Pathogen Host Interaction and Disease Process Flashcards

1
Q

Host provides what for bacteria

A
  • Physical requirements

- Chemical requirements

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2
Q

Bacterial flora

A

Different in different locations

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3
Q

Where is there no natural bacterial flora

A

Internal organs, lymph, blood, or nerve tissue

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4
Q

Types of interactions between host and bacteria

A
  • Mutualism (symbiosis)
  • Commensalism
  • Parasitism
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5
Q

Commensals

A

Don’t harm but can help through bacterial antagonism

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6
Q

Bacterial antagonism

A

Compete for attachment nutrients or produce substances that inhibit other bacteria

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7
Q

Colonization Resistance

A

Concept used to prevent bacterial infections or diseases (probiotics)

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8
Q

Probiotics

A

Beneficial bacteria through competitive exclusion/ bacterial antagonism

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9
Q

Saprophyte

A

Organisms that don’t cause disease

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10
Q

Etiology

A

Cause of disease

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11
Q

Koch’s postulates

A
  1. Pathogen must be present if there is disease
  2. Pathogen must be isolated from host and grown in culture
  3. Pathogen must cause disease when inoculated into host
  4. Pathogen must be recover from inoculated host
    * exceptions to these rules
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12
Q

Molecular Postulates

A

Gene level

  1. Virulence gene or product found in pathogenic strains
  2. loss of virulence gene should convert to nonpathogenic strains
  3. Incorporation of virulence gene should convert nonpatho to pathogenic strain
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13
Q

