Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Microbiology (DEN 303) > Anaerobic bacteria > Flashcards

Anaerobic bacteria Flashcards

You may prefer our related Brainscape-certified flashcards:
Biology 101 flashcards
1
Q

What are anaerobic organisms

A

Do not require oxygen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

2 main categories of anaerobic micro-organism

A

Obligate anaerobes, which are harmed by the presence of oxygen
Facultative anaerobes, which can grow without oxygen but use oxygen if it is present
(Microaerophiles- grow in atmosphere of low oxygen <5%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Anaerobosis

A

Anaerobic respiration/ fermentation

  • production of energy (ATP) without involvement of oxygen
  • anaerobes may use fermentation or anaerobic respiration
  • in presence of oxygen, facultative anaerobes can use aerobic respiration
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Aerobic respiration

A

Glucose comes in –> glycolysis –> acetyl CoA –> TCA cycle –> electron transport chain
Max ATP = 38/mol glucose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Anaerobic fermentation mechanism

A

Organic electron acceptor in the absence of oxygen
-e.g. lactic acid/ lactate
2ATP + acids (VFAs) /alcohols > incomplete breakdown products
-less energy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Fermentation products

A 
Lactic acid
-degrades enamel over time
Acetic acid
Enteric bacteria (propionic acid)
Butyric acid (produced by many oral anaerobes e.g. Clostridium)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Propionic acid

A

Propionibacterium first isolated from Emmentaler cheese
Fermentative production of CO2 creates holes
Propionic acid adds to the flavour!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Aerobic respiration

A

Converting energy from, e.g., glucose, into a ‘usable form’
Aerobic respiration - ATP is released as electrons are transported along chain to final acceptor O2 (forms water)
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+)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Anaerobic respiration - energy available = less

A

Inefficient process e.g. Sulphate:
glucose + 3SO42- + 3H+  6HCO3- + 3SH-, ΔG0’ = -453 kJ
ΔG0’ of aerobic respiration of glucose is -2844 kJ
Anaerobes often slower growth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Anaerobic lifestyle - WHY

A

Allow growth in low O2 tension environments…. E.g. Gut/ sub-gingival biofilm plaque
Drawbacks for obligate anaerobes: no ability to resist presence O2 or other radicals that are by-products of aerobic life

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Lab diagnosis/ study of anaerobes

A

Special culture methods to exclude O2 - Jars, cabinets
Gram stain, spore stain, sensitivity to metronidazole
-only obligate anaerobes sensitive to metronidazole
Sugar fermentation- species specific?
Toxin production- Clostridia
Gas-liquid chromatography
- fatty acid end products (VFAs)
16s RNA sequencing
Maldi-TOF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Major anaerobic bacteria in humans

A 
Clostridia
Bacteroides
Fusobacterium
Porphyromonas and Black-Pigmenters
Gerdnerella and GPACs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Clostridium species

A 
Large, straight, gram-positive bacilli
Produce endospores
Produce endospores
Produce exo-toxins
Important species in prominent diseases
-Cl. perfringens - gas gangrene, food poisoning
-Cl. botulinum - botulism (food)
-Cl. tetani - tetanus (environmental)
-Cl. difficile - pseudomembranous colitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Cl. perfringens

A

Capsulate, non-motile, Gram positive Rod
-polysaccharide capsule, repeating units of 6 sugars:
[→ 4)Glc pβ(1 → 3)Gal pNAcβ(1 → 4)Glc pAβ(1 → 3)Glc pNAcβ(1 → 2)Gal pα(1 → 3)Man pβ(1 →)]n)
-spreading, fast growing, BETA hemolytic colonies on BA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

5 types of exo-toxins (Cl. perfringens)

A

A-E

Differentiated based on production of ‘major lethal’ toxins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Major exo-toxin (Cl. perfringens)

A 
alpha-toxin:
Phospholipase  C/ lecithinase
Lyses RBCs, platelets, Leukocytes and endothelial cells
Inflammation &amp; major swelling
oedema, bleeding (anti-platelet activity)
Haemolysis
Kidney damage- renal failure
Myocardial dysfunction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Other VFs (Cl. perfringens)

A

Proteases and hyaluronidase destroy tissue
Enterotoxin - pore forming, heat labile
-produced upon sporulation of ingested bacteria in stomach acid reaction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Toxin detection (Cl. perfringens)

