anaerobic organisms

Question 1

categories of anaerobic organsims

Answer 1

obligate anaerobes
faculatative anerobes
microaerophiles

Question 2

obligate anerobes

Answer 2

harmed by the presence of oxygen

Question 3

facultative anerobes

Answer 3

can grow without oxygen but uses oxygen if present

Question 4

microaerophiles

Answer 4

grow in atmosphere of low oxygen less than 5%

Question 5

what is the terminal e- acceptor in anaerobic respiration

Answer 5

lactic acid (organic)
inorganic (sulphate nitrate)

Question 6

fermentation products and products from incomplete fermentation

Answer 6

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

Question 7

aerobic respiration vs anaerobic respiraton

Answer 7

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+)

Question 8

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

Answer 8

superoxide dismutase
catalase
perioxdase

convert radicals to water

Question 9

what can be used for study of anaerobes

Answer 9

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

Question 10

lab diagnosis of anaerobes

Answer 10

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

Question 11

major anaerobic bacteria in humans

Answer 11

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

Question 12

clostridium species

Answer 12

• large, straight, gram + bacilli
• produce endospores
• produce exo toxins

Question 13

important clostridium species in prominent diseases

Answer 13

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

Question 14

cl perfringens

Answer 14

• 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

Question 15

exo toxins of cl perfringens

Answer 15

5 toxigenic types A-E

major toxin is alpha toxin

Question 16

what can exo toxins lead to

Answer 16

• 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

Question 17

enterotoxin

Answer 17

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

Question 18

toxin detection what is used and positive test

Answer 18

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

Question 19

treatment of gas gangrene and what causes it

Answer 19

cl perfringens

surgery(amputation) antibiotic

Question 20

what causes food poisoning

Answer 20

clos perfrigens enterotoxins

Question 21

what causes tetanus / what is tetanus

Answer 21

cl tentant

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

Question 22

cl tentani and how does it spread/track

Answer 22

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

toxin released into body, tracks along nerves to CNS

Question 23

tetanus toxin and how it works etc

Answer 23

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

Question 24

treatment and prevention of tetnus

Answer 24

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

Question 25

botulism and symptoms

Answer 25

``` 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 ```

Question 26

cl botulinum type of bacteria

Answer 26

Endospore that is subterminal - motile gram + bacillus - subterminal spores Toxin released as progenitor complex to protect during passage through stomach, intestine then bloodstream

Question 27

botulinum toxin and how it works

Answer 27

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

Question 28

treatment of botulism

Answer 28

- remove toxin | - polyvalent antitoxin

Question 29

antibiotic/hospital associated diarrhoea

Answer 29

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

Question 30

psudomembranous colitis

Answer 30

Antibiotic associated diarrhoea | Adherent membrane of inflammatory cells and necrotic debris

Question 31

cl difficile toxins and how do they work

Answer 31

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

Question 32

treatment and prevention of c difficile

Answer 32

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

Question 33

bacteroides fragilis

Answer 33

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

Question 34

what is bactericides fragilus resistant to

Answer 34

- clindamycin | - metronidazole (some strains)

Question 35

prevotella

Answer 35

black pigmented anaerobe gram - non motile rod shaped

Question 36

porphyrumonoas

Answer 36

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

Question 37

fusobacterium and treatment

Answer 37

- 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

Question 38

black pigmented anerobe examples

Answer 38

``` prevotella porphymonas fusobacterium GPAC- peptostreptococcus eubacteria and bifidobacterium ```

Question 39

b fragilis

Answer 39

causes 25% of non clostridia anaerobic infections