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Infectious Agents > Host-Parasite Relationships > Flashcards

Host-Parasite Relationships Flashcards

1
Q

In any host-pathogen encounter, there are 2 principal determinants of the outcome

A
  • virulence of the parasite (know the enemy)

- resistance of the host (know thyself)

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2
Q

Opportunistic pathogen

A

Bacteria or fungi that are generally harmless in their normal habitat but can cause disease when they gain entrance to other sites or tissues
- have low potential to cause disease, but once disease is established they can be difficult to treat

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3
Q

Obligate pathogen

A

Organisms that always cause disease when it encounters a host
- ex: streptococcus equi, brucella abortus, yersinia pestis

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4
Q

Pathogenicity

A

Capacity of an organism to cause disease

- variation in this capacity is referred to in terms of virulence

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5
Q

Virulence

A

Measure of the degree of pathogenicity

  • ex: pathogenic strains of S. equi may vary in their capacity to produce strangles
  • all strains cause disease but some may cause more severe disease
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6
Q

Infectivity

A

Capacity of an organism to become established in the tissues of the host
- involves the ability to penetrate the tissue, survive the host’s defenses, and disseminate within the animal

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7
Q

Toxicogenicity

A

Ability of certain organisms to produce exotoxins

- there are both toxigenic and nontoxigenic strains of C. perfringes (only the former can cause disease)

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8
Q

Virulence factor

A

Bacterial product or strategy that contributes to its ability to cause infection

  • sometimes several virulence factors are required to act in concert for a pathogen to accomplish a pathogenic event
  • sometimes a pathogen will have virulence factors with overlapping function
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9
Q

Koch’s postulates definition

A

Method to definitively determine whether an agent is causing a disease

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10
Q

Koch’s postulates

A
  • suspected agent is present in all cases of the disease
  • agent is isolated from such disease and propagated serially in pure culture, apart from its natural host
  • upon introduction into experimental host, the isolate produces the original disease
  • agent can be reisolated form this experimental infection
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11
Q

Exceptions to Koch’s postulates

A
  • pathogens that cannot grow outside of the host, so cannot be isolated (obligate)
  • some bacteria can be isolated and not cause infection in a healthy host
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12
Q

What are the 2 basic mechanisms by which bacteria can cause disease?

A
  • direct damage of host cells

- indirectly by stimulating exaggerated host inflammatory/immune response (host response is what causes pathology)

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13
Q

Direct damage of host cells occurs from ______

A
  • extracellular pathogens: secreted exotoxins or effector proteins cause damage
  • intracellular pathogens: destruction of host cells or alteration of host cells’ function
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14
Q

Virulence factors are divided into 2 categories

A
  • those that cause damage to the host (exotoxins)

- those that do not directly damage the host but promote colonization and survival of infecting bacteria

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15
Q

Exotoxin

A

Protein molecule liberated from intact living and lysed bacteria

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16
Q

Exotoxins are _______

A

Antigenic

- elicit protective antitoxic antibodies

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17
Q

Toxoids

A

Nontoxic immunizing agents that exotoxins can be converted into via treatment with formalin

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18
Q

3 roles of exotoxin in disease

A
  • ingestion of preformed toxin (botulism)
  • colonization of wound or surface followed by toxin production (cholera, diptheria)
  • exotoxin produced by bacteria in tissues to aid growth and spread (c. perfringens)
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19
Q

A-B exotoxin

A

Intracellular acting

  • B portion mediates binding to a specific host cell receptor
  • after binding to host cell, A portion is translocated into host cells = biological activity against an intracellular target
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20
Q

The B portion can be used as a _____

A

Toxoid

- if you block the binding, then you prevent the pathology

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21
Q

Membrane disrupting

A

Cause damage/disruption of plasma membranes = osmotic lysis and cell death
- known to cause damage to host tissues and contribute to virulence

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22
Q

Membrane disrupting were originally termed _______

A

Hemolysins

- lysis of RBC is easily detected, but cytotoxin is a more appropriate term

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23
Q

3 types of membrane disrupting toxins

A
  • enzymes that hydrolyze phospholipids (phospholipase, sphingomyelinase)
  • toxins with detergent-like surfactant activity that disrupt by membrane solubilization
  • pore forming toxins (common) = form hydrophilic pore
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24
Q

Superantigens

A

Toxins that bind directly to MHC 2 on macrophages and form a crosslink with TCRs

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25
Q

Crosslinking of superantigens causes

A

Stimulation of up to 1 in 5 T cells (massive overstimulation)

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26
Q

What is the result of excessive T cell stimulation?

A

Excessive IL-2 production

  • causes nausea, malaise, fever
  • stimulation of other cytokines by IL-2 leads to shock
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27
Q

Superantigens cause a ______ which leads to _______

A

localized infection; powerful systemic side effects

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28
Q

Extracellular enzymes

A

Break down host macromolecules

  • important role in disease development by providing a source of carbon and energy, or aid in dissemination
  • cause excessive tissue damage
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29
Q

Coagulase

A

Extracellular enzyme that clots fibrin, thus protecting the bacteria
- cell free or surface bound forms

30
Q

Endotoxin

A

LPS produced by pathogenic and nonpathogenic gram-neg bacteria

31
Q

What is an endotoxin produced in gram-pos bacteria?

A

Peptidoglycan, teichoic acids, or a combo

32
Q

What is the toxic portion of LPS?

A

Lipid A

- is not exposed until bacteria is lysed

33
Q

Method of bacteria lysis

A

Released LPS is bound by LPS binding proteins in plasma —> binds to CD14 –> CD14-LPS complex binds to TLR4 on macro/monocytes –> macrophages release cytokines = prostaglandin and leukotriene release –> complement and coagulation cascades are activated

34
Q

Bacterial sepsis

A

Inflammatory response is triggered throughout the body and septic (endotoxic) shock occurs when bacterial products reach high enough levels in the blood
- must trigger complement activation, cytokine release, and coagulation cascade activation throughout the body

35
Q

Limulus amebocyte lysate assay

A

Determines amount of endotoxin by detecting nanogram amounts

- endotoxin reacts with proteins from horseshoe crab blood cells to produce a gel

36
Q

TLR2 causes septic shock response to _____

A

Gram-positive bacteria

- binds to lipoproteins/teichoic acids

37
Q

Host damage is caused during invasion by either _____

A
  • direct disruption of function

- an exaggerated immune response that compromises tissue function or homeostasis (manifests as inflammation)

38
Q

FIPs

A

Facultative intracellular parasites

  • are not confined to cells
  • could multiply in professional phagocytes
  • may survive in intracellular state of equilibrium with phagocytes (ex: salmonella, brucella, mycobacterium)
39
Q

OIPs

A

Obligate intracellular parasites

  • can only propagate inside host cells
  • chlamydia, rickettsia
40
Q

Extracellular parasites

A

Cause tissue damage while they are outside phagocytes and other cells
- do not have ability to survive long periods in cells (have mechanisms to prevent phagocytosis)

41
Q

Flagella

A

Adapted for low viscosity fluids

- work best in urinary, GIT

42
Q

Other types of motility

A

Corkscrew, gliding motility

43
Q

Chemotaxis

A

Directional swimming using a gradient (esp nutrients)

44
Q

Rotation of flagella toward a stimulus

A

Peritrichous flagella twist together, and rotate as one large propeller in a counterclockwise direction

45
Q

How do flagella rotate in a clockwise direction?

A

Flagella spread apart, and the force pulls the cell in many directions = tumbling motion to occur

46
Q

Fimbriae

A

Attachment receptors are usually carb residues of glycoproteins or glycolipids

  • attachment is more fragile
  • highly specific binding, mediated by adhesins
  • could be blocked by antibodies
  • specific for host tissue type/location
47
Q

Monomeric protein adhesins

A

Mediated by cell surface proteins

  • tighter binding to host cell
  • may recognize proteins on host cell surface, may follow looser fimbrial attachment
48
Q