A

Nagler reaction/ plate

  • opacification due to phospholipase activity of alpha toxin (no anti-toxin)
  • clostridial innoculation where alpha toxin on other half of plate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Diseases caused by Cl. perfringens

A 
Gas gangrene (Clostridial myonecrosis)
Food poisoning
20
Q

Gas gangrene (clostridial myonecrosis)

A

Spore contamination of wounds
-source – soil, animal & human excreta
Oedema, gas formation, necrosis, toxaemia, cellulitis
-treatment: surgery (amputation), antibiotics

21
Q

Food poisoning (Cl. perfringens)

A

2nd/3rd most common cause of food poisoning
Incubation 10-12 h.
abdominal cramps, diarrhoea, (vomiting and fever unusual); resolves within 24 hours.
many cases subclinical
-antibodies to the toxin common in the population

22
Q

Food poisoning in terms of Cl. perfringens

A

C. perfringens/ spores in soil and animal gut
C. perfingens grows in food- meats
Spores survive cooking, germinate in food.
Food ingested
Bacteria sporulate and produce Enterotoxin in stomach
Intestinal epithelim damage, inhibition of glucose transport
Diarrhoea (self-limiting)

23
Q

Tetanus

A

Acute spastic paralysis caused by a potent bacterial neuro-exotoxin
Only ngs needed to cause disease and death
Characterised by Lockjaw (trismus), ricus sardonicus
Caused by uncontrolled contraction of muscles- mostly in CNS

24
Q

Cl. tetani

A

Incubation 10-14 days
Enters body through wounds, splinters, cuts
Spores ubiquitous in the environment (soil etc.)
Spores in soil, contaminates wounds
Grows in wound, toxin released into bloodstream…
Motile - thin spreading film on agar - drum stick spores

25
Q

Tetanus toxin

A 
Classic A-B neurotoxin
Tetanospasmin, TeNT
A domain contains active site
B domain> Carbohydrate receptor binding- Sialic acid containing poly-sialic-gangliosides
Zinc endopeptidase (A-domain)
Breaks down synaptobrevins
Prevents release of inhibitory transmitter (Gamma-aminobutyric acid- muscle relaxant)
Absorbed from infectious focus
Travels along a-fibres to CNS
0.1ng kills a mouse
26
Q

Treatment for tetanus

A

Anti toxin + penicillin + metranidazole

27
Q

Prevention of tetanus

A

Immunisation - toxoid

28
Q

Tetanus worldwide

A

still kills 30-50% in resource poor countries
Most cases neonates, small children, post-birth mothers
15-30,000 per year

29
Q

Botulism (contaminated sausage - botulus is latin for sausage)

A

Caused by ingestion of preformed toxin from contaminated food containing Cl. Botulinum bacteria
Mostly in food that has been heated, then cooled and stored for long-periods
Historically associated with Tinned food (home).
Flaccid paralysis
Drooping eyelids, progressive
motor loss, flaccid paralysis;
Neurological symptoms- dizziness
respiratory & cardiac failure

30
Q

Cl. botulinum

A 
Motile Gram-positive bacillus
-sub-terminal spores
-widely distributed saprophyte e.g. soil
-optimum growth 35°C, some can grow 1-5°C
Causes botulism
-severe form of food poisoning
-incubation 1-2 days
Toxin released as Progenitor complex to protect during passage through stomach>> intestine> bloodstream
31
Q

Botulinum toxin

A

Potent neurotoxin – BoNT, (BoTox)
-7 types A – G; A, B & E most common
-A domain contains active site
-B domain> Carbohydrate receptor binding- Sialic acid containing DI-sialic-gangliosides (
-Zinc endopeptidase
–>affects peripheral cholinergic synapses
–>blocks release of
acetylcholine
–>IRREVERSIBLE BINDING!

32
Q

Botulism treatment

A

Remove toxin

-polyvalent anti-toxin

33
Q

Bolutism outbreaks

A

April - May 2017
traced the outbreak to a gas station in California’s Sacramento County
1 dead, 9 sick
BUT, could have been prevented if sauce heated above 75C, 20mins…..

