Forensic biology - Bacteria: disease and antibiotics

  • Created by: aarafa11
  • Created on: 01-06-20 22:02
Virulence Factors include
Pili for adhesion to cells, tissues and surfaces; Enzymes to evade host’s defences Toxins;; The capsule
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after bacteria invades/enters/attached host cells, what is next?
infection & colonisation
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what are the adhesion factors
Proteins or glycoproteins; Found on end of Fimbriae – attachment pili; Often adhere to receptors on host cells surface; Adherence to specific tissues – lining of lungs, GI tract, GU tract, etc.
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Spreading factors
digestive enzymes; Breakdown tissues and allow rapid invasion; And disease
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type of digestive enzyme used to spread disease
hyaluronidase ; collagenase
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what does hyaluronidase do
Breaks down hyaluronic acid, an important part of the extracellular matrix
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what produces hyaluronidase
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what does collagenase do
– break down collagen; Allowing bacteria to invade between cells; Necrotizing fascitis – highly virulent form of Streptococcus pyogenes; Can invade tissues at a rate of 2.5 cm h-1
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how pathogens invade through basement membrane
reach epithelial surface; produce hyaluronidase; invade deeper tissue;
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how pathogens invade through blood vessesl
produce coagulase; blood clot forms around pathogens; produce streptokinase - dissolving clot and release bacteria
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types of toxins
Endotoxins and Exotoxins
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where are endotoxis released
Released into bacteria’s environment; Often released when bacteria die or divide
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what does endotoxins do
Generally induce the same symptoms, e.g. fever and aches
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examples of endotoxins
lipid A and lipopolysaccharides (LPS) complexes of gram –ve bacteria
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what produced exotoxins
both Gram +ve and –ve bacteria; generally specific to a particular bacterial species
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where is exotoxins released
bacterial cell
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what are the symptoms of exotoxins
Very high potency, amongst the most toxic substances to man
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which is more potent between exotoxins and endotoxins
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how much heat can exotoxins and endotoxins withstand
ENDO)Relatively heat stable – withstand several hours at 60 oC; EXO) Often Denatured by heat and proteolytic enzymes
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what is the mode of action for exotoxins
SPECIFIC - affected by cell signalling; Pore forming toxins (‘punch’ hole in plasma membrane); AB toxins (two part toxins); Enzymes
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how is exotoxins affected by cell signalling
Directly affects signal receptors; Altered cell membrane permeability to Ca2+; Increased in production of cAMP
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how does Pore forming toxins (PFTs) attack the membrane
Proteins form pores on host membrane; Alter permeability of membrane; Leads to ions K+, amino acids and other small molecules leaking out; & others leaking in, (Ca2+, water); Diverse cellular responses – death, senescence, activation of signal cascad
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how does virulence factors of Pore forming toxins (PFTs) Contribute to pathogen growth and colonisation
Disruption of epithelial barriers; Avoidance of host immune system; Facilitaing invasion of cells; Release of nutrients; Eliminate competing bacterial species
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how does Pore forming toxins (PFTs) work
Toxin receptor on cell membrane; PFT protein Binds to receptor; Another PFT protein is recruited; Oligomerisation;reveals hydrophobic surface; insert pft comp into plasma; trans membrane formed; pore alters permiability=leaks;
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examples of exotoxins
Leukocidins & haemolysin & Clostridium perfringens β toxin
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what is Leukocidins
virulence factor and Pore forming toxins (PFT)
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what does Leukocidins do
Damage neutrophil and macrophage white blood cells (WBCs); Both types of WBC are phagocyctic and leukocidins most effective after the fact; Release cells own lysosomal enzymes
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what is haemolysin
lysis blood cells by forming channels
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what does haemolysin do
Important in nutrient acquisition
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what is Clostridium perfringens β toxin
channel forming toxin that forms a small pore
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what does Clostridium perfringens β toxin do
Pore allows efflux K+ and influxes of Ca2+, Cl− and Na+; PFTs differ between species, but pathogenic species tend to have several PFTs in their arsenal
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what is AB toxins
exotoxins; 2 part protein; A) active toxin; B) binding protein
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what is the purpose of the binding protein in AB toxin
to get A into the cell
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What is the role of AB toxin
