Term
|
Definition
STRICT ANAEROBES, gram -ve
-generally mixed infections in order to establish damage and anaerobic conditions
-Fusobacterium necrophorum
-Dichelobacter nodosus |
|
|
Term
| Oxidation-reduction potentials of different tissues and anaerobic bact. |
|
Definition
Healthy tissues +120mV --> +240mV
Damaged tissues -150mV --> -250mV
Anaerobe bact. survival <-100mV
i.e. anaerobes metabolism incr. in resp. to damage / decr blood supply |
|
|
Term
| Fusobacterium necrophorum - source |
|
Definition
-primarily commensal of gut of warm-blooded animals
-can survive in pasture for months in anaerobic pockets/faeces (gen. needs wet pastures)
-often w. Arcanobacterium pyogenes - uses O2 so establishes anaerobic environment |
|
|
Term
| Fusobacterium necrophorum - main dz |
|
Definition
necrobacillosis - necrotic pus lesions and infections
-of feet, mouth, liver |
|
|
Term
| Fusobacterium necrophorum - main dz sheep |
|
Definition
-ovine sheep necrosis
-interdigitial dermatitism (which predisposes to foot rot caused by D. nodosus) |
|
|
Term
| Fusobacterium necrophorum - main dz horse |
|
Definition
|
|
Term
| Fusobacterium necrophorum - main dz cattle |
|
Definition
| foul of foot (foot rot), mixed w. Arcanobacterium pyogenes |
|
|
Term
| Dichelobacter nodosus - source |
|
Definition
-obligate hoof parasite, esp sheep
(no evidence that acts as gut commensal)
-survives in pasture for 2-3weeks
-often mixed inf (once other bact. have caused initial damage) |
|
|
Term
| Dichelobacter nodosus - main dz |
|
Definition
primary cause of ovine foot rot
poss cause of CODD (contagious ovine digital dermatitis - v. similar but starts at coronet band) |
|
|
Term
| Dichelobacter nodosus - pathogenesis |
|
Definition
wet --> soft interdigital tissue --> Fusobacterium necrophorum causes tissue damage (w. aid of A. pyogenes) --> D. noduses able to establish (again w. aid of A. pyogenes) --> foot rot
NB: spirochaetes also often involved |
|
|
Term
| Dichelobacter nodosus - difference in virulence characteristics |
|
Definition
Foot rot can be benign (avirulent) or virulent
-Horn separation - little/none --> extensive
-Necrotic exudate/foul smell - none--> extensive
-Lameness - mild --> severe
-Resolution w. onset of dry conditions is rapid in avirulent strains, but not possible in virulent strains
-Resolution w. treatement - rapid if avirulent, slow if virulent |
|
|
Term
|
Definition
-simple!
-trim feet yearly to maintain shape and balance
-footbath - make sure allow to dry before turn out and turn out on to fresh pasture
-vaccines - footvax is formalin killed whole cell |
|
|
Term
|
Definition
-trim feet to keep clean and expose to O2
-foot bath - formalin / CuSO4 / ZnSO4
-antibiotics - IM or topical
-isolation |
|
|
Term
|
Definition
-gut commensals i.e. endogenous inf.
-soil survivors - ingestion or deep wound entry
i.e. not contagious! no animal-animal spread so don't see outbreaks |
|
|
Term
| Classification of Clostridium spp |
|
Definition
-Non-invasive potent neurotoxins
-Non-invasive enterotoxins
-Invasive, less potent, histotoxins |
|
|
Term
| Clostridia spp. - non-invasive potent neurotoxins |
|
Definition
Clostridium tetani
Clostridium botulinum |
|
|
Term
| Clostridium tetani - source |
|
Definition
| enter via deep puncture wounds / surgery |
|
|
Term
| Clostridium tetani - toxins |
|
Definition
-Tetanolysin - aids necrosis so promotes anaerobic environment
-Tetanospasmin - neurotoxin which causes paralysis (spastic) |
|
|
Term
| Clostridium tetani - consequence |
|
Definition
spastic paralysis and death
-desdending paralysis in man and horse, neurotoxins enter motor neuron terminals in SC via blood / lymph
-ascending paralysis in all other spp, neurotoxins enter motor neuron terminals in SC via peripheral nn. |
|
|
Term
| Clostridium tetani - pathogenesis / sequence of events |
|
Definition
soil/faeces + C. tetani spores + fac. anaerobe --> enter wound --> necrosis --> germination --> tetanolysin --> necrosis i.e. vicious circle
--> germination --> tetanospasmin --> spastic paralysis and death |
|
|
Term
| Clostriudium tetani - prevention and tx in horse |
