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
Enteropathogenic bact and classification of it
C perfringens
Based on toxins (determine dis type)
CW and capsular antigens distrib accross all so not a diagnostic tool
C perfringens A
Alpha tox
Food poisoning (man)
Gangrene
Pig/calf enteritis
C perfringens B
Alpha Beta Epsilon Lamb dysentry Also foal and calf
C perfringens C
Alpha beta toxs
Struck (sheep goats)
Dysentry lamb calf pig
C perfringens D
Alpha epsilon toxs
Enterotoxaemia
Pulpy kidney (sheep goats)
C perfringens E
Alpha iota toxs
Doubtful pathogen
Possibly enteritis in rabbits and calves
Alpha tox c perfringens
Lecithinase act directly on CM
Beta tox c perfringens
Common to strains causing enteritis
Reduces intestinal motility
Epsilon tox c perfringens
Act on endo
Iota tox c perfringens
Target host cell cytoskel
Alter epi perm
C perfringens dis diagnosis
Demonstr spec tox in intestinal tract at necropsy
Detect tox in faeces
Occassional isolation of bact and demo of tox type in culture
Tox detection by ELISA or bioassay ir genes by PCR
Perfringens D enterotoxaemia or pulpy kidney risk grp and pathogenesis
Small no of commensal in intestine
Most in nursing (3-10wk) lambs with rich pasture access as excess digestible carb entering s intestine initiate dis as stim growth of bact
Epsilon tox is a protox act by trypsin. Local epi dam facilitating tox absorption and endo dam esp kidney and brain
Hyperglycaemia due to enhanced glycogenolysis causing glucosuria and large no of non sporing clostridia found in intestinal tract.
Dead animals of enterotoxaemia putrefy quickly
Perfringens B and C dysentry and enteritis
Intestinal lesion due to beta tox
Pathogenesis similar to D infection
Mostly lowland breed single lambs adult sheep and suckling piglets
Muc surf of s intestine colonised
Beta tox cause muc necrosis and ulceration
Perfringens A food poisoning
Commensal in most animals occassionally cause intestinal disease but cause food poisoning in man
Elaborate an enterotox upon sporulation
Strains contam meat and due to spore form and undercooking aren’t elim by heating process
C difficile
Common in hum neonate faeces
Used to be implicated with antibio assoc colitis in hum
Main problem as nosocomial infect in elderly patients treated with antibios
Possibly zoonotic
C botulinum description
Stric anaerobe
G+ve rod
Motile via flagella
Highly res Spore form (widely distribute in soil, veg, fruit, silage, manure, sea and lake sediment)
Cause foodborne botulism, wound botulism and toxicoinfectious botulism
Prod potent neurotox
C botulinum tox
Potent heat labile tox
Most potent known natural tox
(Opposite to tetanus - muscle relaxed paralysis)
C botulinum classification
Subdivised on basis pf 6 main tox types recog A-F
C and D prod 2nd tox -C2
Tox potency varies and are antigenically distinct but pharmacologically similar
Have shared cellular antigens with sporogenes an novyi so may x react in tests
Tox assoc with location
E with marine source
A and B with soil
All found in range of places incl spoiled food, animal carcasses, spoiled hay and silage etc
Tox production and composition of botulinum
Vegetative cells prod toxin released by autolysis
Chrom encoded: A B C2 E
Phage encoded: C1 D
Protoxin - H chain - disulphide bond - L chain
H binds
L is Zn dep endopeptidase (proteolysis of spec pros forming synaptic vesicle docking and fusion complex)
Botulism pathogenicity (Not truly an infectious dis as bact dont need to enter only the preformed toxins)
Preformed tox in food is absorbed in GIT
Tox not inact by proteolytic enz, sometimes act
Tox travel to neurons in blood
Tox affect maily cholinergic system - block Ach release mainly in periphNS esp at neuromusc jctn
Cause flaccid paralysis
Death usually from cardiac or resp failure
Main types affecting animals
C and D
Most frequently in farmed and wild birds
Wound botulism is rare (increased in drug injecting humans
Botulism lab diagnosis
Isolate and ID organism or tox from suspected food, demo tox in blood by tox- antitox neutralisation test in mice
Faeces and vomit may cont tox
Botulism treatment
Remove tox source or unabsorbed tox
Neutralise tox
Botulism control
Reduce tox prod/tox access
Hygiene
Toxoid vacc
Antitox i/v
Horse botulinum types
A b c d
Cattle botulinum types
C d
Sheep botulinum types
C
Birds botulinum types
C d
Fishbotulinum types
E
Human botulinum types
A b e f
Equine grass sickness/dysautonomia/toxico-infectious botulism hypothesis
Natural c and d botulism type carried in equine pop
Unknown trigger alter GI enviro cause overgrowth of C (or maybe D) in gut and incr tox production causing symptoms and pathology of EGS
Severity dep on imm status and toxic insult
Shaker foal syndrome
Rare form of toxico-infectious botulism
Similar to infant botulism in humans