Pathogenesis

A

Process in which pathogen causes disease

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14
Q

Pathogenicity

A

Capacity of an organism to cause disease

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15
Q

Virulence

A

Relative pathogenecity

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16
Q

Virulence factors

A

Substances contained in or secreted by the bacteria that damage the host

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17
Q

Attenuation

A

Reduction in virulence

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18
Q

Invasiveness

A

Ability to enter, establish and spread in the body

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19
Q

Primary pathogen

A

Causes disease on its own

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20
Q

Secondary pathogen

A

Follows a primary pathogen and on its own, may or may not, cause disease

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21
Q

Opportunistic pathogen

A

Causes disease only when conditions are favorable

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22
Q

Obligate intracellular pathogen

A

Grows and multiplies only inside cells

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23
Q

Facultative intracellular pathogen

A

Grows and multiplies inside and outside cells

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24
Q

Mechanisms of intracellular survival

A
  1. Escape phagosome
  2. Inhibit phagosome-lysosome fusion
  3. Survive harsh conditions
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25
Infection
Invasion or colonization by a pathogen may not result in disease
26
Disease
Change from a state of health
27
Infectious disease
Caused by a microorganism
28
Contagious disease
Spread readily by contact
29
Primary infection
Infection in a previously healthy host
30
Secondary infection
Occurs along or following an infection
31
Exogenous infection
Bacteria originate outside of animal
32
Endogenous infection
Bacteria originate within the animal
33
Latent infection
Pathogen remains inactive until the conditions are favorable
34
Zoonotic infection
Animal infects human
35
Nosocomial infection
Acquired in hospital
36
Sporadic disease
Occurs occasionally
37
Endemic disease
Consistently present in a population
38
Epidemic disease
Occurs in a large number of individuals in a population
39
Pandemic
Worldwide
40
Peracute
Higher degree of acute disease
41
Acute
Rapid onset, usually sever and last for short period of time
42
Chronic
Slow onset, less severe lasts longer
43
Subacute or subclinical
Mild with no overt signs or symptoms
44
Localized
Confined to small area
45
Systemic
Spreads through body via blood or lymph
46
Focal infection
Bacteria from local infection enter lymph or blood to set up local infection in other parts of the body
47
Bactermia
Bacteria circulating in blood
48
Septicemia
Bacteria multiplying in the blood
49
Toxemia
Toxin is circulating in the blood
50
Illness
Disease state see signs and symptoms
51
Symptoms
Effects of disease from patient
52
Signs
Effects observed from pt
53
Convalescence
Period of recovery
54
Requirements for infection
- Enter host - Evade or compromise host defenses - Multiply and get established - Damage host
55
Portals of entry
1. Skin 2 Mucous membrane 3. Direct deposit below skin or mucous membrane
56
Modes of infection
- Ingestion - Inhalation - Venereal - Vector-born - Direct entry
57
Colonization
Growth after attachment
58
Invasion
Internal spread beyond site of entry
59
Quorum sensing
Cell to cell communication to control cell density mediated by small molecules that once at high enough numbers virulence genes are expressed
60
Mechanisms of invasion
- Enzymes (proteases, hyaluronidase, collagenase) | - Penetration of mucous membranes between cells (endocytosis, M cells)
61
Ways to cause cell death
- Disrupt cell membrane - Inhibit protein synthesis - Cell lysis by intracellular bacteria - Recruitment of NK cells
62
Hyaluronidase
Break down hyaluronic acid in cell matrix
63
Mechanisms of adherence to host cells
- Pili adhesions - Outer membrane proteins adhesions - Capsular attachment
64
Coagulase
Causes fibrin formation and protects bacteria from host
65
Streptokinase
Fibrinolytic enzyme breaks down blood clots
66
Toxins
Cause damage to tissues or trigger immune response that causes damage. Endotoxin or exotoxins
67
Exotoxins
Produced by both Gram positive and negative. Genes usually carried on bacteriophages or plasmids. Many have enzyme activity. Cell secretes it
68
Endotoxins
Only gram negative make. Part of the cell
69
Groups of exotoxins based on mechanism of action
- Cell membrane disruption - protein synthesis inhibitor - Second messenger pathway disruption - Superantigens - Proteases
70
What are the names of exotoxins based off of
- Target cell (hemolysin) - Target tissue or system (neurotoxin) - Based on disease (tetanus toxin) - Named after bacteria (botulinum)
71
Toxins that cause cell membrane damage
- Hemolysins - Leukotoxins - Cytotoxins - Pore forming toxins
72
Toxins that disrupt protein synthesis
Cytotoxic - Shiga toxins - Diphtheria toxin
73
Toxins that disrupt second messenger path
Interfere with cAMP and cGMP | -Enterotoxins
74
Toxins that form superantigens
Activate immune system in intense way. Stimulate T cells and release cytokines - S aureus-toxic shock protein - Enterotoxins in food poisening
75
Protease toxins
- Tetanus toxin from C. tetani | - Botulinum from C. botulinum
76
Types of exotoxins based on structure
A-B toxin | RTX toxin
77
A-B toxins
- Shiga toxin - Enterotoxin - Neurotoxins
78
Shiga toxin
Inhibit protein synthesis made by Shigella dysenteriae and some E. coli A-B toxin
79
Enterotoxins
Has enzyme ADP-ribosyl transferase and causes diarrhea found in E. coli and Salmonella enterica. Disrupts second messengers. A-B toxin
80
Neurotoxins
A-B toxin. Proteases that block release of neurotransmitters - Tetanus toxin - Botulinum toxin
81
RTX toxin
Produced by some gram negative. Have repeated glycine or aspartic rich sequences - Hemolysins - Leukotoxins - Etc
82
Targets for diagnosis by PCR
Virulence genes
83
Pathogenicity islands
Cluster of multiple genes that code for virulence factors. Don't see in nonpathogenic bacteria. Inherit through horizontal transmission
84
Endotoxin
Lipopolysaccharide from gram negative cell
85
Major effects of endotoxins
- Fever (IL 1 and prostaglandins) - Intravascular coagulation - Shock
86
Disseminated intravascular coagulation
Activation of blood clotting proteins that block capillary blood flow resulting in decreased blood supply and tissue necrosis
87
Endotoxic shock
- Loss of blood pressure - release TNF causes damaged capillaries - Increased permeability and loss of fluids
88
Assay for endotoxins
Use limulus amoebocyte lysate that forms a gel in the presence of endotoxin and is very sensitive
89
When is Endotoxin secreted
Released upon cell death
90
Portals of exit
Related to site of infection and same as the portals of entry