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Microbiology > Block 2.4 Host-Microbe Relationship > Flashcards

Block 2.4 Host-Microbe Relationship Flashcards

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1
Q

Types of Host-Microbe Relationships

A
  1. Symbiosis
  2. Normal Flora
  3. Commensalism
  4. Mutualism
  5. Opportunism
  6. Parasitism
  7. Vector
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2
Q

Symbiosis

A

Close association/interaction of 2 different organisms living together

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3
Q

Normal Flora

A

Microorganisms normal found in/on body WITHOUT disease

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4
Q

Characteristics of Normal Flora

A
  1. Resident vs. Transient
  2. Nature & Variety of microbes distinctive for different parts of body
  3. Normal Flora in 1 area can cause infection in another area
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5
Q

Normal Flora Chart

A

Mouth > GI > Vagina > Skin > Urethra & Nose

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6
Q

Commensalism

A

Relation between organisms where 1 benefits, and the other neither benefitted nor harmed

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7
Q

Mutualism

A

Microbe AND Host benefit

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8
Q

Opportunism

A

Host-Microbe relationship is altered because Resident Flora shows disease traits

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9
Q

Causes of Opportunism

A
  1. Prolonged antibiotic therapy alters flora
  2. Traumatic Injury, Surgery
  3. Immunity Compromise
  4. Hormonal/Chemical Changes
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10
Q

Parasitism

A

Microorganism lives in host & Host is harmed

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11
Q

Vector

A

Carrier of microbes from one host to another

-The Microbe Taxi

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12
Q

Examples of Vectors

A
  1. Insects & Other small animals

2. Inanimate Articles (fomites)

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13
Q

Infectious Disease

A
  • Growth/Spread of pathogen in/on a host

- Results in injury to the host

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14
Q

Pathogen

A

Microbe capable of causing disease by:

  1. Invading tissues
  2. Producing Toxins
  3. Both
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15
Q

Virulence

A

The DEGREE of pathogenicity

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16
Q

2 Categories of Virulence

A
  1. Infectivity- how EASILY microbe survives normal host defenses & establishes infection
  2. Severity- DAMAGE it causes the host
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17
Q

Modes of Transmission

A
  1. Direct Contact- w/ or w/out penetration into skin or mucous membranes
  2. Inhalation- droplets of particles in the air
  3. Ingestion- food/water
  4. Parenteral- direct contamination of blood, body fluids(by animal vectors & nonsterile needles)
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18
Q

Virulence Factors

A
  1. Attachment & Establishment Factors
  2. Antiphagocytic Factors
  3. Invasive Enzymes
  4. Exotoxins
  5. Endotoxins
  6. Genetic Alterations
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19
Q

2 Attachment & Establishment Factors

A
  1. Portal of Entry

2. Attachment

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20
Q

Portal of Entry

A
  1. Organism must enter correct body part (ingested vs inhaled vs wound)
  2. Overcome Local Defenses
  3. Find the best environment for growth/survival
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21
Q

Attachment of Microbe to Host (5)

A

Attachment is required to establish an infection
1. Fibrae
-attach to specific receptor sites on specific tissue
2. Surface Chemicals-
-dissolve cell covering / aids chemical attachment
3. Adhesive Matrix Molecules
-produce BIOFILMS…“protection” for bacteria in harsh
human environments
4. Quantity
-Min # of microbes required for infection
5. Quorum-Sensing Regulators
-Chemicals that: 1) Pause the microbe’s disease-actions
until microbe quantity is met & 2) Switch on the
disease actions all at once (Red Light, Green Light)

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22
Q

Antiphagocytic Factor Action

A

Prevent microbe from being englufed/destroyed by WBCs

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23
Q

Examples of Antiphagocytic Factors (4)

A
  1. Capsule
  2. Leukocidin- destroy WBCs
    • Staph, Strep, & Bacili
  3. Coagulase- makes fibrin clot to form around microbes
    • Staph aureus
  4. Survive Phagocytosis
    • Mycobacteria, Gonococcus, Listeria
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24
Q

What are Invasive Enzymes?

