microbio chapter 19 (G+) Flashcards
Characteristics of Staphylococcus
- normal member of microbiota
- found on our skin
- opportunistic pathogen
- SALT TOLERANT
- tolerant of desiccation
What characteristics allow Staph to live on our skin?
- it is salt tolerant
- it is tolerant to desiccation
- has many forms of innate immunity resistance
How is Staph resistant to our innate immunity?
- interference with the complement system
- SCIN
- oxidative active catalase
- protein A
- PNAG
- CHIPS
How does Staph interfere with complement system?
Staph produces Efb protein (extracellular fribrogen protein)
- Efb binds to C3B before C3B makes its way to the cell surface
- this makes Staph cells less easily phagocytized
What does SCIN do?
SCIN binds to C3 convertase in the Staph cell
- inhibits C3 convertase from making C3A and C3b
- this makes the cell less easily phagocytized
- also inhibits C3A working as an anaphylatoxin to traffic immunity cells to the damaged area
What do oxidative active catalases do to help Staph survive?
Catalases are utilized if a Staph cell is engulfed into a macrophage
- when phagosome binds with lysosome, Catalase responds to the harsh environment by breaking down toxins
- makes the phagolysosome less toxic and increases survival of Staph
What is the function of protein A and on what bacteria cell is it found?
- protein A is found on the surface Staph cells
- protein A functions to grab antibodies and flip them around (arms out)
- this prevents NKC from binding to bacteria cell and killing it
-flipped antibodies cover LESS cell surface allowing more space for Staph to work
What can protein A be used for to help sick people?
protein A can be used to gather antibodies that can then be used as doner antibodies for people that are sick with COVID
- this works because protein A gathers antibodies very well
What is the function of PNAG?
- poly-N-acetylglucosamine
- Covers any C3B on surface of Staph cell with a polysaccharide made by the cell
- covering C3B makes it harder for bacteria cell to be engulfed
What is the function of CHIPS?
- chemotaxis inhibitor proteins of staph
- CHIPS bind to anaphylatoxins
- this inhibits trafficking movement of immune response cells to damaged area
- bind to C5A primarily
What is Stpah the result of?
It is the result of MRSA resistance
What enzymes does Staph produce?
- Lipases
- beta-lactamase
What is the function of lipases produced by Staph?
digest lipids and allows Staph to grow on skin/ in oil glands
What is the function of beta-lactamase?
**break down beta lactams
- beta lactams include antibiotics that end in ‘cillin’ (penicillin)
Why are beta-lactamases significant?
They are significant because they break down beta lactams that can bind to transpeptidase proteins.
- when penicillin is present it binds to the transpeptidase and inhibits its function of forming NAM-NAM alanine bridges which interferes with cell wall production
What is MecA?
MecA is the unique transpeptidase found in Staph cell.
- penicillin does NOT bind to MecA so it can still makes bonds to form cell wall
How did Staph become a resistant bacterium?
It is a very competent cell that has picked up DNA from other cells.
What main toxin is produced by Staph?
Toxic Shock Syndrome Toxin
- prevalent in feminine hygiene products
- causes toxic shock syndrome
Diagnosis of Staph
detection of G+ bacteria in grapelike clusters
Treatment of Staph
-methicillin
- vancomycin to treat MRSA infection
- penicillin and similar antibiotics are not effective
Prevention of Staph?
- hand antisepsis
Staph Antigen
- super antigen that binds to MHC2 protein and increases T-helper cells to bind
- leads to increase in cytokine production and release
- this stimulates the vagus nerve endings and causes vomiting (how it spreads)
Streptococcus pyogenes
- causes strep throat
- step=strips; found in strips of cocci
What makes Streptococcus pyogenes so pathogenic?
It contains protein M on its surface
- protein M undergoes many small mutations from cell to cell
- this is due to low rates of proofreading in the cell
- makes it so memory B cells cannot recognize new bacteria cells with slightly modified protein M on the surface
- body has to make new antibodies which takes 10-14 days allowing it to cause infection more regularly
What enzyme does Step make and what does it do?
Step makes C5A peptidase
- this protein breaks down C5A produced in the cell
- which lowers anaphylatoxin trafficking of immune cells to damaged area
What occurs due to lack of immune response to damaged areas of Step?
- lack of C5A trafficking leads to streptolysins and exotoxin A being produced
What toxins does Step make?
- streptolysin
- can kill neutrophils - exotoxin A
- over stimulates inflammation and cytotoxin release
**these grow subcutaneously and kill cells can lead to necrotizing fasciitis
Bacillus anthracis
- causes anthrax
- taken in as a spore
What are the three types of anthrax?
- GI anthrax: rare in humans but common in grazing animals (animals eat it as a spore)
- Cutaneous anthrax: occurs on the skin with open wounds allowing spores to enter bloodstream
-called wool sorters disease
-causes eschar ulcers on skin - Inhalation anthrax: occurs when anthrax is inhaled and deposited in the lungs
Inhalation anthrax (more detail)
-inhaled into lungs, not detectable early on
- leads to high mortality rates
- not common in humans
- spores reach lungs and germinate
**upon germination they can produce edema factor, lethal factor, and protective antigen
What toxins does Bacillus anthrax make when germinated?
- edema factor: increase cAMP levels
- lethal factor: zinc protease
- protective agent (not an actual toxin)
How does the toxins produced by Bacillus anthrax affect cells?
The protective agent (PA heptamer) lodges itself in our cells membrane and creates barrel shaped pores. These pores allow edema and lethal factor to enter the cell causing them to lyse.
What happens when our cells lyse due to inhalation anthrax?
When the cells lyse, they release all the fluid that was in them, leading to drowning in the lungs.
2001 anthrax situation
envelopes with anthrax were sent out and when opened it was inhaled. This infected 22 people and killed 5 of them. The anthrax cells were modified with silicon to prevent them from sticking together. This allowed them to float in the air longer and infect others. The building was filled with chlorine to kill any remaining spores.
Diagnosis of Bacillus anthrax
large, non-motile =, G+ bacillus cells in lungs or skin samples
Treatment of Bacillus anthrax
ciprofloxacin and many other antimicrobials
Prevention of Bacillus anthrax
-control of animal disease
- use of effective vaccine available
- multiple doses and boosters
Clostridium characteristics
- G+, anaerobic
- endospore forming bacillus
- can survive in harsh areas because of endospore formation
- ubiquitous in soil, water, and GI tracts of animals
Clostridium botulinum
- results when spores germinate and produce botulinum toxins
- A-B toxin; A= active zinc protease that affects release of Ach
How does A-B toxin of botulinum affect the body?
The A-B toxin causes our body to lose the ability to contract muscles by inhibiting the release of Ach onto muscles
- appears quickly in the face and can affect talking/eating
- inhibition of muscle contraction leads to death
What are the three intoxications of botulism
- Foodborne botulism
- Infant botulism
- Wound botulism
Foodborne botulism
- toxin is consumed in food
- death can result from asphyxiation
- common in canning business when autoclave would not reach entire can
- allowed Clostridium botulinum to grow in can and produce gas
- gas produced causes bulging cans and black areas on food
- ONLY deadly if consumed as a toxin not a spore
Why is foodborne botulism only deadly if consumed as a toxin and not a spore?
Our gut prevents spores from germinating and prevents the production of A-B botulinum toxin
Infant botulism
- results from ingested spores in infants
- infants gut cannot prevent germination of spores
- infants should not eat honey
Wound botulism
An open wound allows spore entrance into bloodstream where it can germinate and produce A-B botulinum toxin leading to death
BOTOX
botulinum toxin can be diluted enough to be used as BOTOX, it prevents contraction of muscle to limit wrinkles
Diagnosis of Clostridium botulinum
symptoms are diagnostic
- face drop
- impaired talking and eating
Treatment of Clostridium botulinum
- neutralizing antibodies against botulinum toxin
- antibodies bind to A-B toxin preventing it from binding to nerve ending - antimicrobial drugs in infant botulism
- this works in infants because the spores need time to germinate
Prevention of Clostridium botulinum
- proper food canning
- no honey fed to infants
Clostridium tetani
- blocks stimulants that release contraction
- muscles stay contracted
- muscles cannot relax
- causes lock jaw
Listeria characteristics
- G+, nonspore forming
- coccobacillus
- enters body by infected foods/drinks
- DOES NOT PRODUCE TOXINS
- 2000 cases/yr with ~500 deaths
Listeria breakout Canada 1981
Listeria grew on coleslaw that was sitting out causing 9 still births, 25 infected infants, and 77 non-pregnancy related cases (1/3 of the infants died and 1/3 of the 77 died)
Listeria monocytogenes
- causes listeriosis that can be treated with antibiotics
- dangerous for infants and pregnancy
- causes liver infection that kills our liver cells
Why is listeriosis not diagnosed right away?
