Clostridia Flashcards

1
Q

What are the three main subtypes of clostridia?

A

neurotoxic clostridia,
histotoxic clostridia,
enteropathogenic and enterotoxaemia producing clostridia

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2
Q

Name the bacterium that causes Tetanus, which subtype is this classed under?

A

Clostridium tetani- neurotoxic

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3
Q

Which species are susceptible to C.tetani?

A

horses and man, highly susceptible, ruminants and pigs moderately so, carnivores comparatively resistant, poultry resistant.

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4
Q
Clostridium species: 
Gram + or -? 
Shape? 
Rate of growth? 
Aerobic or anaerobic? 
Biochemically active or not? To which test? 
Spore forming? 
What substances do they produce? (3)
Are they sensitive to antimicrobials?
A
Gram positive
Large Rods
Fast growth
Strict Anaerobes
Biochemically active- API I
Form resistant spores
Produce- VFAs, Enzymes (proteases, saccharases), Toxin- Tetanus toxin on plasmid, botulism toxin on lysogenic phage
Antimicrobial sensitivity, may be some resistance, however you generally can't use them fast enough for them to have an effect
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5
Q
How does tetanus infection occur? 
What are the most likely routes of infection in-
horse
sheep
cows and sheep
other
A

Infection occurs when endospores are introduced into tissue traumatised or not from soil or faeces. Vegetative bacteria develops from spore in wound
Vegetative bacteria produce toxin

Deep penetrating wounds in the horse
Castration and docking in sheep
Abrasions in cows and ewes
Umbilicus in all animals

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6
Q

Culture appearance on blood agar of tetani?

A

Shows a little haemolysis, growth spreads across the plate and each bacterium looks like a matchstick

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7
Q

Tetanus- pathogenesis

A

Tetanus toxin consists of 2 chains joined by disulphide bridge
Light chain is toxic, heavy chain is for receptor binding and internalisation

Binds irreversibly to ganglioside receptors on motor neuron terminals and transported to CNS by intra axonal flow

Toxin blocks pre-synaptic transmission of inhibitory signals

Hydrolyses synaptobrevins – proteins of vesicles containing neurotransmitters

Inhibitory neurotransmitter (glycine and GABA) release is prevented results in SPASTIC paralysis

Bound toxin not neutralised by antitoxin

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8
Q

BOTULISM- which species of bacteria causes this disease?

Overview

A

C. botulinum
Toxin types A-G, they affect different species
Rotting carcasses provide a place for the germination of endospores, growth of vegetative bacteria cells and toxin production. Decaying vegetation and contaminated canned food can also act as sites for this.

Types C and D cause outbreaks in domestic animals

Outbreaks in waterfowl, cattle, horses, sheep, mink, poultry, farmed fish

Toxin types A, B and E account for most human cases

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9
Q

What caused the marked increase in cases of cattle suffering from botulism in 2003?
How would you diagnose it?

A

Deep litter containing poultry carcasses on pasture involved
Detection of toxin in serum difficult – not much present, test GI contents in mouse assay
Toxin types C and D (B has also affected cattle)

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10
Q

Give the structure of the botulism toxin

A

Botulinum toxin synthesized as a single polypeptide chain; The toxin is then nicked by a bacterial protease to produce two chains

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11
Q

Pathogenesis pathway for C. botulinum

A

Preformed toxin in food is absorbed from GI tract, circulates in blood
Acts at neuromuscular junctions of cholinergic nerves and peripheral autonomic synapses.
Remains at junction
Irreversible interference with acetylcholine resulting in FLACCID paralysis
Death from paralysis of respiratory muscles

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12
Q

How does botulism causes tissue damage?

A

Histotoxic:
Ingested endospores are excreted but some may leave the intestine to lie dormant in tissues.
Tissue injury allows them to colonise- reduced oxygen tension is required for germination and negative replication.
Local necrosis is produced by exotoxins of the replicating bacteria, this allows for further proliferation and tissue damage.

