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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
Q

Action of Invasion Factors

A

Allow pathogens to invade tissue or site of infection to spread

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26
Q

Examples of Invasive Factors (8)

A
  1. Collagenase
  2. Lecithinase
  3. Hyaluronidase
  4. Fibrinolysin & Streptokinase
  5. Hemolysins
  6. Lipase
  7. Proteases
  8. Super Antigens
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27
Q

Collagenase Function

A

IF- destroys tissue integrity by breaking down collagen

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28
Q

Lecithinase Function

A

IF- destroys RBC & other tissue’s membranes

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29
Q

Hyaluronidase Function (& types)

A

IF- breaks down hyaluronic acid in cell membranes

-Staph, Strep, & Clostridium perfringens

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30
Q

Fribrinolysin & Streptokinase Functions

A

IF- lyses fibrin in blood clots which prevents isolation of infection

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31
Q

Hemolysin Functions (& examples)

A

IF- dissolve RBC membranes

-Staph, Strep, Clostridium perfingens

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32
Q

Lipase Function

A

IF- digests lipids allowing bacteria to enter

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33
Q

Protease Function

A

IF- digest proteins (IgA) so bacteria does not become opsonized

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34
Q

Super Antigen Function

A

IF- cause exacerbated immune/inflammatory response

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35
Q

What are Exotoxins

A
  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
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36
Q

Exotoxin Function

A
  1. Cause specific & widespread biological effects on body
  2. Highly Potent
  3. Makes protective antibodies
37
Q

Examples of Exotoxins (5)

A
  1. Tetanus neurotoxin
  2. Staphylococcal enterotoxin
  3. Cholera toxin
  4. Diphtheria Toxin
  5. Streptococcal erythrogenic toxin
38
Q

What does Tetanus neurotoxin do?

A
  1. Attacks motor nerves

2. Triggers involuntary muscle contractions

39
Q

What does Staphylococcal enterotoxin cause?

A

Diarrhea & Vomiting

40
Q

What does Cholera toxin cause?

A

Massive Diarrhea

41
Q

What does Diphtheria toxin do?

A

Interferes with protein production in bronchial epithelial cells

42
Q

What does Diphtheria cause?

A
  1. Mucous production
  2. Fibrous blockage of respiratory tract
  3. Inactivation of protein production in heart muscles
43
Q

What does Streptococcal erythrogenic toxin cause?

A

Scarlet fever rash

44
Q

What special feature do Endotoxins contain?

A

Lipid A- lipopolysaccharide part of Gram Negative cell walls

45
Q

When is Lipid A released?

A

Upon disintegration of the cell

46
Q

What does Lipid A do?

A
  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
Q

Are endotoxins potent?

A

No per unit weight, but high levels of endotoxins can trigger huge effects (shock & death)

48
Q

Do endotoxins make protective antibodies?

A

No

49
Q

Example of Endotoxin (1)

A

Gram Negative bacillus cell wall sloughs off or disentigrates

50
Q

Difference between Exotoxins and Endotoxins

A
  • 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
Q

3 Ways Microbes undergo Genetic Alteration

A
  1. Plasmid
  2. Lysogeny
  3. Gene Recombination
52
Q

What is a Plasmid

A
  • A small, separate piece of extrachromosomal DNA in Bacteria
  • Main form of bacterial virulence
53
Q

What do plasmids code for?

A

Exotoxins, antibiotic resistance, invasive enzymes, etc (ways to infect the host)

54
Q

How are plasmids transmitted?

A
  1. Passed to daughter cells during cell division

2. Passed to other bacteria during conjugation

55
Q

What is Lysogeny

A

Viral DNA incorporated in Bacterial DNA

56
Q

What does lysogen code for?

A

Exotoxins & invasive enzymes

57
Q

How is lysogen transmitted?

A
  • Starts by versus infection bacteria

- Then passed to daughter cells during bacterial division

58
Q

What is Genetic Recombination?

A

Pieces of genetic info from one organism are incorporated into genetic info of another organism

59
Q

What does Genetic Recombination result in?