|
Definition
NB: incubation in 5-21 days
If wounded and vacc: clean wound and boost vacc. (creates Abs)
If wounded and unvacc: clean wound, give antiobiotics (not aminoglycosides) and give anti-toxin OR vacc
If clinically affected: tx quickly, death is rapid! clean wound if poss, give antibiotics (not aminoglycosides), anti-toxin, traquilisers and aid resp. (will get resp. failure) |
|
|
Term
| Clostridium botulinum - source |
|
Definition
| enter via wounds or ingestion |
|
|
Term
| Clostriudium botulinum - consequences |
|
Definition
| flaccid paralysis and death |
|
|
Term
| Clostriudium botulinum - pathogenesis / sequence of events |
|
Definition
toxin production in wound --> blood
OR
ingested toxin / local toxin production --> absorption in gut --> blood
blood --> peripheral nn. --> flaccid paralysis and death |
|
|
Term
| Clostriudium botulinum - prevention |
|
Definition
-cook food - 100C 20-30mins
-avoid spoiled feed
-vacc - polyvalent toxoid (based on 8 antigenic forms of neurotoxin) |
|
|
Term
| Clostriudium botulinum - treatment |
|
Definition
| If clinical signs: anti-toxin, purge gut (normally due to ingestion), artifical resp. |
|
|
Term
| Clostriudium tetani and botulinum - comparison |
|
Definition
Both enter via wound, C. botulin also by ingestion (and more than via wound)
C. tetani = spastic paralysis
C. botulinum = falccid paralysis |
|
|
Term
| Clostridium spp. -non-invasive enterotoxins |
|
Definition
| Clostridium perfringens type A-E |
|
|
Term
| Clostridium perfringens - source |
|
Definition
-ubiquitous in environment
-predisposition = change in gut conditions |
|
|
Term
| Clostridium perfringens - toxins |
|
Definition
| Affect gut mucosa and travel in blood to other sites
All necrotising and lethal
alpha - all strains can produce this, haemolytic
beta - associated w. neonates on colostrum
epsilon - animals <3wks old, esp calves |
|
|
Term
| Clostridium perfringens - types |
|
Definition
5 types (A,B,C,D,E) - B,C,D most important
B and C main toxin is beta i.e. associated w. neonates on colostrum
D main toxin is epsilon - animals <3wks old, esp calves |
|
|
Term
| Clostridium perfringens - main dz. |
|
Definition
-dysentery in lambs <3weeks old (type B)
-haemorrhagic / necrotic enteritis - young of most spp (type B,C,E)
-struck / sudden death - adult sheep (type C)
-pulp kidney dz in non-neonate sheep (D) |
|
|
Term
| Clostridium perfringens - diagnosis |
|
Definition
-bulls eye haemolysis
-stormy clot formation i.e. lactose fermentation
-Naglar reaction (due to alpha-toxin)
-gelatin liquefaction
NB: not motile c.f. all other Clostridium spp. |
|
|
Term
| Clostridium perfringens - treatment |
|
Definition
antitoxin i.e. anti-B, C, D
-and toxoid and antibiotics |
|
|
Term
| Clostridium spp - invasive, less-potent histotoxins |
|
Definition
Clostridium haemolytica
Clostridium novyi
Clostridium septicum
Clostridium chauvoei
Clostridium perfringens type A |
|
|
Term
| Invasive, less-potent histotoxins - source |
|
Definition
| -spores enter via wounds or GIT |
|
|
Term
| Clostridium haemolytica - main dz. |
|
Definition
red water (cattle>sheep)
i.e. bacillary haemoglobinuria |
|
|
Term
| Clostridium haemolytica - source |
|
Definition
-spores in soil ingested
-associated w. flukes damaging liver and creating anaerobic pockets |
|
|
Term
| Clostridium novyi type B - main dz. |
|
Definition
black dz (sheep > cattle)
i.e. infectious necrotic hepatitis |
|
|
Term
| Clostridium novyi type B - source |
|
Definition
-spores in soil ingested
-associated w. flukes damaging liver and creating anaerobic pockets |
|
|
Term
|
Definition
| bighead from head butting rams |
|
|
Term
|
Definition
braxy in sheep (and calves)
associated w. grazen frozen pastures - damages int. mucosa
also causes inf. at inj. sites in horses, and necrotic dermatitis in chickens |
|
|
Term
|
Definition
| black leg in cattle (3-24mnths) |
|
|
Term
| Mixed Clostridium infection |
|
Definition
| gas gangrene in many spp - varies from mild malignant oedema to severe gas gangrene and death |
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