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13
Q

Give 3 examples of ENDOGENOUS INFECTION of C. botulinum

A

Blackleg, infectious necrotic hepatitis and bacillary haemoglobinuria result from activation of dormant spores in muscle or liver

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14
Q

Give an example of an EXOGENOUS INFECTION with C. botulinum and describe how growth is possible

A

Gas gangrene (myositis) results from introduction of clostridia into wounds. Anaerobic environment of necrotic tissue allows replication, local and systemic toxin production

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15
Q

HISTOTOXIC CLOSTRIDIA

A

C. chauvoei - Blackleg in cattle
C. septicum - Malignant oedema in cattle pigs and sheep, braxy (abomasitis) in sheep
C. novyi type A - Big head in rams, wound infection
C. perfringens type A - Necrotic enteritis in chickens, Gas gangrene (myositis)
C. sordellii - Myositis in cattle, sheep, horses, abomasitis in lambs
C. novyi type B- Black disease in sheep (necrotic hepatitis
C. haemolyticum- Bacillary haemoglobinuria in cattle and occasionally sheep

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16
Q

Cl. chauvoei- Blackleg

Pathogenesis

A

1) commensal / ingestion
2) relocalisation to muscle
3) bruising
4) spore germination and toxinogenesis
5) haemolysis, crepitation, necrosis

17
Q

Cl. novyi Type B- Black’s Disease Pathogenesis

A

1) commensal / ingestion
2) relocalisation to liver
3) fluke migration
4) spore germination and toxinogenesis
5) oedema, shock, necrosis

Liver lesions look like Aero chocolate

18
Q

Cl. septicum has two routes. Describe the ENDOGENOUS PATHWAY:

A

1) Injury to abomasum (from feeding frozen food)
2) Colonisation by commensal/ ingested Cl.sep
3) Toxinogenesis
4) Localised mucosal haemorrhage and necrosis
5) Toxaemia
6) Braxy

19
Q

Cl. septicum has two routes. Describe the EXOGENOUS PATHWAY:

A

1) Wound
2) Inoculation with Clostridia
3) toxicogenesis
4) Cellulitis and Myositis
5) Gangrene

20
Q

What role do antibiotics have in treating Histotoxic Clostridia?

A

They are usually ineffective unless given very early

21
Q

Name the three components of Histotoxic Clostridial Vaccine

-How often would these need to be administered?

A

bacterin + toxoid + adjuvant

Multicomponent vaccines + boosters + annual re-vaccination

22
Q

Enteropathogenic and enterotoxaemic Clostridia- NAME THE SPECIES WE NEED TO KNOW, YO

A

C. perfringens

23
Q

How many types of C.perfringens are there? What are they called?

A

5

A-E

24
Q

Where do C. perfringens replicate?

Do they cause local or systemic effects?

A

Intestinal Tract

Both

25
Q

Predisposing factors for C. perfringens (3)

A

inappropriate husbandry, dietary changes, local environmental influences

26
Q

C. perfringens Toxins

A

Pattern of toxin production varies with each C. perfringens type and determines clinical syndrome observed
Types A-E produce a number of potent immunologically distinct exotoxins

27
Q

Type A C. perfringens toxin: name? actions?

A

Alpha
Gas gangrene of humans and animals, fowl and porcine necrotic enteritis, bovine and ovine enterotoxaemia, food poisoning in man, colitis in horses, canine haemorrhagic gastroenteritis

28
Q

Type B C. perfringens toxin: names? actions?

A

Alpha, Beta, Ypsilon

Lamb dysentery, enterotoxaemia of foals, sheep, goats

29
Q

Type C C. perfringens toxin: names? actions?

A

Alpha, beta

Pig-bel (necrotic enteritis) in man, enterotoxaemia of sheep (struck), calves, lambs, piglets

30
Q

Type D C. perfringens toxin: names? actions?

A

Alpha, Ypsilon

Enterotoxaemia of lambs and sheep (pulpy kidney), goats, cattle (human)

31
Q

Type E C. perfringens toxin: names? actions?

A

Alpha, Iota

Rabbit enteritis, enterotoxaemia of calves and lambs

32
Q
Species of Clostridia associated with disease, what do they cause?
C. difficile-
C. haemolyticum-
C. spiroforme-
C. colinum
A

C. difficile- Enteritis
C. haemolyticum- Bacillary Haemoglobinuria
C. spiroforme- Rabbit Diarrhoea
C. colinum- Quail disease