34
Q

Botox

A

Because it can weaken muscles temporarily when injected in small amounts, used for treatment of spasms and dystonias, e.g

  • strabismus (Cross-eyes)
  • bruxism (tooth grinding)> linked to bone loss
  • torticolis (neck spasms)
  • muscle spasms in cerebral palsy
35
Q

C. difficile

A

Antibiotic/ hospital associated diarrhoea:
Associated with broad-spectrum antibiotic use, clindamycin and ampicillin
Outcompetes rest of population after antibiotic course complete
Hospital outbreaks, risk in elderly, care homes
Spore forming- resistant to heat and disinfectants, shed in faeces
Severe diarrhoea
Two exotoxins A and B
Pseudomembranous colitis: bowel disease- can lead to rupture

36
Q

Pseudomembranous colitis

A

Adherent membrane of inflammatory cells and necrotic debris

Antibiotic-associated diarrhoea

37
Q

C. difficile toxins (skipped over in lecture)

A

Produces TcdA and TcdB
-glucosyltransferases
-toxin present in patient’s stool
–>primary diagnostic marker
Cell receptor for TcdA is disaccharide Galß1-4GlcNac
Inactivates Rho (family of GTPases)
-actin condensation, rounding of the cells, membrane blebbing, and apoptosis of cell
-leads to neutrophil infiltration, disruption of tight junctions, fluid accumulation

38
Q

C. difficile toxin mechanism

A 
2x toxins encoded by tcdA and tcdB
 A-B toxins> glycosylate G-protein
 Bind disaccharide receptor on intestinal cells 
internalised and Catalytic domain (A) 
released into cytoplasm
Activate host neurons >>> diarrhoea
Induce cytokines>>> attract PMNs >>> 
disrupts cell junctions>>> Tcd-B damages underlying mucosa and tissues
 Septicaemia and bowel damage
Toxin present in patient’s stool
primary diagnostic marker of infection
39
Q

C. difficile treatment

A

Common in faeces of neonates, not adults
Antibiotic-associated diarrhoea increased
-epidemics amongst elderly (transmission of spores)
Therapy is vancomycin or metronidazole
-+ remove offending selective antibiotic e.g. clindamycin
Prevention measures: cleaning, hand-washing, quarantine
Limit use of broad-spectrum antibiotics in ‘at-risk’ patients
Treatment: - removal of broad-spectrum antibiotic
- metronidazole or vancomycin

40
Q

Gram negative anaerobes

A 
Bacteroides
-abdominal wound infections
-peritonitis
Prevotella
-oral and genital infections
Porphyromonas
-oral infections
Fusobacterium
-F.nucleatum - oral and vaginal infections
-F.necrophorum - Necrobacillosis - systemic sepsis and multisystem abscesses
41
Q

Gram-positive anaerobes

A

Peptostreptococcus (Parvimonas)
Eubacterium
Bifidobacterium
Gardnerella

42
Q

Bacteroides fragilis

A 
Most common anaerobe recovered from non-oral clinical infections
-abdominal, pelvic, brain, liver
-often mixed infections 
-involved in bacterial vaginosis
Gram-negative bacillus 
-capsulate (CPA, LPS)
Toxigenic strains- some cause diarrhoea
-toxin cleaves E-cadherin
Resistant to numerous antibiotics
clindamycin, metronidazole (some strains)
43
Q

Prevotella

A

Gram-negative, non-motile, rod-shaped
In the oral cavity, Prevotella colonize by binding or attaching to other bacteria in addition to epithelial cells, creating a larger infection in previously infected areas.
Abscesses, bacteraemia, wound infection, bite infections, genital tract infections, and periodontitis

44
Q

Porphyromonas

A

Non motile, Gram negative, rod-shaped
Periodontal disease – P.gingivalis is commonly found in biofilm with other spp.
(e.g, T.forsythia, T.denticola- RED COMPLEX)
Forms black colonies on blood agar
-P.gingivalis releases cysteine proteases – ‘gingipains’ that bind and degrade erythrocytes, destroy receptors, degrade complement components, subvert cell signalling

45
Q

Fusobacterium

A

LONG Rod shaped spindle-shaped
bacillli, Gram negative
Associated with periodontal disease (F.nucleatum), skin ulcers, respiratory infections, BV, ANUG- often in mixed infection
Highly effective at biofilm formation
Treatment – antibiotics (Clindamycin, Chloramphenicol)
main spp.
-F.nucleatum - oral and vaginal infections, PTB
-F.necrophorum - Necrobacillosis - systemic sepsis and multisystem abscesses- Lemierres syndrome- rare head and neck origin

46
Q

F. nucleatum linked to

A

Colon cancer

-FadA adhesin stimulates oncogenic response in colon- BIG news in microbiology- READ about it….

Microbiology (DEN 303) (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions