Gram + anaerobes Flashcards
Clostridium spp. morphology + metabolic requirements/characteristics
Large gram + rods
Anaerobic, spore-forming, motile
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
Which Clostridia spp possess neurotoxins? (2)
C. tetani - spastic paralysis
C. botulinum - flaccid paralysis
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
Tetanus VFs (3)
Tetanospasm (exotoxin) = Zn endoproteinase activated by bacterial proteases (unstable in GIT)
Tetanolysin (haemolysin)
Non-spasmogenic toxin
Tetanus route of infection
Deep wounds
- anaerobic environment required for spore germination
- tetanospasm is destroyed in intestine
Tetanus immunity
Ab mediated immunity to toxin > toxoid vax/passive immunity
Tetanus tx
Penicillin - may not reach wound in necrotic tissue
Tetanux dx
clinical observations = tetanic muscle spasm
hard to find wound + can’t demonstrate toxin
Tetanus source of infection
Common in environment
Botulism source of infection
Ubiquitous in poor quality food
Species susceptibility to tetanus
Horse > pig/rum/carn
Species susceptibility to botulism
Rum > others
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
Botulism VFs (1)
7 distinct toxins (A-G)
- C/D are most animal cases = obligate intestinal parasites
- Zn-endoproteinase cleaves synaptobrevin in peripheral nn.
Botulism immunity
Anti-toxin Ab > toxoid vax (type C/D toxins)
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
Botulism route of infection
Oral
Botulism Dx (2)
food/GIT specimens inoculated into mice
ELISA on serum
Invasive Clostridial spp.
C. chauvoei
C. novyi (type A/B)
C. septicum
C. perfringes
Malignant oedema - agent
Clostridium perfringes type A
± C. chauvoei, C. novyi type A, C. septicum
C. perfringens toxins (4)
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
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
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