A

Factors that promote invasion & spread of pathogen in/on tissue

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25
Action of Invasion Factors
Allow pathogens to invade tissue or site of infection to spread
26
Examples of Invasive Factors (8)
1. Collagenase 2. Lecithinase 3. Hyaluronidase 4. Fibrinolysin & Streptokinase 5. Hemolysins 6. Lipase 7. Proteases 8. Super Antigens
27
Collagenase Function
IF- destroys tissue integrity by breaking down collagen
28
Lecithinase Function
IF- destroys RBC & other tissue's membranes
29
Hyaluronidase Function (& types)
IF- breaks down hyaluronic acid in cell membranes | -Staph, Strep, & Clostridium perfringens
30
Fribrinolysin & Streptokinase Functions
IF- lyses fibrin in blood clots which prevents isolation of infection
31
Hemolysin Functions (& examples)
IF- dissolve RBC membranes | -Staph, Strep, Clostridium perfingens
32
Lipase Function
IF- digests lipids allowing bacteria to enter
33
Protease Function
IF- digest proteins (IgA) so bacteria does not become opsonized
34
Super Antigen Function
IF- cause exacerbated immune/inflammatory response
35
What are Exotoxins
1. Proteins excreted from the cell (cytolytic & receptor- binding 2. Dimeric- A&B subunits; allows entry into cells 3. Affects only specific and limited tissues 4. Superantigens = special group of exotoxins 5. Has Genetic Code- coded on the plasmid or during the lysogenic phase
36
Exotoxin Function
1. Cause specific & widespread biological effects on body 2. Highly Potent 3. Makes protective antibodies
37
Examples of Exotoxins (5)
1. Tetanus neurotoxin 2. Staphylococcal enterotoxin 3. Cholera toxin 4. Diphtheria Toxin 5. Streptococcal erythrogenic toxin
38
What does Tetanus neurotoxin do?
1. Attacks motor nerves | 2. Triggers involuntary muscle contractions
39
What does Staphylococcal enterotoxin cause?
Diarrhea & Vomiting
40
What does Cholera toxin cause?
Massive Diarrhea
41
What does Diphtheria toxin do?
Interferes with protein production in bronchial epithelial cells
42
What does Diphtheria cause?
1. Mucous production 2. Fibrous blockage of respiratory tract 3. Inactivation of protein production in heart muscles
43
What does Streptococcal erythrogenic toxin cause?
Scarlet fever rash
44
What special feature do Endotoxins contain?
Lipid A- lipopolysaccharide part of Gram Negative cell walls
45
When is Lipid A released?
Upon disintegration of the cell
46
What does Lipid A do?
1. Binds to CD14 & TLR4 on macrophages & B-cells 2. Stimulates production/release of acute cytokines - I.e. triggers WBCs to induce fever, pain, hemorrhage, etc
47
Are endotoxins potent?
No per unit weight, but high levels of endotoxins can trigger huge effects (shock & death)
48
Do endotoxins make protective antibodies?
No
49
Example of Endotoxin (1)
Gram Negative bacillus cell wall sloughs off or disentigrates
50
Difference between Exotoxins and Endotoxins
- Exotoxins release toxins as part of their growth, are normally Gram positive, and make antibodies - Endotoxins release their lipid A toxins once they die, are Gram negative, and do not make antibodies
51
3 Ways Microbes undergo Genetic Alteration
1. Plasmid 2. Lysogeny 3. Gene Recombination
52
What is a Plasmid
- A small, separate piece of extrachromosomal DNA in Bacteria - Main form of bacterial virulence
53
What do plasmids code for?
Exotoxins, antibiotic resistance, invasive enzymes, etc (ways to infect the host)
54
How are plasmids transmitted?
1. Passed to daughter cells during cell division | 2. Passed to other bacteria during conjugation
55
What is Lysogeny
Viral DNA incorporated in Bacterial DNA
56
What does lysogen code for?
Exotoxins & invasive enzymes
57
How is lysogen transmitted?
- Starts by versus infection bacteria | - Then passed to daughter cells during bacterial division
58
What is Genetic Recombination?