______ mediate attachment

A

Fimbriae

49
Q

Bacterial-mediated host cell invasion

A

Zippering or triggering

  • following attachment, pathogens cause changes in host cell cytoskeleton (actin) that cause pathogen internalization
  • some utilize actin fibers intracellularly to transcytose
  • invasins may mediate uptake of bacteria into professional phagocytes that bypasses normal phagosome formation
50
Q

Zippering

A

Bacteria present ligands on their surface, allowing them to bind to host cells and initiate entry process
- similar to FcR and CR3 mediated phagocytosis

51
Q

Triggering

A

Bacteria inject effectors into host cells via T3SS to regulate phagocytosis

52
Q

Manipulation of host cell functions

A

Bacterial pathogens are manipulative of host cell functions
- extra and intracellular pathogens will cause host cells to perform functions favorable to the pathogen (use their own proteins to manipulate the environment)

53
Q

TTSS

A

Specialized type 3 secretion system that forms a needle-like structure that injects effector proteins directly into the host cell cytoplasm

  • could serve as receptors in host membrane for bacterial attachment
  • could mobilize cytoskeleton to cause phagocytosis
  • could induce or prevent apoptosis
54
Q

TTSS forms a direct connection between

A

The cytoplasm of the bacteria and the cytoplasm of the host

- only produced in the course of infection

55
Q

Host cytoplasm is a very ______ environment

A

Nutrient-rich

  • extracellular pathogens will lyse host cells to obtain nutrients
  • intracellular pathogens will escape from phagosomes or modify vacuole to get nutrients thru the cytoplasm
56
Q

Why are host tissues low in iron?

A

It is usually bound to transferrin, lactoferrin, ferritin, and heme

57
Q

Iron is part of the ______

A

Non-specific immune response

- it should not be freely available in the body

58
Q

Siderophores

A

Low MW compounds that chelate iron with very high affinity

- secreted and taken up by bacterial surface receptors

59
Q

What is one method of iron uptake by bacteria?

A

Direct binding of host transferrin, lactoferrin, ferritin, or heme by bacterial surface receptors

60
Q

Serum resistance

A

Ability to prevent bacterial lysis by the C5b-C9 membrane attack complex

61
Q

How does the capsule mediate resistance to complement

A
  • preventing C3b binding and opsonization

- promoting C3bH complex formation instead of C3bBb (mediated by sialic acid in capsule)

62
Q

How does LPS mediate resistance to complement

A

Binds C3b and C5b

63
Q

How does O polysaccharide mediate resistance to complement

A
  • sialic acid attached to promote C3bH formation

- long O polysaccharide side chains that prevent MAC killing after C5b binds

64
Q

What are the 3 components of serum resistance?

A
  • capsule
  • LPS and O polysaccharide
  • S-layer (same effect as capsule, but is a protein)
65
Q

Extracellular products that resist opsonization/phagocytosis

A
  • enzymes that inactivate C5a chemoattractant
  • toxins that kill phagocytes
  • inhibit migration, or reduce oxidative burst
66
Q

3 strategies for surviving phagocytosis

A
  • escape from phagosome before fusion with lysosome
  • prevent phagosome-lysosome fusion
  • express factors that allow survival in harsh phagolysosome conditions
67
Q

Evading antibody response

A
  • slgA proteases (human pathogens)
  • phase variation or antigenic switching
  • masking
68
Q

Virulence gene regulation

A

Regulon-coordinated control of group of virulence factors that are activated or deactivated in response to environmental signal
- allows bacterial pathogens to adapt to varying host conditions

69
Q

What triggers virulence gene expression?

A

Triggered when a pathogen senses environmental cues from the host environment
- ex: pH, iron concentration

70
Q

Quorum sensing

A

Triggers virulence gene expression when a pathogen detects sufficient bacterial numbers

  • bacteria with quorum sensing ability secrete a small molecule –> when the molecule reaches a critical concentration gene expression is stimulated
  • sometimes regulates virulence genes
71
Q

Mutations in regulatory genes

A

Can either deactivate multiple virulence genes or cause inappropriate expression

72
Q

If little or no tissue invasion is involved, _____ manipulate the host to the bacteria’s advantage

A

Toxins

Infectious Agents (44 decks)

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