granules contents

24
Q

Phagocytes

A

Neutrophils and macrophages secrete cytotoxic factors externally that kill parasites within the need to ingest them

25
Q

What defense is used against protozoa?

A

TH1 cell-derived cytokines

26
Q

Helminthic infection

A

Activation of TH2 cells (IL-4 & 5) and naive CD4+
Production of IgE Abs and activates eosinophils
Ab dependent cell-mediated cytotoxicity

27
Q

Innate Immunity to parasites

A

Platelets can kill by releasing cytotoxic factors
Mast cells triggered by IgE release histamine

28
Q

Abs response to parasites

A

Impt. against blood parasites
Damage parasites directly
Enhance phagocytosis (opsonization)
Activate complement
Blocks entry to parasite into host cell

29
Q

Mycobacterium Avium (MAP)

A

Etiological agent of John’s disease
Chronic, fatal, debilitating granulomatous enteritis
Ruminants and zoonotic

30
Q

Prevalence of Mycobacerium avium (John’s disease)

A

US dairy herd: 91.1%
US beef herd: 7.9%

31
Q

John’s disease pathogenesis

A
  1. Ingestion of MAP from milk, colostrum, water
  2. Invasion of M or intestinal cells
  3. Uptake into subepithelial macrophages
  4. Release 2-5 years later
  5. Return to epithelial cells and shedding
    Dissemination throughout body lymphatics
32
Q

Immune evasion strategies of bacteria

A
  1. Secrete modulators (toxins, proteases, leukotoxins)
  2. Modulate surface proteins (modify lipid profiles)
  3. Hide form immune surveillance
  4. Block/ modify acquired immunity
  5. Inhibit cytokines/ interferon/ chemokines
  6. Modulate apoptosis (inhibit/ activate death signaling)
  7. Interfere in pathogen recognition receptors
  8. Block antimicrobial peptides
33
Q

Viral Immune Evasion

A
  1. Mimic receptors or ligands
  2. Hide from immune surveillance
  3. Antigenic hypervariability
  4. Subvert or kill immune cells/ phagocytes
  5. Inhibit/ alter complement/ cytokines
  6. Modulate apoptosis
  7. Block antimicrobial
34
Q

FELINE INFECTIOUS PERITONITIS

A

Fatal viral disease in cats (young and old)
12% feline deaths associated
Most organs infects

35
Q

Pathway of feline infectious peritonitis

A

Mutated enteric coronavirus –> lymphoid system –> macrophages –> systemic spread

36
Q

Evasion of immunity by parasites

A
  1. Resist destruction by complement
  2. Escape into cytoplasm before they’re killed in phagolysosome
  3. Antigenic variation (trypanososmes)
  4. Acquire surface layer of host antigens
  5. Shedding of soluble antigens
  6. Eosinophils promote Th2