1.1 Intro to infection Flashcards
Name the 7 types of microorganisms
Bacteria, fungi, viruses, protozoa, algae, archaea, multicellular animal parasites
What classification system exists for viruses?
How does replication differ between the classes (1 +2 and 3-7)
The Baltimore system:
Class 1 + 2 DNA viruses replicate within the nucleus
Class 3-7 RNA viruses replicates in the cytoplasm
Explain the process of gram staining
1) apply crystal violet to bacteria on dish
2) apply iodine to bind crystal violet and trap it in cell
3) add acetone or methanol to wash away the stain
- gram (+) fixes crystal violet
- gram (-) turn colourless (thin PGN)
4) add pink counterstain (safranin) leaving:
- gram (-) pink
- gram (+) purple
What are the structural differences between gram (-) and (+) bacteria
Gram (-) has a thin peptidoglycan layer and a lipopolysaccharide layer which holds antibodies
Gram (+) has a thick peptidoglycan layer and no lipopolysaccharide layer
What stain would you use to identify mycobacterium and why?
Ziel Neilson stain because the mycolic acid prevents the crystal violet stain from washing away
Compare the terms pathogenicity and virulence
What determines these factors?
Pathogenicity is the ability of a microorganism to cause disease and damage
Virulence is the degree of pathogenicity.
They are both determined by the composition of the genome (virulence can also depend on how the bacteria entered the host)
Compare the terms parasite and pathogen
A parasite is an organism that can live on or within a secondary organism/’host’
A pathogen is an organism that can cause damage to the host, cause disease
What is a plasmid?
An extra piece of DNA often carrying the bacteria’s virulent factors
Define attenuation
When a pathogen’s virulence is reduced
What 5 key steps do virulence factors help bacteria to do? (ACTII)
- Attach to the host (Via adhesins)
- Colonization (and enzymes)
- Invade
- Toxins (and enzymes) aid deeper penetration to avoid host defences
- Inhibit phagocytosis
Define the following terms:
a) Toxin
b) Toxigenicity
c) Toxemia
d) Toxoid
e) Anti-toxin
Toxin: substances produced by pathogens that contribute to pathogenicity
Toxigenicity: ability to produce a toxin
Toxemia: Presence of toxin in the host’s blood
Toxoid: inactivated toxin used in a vaccine
Anti-toxin: antibodies against a specific toxin
What are the 2 types of toxins and what is their key difference?
Exotoxins: toxins produced/secreted extracellularly as the organism grows
Endotoxins: lipopolysaccharides present on part of the outer layer of gram negative bacteria
Where are endotoxins released from and describe how they are released into the blood stream
Why are they so damaging?
Endotoxins are released from the lipid portion of the outer membrane from gram (-) bacteria
Process:
1) gram (-) bacteria is engulfed by a phagocyte and ingested by lyososmes
2) the dead debris is released into the bloodstream
3) once detected by the immune systems ➞ triggers an immune response
Endotoxins are highly antigenic and provoke a strong immune response, quickly causing heightened inflammation, fever and possible shock
What are exotoxins released from?
Both gram-positive and negative bacteria BUT all major gram-positive will produce it
Name the 3 types of exotoxins and their method of causing damage/dysfunction
Type I: Signalling at the host cell
Type II: Damaging the membrane/phospholipid bilayer by making protein channels in it
Type III: Entering the target cell and directly altering the function
Name the 3 classes of toxins
1) Neurotoxin (acts on nervous system)
2) Enterotoxin (acts on gut)
3) Superantigen
What type of exotoxins are superantigens?
Give the MoA?
Name 4 symptoms associated
Type I exotoxin
Causes an intense response due to release of cytokines from host cell. They are unspecific and bind to any T cell causing a heightened intense immune response
Symptoms = nausea, vomiting, fever, shock and death
Which Superantigen causes Toxic shock syndrome?
Name 3 major signs
Toxic shock syndrome toxin is caused by TSST-1 superantigen.
Causes hypotension, organ dysfunction and desquamative (peeling) skin lesions
What bacterium causes Staphlococcal scalded skin syndrome?
What toxin is released?
