7 distinct toxins (A-G) - C/D are most animal cases = obligate intestinal parasites - Zn-endoproteinase cleaves synaptobrevin in peripheral nn.

Gram + anaerobes Flashcards by Fjørdan Slümnòdl

Clostridium spp. morphology + metabolic requirements/characteristics

Large gram + rods

Anaerobic, spore-forming, motile

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Clostridial diseases by species (12)

C. tetani - tetanus
C. botulinum - botulism
C. perfringens - enterotoxaemia/haemorrhagic enteritis, malignant oedema, lamb dysentery
C. novyi - malignant oedema, big head, black disease 
C. haemolyticum - bacillary haemoglobinuria
C. septicum - braxy, malignant oedema
C. chauvoei - black leg
C. spiroforme - enterotoxaemia
C. villosum - cat fight abscess
C. difficile - enterocolitis
C. colinum - necrotic enteritis
C. piliforme - acute hepatic necrosis

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Which Clostridia spp possess neurotoxins? (2)

C. tetani - spastic paralysis

C. botulinum - flaccid paralysis

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Pathogenesis of tetanus

Local infection of wound by spores
> infection/necrosis = ↓ redox potential/↓ [oxygen]
> spore germination/growth 
> exotoxin disseminates via blood/nerves
> binds to pre-synaptic membrane of inhibitory neurons 
> blocks GABA/Gly release 
> tetanic spasm 
> respiratory paralysis/death

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Tetanus VFs (3)

Tetanospasm (exotoxin) = Zn endoproteinase activated by bacterial proteases (unstable in GIT)

Tetanolysin (haemolysin)

Non-spasmogenic toxin

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Tetanus route of infection

Deep wounds

anaerobic environment required for spore germination
tetanospasm is destroyed in intestine

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Tetanus immunity

Ab mediated immunity to toxin > toxoid vax/passive immunity

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Tetanus tx

Penicillin - may not reach wound in necrotic tissue

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Tetanux dx

clinical observations = tetanic muscle spasm

hard to find wound + can’t demonstrate toxin

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Tetanus source of infection

Common in environment

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Botulism source of infection

Ubiquitous in poor quality food

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Species susceptibility to tetanus

Horse > pig/rum/carn

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Species susceptibility to botulism

Rum > others

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Pathogenesis of botulism

Agent multiplies in feed
> cell lysis = toxin release
> toxin ingestion
> toxin cleaved by trypsin in GIT + absorbed
> binds NMJ = blocks ACh release
> flaccid paralysis (can’t initiate muscle contraction)
> Respiratory paralysis/death

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Botulism VFs (1)

7 distinct toxins (A-G)

C/D are most animal cases = obligate intestinal parasites
Zn-endoproteinase cleaves synaptobrevin in peripheral nn.

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Botulism immunity

Anti-toxin Ab > toxoid vax (type C/D toxins)

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Botulism epidemiology (2)

Multiplies in carcasses, ↓ quality/poorly stored feed, spoiled silage, decomposing plant material

Outbreaks in water birds dt ingestion of decomposing plant material/snails eating it

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Botulism route of infection

Oral

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Botulism Dx (2)

food/GIT specimens inoculated into mice

ELISA on serum

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Invasive Clostridial spp.

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C. chauvoei
C. novyi (type A/B)
C. septicum
C. perfringes

Malignant oedema - agent

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Clostridium perfringes type A

± C. chauvoei, C. novyi type A, C. septicum

C. perfringens toxins (4)

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Alpha = splits lecithin in cell wall

Beta = intestinal inflamm/mucosal sloughing
- destroyed by trypsin

Epsilon = ↑ permeability of gut epithelium/ brain endothelium TF necrotising
- activated by trypsin/pepsin

Iota = cytotoxin

Malignant oedema - pathogenesis

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C. perfringens type A

Wound contamination by spores
> germination in anaerobic conditions
> alpha toxin elaboration = muscle damage
> further replication
> exotoxins absorbed into circulation = endothelial damage
> hepatic/muscle damage