It is not common enough to be diagnosed right away, longer waits for diagnosis can lead to death
- ~30% mortality rate
What genes does Listeria have that helps it avoid out immune system?
- internalin A and B
- hemolysin Listeriosin O
- Act-A
- catalases
What is the function of InlB in Listeria?
InlB is a surface protein on Listeria that comes onto contact with liver cell surfaces. It tricks the liver cell into rearranging its actin. The change in its actin causes the liver cell to make a phagosome and engulf Listeria cell.
What is the function of hly listeriosin O?
hly permeabilizes the phagosomes membrane allowing the Listeria cell to escape before its phagosome binds to a lysosome.
Why is Listeria escaping the phagosome significant?
It leaves Listeria in our cells cytoplasm where nutrients are available, and no competition is present. This allows Listeria to grow and replicate.
What is the function of Act A in Listeria?
Act A is produced on one pole of the Listeria cell, it causes our cells actin to polymerize upon contact. The polymerization of actin causes bacteria cell to be pushed up against adjacent cell forcefully. Listeria is pushed in to new cell. Listeria enters in a phagosome and the process continues.
Function of catalase in Listeria
Listeria utilizes catalase to survive harsh environments
What kind of pathogen is Listeria?
Listeria is an emerging pathogen because new technology has made it more prominent than before
In what conditions can Listeria live?
psychotropic and mesophilic conditions
- this is due to the prfA protein in its operon that is turned on as a response to heat increase
Listeria Operon
codes for a set of unique genes including prfA protein
- prfA protein is heat responding and is expressed when Listeria cells go from warmer to colder temps
- prfA can then bind to DNA and turn on operon to express all genes
Diagnosis of Listeria
bacteria in cerebrospinal fluid
Treatment of Listeria
most antimicrobial drugs
Prevention of Listeria
hard to prevent because its ability to survive in different temps
Mycobacterium tuberculosis
- cell wall contains MYCOLIC ACID
- this is a waxy lipid layer
What characteristics does mycolic acid give to Mycobacterium TB?
- slow growth that prevents antibiotics from being effective
- protection of lysis after phagocytosis
- capacity for intracellular growth
- highly antibiotic resistant
Why are antibiotics ineffective to TB?
antibiotics break down before cells replicate
What disease does Mycobacterium tuberculosis causes?
It causes tuberculosis, a respiratory disease that affects the lungs
What happens when a person develops TB?
Mycobacterium tuberculosis makes its way into the lungs but because it has the waxy lipid layer phagosomes do not do a good job of breaking it down.
- as phagocytes fail and bacteria stays in the lungs, out lungs begin to deposit fibers around macrophages
- eventually the fiber covered tissue dies
- our skin grows around the macrophage and creates scars in out lungs
Why is TB hard to treat?
Because the scars are developed in our lungs, it is hard to access them and remove them. This is due to the small size out our bronchioles.
Diagnosis of Mycobacterium tuberculosis
tuberculin skin test based on type 1 hypersensitivity reaction
Components of a tuberculin skin test
- based on a type 1 hypersensitivity rxn
- our plasma cells should have already made antibodies and have memory B cells stores
- IgE likes to adhere to our cells with the antibody arms out
How is a tuberculin skin test done?
- take a bifribricated need and dip into mycobacterium skin
- if TB is present, we will have B cells with IgE present
- TB protein will stick to both antibodies and cause degranulation
- this causes the immediate release of leukotrienes and histamines
- creating immediate inflammation to the area (leukotrienes)
Treatment of TB
months of therapy to treat disease
- antimicrobials are ineffective
Prevention of TB
BCG immunization where TB is prevalent
Propionibacterium
- small, G+ rods often in skin
-causes acne in young adults and adolescents - many cases do not require treatment
- can be controlled with antimicrobial drugs
