anaerobic organisms Flashcards

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1
Q

categories of anaerobic organsims

A

obligate anaerobes
faculatative anerobes
microaerophiles

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2
Q

obligate anerobes

A

harmed by the presence of oxygen

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3
Q

facultative anerobes

A

can grow without oxygen but uses oxygen if present

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4
Q

microaerophiles

A

grow in atmosphere of low oxygen less than 5%

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5
Q

what is the terminal e- acceptor in anaerobic respiration

A
lactic acid (organic)
inorganic (sulphate nitrate)
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6
Q

fermentation products and products from incomplete fermentation

A
lactic acts
(feeds NAD back into muscles when there is oxygen starvation 

products from incomplete fermentation

1) Vingear
2) propionic acid
3) some yeast produce alcohol

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7
Q

aerobic respiration vs anaerobic respiraton

A

1) Aerobic respiration - ATP is released as electrons are transported along chain to final acceptor O2 (forms water)
2) Anaerobic respiration uses electron transport chain but the final electron acceptor is not O2
• Nitrate (NO3- reduced to nitrite NO2-, or N2)
• Ferric iron (Fe3+ reduced to Fe2+)

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8
Q

what do organisms have to stop oxygen radicals and what do they do

A

superoxide dismutase
catalase
perioxdase

convert radicals to water

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9
Q

what can be used for study of anaerobes

A

Obligate anaerobes can process the metronidazole, allows diagnosis of anaerobic organisms

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10
Q

lab diagnosis of anaerobes

A
Sugar fermentation (species specific?)
Toxin production (clostridia)
Gas liquid chromatography measures fatty acid end products (VFAs)
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11
Q

major anaerobic bacteria in humans

A

1) clostridia
2) Bacteroides
3) fusobacterium
4) porphryromonas and black pigmenters
5) Gardnerella and GPACs

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12
Q

clostridium species

A
  • large, straight, gram + bacilli
  • produce endospores
  • produce exo toxins
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13
Q

important clostridium species in prominent diseases

A

1) Cl. perfringens
- gas gangrene
- food poisoning
2) Cl. Botulinum
- botulism (food)
- uses in botox
3) Cl. tetani
- tetaus (Environmental)
4) Cl. difficile
- pseudomembranous colitis

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14
Q

cl perfringens

A
  • Capsulate
  • non motile
  • gram + rod
  • polysaccharide capsule
  • spreading, fast growing, double BETA hemolytic colonies on BA (also has some alpha hemolysis)
  • i.e. several types of hemolysis
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15
Q

exo toxins of cl perfringens

A

5 toxigenic types A-E

major toxin is alpha toxin

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16
Q

what can exo toxins lead to

A
  • phospholipase C/lecithinase
  • lyses RBCs, platelets, leukocytes and endothelial cells
  • inflammation and major swelling
  • oedema, bleeding (antiplatelet activity)
  • haemolysise
  • kidney damage- renal failure
  • myocardial dysfunction
17
Q

enterotoxin

A
  • pore forming
  • heat labile
  • produced upon sporulation of ingested bacteria in stomach acid reaction (important in diarrhoeas)
  • activated in the stomach
18
Q

toxin detection what is used and positive test

A

nagler reaction/plate
Alpha toxin – used to confirm perfringens
- Antitoxin on one side of plate, not on the other side
- presence of the toxin leads to precipitate when toxin is present
- neutralised with antitoxin, no ppt
- sporogenes does not produce toxin therefore no difference

19
Q

treatment of gas gangrene and what causes it

A

cl perfringens

surgery(amputation) antibiotic

20
Q

what causes food poisoning

A

clos perfrigens enterotoxins

21
Q

what causes tetanus / what is tetanus

A

cl tentant

Acute spastic paralysis caused by a potent bacterial neuro-exotoxin (muscles contract uncontrollably)

