Clostridium Flashcards

1
Q

smell of culture

A

putrid due to volatile fatty acids

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2
Q

gram, size, shape, spore, respiration, catalase, oxidase, motility, media, hemolysis, habitat

A

-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

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3
Q

groupings

A

-neurotoxic
-histotoxic
-enteropathogenic and enterotoxaemia

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4
Q

C perfringens morphology

A

large, wide rods
rarely form endospores

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5
Q

C tetani morphology

A

thin rods
produce terminal endospores
drumstick appearance

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6
Q

C chauvoei morphology

A

medium sized rods
lemon shaped endosomes

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7
Q

C tetani – neurotoxic

A

-infection through wound contamination
-genes that regulate production in plasmids
-antigenic type – tetanospasmin
-mode of action – synaptic inhibition
-musclular patterns

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8
Q

C botulinum – neurotoxic

A

-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

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9
Q

C tetani toxin

A

never changes
can be used in vaccine

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10
Q

C tetani adjuvant

A

aluminum hydroxide – very painful

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11
Q

C tetani reservoir

A

-widely distributed in soil
-transient in intestines
-horses have normal amount in intestines

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12
Q

tetanus

A

introduction of spore into traumatized tissue

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13
Q

what is more important in tetanus

A

amount of toxin more important than amount of bacteria

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14
Q

tonic clonic convulsions in tetanus

A

-neuroparalytic intoxication
-protien neurotoxin
-poultry highly resistant

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15
Q

tetanus toxin – tetanospasim

A

-zinc endopeptidase binds to neurons, release gamma aminobutyric acid (GABA) and glycine
-once docking proteins hydrolyzed, synapse degenerates – weeks to months to regenerate

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16
Q

which species highly resistant to C tetani

A

poultry

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17
Q

spore germination in C tetani

A

-anaerobic environment allows spores to germinate

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18
Q

toxin diffusion and attachment in C tetani

A

-toxin diffuses via vascular channels or peripheral nerve tracks
-toxin attaches to receptors on nearest cholinergic nerve and is internalized within vesicle

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19
Q

travel of vesicle containing toxin in C tetani

A

-travels retrograde inside axon to cell bodeis of ventral horns of spinal cord

20
Q

spastic paralysis in C tetani

A

malachite green???

21
Q

early signs of disease in C tetani

A

-stiffness
-muscular tremor
-increased responsiveness to stimuli

22
Q

signs in horses, ruminants, swine in C tetani

A

-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

23
Q

gross lesions in C tetani

A

none in brain or muscle
clinical diagnosis only

24
Q

pathogenesis in C tetani

A

exotoxin (tetanospasim) blocks inhibitory neurotransmitter in upper motor neurons – spastic paralysis

25
Q

lab diagnosis in C tetani

A

-hemolytic due to tetanolysin
-gram stain – drumstick shape

26
Q

treatment – neutralization of circulating toxin in C tetani

A

-antitoxin

27
Q

treatment – suppression of toxin production in C tetani

A

-wound care, parenteral penicillin or metronidazole
-flushing of hydrogen peroxide to create aerobic conditions

28
Q

treatment – life support and symptomatic relief in C tetani

A

-sedatives, muscle relaxants, exclusion of external stimuli
-artificial feeding
-nursing care

29
Q

prevention of C tetani

A

-clean and dress wounds
-hygienic precautions during surgery
-horses get antitoxin after injury or surgery

30
Q

what causes botulism

A

Clostridium botulinum

31
Q

what is botulism

A

neuroparalytic intoxication characterized by flaccid paralysis

32
Q

most common C. botulinum type in domestic animals

A

type D and D

33
Q

mainly affected animals of botulism

A

ruminants, horses, mink, waterfowl

34
Q

C botulinum toxins – Botulinum neurotoxins (BoNT)

A

-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

35
Q

reservoir of C. botulinum

A

-soil and aquatic sediments
-contaminated cans of meat and veggies
-spores contaminate environemnt

36
Q

transmission of C botulinum

A

-toxin ingestion
-spore ingestion – human infant botulism
-wound contamination – rarely in humans and horses

37
Q

pathogenesis of C botulinum

A

-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

38
Q

clinical signs of botulism

A

-muscular incoordination
-recumbency
-extrusion of tongue
-no change in consciousness
-temperature remains normal
-recovery slow and residual signs persist in non fatal cases
-limberneck

39
Q

gross lesions in botulism

A

no gross lesions in brain or msucle

40
Q

lab diagnosis

A

-toxin in plasma or tissue
-isolation of organism not definitive
-toxin in feedstuffs, stomach contents, vomit
-serological and molecular techniques to support diagnosis

41
Q

only accepted method of confirmation of botulism

A

-toxin extracted from material and injected into guinea pigs or mice
-death in 10hrs-3wks preceded by muscular weakness, limb paralysis, respiratory difficulties

42
Q

growth of C botulinum in differnet media

A

-egg yolk agar – lipase reaction after 72 hrs
-blood agar – colony growth after 72 hrs

43
Q

treatment for recent injections of C botulinum

A

-evacuation of stomach and purging

44
Q

treatment after onset of signs of botulism

A

-antitoxin treatment may be beneficial (minks, ducks)

45
Q

control of c botulinum

A

-remove affected waterfowl
vaccination (toxoid) in endemic areas
-placing feed on dry ground attracts birds form contaminated areas