Bacteriology Flashcards
Shape of bacteria
Gram positive cocci: Anything that has ‘cocci’ in its name.
Gram positive bacilli/rods:
ABC: Actinomyces, Bacillus, Clostridium; Clostriduim starts with ‘C’, then ‘L’, so Cornybacterium, Listeria.
Gram negative cocci: NEisseria
Gram negative bacilli/rods:
All that have ‘-ella’ in their names.
Get ill at a camp (Camptobacter). Air-lifted by helicopter on which there’s contaminated water (E.Coli, Vibrio cholerae). Arrive at hospital where you can pee pee (Pseudomonas, Proteus).
Also: Yersinia pestis, Bateroides, Haemophilus (Yeonj Bae hey)
Note that vibrio cholerae is a CURVED rod.
Spiral shaped: Helicobacter, treponema (causes syphilis).
Endospore formers
BC
Bacillus anthracis, ALL Clostridium (tetani, perfringens, botulinum, difficile).
Do not gram stain
Microbes May lack Colour
Mycobacteria: Mycolic acid layer outside cell wall makes them ‘acid-fast’. Use Ziehl-Neelson stain for ‘acid-fast’ organisms.
Mycoplasma + Chlamydia lack cell wall. They both cause NGU (non-gonococcal urethritis).
Encapsulated bacteria
Yo! Such a Shit HIt Sir!
Yersinia Pestis, Streptococcus pneumoniae, Streptococcus pyogenes, Haemophilus influenza, Staphylococcus aureus
(1) Steric hindrance - anti-phagocytic
(2) Made of a non-immunogenic polysaccharide (not necessarily sialic acid!)
(3) Lack affinity for complement factor B (just learn this)
Obligate Aerobes
Pests Must Die
Pseudomonas aeruginosa, Mycobacterium tuberculosis, c.Diphtheria.
Obligate Anaerobes
anaerobes Can’t Breathe
Clostridium (whole genus), Bacteroides fragilis.
Facultative anaerobes
ALL ‘-coccus’ + E.coli + Salmonella
They grow less well without oxygen.
Urease activity
PuncH
Proteus, Helicobacter pylori
H.pylori and Shigella also pumps H+ out of their cells.
Biofilms
So Much Stuff to Prepare/Produce (again)
Streptococcus mutans, Staphylococci, Pseudomonas aeruginosa.
Biofilm production regulated by quorum sensing.
Streptococcus pyogenes cause what diseases
Acute suppurative (pus forming) infections: NIPPLES + Tonsilitis Necrotising fasciitis, Impetigo, Pharyngitis, Puerperal fever, (lymphangitis), erysipelas, scarlet fever.
Staphylococcus aureus can also cause erysipelas and impetigo (has similar virulence factors).
Facultative intracellular bacteria that survives inside macrophages
M&S Lied
Mycobacterium tuberculosis, Salmonella, Legionella pneumophila (facultative intracellular in amoebae).
They inhibit phagosome-lysosome fusion and resists oxidative burst.
Legionella pneumophila inhibits phagosome-lysosome fusion, which causes cytokine release and vigorous inflammation in lungs, which is the main pathology in Legionnaries’ disease.
IgA protease
NHS
Neisseria (gonorrhoea and meningitidis), Haemophilus influenzae, Streptococcus pneumoniae.
Cytolysins (target membranes)
(1) Phospholipases that enzymatically degrade membrane phospholipids:
Listeriolysin O phospholipase allows Listeria to escape vacuole.
Clostridium perfringens alpha-toxin degrades host cell membrane.
(2) These form pores in membrane: Streptococcus pneumoniae's penumolysin E.coli's haemolysin Streptococcus pyogenes' streptolysin O and S Helicobacter's VacA
B.pertussis also makes cytolysins.
A-B toxins (enzymatic intracellular toxins)
(1) Cholera toxin + ETEC’s labile toxin ADP-ribosylates alpha-S, causing Gs protein to be always active. Pertussis toxin ADP-ribosylates alpha-I, causing Gi protein to be always inactive.
(2) Diphtheria toxin from Cornybacterium diphtheria ADP-ribosylates eEF-2 (equivalent of EF-G), blocking protein synthesis.
(3) Bordetella pertussis and Bacillus anthracis produce toxins that mimics adenylate cyclase.
(4) Shiga toxin (from Shigella which cause bacterial dysentery - bloody, low-volume diarrhoea with mucous and PMNs) is a glycosidase that depurinates 28S rRNA and blocks protein synthesis.
(5) Clostridium difficile’s TcdA + TcdB toxins glucosylates small GTPases involved in signal transduction - disrupt cytoskeleton, epithelium becomes leaky, cell destruction.
(6) SEC (Salmonella typhi, E.coli, Campylobacter) produce CDTs (cytolethal distending toxins) that cleave DNA. ‘SEC DTs’
(7) UPEC and meningitis-causing E.coli produce cytotoxic necrotising factor, a deamidase against GTPases involved in signal transduction - disrupt cytoskeleton, epithelium becomes leaky, cell destruction.