Clostridial enterotoxaemia - agent + source of infection

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C. perfringens type D

Commensal of intestine > overgrows w ↑ undigested starch contents

Clostridial enterotoxaemia - pathogenesis

C. perfringens type D Change in food = ↑ undigested starch > proliferation of agent > epsilon toxin accumulates = ↑ GI permeability > toxin absorbed into circulation > ↑ vasc perm of brain = focal symmetrical encephalomalacia > renal tubule dmg = glycosuria > death w hypovolaemia + pulmonary oed/hydropericardium

Pulpy kidney

Post-mortem change dt rapid autolysis following death from clostridial enterotoxaemia

Haemorrhagic enteritis - agent

Clostridum perfringens type B/C

Haemorrhagic enteritis - pathogenesis

C. perfringens type C Agent binds to jejunal mucosa > Beta toxin elaborates (if no trypsin) > necrosis/sloughing of mucosa > haemorrhagic enteritis

Malignant oedema/enterotoxaemia/haemorrhagic enteritis - immunity

Toxoid (type B + D) = protective Ab to types A-D Enterotoxaemia requires Ab in circulation Enteric dz requires Ab in intestinal lumen (colostrum)

C. perfringens dx (3)

serum/intestinal contents inoculated into mice to demonstrate toxin presence ELISA Lots of agent in upper SI

C. novyi types + associated dz's (2)

C. novyi type A = malignant oedema including big head (rams dt fighting) C. novyi type B = black disease (infectious necrotic hepatitis)

C. novyi VFs (1)

Alpha = lethal, ↑ capillary permeability causing oedema

Black disease (infectious necrotic hepatitis) - agent + pathogenesis

C. novyi type B Agent ingested + spores lodge in liver > local hepatic necrosis dt F. hepatica larval migration (or other causes) > ↓ redox = spore germination/multiplication > toxin elaborate = further local necrosis > toxins enter circulation > ↑ vasc perm + muscle dmg (incl heat) + congestion

Black disease - immunity

Toxoid of type B = Ab protective against C. novyi type A + B

Black disease - dx (2)

Focal hepatic necrosis | Evidence of F. hepatica migration

Braxy - agent What other disease does this agent cause?

Clostridium septicum Also malignant oedema

Braxy - pathogenesis

C. septicum Eating frozen pasture = dmg to abomasal wall > local replication of agent > toxaemia

Blackleg - agent + route of infection

Clostridium chauvoei oral route (ingested)

Blackleg - pathogensis

C. chauvoei Ingestion + replication in intestine > spores reach muscle via circulation (no external wounds) > Muscle damage (bruising) = anaerobic conditions/↓ redox = germination/replication > local muscle dmg dt toxins > toxins enter circulation = lameness, fever, depression, death

Blackleg - immunity (1)

Ab against bacterin (cells) + toxin

Blackleg - dx

agent demonstrated by fluorescent Ab staining of muscle smears (ddx pos-mortem invasion)

Enterocolitis in horses, rabbits, guinea pigs - agent + clin signs

Clostridium difficile Toxin elaboration = GI epithelial necrosis/inflamm > severe diarrhoea + necrotising enteritis

Enterocolitis (eq/rabbits) - risk factors/associations

C. difficile Broad-spectrum antibiotic use = overgrowth of agent dt destruction of competing flora Assoc w tx for rattles

Enterocoloitis - tx (2)

Metronidazole | Vancomycin

Tyzzer's disease (foals) - agent/morphology/habitat

Clostridium piliforme - gram neg Obligate intracellular parasite of hepatocytes, epithelial cells, GI SM cells

Tyzzer's disease (foals) - disease

C. piliforme Acute hepatic necrosis + necrotic enterocolitis

Cystitis/pyelonephritis in sows - agent + morphology

Actinobaculum suis - gram + anaerobic, pleomorphic rod

Cystitis/pyelonephritis in sows - source of infection

A. suis Carried by boars in prepuce > infection of sows during coitus > ascending UTI Urease + = NH3 prod'n > mucosal ulceration + haemorrhagic cystitis

Cystitis/pyelonephritis in sows - tx

penicillin

Gram + anaerobes Flashcards

(49 cards)