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Bacteriology Flashcards

1
Q

Shape of bacteria

A

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).

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2
Q

Endospore formers

A

BC

Bacillus anthracis, ALL Clostridium (tetani, perfringens, botulinum, difficile).

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3
Q

Do not gram stain

A

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).

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4
Q

Encapsulated bacteria

A

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)

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5
Q

Obligate Aerobes

A

Pests Must Die

Pseudomonas aeruginosa, Mycobacterium tuberculosis, c.Diphtheria.

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6
Q

Obligate Anaerobes

A

anaerobes Can’t Breathe

Clostridium (whole genus), Bacteroides fragilis.

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7
Q

Facultative anaerobes

A

ALL ‘-coccus’ + E.coli + Salmonella

They grow less well without oxygen.

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8
Q

Urease activity

A

PuncH
Proteus, Helicobacter pylori
H.pylori and Shigella also pumps H+ out of their cells.

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9
Q

Biofilms

A

So Much Stuff to Prepare/Produce (again)
Streptococcus mutans, Staphylococci, Pseudomonas aeruginosa.
Biofilm production regulated by quorum sensing.

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10
Q

Streptococcus pyogenes cause what diseases

A 
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).

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11
Q

Facultative intracellular bacteria that survives inside macrophages

A

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.

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12
Q

IgA protease

A

NHS

Neisseria (gonorrhoea and meningitidis), Haemophilus influenzae, Streptococcus pneumoniae.

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13
Q

Cytolysins (target membranes)

A

(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.

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14
Q

A-B toxins (enzymatic intracellular toxins)

A

(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.

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15
Q

What does Streptococcus pneumoniae cause

A

MOPS: Meningitis, Otitis media, Pneumonia, Sinusitis.

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16
Q

What pathogens cause Meningitis

A

Easy! NHS!

E.coli K1, Neisseria meningitidis, Haemophilus influenzae type B, Streptococcus pneumoniae

17
Q

Sialic acid capsule

A

E.coli K1 and Neisseria meningitidis.

18
Q

Chronic inflammation

A

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’.

19
Q

Hypersensitivty and autoimmune conditions caused by pathogens

A

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)

20
Q

Diphtheria

A

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.

21
Q

Streptococcus pyogenes virulence factors

A

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.

22
Q

Streptococcus pneumoniae

A

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.

23
Q

Bordetella pertussis

A

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.

24
Q

TB

A

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.

25
Q

Food Intoxications

A

C.botulinum, C.perfringens, Staph aureus.

No bacterial colonisation. Symptoms seen after a few hours. Contrast with food INFECTIONs (symptoms after a few days caused by invasive bacteria).

26
Q

Cholera

A

CTX toxin carried by bacteriophage and integrated into bacterial chromosome.
Cholera uses a HAP system for global regulation.

AB5 toxin structure. B binds to GM1-ganglioside, A-B toxin transported to ER. A subunit goes out of ER to the cytosol. ADP-ribosylates alpha-S.
Too much cAMP increases opening of CFTR. More Cl- secretion, allowing Na+ and H2O to follow out. Causes electrolyte loss and watery diarrhoea.

27
Q

Salmonella

A

S.enterica causes salmonellosis. It invades apical surface of epithelial cells of ileum/colon junction via trigger mechanism (SipA, SipC, SptP on SPI-1).
Remains in a vacuole (unlike Listeria) and replicates.
Released from vacuole and epithelial cell and causes inflammation (gastroenteritis).
Taken up by macrophages and survives inside by switching on SPI-2 genes, allowing it to inhibit phagosome-lysosome fusion, resist oxidative burst.

Host response to salmonella is to increase cAMP production which causes diarrhoea.

Campylobacter also causes food-borne infections and behaves like salmonella.

S.typhi has no animal reservoir unlike S.enterica (present in chicken). Replicates in macrophages and spreads to liver + spleen, secreting CDT toxin and causing typhoid fever. Bacteria shed in bile (like hepatitis A virus). Carriers are important (typhoid Mary).

28
Q

E.coli and Listeria

A

ETEC produces labile toxin. Causes traveller’s diarrhoea. Important disease in pigs.
EPEC and EHEC initially attach via adhesins like ETEC, but it then also injects TIR which causes host cell pedestal formation.
EHEC produces shiga-like toxin which causes renal failure, HUS (haemolytic uraemic syndrome) (mechanism don’t care), bloody diarrhoea. O157 serotype is from beef.
UPEC attaches to bladder via type 1 pili (cause cystitis) and to kidney via P-pili (cause pyelonephritis) and causes UTI.
E.coli also cause meningitis.

Listeria (food-borne bacteria) can cause meningitis and cross placenta.

29
Q

Clostridium difficile

A

TcdA + TcdB toxins glucosylates small GTPases. Colonises colon after eradication of normal microflora by antibiotics. Causes ‘antibiotic-associated diarrhoea’.
Also forms pseudomembrane. Also an issue in horses.
Can treat with faecal transplants.

30
Q

Helicobacter pylori

A

Colonises mucin layer of antrum (lower part of stomach). Very motile (unlike M.TB). Secretes urease to neutralise acid.
Induces IL-8 (a.k.a CXCL8) production by epithelial cells, secretes pore-forming vacuolating cytolysin called VacA.
VacA is hexameric and causes endosomes to swell to become vacuoles. This leads to apoptosis.

Infection leads to cancer due to chronic inflammation and bacterial effector CagA causing increased cell proliferation.

31
Q

Bacteria Vaccines

A

DPT vaccine: Diphtheria toxoid, tetanus toxoid, killed bordetella pertussis.
Pneumonia: polysaccharide from S.pneumoniae, H.influenzae.
Meningitis: polysaccharide from N.meningitides, or from H.influenzae type B coupled to tetanus toxoid
Typhoid: Live attenuated bacteria, or polysaccharide.
Cholera: Killed bacteria.
TB: BCG vaccine from LIVE attenuated M.bovis.

32
Q

Staphylococcus aureus complement evasion strategies

A

‘An AI Committed A SCIN’
Anti-C3 proteins
clumping factor A recruits factor I
Chemotaxis inhibitor protein blocks C5a receptor on neutrophils and macrophages (C5a binding to C5 need to trigger phagocytosis, as well as CR1 bonding C3).
Staphylococcus protein A binds Fc region of IgG to prevent complement activation via classical pathway
Stapylococcus complement inhibitor (SCIN) inhibits C3 convertases.

33
Q

Neisseria gonorrhoea

A

AEIoU
Arthritis, Endocarditis, Infertility, acute Urethritis.
In newborns: conjunctivitis, blindness.
Gonorrhoea of course…

Neisseria meningitidis causing meningitis does NOT aid bacterial survival. Like polio virus, this bacteria would rather not go to the meninges.

34
Q

Yersinia Pestis

A

High Nose Punch Ball

Haemorrhagic inflammation, Necrotic lesions, Pneumonic plague, Buboes

35
Q

CLEan TAGS

A

Chloramphenicol and Clindamycin, Linezolid, Erythromycin – 50S; Tetracycline, AminoGlycosides, Spectinomycin

BOD (5 decks)

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