Clostridium Flashcards
smell of culture
putrid due to volatile fatty acids
gram, size, shape, spore, respiration, catalase, oxidase, motility, media, hemolysis, habitat
-gram positive
-large
-rods – straight or slightly curved
-endospores produces – terminal, central, subterminal
-anaerobic
-catalase negative
-oxidase negative
-motile except for C perfringens
-requires enriched media
-zones of double hemolysis in C perfringens
-present in soil, alimentary tracts of animals, feces
groupings
-neurotoxic
-histotoxic
-enteropathogenic and enterotoxaemia
C perfringens morphology
large, wide rods
rarely form endospores
C tetani morphology
thin rods
produce terminal endospores
drumstick appearance
C chauvoei morphology
medium sized rods
lemon shaped endosomes
C tetani – neurotoxic
-infection through wound contamination
-genes that regulate production in plasmids
-antigenic type – tetanospasmin
-mode of action – synaptic inhibition
-musclular patterns
C botulinum – neurotoxic
-ingestion of bacteria, spore, toxin
-in carcasses, decaying vegetation, canned food, wounds, intestines
-genes that regulate production in chromosome, plasmids, bacteriophage
-antigenic type – A, B, C, D, E, F, G
-mode of action – inhibition of neuromuscular transmission
C tetani toxin
never changes
can be used in vaccine
C tetani adjuvant
aluminum hydroxide – very painful
C tetani reservoir
-widely distributed in soil
-transient in intestines
-horses have normal amount in intestines
tetanus
introduction of spore into traumatized tissue
what is more important in tetanus
amount of toxin more important than amount of bacteria
tonic clonic convulsions in tetanus
-neuroparalytic intoxication
-protien neurotoxin
-poultry highly resistant
tetanus toxin – tetanospasim
-zinc endopeptidase binds to neurons, release gamma aminobutyric acid (GABA) and glycine
-once docking proteins hydrolyzed, synapse degenerates – weeks to months to regenerate
which species highly resistant to C tetani
poultry
spore germination in C tetani
-anaerobic environment allows spores to germinate
toxin diffusion and attachment in C tetani
-toxin diffuses via vascular channels or peripheral nerve tracks
-toxin attaches to receptors on nearest cholinergic nerve and is internalized within vesicle
travel of vesicle containing toxin in C tetani
-travels retrograde inside axon to cell bodeis of ventral horns of spinal cord
spastic paralysis in C tetani
malachite green???
early signs of disease in C tetani
-stiffness
-muscular tremor
-increased responsiveness to stimuli
signs in horses, ruminants, swine in C tetani
-third eyelid retraction, erect ears, stiff tail
-bloat in ruminants
-lockjaw
-rigidity of extremities – sawhorse attitude, recumbency
-fecal and urinary retention
-death due to respiratory arrests
gross lesions in C tetani
none in brain or muscle
clinical diagnosis only
pathogenesis in C tetani
exotoxin (tetanospasim) blocks inhibitory neurotransmitter in upper motor neurons – spastic paralysis
lab diagnosis in C tetani
-hemolytic due to tetanolysin
-gram stain – drumstick shape
treatment – neutralization of circulating toxin in C tetani
-antitoxin
treatment – suppression of toxin production in C tetani
-wound care, parenteral penicillin or metronidazole
-flushing of hydrogen peroxide to create aerobic conditions
treatment – life support and symptomatic relief in C tetani
-sedatives, muscle relaxants, exclusion of external stimuli
-artificial feeding
-nursing care
prevention of C tetani
-clean and dress wounds
-hygienic precautions during surgery
-horses get antitoxin after injury or surgery
what causes botulism
Clostridium botulinum
what is botulism
neuroparalytic intoxication characterized by flaccid paralysis
most common C. botulinum type in domestic animals
type D and D
mainly affected animals of botulism
ruminants, horses, mink, waterfowl
C botulinum toxins – Botulinum neurotoxins (BoNT)
-act in neuromuscular junction
-zinc endopeptidases bind to cholinergic nerve cells
-decreased release of acetylcholine
-synapse degenerates and takes weeks-months to regenerate
-secreted with accessory proteins – survival in GI tract
reservoir of C. botulinum
-soil and aquatic sediments
-contaminated cans of meat and veggies
-spores contaminate environemnt
transmission of C botulinum
-toxin ingestion
-spore ingestion – human infant botulism
-wound contamination – rarely in humans and horses
pathogenesis of C botulinum
-BoNT ingested and absorbed in GI tract
-circulates in blood to neuromuscular junction of cholinergic nerve
-synapse degenerates, flaccid paralysis due to lack of neurotransmitter acetylcholine
-can affect respiration muscles – death form respiratory failure
clinical signs of botulism
-muscular incoordination
-recumbency
-extrusion of tongue
-no change in consciousness
-temperature remains normal
-recovery slow and residual signs persist in non fatal cases
-limberneck
gross lesions in botulism
no gross lesions in brain or msucle
lab diagnosis
-toxin in plasma or tissue
-isolation of organism not definitive
-toxin in feedstuffs, stomach contents, vomit
-serological and molecular techniques to support diagnosis
only accepted method of confirmation of botulism
-toxin extracted from material and injected into guinea pigs or mice
-death in 10hrs-3wks preceded by muscular weakness, limb paralysis, respiratory difficulties
growth of C botulinum in differnet media
-egg yolk agar – lipase reaction after 72 hrs
-blood agar – colony growth after 72 hrs
treatment for recent injections of C botulinum
-evacuation of stomach and purging
treatment after onset of signs of botulism
-antitoxin treatment may be beneficial (minks, ducks)
control of c botulinum
-remove affected waterfowl
vaccination (toxoid) in endemic areas
-placing feed on dry ground attracts birds form contaminated areas
