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MICROBIOLOGY PART 1 303 > Anaerobic Bacteria > Flashcards

Anaerobic Bacteria Flashcards

1
Q

What do anaerobic organisms not require?

A

Anaerobic organisms do not require oxygen

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2
Q

What are the main categories of anaerobic microorganisms?

A

Obligate anaerobes = harmed by presence of oxygen
Facultative anaerobes = can grow without oxygen but use oxygen if it’s present
Microaerophiles = grow in atmosphere of low oxygen <5%

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3
Q

Features of anaerobiosis?

A

Anaerobic respiration/fermentation

  • Produce energy without oxygen
  • May use fermentation or anaerobic respiration
  • In presence of oxygen = faculative anaerobes can use aerobic respiration
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4
Q

What occurs in anaerobic fermentation?

A

Organic electron acceptor in the absence of oxygen

Glucose - pyruvate (organic e receptors, 2ATP plus acids > incomplete breakdown products) - TCA cycle

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5
Q

What are the fermentation products?

A

Lactic acid
Acetic acid
= streptococcus, lactobacillus

H2, CO2, acetic acid, ethanol, lactic acid, propionic acid
= Enteric bac (E.coli)

H2, CO2, Ethanol, butanol, acetone
= Clostridium
= Live in mouth

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6
Q

How much glucose is produced by aerobic respiration?

A

38/mol glucose

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7
Q

What is respiration?

A

Converting energy from e.g. glucose into a usable form

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8
Q

What is aerobic respiration?

A

ATP is released as electrons are transported along chain to final acceptor O2 (forms water)

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9
Q

What is anaerobic respiration?

A

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+)

Allows growth in low O2 environs
Drawbacks for obligate anaerobes; no ability to resist presence O2 or other radicals that are by-products of aerobic life
Inefficient process
Anaerobes often slower growing

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10
Q

How are anaerobes diagnosed/studied?

A

Jars/cabinets to exclude O2 subculture
Gram stain, spore stain, anaerobes = sensitivity to metronidazole
Sugar fermentation
Toxin production - Clostridia
Gas-liquid chromatography - fatty acid end products
16s RNA sequencing

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11
Q

Give examples of major anaerobic bac in humans?

A 
Clostridia
Bacteriodes
Fusobacterium 
Porphyromonas and black pigmented
Gardnerella
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12
Q

Features of clostridium species?

A 
Large, straight, gram pos bacilli
Produce endospores and exo-toxins
Cl.perfringens - food poisoning 
Cl.botulinum = botulism (food)
Cl.tetani - tetanus
Cl.difficile - pseudomembranous colitis
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13
Q

Cl. perfringens features?

A

Capsulated, non-motile, gram pos rod
Polysaccharide capsule, repeating units of 6 sugars
Fast growing, spread, BETA hemolytic colonies on BA

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14
Q

Exo-toxins are differentiated based on? What are the types of exo-toxins?

A

Differentiated based on production of major lethal toxins

5 toxigenic types; A-E

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15
Q

Features of the major exo-toxin?

When are enterotoxins formed? Features?

A

Alpha-toxins;

  • Phospholipase C
  • Luses RBCs, platelets, leukocytes, endothelial cells
  • Inflam and major swelling
  • Oedema, bleeding
  • Haemolysis
  • Kidney damage - renal failure
  • Myocardial dysfunction

Other VFs; proteases and hyaluronidase - destroy tissue
Enterotoxin - pore forming, heat labile - produced upon sporulation of ingested bac in stomach acid secretion

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16
Q

How to test for toxins?

A

Nagler test - half plate infiltrated with antitoxin, rxn = fuzzy area, no rxn = colonies grown
clowdiness on side without alpha antitoxin

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17
Q

Name the diseases caused by Cl.perfringens? Treatment?

A

Gas gangrene

  • Spore contamination of wounds - source - soil, animal and human excreta
  • Oedema, gas formation, necrosis, toxaemia, cellulitis
  • Treatment - surgery (amputation), antibiotics
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18
Q

Features of food poisoning?

A

Incubation 10-12hrs
Abdominal cramps, diarrhoea
Resolves in 24hrs

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19
Q

How is diarrhoea from food poisoning caused?

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

20
Q

Tatanus features? What causes it?

A

Acute spastic paralysis caused by potent bacterial neuro-exotoxin
Trismus, rictus grin
Caused by uncontrolled contraction of muscles - mostly in CNS

21
Q

Cl.tetani features?

A

Incubation 10-14 days
Enters body through wounds, splinters, cuts
Spores ubiquitous in environment
Spores in soil, contaminates wounds
Grows in wounds, toxin released into bloodstream
Motile - thin spreading film on agar (drumstick)

22
Q

Name the tetanus toxins and their features? (How does Cl.tenani cause disease)

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 (muscle relaxant)
Absorbed from infectious focus 
- Travels along alpha fibres to CNS
-2.5ng/kg kills a human
23
Q

What treats tetanus?

