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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
Crosslinking of superantigens causes
Stimulation of up to 1 in 5 T cells (massive overstimulation)
26
What is the result of excessive T cell stimulation?
Excessive IL-2 production - causes nausea, malaise, fever - stimulation of other cytokines by IL-2 leads to shock
27
Superantigens cause a ______ which leads to _______
localized infection; powerful systemic side effects
28
Extracellular enzymes
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
29
Coagulase
Extracellular enzyme that clots fibrin, thus protecting the bacteria - cell free or surface bound forms
30
Endotoxin
LPS produced by pathogenic and nonpathogenic gram-neg bacteria
31
What is an endotoxin produced in gram-pos bacteria?
Peptidoglycan, teichoic acids, or a combo
32
What is the toxic portion of LPS?
Lipid A | - is not exposed until bacteria is lysed
33
Method of bacteria lysis
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
Bacterial sepsis
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
Limulus amebocyte lysate assay
Determines amount of endotoxin by detecting nanogram amounts | - endotoxin reacts with proteins from horseshoe crab blood cells to produce a gel
36
TLR2 causes septic shock response to _____
Gram-positive bacteria | - binds to lipoproteins/teichoic acids
37
Host damage is caused during invasion by either _____
- direct disruption of function | - an exaggerated immune response that compromises tissue function or homeostasis (manifests as inflammation)
38
FIPs
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
OIPs
Obligate intracellular parasites - can only propagate inside host cells - chlamydia, rickettsia
40
Extracellular parasites
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
Flagella
Adapted for low viscosity fluids | - work best in urinary, GIT
42
Other types of motility
Corkscrew, gliding motility
43
Chemotaxis
Directional swimming using a gradient (esp nutrients)
44
Rotation of flagella toward a stimulus
Peritrichous flagella twist together, and rotate as one large propeller in a counterclockwise direction
45
How do flagella rotate in a clockwise direction?
Flagella spread apart, and the force pulls the cell in many directions = tumbling motion to occur
46
Fimbriae
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
Monomeric protein adhesins
Mediated by cell surface proteins - tighter binding to host cell - may recognize proteins on host cell surface, may follow looser fimbrial attachment
48
______ mediate attachment
Fimbriae
49
Bacterial-mediated host cell invasion
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
Zippering
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
Triggering
Bacteria inject effectors into host cells via T3SS to regulate phagocytosis
52
Manipulation of host cell functions
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
TTSS
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
TTSS forms a direct connection between
The cytoplasm of the bacteria and the cytoplasm of the host | - only produced in the course of infection
55
Host cytoplasm is a very ______ environment
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
Why are host tissues low in iron?
It is usually bound to transferrin, lactoferrin, ferritin, and heme
57
Iron is part of the ______
Non-specific immune response | - it should not be freely available in the body
58
Siderophores
Low MW compounds that chelate iron with very high affinity | - secreted and taken up by bacterial surface receptors
59
What is one method of iron uptake by bacteria?
Direct binding of host transferrin, lactoferrin, ferritin, or heme by bacterial surface receptors
60
Serum resistance
Ability to prevent bacterial lysis by the C5b-C9 membrane attack complex
61
How does the capsule mediate resistance to complement
- preventing C3b binding and opsonization | - promoting C3bH complex formation instead of C3bBb (mediated by sialic acid in capsule)
62
How does LPS mediate resistance to complement
Binds C3b and C5b
63
How does O polysaccharide mediate resistance to complement
- sialic acid attached to promote C3bH formation | - long O polysaccharide side chains that prevent MAC killing after C5b binds
64
What are the 3 components of serum resistance?
- capsule - LPS and O polysaccharide - S-layer (same effect as capsule, but is a protein)
65
Extracellular products that resist opsonization/phagocytosis
- enzymes that inactivate C5a chemoattractant - toxins that kill phagocytes - inhibit migration, or reduce oxidative burst
66
3 strategies for surviving phagocytosis
- escape from phagosome before fusion with lysosome - prevent phagosome-lysosome fusion - express factors that allow survival in harsh phagolysosome conditions
67
Evading antibody response
- slgA proteases (human pathogens) - phase variation or antigenic switching - masking
68
Virulence gene regulation
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
What triggers virulence gene expression?
Triggered when a pathogen senses environmental cues from the host environment - ex: pH, iron concentration
70
Quorum sensing
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
Mutations in regulatory genes
Can either deactivate multiple virulence genes or cause inappropriate expression
72
If little or no tissue invasion is involved, _____ manipulate the host to the bacteria's advantage
Toxins

Infectious Agents (44 decks)

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