22
Q

cl tentani and how does it spread/track

A

Motile
Gram + rods
- thin spreading film on agar
- drum stick spores

toxin released into body, tracks along nerves to CNS

23
Q

tetanus toxin and how it works etc

A
Classic A-B neurotoxin
-	Tetanospasmin, TeNT
2 domains
–	A domain contains active site
–	B domain> Carbohydrate receptor binding- Sialic acid containing poly-sialic-gangliosides (found on the outside of nerve cells)
Zinc endopeptidase (A-domain)
-	Prevents release of inhibitory transmitter (Gamma-aminobutyric acid- muscle relaxant)
Absorbed from infectious focus
–	Travels along a-fibres to CNS
24
Q

treatment and prevention of tetnus

A
Treatment
-antitoxin/immunoglobulin +penicillin +metronidazole
Prevention
-	immunisation
-	tetanus toxoid
25
Q

botulism and symptoms

A
Caused by ingestion of preformed toxin from contaminating Cl.Botulinum 
Symptoms
-	drooping eyelids
-	progressive motor loss
-	flaccid paralysis
Neurological sypmtoms
-	diziness
-	respiratory and cardiac failure
26
Q

cl botulinum type of bacteria

A

Endospore that is subterminal

  • motile gram + bacillus
  • subterminal spores

Toxin released as progenitor complex to protect during passage through stomach, intestine then bloodstream

27
Q

botulinum toxin and how it works

A

7 types A-G
A B and E most common
- A domain contains active site
- B domain – carbohydrate receptor binding – sialic acid containing DL – sialic- gangliosides
Zinc endopeptidase
- affects peripheral cholinergic synapses
- blocks release of acetylcholine (blocks stimulatory molecule)
- irreversible binding, relaxation
- stronger binding than tentaus toxin

28
Q

treatment of botulism

A
  • remove toxin

- polyvalent antitoxin

29
Q

antibiotic/hospital associated diarrhoea

A

Cl. difficle
- spores of the organisms germinate and can overwhelm gut flora can cause psudomemntanous colitis (lesiosn in the gut)
- need to give a narrow rather than broad antibiotic
Antibiotic associated diarrhoea
- associated with broad spectrum antibiotic use, clindamycin and ampicillin
- outcompetes rest of population after antiobtic course complete

30
Q

psudomembranous colitis

A

Antibiotic associated diarrhoea

Adherent membrane of inflammatory cells and necrotic debris

31
Q

cl difficile toxins and how do they work

A

Produces TcdA and TcdB
- glucosyltransferases
- toxin present in patients stool (primary diagnostic marker)
Cell receptor for TcdA disaccharide GalB I – 4GlcNac (bind via glycoproteins)
Inactivates Rho (family of GTPases)
- actin condensation, rounding of cells, membrane blebbing and apoptosis of cell
- leads to neutrophil infiltration, disruption of tight junctions, fluid accumulation

32
Q

treatment and prevention of c difficile

A

Therapy is vancomycin or metronidazole
- + remove offending broad spectrum, selective antibiotic eg clindamycin

  • cleaning
  • hand washing (to remove transmission of spores)
  • quarantine
    Limit use of broad spectrum antibiotics in at risk patients
33
Q

bacteroides fragilis

A
Gram – bacillus
-	capsulate (CPA, LPS)
Toxigenic strains
-	some cuase diarrhoea
-	toxin cleaves E- cadherin
34
Q

what is bactericides fragilus resistant to

A
  • clindamycin

- metronidazole (some strains)

35
Q

prevotella

A

black pigmented anaerobe
gram -
non motile
rod shaped

36
Q

porphyrumonoas

A

black pigmented anaerobe

  • non motile
  • gram –
  • rod shaped
  • PDD – gingivalus commoly found in biofilm with other spp (eg T forsythia)
  • forms black colonies on blood agar
37
Q

fusobacterium and treatment

A
  • long rod shaped spindle shaped bacilli, gram –
  • associated with PDD, skin ulcers, respiratory infections
  • highly effective at biofilm formation
    black pigmented anerobe

treatment
- antibiotics clindamycin

38
Q

black pigmented anerobe examples

A
prevotella
porphymonas
fusobacterium
GPAC- peptostreptococcus
eubacteria and bifidobacterium
39
Q

b fragilis

A

causes 25% of non clostridia anaerobic infections