A

Anti-toxin/immunoglobulin plus penicillin and metronidazole

Prevention - immunisation; toxoid

24
Q

What causes botulism?

A

Ingestion of preformed toxin from contaminated food containing Cl.Botulinum bacteria
- Mostly in foods that have been heated, then cooled and stored for long periods

25
Q

Symptoms/signs of botulism?

A

Flaccid paralysis
Drooping eyelids, progressive motor loss, flaccid paralysis
Neurological symptoms - dizziness, resp and cardiac failure

26
Q

Cl.botulinum features?

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

27
Q

Botulinum toxin features?

A

Potent neurotoxin - BoNT

  • 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
28
Q

How to treat botulinum toxin?

A

Remove toxin

Polyvalent anti-toxin

29
Q

What can botox do? How?

A

Can weaken muscles temporarily when injected in small amounts
Uses botulinum toxin

30
Q

What can botox treat?

A

Used to treat spasms and dystonias e.g.

  • Strabismus (cross eye)
  • Bruxism = bone loss
  • Toricolis (neck spasms)
  • Muscle spasms in cerebral palsy
31
Q

Antibiotic associated diarrhoea C.difficile features?

A

Associated with broad spectrum antibiotic use - clindamycin and ampicillin
Outcompetes rest of pop after antibiotic course complete
Risk in elderly
Spore forming - resistant to heat and disinfectants, shed in faeces
Severe diarrhoea
2 exotoxins A and B
Pseudomembranous colitis; bowel disease - can lead to rupture

32
Q

What is Pseudomembranous colitis?

A

Antibiotic-associated diarrhoea

33
Q

Cl. Difficile- treatment?

A

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

34
Q

Name the other gram pos and gram neg anaerobes

A

Gram-negative anaerobes

  • 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

Gram-positive anaerobes

  • Peptostreptococcus (Parvimonas)
  • Eubacterium
  • Bifidobacterium
  • Gardnerella
35
Q

List the black pigmented anaerobes

A

Prevotella
Porphyromonas
Fusobacterium

36
Q

Features of prevotella? What can it cause?

A

Gram neg, non-motile, rod shaped
Colonise in oral cavity by binding or attaching to other bacteria in addition to epi cells = larger infection in previously infected areas
Abscesses, bacteraemia, wound infections, bite infections, periodontitis

37
Q

Porphyromonas features?

A

Non motile, Gram negative, rod-shaped
PD - P.gingivalis = commonly found in biofil with other spp.
Forms black colonies on blood agar

38
Q

What does P.gingivalis do?

A

Releases cysteine proteases - gigipains = bind and degrade erythrocytes, destroy receptors, degrade complement components and subvert cell signalling

39
Q

Fusobacterium features? Treatment?

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

40
Q

What is F. nucleatum linked to?

A

Colon cancer - FadA adhesin stimulates oncogenic response in colon

41
Q

What is GPAC?

A

‘GPAC’- Peptostreptococcus-
normal flora of all mucocutaneous surfaces (inc. oral)
Often isolated from infections such as chronic deep organ abscesses, obstetric and gynecological sepsis + intraoral infections.
Not well studied: difficulties with laboratory identification, isolated from mixed infections.

42
Q

Features of Eubacterium and Bifidobacterium?

A

Gram Positive rods, rarely isolated from abdominal infections POST oral/ genital trauma.

43
Q

Features of Gardnerella and Mobilincus?

A

Bacterial Vaginosis in females, associated with dysbiotic communities and PreTerm Birth

44
Q

Cl.difficile toxins?

A

Produces TcdA and TcdB
- GluActivate host neurons&raquo_space;> diarrhoea

Induce cytokines»> attract PMNs&raquo_space;>
disrupts cell junctions»> Tcd-B damages underlying mucosa and tissues

Septicaemia and bowel damage cosyltransferases
- Toxin present in pt’s stool (primary diagnostic marker)

Cell receptor for TcdA is disaccahride Gallß1-4GlcNac

Inactivates Rho (family of GTPases)

  • Actin condensation, rounding of the cells, membrane blebbing, cell apoptosis
  • Leads to neutrophil infiltration, disruption of tight junctions, fluid accumulation
45
Q

Cl.difficile toxin mechanisms?

A

TcdA and TcdB:
- Activate host neurons&raquo_space;> diarrhoea
- Induce cytokines»> attract PMNs&raquo_space;>
disrupts cell junctions»> Tcd-B damages underlying mucosa and tissues

Septicaemia and bowel damage

46
Q

Bacteriodes Fragilis features?

A

Most common anaerobe recovered from non-oral clinical infecs

  • Abdominal, pelvic, brain, liver
  • Involved in bacterial vaginosis

Gram neg bacillus
Toxigenic strains - some cause diarrhoea
- Toxin cleaves E-cadherin

Resistant to numerous antibiotics - clindamycin, some strains of metronidazole

MICROBIOLOGY PART 1 303 (12 decks)

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