Host Microbe Interactions Flashcards
Immuncompromised
What are they most affected by?
- Malnutrition
- Cancer/AIDS
- Genetics
- Surgery / Wounds
- Substances
- Immunosuppressants
Disbiosis
Imbalance of microbiota
Microbiota
What benefits do they bring?
- Covering Binding sites
- Toxins
- Nutrient hoarding
- Immune system activation
- Oral tolerance
Microbiome
Composition
- @ Birth
- Breast milk
- Physical state
Microbiota
Oral Tolerance
- Teaching immune sys which microbes safe in food + environ and not atk
MB
Hygiene Hypothesis
Too little exposure to antigens leads to higher occurance of allergies
Colonization
establishment and growth of colonies
Infection
- Pathogens colonating
- First step of primary infection –> Exponential growth
Infection types
Subclinical
No symptoms
Infection Types
Infectious
Lowered host fuctions
Characteristics of Infections
Communicable or Contagious
- Can spread from host to host
Infectious Dose
- Enough microbes to cause an infection
- ID50 = enough to cause 50% of the population to become infected
Illness Progression
Inoculation
- Time between onset and first symptoms
Illness Progression
Illness
- First sign of symptoms
Illness Progression
Prodromal
- Vague symptoms
Illness Progression
Convalescence
- Body recovered from illness and memory cells made
Types of infections
Acute
- Quick infection that goes away quickly
Types of Illness
Chronic
- Slower time
- Illness phase lasts a long time/ forever
Types of Illness
Latent
- Microbe remains in tissue until immune system weakened or compromised to attack again
Distribution of Infection
-emia
- blood-based infection
- if bacteremia –> sepsis
Disease
- Body cell Damage
Signs
- Measureable and objective evidence
Symptoms
- subjective and what patient feels
Koch’s postulates
- One microbe causes 1 disease
1. Microorganism in every case
2. Pure culture
3. Same disease in all hosts
4. Can recover
Molecular Kochs
- Studies virulence
Pathogenicity
What is it
- Ability for pathogen to cause a disease
Pathogenicity
Virulence
Degree of pathogenicity
Pathogenicity
Virulence Factors
What contributes to higher Pathogenicity
Pathogenicity
What are some methods for it to occur?
- Producing ingesible toxins
- Colonize on mucous membrane to give toxins
- Invade tissue and deliver toxins(or not!)
Pathogenicity
Balanced Pathogenicity
Has to balance virulence while keeping host alive
Establishing Infection
Adhesins
- Attach to host cell receptors
- species specific
Establishing Infection
Siderphores
- Attach to iron
- Compete with lactoferrin and transferrin
Establishing Infection - Avoiding Ig
Pili Turnover
- Change pili so they cant be recognized
Establishing Infection - Avoiding Ig
Antigenic Variation
- Change antigen to allow for reduced binding
Establishing Infection - Avoiding Ig
IgA proteases
Destroy IgA to avoid recognition on mucous membranes
Establishing Infection - Avoiding Immune System
Avoiding Phages
- C5 peptidase
- Membrane Damaging Toxins
- Allowing for not recognition or attachments
Establishing Infection - Avoiding Immune System
M protein
In cell wall of S pyrogenes –> No functioning C3b
Establishing Infection - Avoiding Immune System
Capsules
no C3b –> No opsonization
Establishing Infection - Avoiding Immune System
Fc receptors
Take some for themselves so they can’t be recognized by cells
Establishing Infection - Avoiding Immune System by using Macrophages
Serum-resistant bacteria
- bind to complement proteins to inactivate them
Establishing Infection - Host Damage
Effector Proteins
Disrupt cell cytoskeleton
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
Establishing Infection - Host Damage
Direct Uptake
- Endocytosis
Establishing Infection - Host Damage
Membrane Ruffling
- ruffles to do direct uptake
Establishing Infection - New Host
How can they get in?
- Mucous Membranes = exploiting antigen-sampling process
- Skin = deep injury
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
Establishing Infection - New Host
What do Exotoxins(direct) exploit with mucous membranes?
- M cells
- Alveolar Macrophages
Establishing Infection - Host Damage
Direct vs Indirect
Toxins vs immune system
Establishing Infection - Host Damage
Exotoxins(Indirect)
- Neuro-; Entero-; Cyto-
- Traits:
- Gram + and -
- Heat inactivated
Types of Indirect exotoxins
A-B
- A = toxin
- B = binding end
Types Indirect Exotoxins
Membrane Damaging Toxins
- cytotoxins
- disrupt cytoplasmic membrane
Membrane Damaging Toxins
Phospholipases
- Hydrolyze phospholipids
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
Establishing Infection - Host Damage
Endotoxins
- Made from Gram
- and can do local or systematic
- Lipid A from LPS
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
