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Microorganisms + Disease > Infections caused by anaerobes L11 > Flashcards

Infections caused by anaerobes L11 Flashcards

1
Q

what is an anaerobe

A

any organism that does not require oxygen for growth OR required reduced oxygen tension and fails to grow on solid media in 10% CO2 (an equivalent of 20% molecular oxygen)

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2
Q

what is aerotolerance

A

tolerate 2-8 % oxygen

degree to which superoxide dismutase expressed

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3
Q

what are the anaerobes that generally cause human infection

A

aerotolerant (ie tolerate 2-8 % oxygen) and can survive sustained periods- but the do not replicate- in an oxygenated atmosphere

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4
Q

what is a feature most anaerobes do not posess

A

catalase

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5
Q

what do the anaerobes that cause human disease often have

A

superoxide dismutase (catalyses partitioning of O2 radical into their molecular O2 or H2O2) and in general the degree to which this enzyme is expressed dictates the aerotolerance of the organism

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6
Q

how are bacteria currently classified

A

This is the scheme that divides the medically important anaerobes by genus. In decreasing frequency we distinguish: 1. GRAM-ve RODS; 2. GRAM+ve COCCI; 3. GRAM+ve spore forming BACILLI (Clostridia) and non sporing bacilli 4. GRAM-ve COCCI (mailny Veillonella spp)

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7
Q

what is the cause of most anaerobic infections

A 
endogenous microbial flora
Normal flora (Skin, Upper airways, genito-urinary tract and gastro-intestinal)
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8
Q

what is the endogenous role in normal flora

A

providing colonisation resistance
Serve nutritional function
Exert effect on host immunity

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9
Q

how do endogenous strains of normal flora gain access to normally sterile sites

A

breach to anatomical barrier

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10
Q

what do ANA infections indicate

A

ANA infections are usually endogenous indicating that they originate from the hosts’s own flora

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11
Q

what is exogenous acquisition

A

relates to either contamination of wound by objects contaminated
ingestion of food containing (C. botulinum and C. perfringens)
colonisation of GIT with spores and toxin production inside host
person to person spread

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12
Q

what are clinical syndromes examples -main clinical features of anaerobic infection

A

Abscess formation/empyema
> Foul-smelling pus or discharge (eg surgical wound)
> Gas formation in tissues
Necrotising fasciitis (myofasciitis/gas gangrene)
Sepsis syndromes
Toxin-mediated disease

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13
Q

what are clostridia

A

Large Gram-positive spore-bearing bacilli

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14
Q

what feature varies in clostridia

A

Vary considerably in O2 tolerance

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15
Q

what are clostridia important for

A

Most are environmental saprophytes important in putrefaction

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16
Q

what does clostridia produce

A

exotoxins

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17
Q

what are exotoxins

A

Biologically active proteins
Antigenic in nature
Neutralised with specific antisera
Detection can be diagnostic

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18
Q

how many types of Clostridium perfringens are there

A

5

A-E

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19
Q

what does Clostridium perfringens make

A

potent toxins
α toxin = lecithinase = phospholipase C
Egg yolk medium

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20
Q

how is clostridium perfringens differentiated on agar

A

Double zone β haemolysis
Where u get precipitate there is no antitoxin
diagnostic way to see if its perfringens

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21
Q

what is Clostridium perfringens like

A

Non motile, freq non spore forming

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22
Q

what does Clostridium perfringens cause

A

gas gangreene (myonecrosis)
it is life threatening
need surgery and antibiotics

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23
Q

how does Clostridium perfringens cause food poisoning

A

enterotoxin production during sporulation

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24
Q

what is Clostridium tetani

A

Straight slender ‘drumstick’ terminal spore (spore at the terminal end)
neurotoxin

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25
Q

what is the Clostridium tetani gram stain feature

A

readily loses gram stain

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26
Q

what oxygen level does Clostridium tetanineed

A

Obligate anaerobe

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27
Q

what is Clostridium tetani like

A

motile, swarms

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28
Q

where is Clostridium tetani

A

Cattle faeces, contaminated soil

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29
Q

what does Clostridium tetani cause

A

Prevents muscle relaxation leading to spasticity = tetanus

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30
Q

what is the clinical diagnosis of Clostridium tetani

A

3 laboratory tests
Isolate organism
Detect toxin in serum (Ref lab)
Low/no ab levels supports diagnosis

31
Q

how is suspected Clostridium tetani - tetanus clinically managed

A

Require ITU observation
Wound cleaned
Antimicrobials including metronidazole or penicillin
Anti-tetanus antibody (TIG)
Vaccination with tetanus toxoid on recovery important to prevent future episodes

32
Q

what are tetanus prone wounds like

A

Puncture-type
Contact with soil/manure
Significant degree of devitalised tissue
Any wound with delay >6 hours before surgery

33
Q

how is Clostridium tetani - tetanus prevented

A

Active immunisation with toxoid introduced in UK 1961 (5 doses)

34
Q

what is the tetanus neurotixin

A

Tetanospasmin

35
Q

what are the symptoms of tetanus

A

Symptoms involve characteristic grin of the face, spastic posture of limbs and trunk

36
Q

how does tetanus neurotoxin work

A

binds to the resynaptic membrane of neuromuscular junction, internalized and transported retro-axonally to
the spinal cord
spastic paralysis induced by the toxin is due to the blockade of neurotransmitter release from spinal inhibitory interneurons

