Host Microbe Interactions Flashcards
1
Q
Immuncompromised
What are they most affected by?
A
- Malnutrition
- Cancer/AIDS
- Genetics
- Surgery / Wounds
- Substances
- Immunosuppressants
2
Q
Disbiosis
A
Imbalance of microbiota
3
Q
Microbiota
What benefits do they bring?
A
- Covering Binding sites
- Toxins
- Nutrient hoarding
- Immune system activation
- Oral tolerance
4
Q
Microbiome
Composition
A
- @ Birth
- Breast milk
- Physical state
5
Q
Microbiota
Oral Tolerance
A
- Teaching immune sys which microbes safe in food + environ and not atk
6
Q
MB
Hygiene Hypothesis
A
Too little exposure to antigens leads to higher occurance of allergies
7
Q
Colonization
A
establishment and growth of colonies
8
Q
Infection
A
- Pathogens colonating
- First step of primary infection –> Exponential growth
9
Q
Infection types
Subclinical
A
No symptoms
10
Q
Infection Types
Infectious
A
Lowered host fuctions
11
Q
Characteristics of Infections
Communicable or Contagious
A
- Can spread from host to host
12
Q
Infectious Dose
A
- Enough microbes to cause an infection
- ID50 = enough to cause 50% of the population to become infected
13
Q
Illness Progression
Inoculation
A
- Time between onset and first symptoms
14
Q
Illness Progression
Illness
A
- First sign of symptoms
15
Q
Illness Progression
Prodromal
A
- Vague symptoms
16
Q
Illness Progression
Convalescence
A
- Body recovered from illness and memory cells made
17
Q
Types of infections
Acute
A
- Quick infection that goes away quickly
18
Q
Types of Illness
Chronic
A
- Slower time
- Illness phase lasts a long time/ forever
19
Q
Types of Illness
Latent
A
- Microbe remains in tissue until immune system weakened or compromised to attack again
20
Q
Distribution of Infection
-emia
A
- blood-based infection
- if bacteremia –> sepsis
21
Q
Disease
A
- Body cell Damage
22
Q
Signs
A
- Measureable and objective evidence
23
Q
Symptoms
A
- subjective and what patient feels
24
Q
Koch’s postulates
A
- One microbe causes 1 disease
1. Microorganism in every case
2. Pure culture
3. Same disease in all hosts
4. Can recover
25
Molecular Kochs
- Studies virulence
26
# Pathogenicity
What is it
- Ability for pathogen to cause a disease
27
# Pathogenicity
Virulence
Degree of pathogenicity
28
# Pathogenicity
Virulence Factors
What contributes to higher Pathogenicity
29
# Pathogenicity
What are some methods for it to occur?
1. Producing ingesible toxins
2. Colonize on mucous membrane to give toxins
3. Invade tissue and deliver toxins(or not!)
30
# Pathogenicity
Balanced Pathogenicity
Has to balance virulence while keeping host alive
31
# Establishing Infection
Adhesins
- Attach to host cell receptors
- species specific
32
# Establishing Infection
Siderphores
- Attach to iron
- Compete with lactoferrin and transferrin
33
# Establishing Infection - Avoiding Ig
Pili Turnover
- Change pili so they cant be recognized
34
# Establishing Infection - Avoiding Ig
Antigenic Variation
- Change antigen to allow for reduced binding
35
# Establishing Infection - Avoiding Ig
IgA proteases
Destroy IgA to avoid recognition on mucous membranes
36
# Establishing Infection - Avoiding Immune System
Avoiding Phages
1. C5 peptidase
2. Membrane Damaging Toxins
3. Allowing for not recognition or attachments
37
# Establishing Infection - Avoiding Immune System
M protein
In cell wall of S pyrogenes --> No functioning C3b
38
# Establishing Infection - Avoiding Immune System
Capsules
no C3b --> No opsonization
39
# Establishing Infection - Avoiding Immune System
Fc receptors
Take some for themselves so they can't be recognized by cells
40
# Establishing Infection - Avoiding Immune System by using Macrophages
Serum-resistant bacteria
- bind to complement proteins to inactivate them
41
# Establishing Infection - Host Damage
Effector Proteins
Disrupt cell cytoskeleton
42
# Establishing Infection - Host Damage
Type III Secretion System(Injectisomes)
- Only in Gram - cells
- activate with proteins in bacteria which disable cell membrane and deliver effector proteins
- allows uptake of bacteria
43
# Establishing Infection - Host Damage
Direct Uptake
- Endocytosis
44
# Establishing Infection - Host Damage
Membrane Ruffling
- ruffles to do direct uptake
45
# Establishing Infection - New Host
How can they get in?
- Mucous Membranes = exploiting antigen-sampling process
- Skin = deep injury
46
# Establishing Infection - Host Damage
Exotoxins(Direct)
- from outside body(pathogen parts?)
- from leaking tissue after bact lysis
- lnclude toxins and LPS and others
- can be local or systematic
47
# Establishing Infection - New Host
What do Exotoxins(direct) exploit with mucous membranes?
1. M cells
2. Alveolar Macrophages
48
# Establishing Infection - Host Damage
Direct vs Indirect
Toxins vs immune system
49
# Establishing Infection - Host Damage
Exotoxins(Indirect)
- Neuro-; Entero-; Cyto-
- Traits:
- Gram + and -
- Heat inactivated
50
# Types of Indirect exotoxins
A-B
- A = toxin
- B = binding end
51
# Types Indirect Exotoxins
Membrane Damaging Toxins
- cytotoxins
- disrupt cytoplasmic membrane
52
# Membrane Damaging Toxins
Phospholipases
- Hydrolyze phospholipids
53
# Indirect Exotoxin Types
Superantigens
- Higher Th
- Higher APCs
- Cytokine storms
-Connect MHC class II and T-cell
- higher IL 1,2, 6 and TNF a and gamma
54
# Establishing Infection - Host Damage
Endotoxins
- Made from Gram
- and can do local or systematic
- Lipid A from LPS
55
# Establishing Infection - Host Damage
How does Lipid A from LPS do it?
- release after cell lysis which leads to higher cytokines from T cells
- T-independent Antigen which allows for B cells to propagate IgM
- Immune response:
- Local is just an infection
- Sysytematic --> Septic and Endotoxic shock
