Clostridium Flashcards
Clostridium summary
G+ve bacilli Anearobes of varying O2 sensitivity Produce spores Commensal and saprophytic present in intestinal tract in soil and in decaying organic matter Produc highly effective exotoxins Not contagious
Disease type: histiotoxic
Wound infection or dis preceded by injury or insult
Disease type: enterotopathogenic
Problems originate in GIT incl ingest of preformed toxins in botulism
Histiotoxic clostridia
Involve trauma to tissues that allows inoc or act of spores
Begetative cells in alimentary tract can lead to spore deposition in tissues
Spores persist until elim
Tissue injury due to bact growth and disease - dep on tissue colonised, trauma type and clostridial species toxigenicity
Histiotoxic clostridia toxins
Lecithinase
Necrotising tox
C novyi type B
Sheep and cattle
Can cause blacks disease of sheep
Spore germ in tract left by migratin immature fluke
Tox prod extends the lesion causing tissue nevrosis and systemic tox release
C novyi type D
Cattle
Liver
Contrib by fascioliasis
C chauvoei
Cattle usually 6mnth to 2 yr and usually restricted to spec pastures
Muscle
Causes blackleg
Without obvious trauma usuaally a non penetrating injury or tooth eruption
Affected muscles are black to dark red and contain gas
C septicum
Sheep
Abomasum
Frosted food
C perfringens, novyi, septicum, chauvoei
Myositis or gas gangrene
Bact intro directly to tissues by trauma
Most in cattle and sheep but other animals too
Colonise putrefying tissues, pathology of lesions( gas form, tissue BD, proteolysis)
Control of clostridium infection
Vacc
C tetani description
Anearobe G+ Straight slender rod with rounded end Spore form with terminal drumstick spores Spores highly res Flagella for motility
C tetani occurrence
Founf in animal and man intestines
1o source is animal faeces and soil
Spires are widespread
Variable species succeptibility
C tetani toxins
Most pathogenic tetanospasmin consist of a H and L chain
Non toxic by oral route as degraded
Strains vary in toxigenicity but only one antigenic type recog
C tetani pathogenesis
Non invasive so stay at original site Spore contam wound Spore germ in wound as low O2 tension and nonviable material Tox prod and release Tox action
C tetani tox action
Absorbed from infect site and move via periph motor neurons within axon to CNS
Tox prev inhib neurotrans release so over stim motor neurons in CNS preventing m relaxation
So interfere with normal inhib and cause tonic spasm
Affects voluntary m - head and neck first affected
Some tox travel bia blood and lymph to all body nerves and reaches CNS by uptake through neuromusc nerve endings and subseq intra-axonal route
Tetanus severity dep on
Toxin amount reaching the CNS
Tetanus lab diagnosis
Gran stained smear
Drumstick appearance
Direct culture onto blood agar
Tetanus treatments
Debride
Relaxants
Antitoxins
Antibios
Tetanus prev and control
Hygeine
Toxoid vacc
Antitox
Horses often 2 priming tetanus toxoid dose vacc with booster after 1 yr and then every 2/3 yrs after that
Antitoxin (tetanus) action
Once toxin bound it can’t be neutralised by antitoxin
Antitoxin provides about 4 wks protection
Ruminant tetanus risk
Less susceptible but can occur following castration
Tail docking
Or dystocia