List 5 symptoms
Caused by staphylococcus aureus which produces an “exfoliating toxin” causing the outer layers of skin to blister and peel
Symptoms: fever, redness, skin exfoliation, skin wrinkles and blisters/lesions
What type of exotoxin does clostridium produce?
How can it lead to gas gangrene?
Clostridium are type II exotoxins -> they cause membrane damage and disruption which leads to:
increased permeability of blood vessels ➞ disrupts blood flow ➞ allows gas to enter tissues
How is spore-forming advantageous to Clostridum
Because they’re anaerobic and particular about where they grow, they create spores as a protective mechanism so they can withstand environments they can’t grow in (aerobic)
Describe the size, shape, (-) or (+), environmental niche and protective features of a clostridia
- Large
- bacilli
- gram (+)
- anaerobic
- spore forming
Explain the ‘A’ and ‘B’ segment of an A-B enterotoxin
1) The B portion binds to the surface receptors of the host cell
2) The entire A-B protein is taken into the cell by endocytosis
3) Once inside the cell the vacuole becomes extremely acidic causing dissociation of A and B portions
4) The A part is active and enters the cytoplasm and can then be incorporated into the host cell.
5) The B part is then recycled out by exocytosis, while A stays and infects
What type of exotoxin does Vibrio Cholera produce?
Give its shape, type (-) or (+), environmental niche and protective features
What part of the body does it commonly affect and why?
It produces a type III A-B enterotoxin
- Bacilli
- gram (-)
- lives in warm water pH >7, salty
- has flagella which allows it to propel forwards
Attaches to the intestinal epithelia and reproduces due to the acidic environment of the gut
What bacteria causes Tetanus?
What type of exotoxin does this produce + incl the specific name of the toxin?
Clostridum tetani
Type III A-B neurotoxin
Toxin = Tetanospasmin
Name one feature of pili
They are antigenic and provoke an immune response
What bacteria causes Botulism and where is it found?
What type of exotoxin does it produce + specific name of toxin?
How does this cause Botulism?
Clostridium botulinum, found in soil and intestinal tract of humans and animals
Produces a Type III A-B neurotoxin ➞ ‘metalloprotease toxin’
Toxin enters PNS, causing proteolysis of key proteins resulting in Inhibition of ACh release
What are the 3 forms of Botulism disease?
1) Food borne
2) Infant borne
3) Wound botulism
What are the main symptoms of Botulism?
Flacid paralysis leading to muscle weakness and respiratory arrest
How do type II exotoxins cause damage
These are membrane disrupting toxins
They lyse the host cells by making protein channels in the plasma membrane (eg. leukocidins, hemolysins) which disrupt the phospholipid bilayer
Give the MoA of how the cholera toxin causes damage (A-B mechanism)
1) One of the B subunits bind to a glycoprotein receptor on the cytoplasmic membrane
2) This results in cleavage of the A subunit which then enters the cytoplasm
3) Once in the cytoplasm it activates adenyl cyclase
4) adenyl cyclase converts ATP into cAMP
5) cAMP stimulates active secretion of electrolytes from cell into intestinal lumen
6) water flows to area with high electrolytes ➞ into intestinal lumen
7) Results in very water diarrhoea
How are the stools in a patient infected with cholera described? (Hint: hallmark of cholera)
Watery diarrhoea with flecks of mucus -> “rice-water stool”
List 4 important signs of cholera infection
1) dehydration
2) thirst
3) tachycardia
4) sunken eyes and flacid skin
Describe the electrolyte/ acid-base imbalances in cholera
Metabolic acidosis ➞ loss of HCO3-
Hypokalemia ➞ loss of K+ (causes muscle cramps)
What type of exotoxin does Clostridium Tetani produce?
Give its shape, type (-) or (+) and environmental niche
Type III A-B neurotoxin
- bacilli
- gram (+)
- anaerobic, found in soil or GI tract of animals
Describe the mechanism of how clostridium tetani causes damage?
1) spores become activated and develop into gram (+) bacteria that produce the toxin tetanospasm
2) this bind motor neurons that control muscles
3) it enters axons, migrates into the synapse of motor nerves and binds to the nerve terminals
4) this inhibits the release of inhibitory neurotransmitters (GABA and glycine)
5) This process intensifies results in severe muscle tightening and spasm