(8) Tetanus toxin from Clostridium tetani made during anaerobic growth in a wound. B chain binds gangliosides on motor neurones. A-B toxin endocytosed and undergoes retrograde transport to CNS (so acts CENTRALLY). Discharged into intersynaptic space. A-chain cleaves synaptobrevin on inhibitory neurones causing violent spasms, spastic paralysis.
(9) Botulinum toxin from Clostridium botulinum. Also made during anaerobic growth (P.36). B chain binds gangliosides on ACh secreting neurones at NMJ (so acts PERIPHERALLY). A-B toxin endocytosed and cleaves SNAREs. Causes flaccid paralysis.
Cholera, Anthrax, Pertussis (CAP) toxins are multimeric.
What does Streptococcus pneumoniae cause
MOPS: Meningitis, Otitis media, Pneumonia, Sinusitis.
What pathogens cause Meningitis
Easy! NHS!
E.coli K1, Neisseria meningitidis, Haemophilus influenzae type B, Streptococcus pneumoniae
Sialic acid capsule
E.coli K1 and Neisseria meningitidis.
Chronic inflammation
Chlamydia cause NGU which leads to pelvic inflammatory disease and infertility.
H.pylori cause gastric ulcers and cancer
Syphilis (caused by Treponema pallidum), M.tuberculosis, Leprosy (caused by Mycobacterium leprae) cause granulomatous inflammation. ‘Small Medium Large’.
Hypersensitivty and autoimmune conditions caused by pathogens
Streptococcus pyogenes: Rheumatic fever (autoimmune disease), glomerulonephritis (type 3 hypersensitivity)
Lyme’s disease can cause type 3 hypersensitivity - immune complex deposited in joints, vasculature, meninges.
Yersinia, Shigella, Chlamydia (YeSH u Can): reactive arthritis (autoimmune disease)
Diphtheria
ABCDEF: A-B toxin made by Cornybacterium diphtheria ADP-ribosylates eEF-2.
B binds HB-EGF receptor. A-B peptide nicked by furin but A-B still attached by disulphide bond. Endocytosed. A leaves endosome after endosome acidified and ADP-ribosylates eEF-2.
C.diphtheria related to C.ulcerans and C.pseudotuberculosis.
DTX diphtheria toxin gene carried by bacteriophage and integrated into chromosome. DTX controlled by transcription factor DtxR, which represses gene expression when bound to iron.
Bacteria colonises nasopharyngeal epithelium and forms pseudomembrane which occludes airway.
Streptococcus pyogenes virulence factors
Lancefield group A. SMASHED:
Streptolysins O and S causes beta-haemolysis (complete haemolysis)
M protein on the surface has 80 serotypes. It activates factor H to inactivate alternative pathway.
Anti-C5a peptidase inhibit macrophage and neutrophil chemotaxis.
Streptokinase lyse clots (used as a drug!) - note that S.aureus uses staphylokinase.
Hyaluronidase breaks down tissue
Exotoxin which cause toxic shock like syndrome
DNAses breaks down DNA in pus to reduce abscess viscosity
Closely related to S.equi (lancefield group C) in horses. S.equi has the siderophore equibactin. Causes strangles and bastard strangles.
Streptococcus pneumoniae
Colonises nasopharynx via adhesins. Produces IgA protease, pneumolysin, carbohydrate capsule resists phagocytosis by alveolar macrophages. Migrates to lower respiratory tract to cause pneumonia.
Following factors predisposes to colonisation: Alcoholism + viral respiratory infections.
Bordetella pertussis
Toxin action and infalmmation by lipid A causes paroxysms of coughing (sudden attacks of coughing), leading to neurological sequelae.
All respiratory pathogens colonise nasopharyngeal epithelium via adhesins, apart form Yersinia pestis which first spreads via lymph (causing buboes), then to bloodstream, then to lungs. All cause damage via lipid A mediated inflammation.
TB
M.bovis is a zoonosis, spreading to humans via non-pasteurised milk.
M.TB is a non-motile obligate aerobe. Grows SLOWLY. Has mycolic acid coat: Hard to destain so ‘acid-fast’. Resistant to drying, disinfectants, immune attack.
Ingested by alveolar macrophages and survive inside by inhibiting phagosome-lysosome fusion, producing ESAT6 which is a pore forming toxin, and downregulates ROS production. Killing of macrophage allows bacteria to spread around body causing ‘miliary TB’.
Tuberculin skin test is a type IV hypersensitivity reaction caused by CD4+ T cells made against M.TB.
In acute infection, TH1 response enough. Chronic infection needs TH2 response. Chronic infection also causes granulomatous inflammation with caseous necrosis.
Secondary TB usually happens at the lung apex, because M.TB is an obligate aerobe, and apex of lung has highest oxygen tension.