Pieces of genetic info from one organism are incorporated into genetic info of another organism
59
What does Genetic Recombination result in?
1. New Types of antigens- influenza virus | 2. Increased resistance to antibiotics
60
How do bacteria gain antibiotic resistance?
1. Mutated Genes 2. Plasmid encoded genes 3. Lysogenic virus
61
What does antibiotic resistance lead to?
1. Survival of microbe 2. Increasing numbers of microbe 3. Disease spreads to other places
62
3 Antimicrobial Resistance Situations
1. Beta Lactamase 2. MRSA: methicillin-resistance staph aureus 3. CRE-CPE: carbapenemase-resistant/producing enterobacteria
63
What is Beta Lactamase?
Bacterial enzyme that inactivates beta-lactam antimicrobics
64
What are beta-lactam antimicrobics
1. Penecillin 2. Cephalosporin 3. Carbapenem 4. Monobactam classes
65
What produces beta lactamase?
Plasmid-endcoded gene carried by enterobacteria (staph, n. gonorrhoeae, & haqmophilus influenza)
66
What do you do if a bacteria is beta-lactamase positive?
Treat with a beta-lactamase resistant antibiotic (not penicillin)
67
What is Extended Spectrum Beta-Lactamase (ESBL)?
Version of beta-lactamase that affects a Larger Group of antibiotics (that aren't normally affected by plain old beta-lactamase) -ESBL is way more intense
68
What is MRSA?
- Mutated mecA gene - Resistant to all beta-lactam antibiotics (regardless of lab results) - Makes PBP
69
What are CRE/CPE
- Mutated genes for outer membrane porins (pore proteins) | - A type of beta-lactamase
70
How is CRE/CPE carried?
By plasmids
71
What does CRE/CPE result in?
1. Loss of drug diffusion into periplasm | 2. Loss of cross-linking of PBP
72
4 Non-Specific (Innate) Host Factors
1. Physical/Mechanical Barriers 2. Chemical Barriers 3. Phagocytosis 4. Inflammation
73
5 Physical Barriers to disease
1. Skin- prevents entry 2. Mucous Membranes- sticky; traps pathogen 3. Respiratory Cilia- move pathogens to throat... swallowed 4. Peristalsis- moves gut contents...prevents overgrowth 5. Normal Flora- occupy attachment sites & compete for nutrients
74
5 Chemical Barriers to disease
1. Acid pH 2. Bile salts 3. Lysozymes 4. Antimicrobial chemicals from normal flora 5. Interferons
75
What does Acidic pH do?
- Stomach, skin, vagina, urine - Denatures organisms EXCEPT: 1. Typhoid & Tubercule bacilli 2. Protozoan cysts 3. Polio 4. Hepatitis A Virus
76
What do bile salts do?
- Intestines | - Inhibit microbes
77
What do Lysozomes do?
- Tears & Saliva | - Digest Gram POSITIVE cell walls
78
What are interferons?
- Type of lymphokine | - Proteins made in response to invasion of viruses
79
What do interferons do?
- Local Defense against certain viruses - Make inhibiting substances that "interfere" with viral reproduction - Tells cells to make antiviral proteins
80
What 3 types of cells phagocytize
1. Polymorphonuclear Leukocytes 2. Monocytes 3. Macrophages
81
Problem with phagocytosis
Can cause local tissue damage due to egestion of waste materials
82
When does inflammation occur?
After mechanical injury or exposure to certain chemicals
83
Main function of inflammation
Limit the extent of injury
84
Inflammation Process
1. Increases capillary permeability... fluid accumulates & large influx of phagocytes & WBCs 2. Neutrophils & macrophages phagocytize pathogen 3. Fibrin clot is formed to enclose pus (macrophages, dead microbes, dead tissue, & plasma)
85
2 Specific Host Factors
1. Cell Mediated Immunity | 2. Antibodies & Complement
86
Cell-Mediated Immunity Process
1. Antigen stimulates release of lymphokines | 2. Lymphokines enhance phagocytosis & killing
87
What do antibodies do?
1. Neutralize the antigen | 2. Opsonize the antigen
88
What does complement do?
1. Assists antibody to neutralize or lyse the bacteria 2. Chemotaxis of Macrophages 3. Opsonizing agents

Microbiology (3 decks)

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