Target of diphtheria toxin- Translation elongation factor 2 (EF2); Release tRNA from the binding site on ribosome to make way for the next tRNA; Inactivate EF2 & translation, thus, protein synthesis stops
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what does Shiga toxin do - exotoxin
acts by cleaving sub-units of the ribosome; no translation; Exploits the difference between prokaryotic and eukaryotic ribosomes
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what does botulinum toxin (Clostridium botulinum ) do
Inhibits secretion of the neurotransmitter acetylcholine (Ach); Cleaves SNARE protein on Ach containing vesicles; Switching off nerve impulse, causing gradual paralysis and death
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what does tetanospasmin toxin (Clostridium tetani) do
cleaves SNARE but of vesicles containing the inhibitory neurotransmitters GABA and glycine; Motor neurons increase rate of firing, resulting in muscle contraction – lock jaw
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what are the type of SNARE protein cleavage
tetanospasmin toxin (Clostridium tetani); botulinum toxin (Clostridium botulinum )
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how can some exotoxins be enzymes
Can act catalytically; Some have a broad cytotoxic activity; Phospholipases, cleave the phospholipids of the cell membrane
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how is antibodies a chemotheraputic drub
Selectively kill prokaryotic cells, but have a far lower toxicity to eukaryotic cells
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how does antibodies Exploit the fact that prokaryotic and eukaryotic cells have differences
Peptidoglycan cell wall; Ribosomes with a different structure to eukaryotes
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Examples of β-lactam class Anitibiotics
penicillins & cephalosporins, generally most effective against Gram +ve bacteria
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where was β-lactam class Anitibiotics extracted
fungi, e.g. Penicillin sp
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what is β-lactam class Anitibiotics
Irreversible inhibitors of the enzyme peptidoglycan transpeptidase
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what does β-lactam class Anitibiotics so
catalyses the formation of peptide bridges between peptidoglycan polymers; stops cell wall formation & therefore bacterial growth; weakens existing cell wall
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why is it bad if β-lactam class Anitibiotics weaken existing cell wall
Gram +ve bacteria have a high osmotic pressure compare to body fluids
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What is not affected by first generation β-lactam antibiotics
Gram -ve bacteria
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why isn't Gram -ve bacteria affected by first generation β-lactam antibiotics
Outer membrane prevents the antibiotic reaching the cell wall;
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what is the purpose of broad spectrum antibiotics
Exploit differences between bacterial and mammal ribosomes
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how does antibodies create action against translation
Principally effecting tRNA binding and ribosomal enzymes that form peptide bonds between amino acids; But still get resistance
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Two modes of action of antimetabolites
Competitive inhibitors of enzymes; Incorporated in biochemical in place of normal metabolite
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which group of antibodies inhibit nucleic acid synthesis
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where is rifamycin found
Fist isolated from soil bacterium Amycolatopsis rifamycinica
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how does rifamycin inhibit nucleic acid synthesis
Bind to bacterial RNA polymerase with high affinity; And thereby inhibiting mRNA synthesis
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problem with rifamycin inhibit nucleic acid synthesis
Have low affinity for mammalian RNA polymerase
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why is rifamycin inhibit nucleic acid synthesis useful
treatment of mycobacteria
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why is antibodies resistant
Enzymic deactivation of the antibiotic; Pumping the antibiotic out of the cell; Suppressing the antibiotic with specific proteins; Altering the shape of the target molecules; Altering membrane permeability to prevent entery
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how does bacteria deactivate antibodies
use enzyme β-lactamase to cleave β-lactam ring
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what should you know about β-lactamase inhibitors
used to over come Penicillin resistance
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Transmission of antibiotic resistance genes
R plasmid; Antibiotics (mis)use naturally selects for bacteria with resistance genes; X10 the quantity of antibiotics used in agriculture than used to treat humans
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How does the R plasmid transmit antibiotic resistance genes
- contain up to 10 genes linked to antibiotic resistance - Transferred during conjugation - and by Transformation
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what does Resistance transfer factor contain
replication function; resistance to lead and mercury; resistance to arsenic antimony;
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after bacteria invades/enters/attached host cells, what is next?


infection & colonisation

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what are the adhesion factors


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Spreading factors


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type of digestive enzyme used to spread disease


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