Host/Parasite Relationships- Bacterial Pathogenesis Flashcards Preview

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Flashcards in Host/Parasite Relationships- Bacterial Pathogenesis Deck (72):

What is an adhesin?

Host cell or microbial external structure (often antigen) that binds to a substrate surface on another cell


What is a biofilm?
Describe its structure.
What is the purpose of having this complex structure?

Bacteria binding to each other and to surfaces within a polysaccharide slime.

It is made of pillars of bacteria surrounded by water channels where they can get nutrients and allow toxins to diffuse out of biofilm

The structure allows the bacteria to be refractory to disinfectants and antibiotics


What is commensalism, parasitism and symbiosis?

Commensalism- bacteria live inside a host (benefit) and cause the host no harm (neutral)

Parasitism- bacteria benefit at the expense of the host

Symbiosis- both organisms benefit


What is a cytotoxin?

A substance from microorganisms that can damage the structure or function of somatic cells of the host


What is the difference between an endotoxin and exotoxin?

Endotoxin is LPS on G- bacteria that is released at cell destruction during the normal growth cycle

Exotoxin is a substance released by the bacteria into the host cell to damage the structure/function of the invaded cell


What host cell surface glycoprotein mediates non-specific adherence of some bacteria (like staph)?



What does it mean if something is pyogenic?

It stimulates the recruitment of PMN white cells (neutrophils, etc)


What are the three major types of bacterial/host associations?
Describe each.

1. Normal flora - symbiosis with the host aiding in digestion, production of vitamins (K) and protecting the host from colonization of pathogenic microbes
2. Pathogenic bacteria- cause disease in the host and cause inflammation
3. Opportunistic bacteria- cause disease in immunocompromised individuals (chemo, HIV, transplants)


What are the three things normal flora do that allow it to have a symbiotic relationship with the host?

1. Digest food
2. Synthesize vitamin K
3. Protect from colonization of pathogenic microbes


What are the four major "natural defense" barriers against microbes?

1. Skin
2. Ciliated epithelium
3. antibacterial secretions (lysozymes, bile)
4. mucin


What are the major ways by which bacteria enter the skin?

They normally cannot (except nematodes) unless there is:
1. broken skin- surgery, catheters, wounds
2. skin trauma- biting arthropods


What are the four major body cavities by which bacteria enter?

1. GI tract
2. Urogenital tract
3. Eyes
4. Respiratory tract


What are four ways bacteria can penetrate the mucin layer (host "natural defense")?

1. Lack receptors for mucin so they don't get trapped in the layer
2. Motile bacteria move through the viscous mucin
3. Secrete mucin-degrading enzymes
4. Enter through M cells where the mucin is thinner


What is the function of the M cell?
What are two pathogens that enter the host through M cell?

To sample material passing through the intestine and deliver it to the immune system.

Shigella and salmonella


What are examples of bacteria that enter the host via ingestion? (6)

1. Salmonella
2. Shigella
3. Vibrio cholera
4. Yersinia enterocolitica
5. E. coli (diarrheagenic)
6. Campilobacter


What are examples of bacteria that are inhaled? (5)

1. Mycobacteria
2. Mycoplasma pneumonia
3. Nocardia
4. Legionella
5. Bordetella purtussis


What are examples of bacteria that enter via trauma? (4)

1. Clostridium tetani
2. Streptococci
3. Staphylococcus aureus
4. Pseudomonas


What are examples of bacteria that enter the host via arthropod bite? (4)

1. Borrelia burgdorferi
2. Rickettsia
3. Erlichia
4. Yersinia pestis


What are examples of bacteria that are transmitted sexually? (3)

1. Treponema pallidum (syphillis)
2. Neisseria gonorrheae
3. Chlamydia trachomatis


What are the three major ways bacteria adhere to hosts?

1. Pili and fimbrae
2. Afimbral adhesins
3. Biofilms


What are pili and fimbrae composed of?
What is their shape?
What portion, specifically, binds to the host?

They are protein structures made of an ordered array of single subunits.
They are rod shaped but different types have different thickness and length.
The tip structure attaches to the receptors on the host cell


What does the tip structure of pili and fimbrae allow the bacteria to do?

Overcome the - to - chemical repulsion of normal cells membranes and bind to glycoprotein or glycolipids on the host cell allowing a loose connection


Pili are constantly _________ and ________ partially due to their fragility.

Lost and reformed


Adhesion with _________ or _________ are generally loose connections while adhesion by ________ is usually stronger.