37
Q

what is Clostridium botulinum

A

Motile

sub-terminal spores

38
Q

where is Clostridium botulinum

A

always present in nature - soil

39
Q

what is Clostridium botulinum known for

A

most powerful toxin known

40
Q

what does Clostridium botulinum cause

A

Descending FLACCID paralysis = Blocks acetylcholine release at neuromuscular synapses
Blurred vision, difficulty swallowing, headaches and muscle weakness

41
Q

what can Clostridium botulinum be used for

A

Relatively heat stable: bioweapon potential

Botox

42
Q

what causes food-borne botulism

A

ingestion of preformed toxin in food that has been contaminated as a result of it being improperly canned or preserved

43
Q

what causes wound botulism

A

wound becomes infected with botulinum spores which then germinate, reproduce and then produce toxins ie growth of the organism

44
Q

what causes infant botulism

A

very rare. Ingestion of spores or organisms followed by colonisation and toxin production in gut. Usually only affects babies < 12 months old. After this, children develop a defence against the spores

45
Q

how are botulism clinical syndromes treated

A

Involve ITU
Polyvalent antitoxin to neutralise unfixed toxin
Wound botulism- surgical debridement and antibiotics

46
Q

how is a reference laboratory of botulism clinical syndrome done

A

mouse bioassay for toxin

Anaerobic culture of food/faeces

47
Q

how is botulism clinical syndromes prevented

A

Prophylactic use of polyvalent antitoxin
Vaccine (not widely used as concerns re effectiveness and adverse effects)
Avoid home canning/adequate food preparation
Do not feed honey to infants <12 months

48
Q

how do the seven serotypes of botulinum neurotoxins work

A

act at the periphery by inducing a flaccid paralysis due to the inhibition of acetylcholine release at the neuromuscular junction

49
Q

what do tetanus and botulinum toxins have in common

A

have specific protease activities
act on proteins in neurones which control neurotransmitter activity
proteins included SNARE proteins

50
Q

what do SNARE proteins do

A

facilitate fusion of vesicles with membranes to a allow delivery of molecules like neurotransmitters to control nerve function

51
Q

PWID

A

people who inject drugs

52
Q

clostridia and PWID

A

PWID can cause tetanus

53
Q

where is Clostridium difficile present

A

normal flora in 3-5% adults

54
Q

how does Clostridium difficile infect

A

administration of broad-spectrum antibiotics in vulnerable patients (e.g. elderly) allows C. diff to grow and produce TOXINS

55
Q

what is Clostridium difficile the leading cause of

A

nosocomial diarrhoea

56
Q

what does Clostridium difficile make

A 
Toxin mediated process
Exotoxin A (enterotoxin)
Exotoxin B (cytotoxin)
57
Q

what does infection with Clostridium difficile lead to

A

morbidity and mortality
mild to severe diarrhea
toxic megacolon
pseudomemranous colitis

58
Q

how is Clostridium difficile treated

A

withholding antibiotics where possible and replacing them with fluids
Fecal bacteriotherapy, also known as a stool transplant
colectomy - section of infected bowel is removed

59
Q

what are the screening methods that can be used to diagnose Clostridium difficile

A

ELISA

PCR

60
Q

what is the problem with using plates to diagnose Clostridium difficile

A

is slow process and need to know ASAP if infected so not regularly used in diagnostic labs

61
Q

what is the problem with using cell rounding assay

A

labour intensive so not ideal

62
Q

how is cell rounding assay performed

A

Take some supernatant from patient put onto eukaryotic cells

Will stop to round up due to the toxin

63
Q

what is usually done first to test for Clostridium difficile

A

quick test
apply sample to plate
will tell if is
- antigen positive (present)
- antigen and toxin(s) positive (present and making toxins)
- negative for antigen and toxin(s) (not present)

64
Q

why does C.difficile not cause problem when there are no antibiotics present

A

Normally in gut with no antibiotics have a mix of different types of bacteria
These bacteria take primary bile salts will be digested into secondary bile acids
Secondary bile acids are inhibitory to C. difficile germination can’t germinate any spores so wont cause problems

65
Q

where are primary bile acids made

A

normally produced as part of the digestive system

66
Q

what is key in the break down of primary bile acids to secondary

A

C. scindens

67
Q

why does C.difficile cause a problem when antibiotics are ingested

A

Take antibiotics will kill off the C. scindens
So no longer get transformation of primary bile acids to secondary
Nothing blocking the C. difficile from forming spores

68
Q

what does C. difficile produce

A

produces two large exotoxins – TcdA and TcdB

69
Q

what do the toxins C. difficile produce do

A

have activity against gut epithelial cell
bind to the cell surface and trigger intracellular signalling pathways that cause changes in the cell cytoskeleton
can lead to cell death

70
Q

what is the effect does death of cells lining the colon

A

can result in changes in fluid absorption and diarrhoea

71
Q

how is C. difficile treated

A

prevention rather than using antibiotics
isolate patient
Antibiotic therapy: Metronidazole, Vancomycin, Fidaxomicin
Some alternative treatment options fall into four main areas:
prebiotics and probiotics;
“faecal transplants” — where stools donated from a healthy donor are placed in the bowel in an attempt to restore the normal microbiota

72
Q

what is metronidazole

A

inhibitor of DNA synthesis

73
Q

what does metronidazole require, why is it only effective against anaerobic bacteria and anaerobic protozoa

A

At low Eh values reduced to a short-lived intermediate which causes DNA strand breakages
Because of this requirement for a low Eh value, only active against anaerobic bacteria and anaerobic protozoa

Microorganisms + Disease (16 decks)

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