A
  1. New Types of antigens- influenza virus

2. Increased resistance to antibiotics

60
Q

How do bacteria gain antibiotic resistance?

A
  1. Mutated Genes
  2. Plasmid encoded genes
  3. Lysogenic virus
61
Q

What does antibiotic resistance lead to?

A
  1. Survival of microbe
  2. Increasing numbers of microbe
  3. Disease spreads to other places
62
Q

3 Antimicrobial Resistance Situations

A
  1. Beta Lactamase
  2. MRSA: methicillin-resistance staph aureus
  3. CRE-CPE: carbapenemase-resistant/producing enterobacteria
63
Q

What is Beta Lactamase?

A

Bacterial enzyme that inactivates beta-lactam antimicrobics

64
Q

What are beta-lactam antimicrobics

A
  1. Penecillin
  2. Cephalosporin
  3. Carbapenem
  4. Monobactam classes
65
Q

What produces beta lactamase?

A

Plasmid-endcoded gene carried by enterobacteria (staph, n. gonorrhoeae, & haqmophilus influenza)

66
Q

What do you do if a bacteria is beta-lactamase positive?

A

Treat with a beta-lactamase resistant antibiotic (not penicillin)

67
Q

What is Extended Spectrum Beta-Lactamase (ESBL)?

A

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
Q

What is MRSA?

A
  • Mutated mecA gene
  • Resistant to all beta-lactam antibiotics (regardless of lab results)
  • Makes PBP
69
Q

What are CRE/CPE

A
  • Mutated genes for outer membrane porins (pore proteins)

- A type of beta-lactamase

70
Q

How is CRE/CPE carried?

A

By plasmids

71
Q

What does CRE/CPE result in?

A
  1. Loss of drug diffusion into periplasm

2. Loss of cross-linking of PBP

72
Q

4 Non-Specific (Innate) Host Factors

A
  1. Physical/Mechanical Barriers
  2. Chemical Barriers
  3. Phagocytosis
  4. Inflammation
73
Q

5 Physical Barriers to disease

A
  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
Q

5 Chemical Barriers to disease

A
  1. Acid pH
  2. Bile salts
  3. Lysozymes
  4. Antimicrobial chemicals from normal flora
  5. Interferons
75
Q

What does Acidic pH do?

A
  • Stomach, skin, vagina, urine
  • Denatures organisms EXCEPT:
    1. Typhoid & Tubercule bacilli
    2. Protozoan cysts
    3. Polio
    4. Hepatitis A Virus
76
Q

What do bile salts do?

A
  • Intestines

- Inhibit microbes

77
Q

What do Lysozomes do?

A
  • Tears & Saliva

- Digest Gram POSITIVE cell walls

78
Q

What are interferons?

A
  • Type of lymphokine

- Proteins made in response to invasion of viruses

79
Q

What do interferons do?

A
  • Local Defense against certain viruses
  • Make inhibiting substances that “interfere” with viral reproduction
  • Tells cells to make antiviral proteins
80
Q

What 3 types of cells phagocytize

A
  1. Polymorphonuclear Leukocytes
  2. Monocytes
  3. Macrophages
81
Q

Problem with phagocytosis

A

Can cause local tissue damage due to egestion of waste materials

82
Q

When does inflammation occur?

A

After mechanical injury or exposure to certain chemicals

83
Q

Main function of inflammation

A

Limit the extent of injury

84
Q

Inflammation Process

A
  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
Q

2 Specific Host Factors

A
  1. Cell Mediated Immunity

2. Antibodies & Complement

86
Q

Cell-Mediated Immunity Process

A
  1. Antigen stimulates release of lymphokines

2. Lymphokines enhance phagocytosis & killing

87
Q

What do antibodies do?

A
  1. Neutralize the antigen

2. Opsonize the antigen

88
Q

What does complement do?

A
  1. Assists antibody to neutralize or lyse the bacteria
  2. Chemotaxis of Macrophages
  3. Opsonizing agents

Microbiology (3 decks)

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