Pili and fimbrae make weak connections where afimbrial structures form stronger connections


The initial weak adhesion of pili trigger mechanisms of _______ and _______ in both the bacterial cell and the host.

1. stronger adhesion
2. signal transduction


How do afrimbrial adhesins form stronger bonds than pili adherence?

Afimbrial adhesins bind to proteins rather than glycoproteins or glycolipids which provides a stronger bond


What are three examples of bacteria that utilize pili and fimbrae for adherence?

1. vibrio cholera
2. E. coli
3. N. gonorrhea


What is an example of a bacteria that utilizes afimbrial adhesin for adherence?

E. coli AIDA and intimin


What are the two functions of the water channels between the bacterial columns in biofilms?

1. Allow nutrients to reach bacteria
2. Allow toxic metabolites from the bacteria to diffuse out


What are the 4 situations where you would typically see a bacterial biofilm?

1. aerosolized bacteria (legionella)
2. on plastic tubing (catheter)
3. on plastic implants (valves, prosthetic joints)
4. on body surfaces (dental plaque, lungs in CF)


What are the three steps in biofilm formation?

1. Attach to a surface and form a monolayer
2. Attach to each other and form a microcolony
3. Mature into polysaccharide slime


What binds Fe in extracellular fluids?
What binds Fe in cells?

Extracellular- lactoferrin, transferrin
Intracellular- Hb, ferritin


What are the 4 major mechanisms used by bacteria to acquire Fe (necessary for their growth)?

1. Siderophores
2. Binding transferrin, lactoferrin, ferritin, Hb
3. Toxins that kill host cells
4. Iron abstinence


What are siderophores?

It is secreted by bacterial cells to chelate Fe. The Fe-siderophore complex is taken back up by the bacterial cell where the complex is cleaved to release the free iron


What is iron abstinence? What is an example of bacteria that does this?

It is when the bacteria lack Fe-dependent enzymes and utilize manganese instead.
Borrelia burgdorferi (Lyme disease) does this


How are some bacteria able to enter cells that do not have phagocytic function?

1. Shigella has a "molecular syringe" which disrupts the host cytoskeleton causing "ruffling" and engulfment
2. Yersinia invades through a "zipper mechanism"


After enter the cell, how do bacteria protect themselves?

1. Prevent phagosome-lysosome fusion so they don't get enzymatically degraded
2. Escape from the phagosome by degrading the membrane lipids or forming pores


What are two examples of bacteria that prevent phagosome-lysosome fusion allowing their preservation intracellularly?

1. mycobacterium tuburculosis
2. salmonella


What Are the two ways by which a bacteria can escape the phagosome once it has entered the host cell?

1. Disrupt the membrane by degrading membrane lipids
2. Form pores in the membrane


What are the three major benefits of living in a host cell cytoplasm (vs. existing extracellularly)?

1. abundance of nutrients
2. protection from Ab and complement
3. partial protection from antibiotics


If a bacteria cannot escape the phagosome or prevent phagosome-lysosome fusion, what is their survival strategy?

They produce enzymes that detoxify ROS and prevent the oxidative burst (ex. catalase + organisms can break down H202)


What two bacteria interact with actin in the host cytoplasm? What does the actin allow them to do?

Ex. are shigella and listeria monocytogenes

They promote actin condensation at one side of the bacteria to propel the bacteria into a neighboring cell so it doesn't need to use energy entering or exiting the cell and doesn't risk immune detection


What is a pathogenicity island?

genes that code for virulence or antibiotic resistance cluster together in the bacterial chromosome


What are the four hallmarks of a pathogenicity island?

1. different CG content from the rest of the chromosome
2. Inserted close to tRNA genes
3. Encode virulence factors
4. Are acquired via horizontal gene transfer (using phages or transposons)


How are pathogenicity islands acquired?

Through horizontal transfer using bacteriophages or transposons


Describe the type 1 secretory system and give an example.

It spans the inner and outer membrane with one channel and has no periplasmic intermediate steps.

The secretory unit is made of 1 protein

Ex. hemolysin


Describe the type 2 secretory pathway.
What are the steps?

It is multiple proteins that have an inner membrane step and a periplasmic step.
It secretes virulence factors and non-virulence factors


What determines that a bacteria will get secreted via the type 2 secretory pathway?
What is an example of a bacteria that gets excreted this way?

Bacteria have a signal sequence on their termini that targets them for type 2 secretion.



Describe type 3 secretory systems.

They have multiple proteins that span the inner and outer membrane forming a single channel.

They also have a "needle" structure that allows bacteria to inject virulence factors directly from within their cytoplasm to the eukaryotic cytoplasm

They are specialized to secrete virulence factors


What is the unique structural feature of type 3 secretory systems?
What does it allow bacteria to do?

