Clostridia Flashcards
What are the three main subtypes of clostridia?
neurotoxic clostridia,
histotoxic clostridia,
enteropathogenic and enterotoxaemia producing clostridia
Name the bacterium that causes Tetanus, which subtype is this classed under?
Clostridium tetani- neurotoxic
Which species are susceptible to C.tetani?
horses and man, highly susceptible, ruminants and pigs moderately so, carnivores comparatively resistant, poultry resistant.
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?
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
How does tetanus infection occur? What are the most likely routes of infection in- horse sheep cows and sheep other
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
Culture appearance on blood agar of tetani?
Shows a little haemolysis, growth spreads across the plate and each bacterium looks like a matchstick
Tetanus- pathogenesis
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
BOTULISM- which species of bacteria causes this disease?
Overview
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
What caused the marked increase in cases of cattle suffering from botulism in 2003?
How would you diagnose it?
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)
Give the structure of the botulism toxin
Botulinum toxin synthesized as a single polypeptide chain; The toxin is then nicked by a bacterial protease to produce two chains
Pathogenesis pathway for C. botulinum
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
How does botulism causes tissue damage?
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.
Give 3 examples of ENDOGENOUS INFECTION of C. botulinum
Blackleg, infectious necrotic hepatitis and bacillary haemoglobinuria result from activation of dormant spores in muscle or liver
Give an example of an EXOGENOUS INFECTION with C. botulinum and describe how growth is possible
Gas gangrene (myositis) results from introduction of clostridia into wounds. Anaerobic environment of necrotic tissue allows replication, local and systemic toxin production
HISTOTOXIC CLOSTRIDIA
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
Cl. chauvoei- Blackleg
Pathogenesis
1) commensal / ingestion
2) relocalisation to muscle
3) bruising
4) spore germination and toxinogenesis
5) haemolysis, crepitation, necrosis
Cl. novyi Type B- Black’s Disease Pathogenesis
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
Cl. septicum has two routes. Describe the ENDOGENOUS PATHWAY:
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
Cl. septicum has two routes. Describe the EXOGENOUS PATHWAY:
1) Wound
2) Inoculation with Clostridia
3) toxicogenesis
4) Cellulitis and Myositis
5) Gangrene
What role do antibiotics have in treating Histotoxic Clostridia?
They are usually ineffective unless given very early
Name the three components of Histotoxic Clostridial Vaccine
-How often would these need to be administered?
bacterin + toxoid + adjuvant
Multicomponent vaccines + boosters + annual re-vaccination
Enteropathogenic and enterotoxaemic Clostridia- NAME THE SPECIES WE NEED TO KNOW, YO
C. perfringens
How many types of C.perfringens are there? What are they called?
5
A-E
Where do C. perfringens replicate?
Do they cause local or systemic effects?
Intestinal Tract
Both
Predisposing factors for C. perfringens (3)
inappropriate husbandry, dietary changes, local environmental influences
C. perfringens Toxins
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
Type A C. perfringens toxin: name? actions?
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
Type B C. perfringens toxin: names? actions?
Alpha, Beta, Ypsilon
Lamb dysentery, enterotoxaemia of foals, sheep, goats
Type C C. perfringens toxin: names? actions?
Alpha, beta
Pig-bel (necrotic enteritis) in man, enterotoxaemia of sheep (struck), calves, lambs, piglets
Type D C. perfringens toxin: names? actions?
Alpha, Ypsilon
Enterotoxaemia of lambs and sheep (pulpy kidney), goats, cattle (human)
Type E C. perfringens toxin: names? actions?
Alpha, Iota
Rabbit enteritis, enterotoxaemia of calves and lambs
Species of Clostridia associated with disease, what do they cause? C. difficile- C. haemolyticum- C. spiroforme- C. colinum
C. difficile- Enteritis
C. haemolyticum- Bacillary Haemoglobinuria
C. spiroforme- Rabbit Diarrhoea
C. colinum- Quail disease