The needle structure allows bacteria to inject virulence factors from their cytoplasm directly into the eukaryotic cells cytoplasm.

(ex. shigella forming ruffles on eukaryotic cell)


Once the "needle structure" of type 3 secretory systems inject virulence factors into the host cell cytoplasm, what are 4 possible effects?

1. alteration of cytoskeleton (shigella, salmonella)
2. inflammation
3. opening of tight junctions (E. coli)
4. electrolyte secretion


Describe type 4 secretory systems.

They form a channel spanning the inner and outer membranes and are composed of multiple proteins.
They transfer bacterial DNA or bacterial effector proteins.
They can also form a pili channel directly from bacterial to eukaryotic cell cytoplasm.


What are the two secretory systems that can form channels directly into host cell cytoplasm?
What is the difference between the two?

Type 3- "needle-like structure"
Type 4- long pili-like structure


What is the only secretory system composed of a single protein?

system 1


What is secreted by:
1. Type 2 secretory systems
2. Type 3 secretory systems
3. Type 4 secretory systems

1. virulence and non-virulence factors
2. Virulence factors
3. bacterial DNA and effector proteins


What is the secretory system that utilizes a periplasmic intermediate step?

type 2


What are capsules typically made of?
What is their major function?

They are a network of polymers (polysaccharides normally, sometimes proteins)
They protect against:
1. complement activation by preventing formation of C3 convertase
2. phagocyte mediated death


What is an effective host response against bacterial capsules?
How have some bacteria evolved to avoid this?

The host will make antibodies against the bacteria capsule.
Some bacteria subvert this by having their capsule closely resemble host polysaccharides like hyaluronic acid or sialic acid


What two host polysaccharides have been mimicked so that a bacterial capsule could avoid Ab?

Hyaluronic acid- Step pyogenes

Sialic acid- N. meningitidis


What are two ways that LPS of G- bacteria can be modified to avoid bacterial phagocytosis and complement activation?

1. Attach sialic acid to O-antigen preventing C3 convertase formation
2. Change length of o-antigen so MAC complex is too far from the cell surface to disrupt the membrane


What are the four ways exotoxins can be named?

1. Based on target (neurotoxin, leukotoxin, hepatotoxin)
2. Bacterial species that produced it (cholera toxin, shiga toxin, botulinum toxin, tetanus toxin)
3. Type of activity ( lecithinase, adenylate cyclase)
4. Letter (exotoxin A)


Where are the majority of bacterial exotoxins encoded?

On mobile elements like plasmids or bacteriophages


What is exotoxin type 1?

Superantigens that bind to the surface of the cell and do not enter.
They bind indescriminately (are not cleaved and processed, thus creating specificity for T cells) to MHC class II macrophages and the receptors on T cells that interact.

Instead of 1/10000 T cells activating, 1/5 are activated creating a cytokine storm


How many T cells are normally activated in response to an antigen?
What about when a superantigen is present?

normal : 1/10,000
superantigen: 1/5


What are symptoms associated with the presence of superantigen?
What ultimately occurs?
What is an example of a bacteria that can produce type 1 exotoxins?

Fever, nausea, vomiting, malaise (inflammatory response bc of elevated IL-2)

It progresses to toxic shock syndrome

Streptococcus, S. aureus


What is the function of type 2 exotoxins?
Give one example.

Toxins that destroy eukaryotic cell membranes by:
1. forming channels in the membrane disrupting osmotic gradients triggering water to rush in
2. Phospholipase to degrade phospholipids in the membrane

S. aureus alpha-toxin is pore forming


What is the structure of type III toxins?

They have two subunits A-B.
B- binds to the host cell receptor
A- has enzymatic activity

Simple have one A and one B
Complex have one A and 5 B


What determines host specificity for a type III toxin?

B subunit binding to the host cell receptor


What do most A subunits of type III toxins do?

They remove ADP-ribosyl groups from NAD and attach it to a host protein (yielding different responses based on what protein they attach it to)


What does the A subunit of diptheria ribosylate?

EF2 . This kills the host cell by stopping protein synthesis


What does the A subunit of cholera ADP-ribosylate?

a regulatory enzyme that controls cAMP.
cAMP cannot be turned off--> no control of ion flow--> loss of host cell water--> diarrhea


How is Shiga toxin A subunit different from most other A subunits?

It does not take ADP-ribosyl from NAD and transfer it to another cell protein.
Instead, it cleaves the host cell rRNA preventing protein synthesis