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Veterinary Bacteriology & Mycology > Clostridium > Flashcards

Clostridium Flashcards

1
Q

What are the main 3 morphological characteristics of Clostridium?

A
  1. straight or slightly curved rods
  2. Gram positive
  3. produce endospores, where the size, shape, and location can be used for ID
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2
Q

What’s unique about Clostridium cultures? What is their most common mode of energy production?

A

typically emit putrid odors

peptide catabolism

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3
Q

What kind of respiration does Clostridium undergo?

A

anaerobes

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4
Q

How does Clostridium respond to catalase and oxidase tests?

A

negative
negative

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5
Q

Clostridium are motile bacteria. What species is the exception?

A

C. perfringens

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6
Q

What is necessary for Clostridium growth on agar? How does C. perfringens grow in blood agar?

A

enrichment of the media

surrounded by zones of double hemolysis

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7
Q

What are the main 3 locations that Clostridium is found?

A
  1. soil (saprophytes)
  2. alimentary tracts of animals (intestinal flora)
  3. feces
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8
Q

How are Clostridium grouped? What are the 3 groups?

A

according to the mode and sites of action of their exotoxins

  1. neurotoxic
  2. histotoxic
  3. enteropathogenic and enterotoxemia-producing
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9
Q

Where are sequestered endospores of Clostridium typically found? What happens when they’re activated?

A

muscle or liver

produce disease

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10
Q

How do Clostridium perfringens, C. tetani, and chauvoei compare morphologically?

A

C. perfringens: large, wide rods that rarely form endospores

C. tetani: thin rods that produce terminal endospores (drumstick)

  1. C. chauvoei: medium-sized rods that produce lemon-shaped endospores
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11
Q

What are the 2 neurotoxic Clostridia? Where do the genes for their neurotoxins come from?

A
  1. C. tetani - plasmids
  2. C. botulinum - chromosomes, plasmids, bacteriophages
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12
Q

What are the 10 serotypes of C. tetani based on?

A

flagellar antigens and geographic strain origin

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13
Q

What makes the C. tetani vaccine efficient?

A

tetanus neurotoxin (TeNT) is antigenically uniform (not altered by mutations)

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14
Q

What are the main 2 reservoirs of C. tetani?

A
  1. widely distributed in the soil
  2. transient in the intestine
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15
Q

What is the occurrence of tetanus commonly linked to? How can this happen?

A

introduction of spores into traumatized tissue
- contaminated syringes
- penetrating nail wounds on foot
- barnyard surgery
- use of rubber bands for castrating and docking
- ear tagging infections
- shearing wounds
- post-partum uteroine infections
- perinatal umbilical infections
- small fights

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16
Q

What is the neuroparalytic intoxication of tetanus characterized by? What causes this?

A

tonic-clonic convulsions

protein neurotoxin (tetanospasmin)

(tetanus = taut)

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17
Q

All mammals are susceptible to tetanus to varying degrees. How do animals compare? How susceptible is poultry? What is true in all animals infected?

A

horses, humans, ruminants, and swine are more susceptible than carnivores

poultry are highly resistant

mortality rate is high

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18
Q

How does tetanospasmin cause spastic paralysis?

A

zinc endopeptidase binds ti the neurons, which releases GABA and glycine, the major inhibitory neurotransmitters that stop muscle contraction

however, tetanoplasmin hydrolyzes the docking protein (VAMP, synaptobrevin) required by inhibitory transmitter-containing vesicles to fuse with the presynaptic membrane, causing the synapse to degenerate which takes weeks to months to regenerate

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19
Q

What are the 5 steps to C. tetani pathogenesis?

A
  1. anaerobic environment allows spores to germinate
  2. toxin diffuses via vascular channels or peripheral nerve trunks
  3. toxin attaches to receptors on nearest cholinergic nerve and is internalized within a vesicle
  4. vesicle travels retrograde inside the axons to the cell bodies in the ventral horns of the spinal cord
  5. toxin causes innervated muscles to remain in sustained clonic or tonic spasms and can travel within the cord to other levels affecting additional muscle groups

(SPASTIC PARALYSIS)

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20
Q

How can the spores of C. tetani be visualized microscopically?

A

Malachite green stain
(Gram positive!)

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21
Q

What is the incubation period of C. tetani? What are the major early signs? When is mortality the highest?

A

few days to several weeks

stiffness, muscular tremor, increased responsiveness to stimuli

mortality is at least 50% and highest in young animals

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22
Q

What are 5 common signs of tetanus is horses, ruminants, and swine?

A
  1. retraction of third eyelid
  2. erectness of ears
  3. teeth grinding
  4. tail stiffness
  5. lockjaw —> feeding impossible
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23
Q

What is the most common sign of tetanus in ruminants? What is sawhorse?

A

bloat

rigidity of extremities that leads to recumbence

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24
Q

How does tetanus affect urinating and defecation? Will the animal remain conscious?

A

fecal and urinary retention

yes

25
Q

What is the ultimate cause of death in animals with tetanus? How does it compare is young animals and older animals? How long does full recovery take?

A

respiratory arrest

LAMBS/PIGLETS: within first week
ADULT ANIMALS: 1-2 weeks

weeks to months

26
Q

What is the only way to diagnose tetanus?

A

clinical diagnosis only —> the injury that allowed for infection will be healed by the time of death and there is no gross lesions in brain or muscle

27
Q

Why do animals with tetanus tend to extend their neck?

A

makes breathing easier

28
Q

What is acquired resistance to tetanus dependent on?

A

the amount of circulating toxin (not the amount of bacteria)

29
Q

Why are survivors susceptible to tetanus reinfection? How is immune protection acquired?

A

survivors most likely survived because there was not enough toxin present, which doesn’t induce a strong immune response (neutralizing antibodies)

passive and active protection is provided by administrating antitoxin or immunization with toxoid

30
Q

What should a Gram stain smear of suspected C. tetani look like?

A

Gram-positive “drumstick” bacteria

31
Q

How should wound exudate from C. tetani plate on blood agar in an anaerobic culture? What would a drop of antitoxin in the culture do?

A

hemolytic due to tetanolysin

inhibit hemolysis

32
Q

What are the 3 major goals of tetanus treatment?

A
  1. neutralization of circulating toxin using antitoxin
  2. suppression of toxin production using parenteral penicillin or metronidazole and flushing with hydrogen peroxide to create an aerobic environment
  3. life support and symptomatic relief
33
Q

What are 3 ways that symptomatic relief of tetanus can be achieved?

A
  1. use of sedatives and muscle relaxants and exclusion of external stimuli
  2. artificial feeding by stomach tube or IV
  3. nursing care is most important (quiet barn with minimal noise and light)
34
Q

What is the main way tetanus is prevented?

A

wounds should be properly cleaned and dressed, especially after surgical procedures and under farm conditions

35
Q

What is given to horses after injury or surgery when they are not actively immunized against tetanus?

A

tetanus antitoxin and/or penicillin

36
Q

What does active immunization against tetanus use? How is passive immunity gained?

A

formalinized toxoid given twice at 1-2 month intervals and annually thereafter

passes from immunized mares to nursing foals to protect them for about 10 weeks

37
Q

What causes botulism? What is neuroparalytic intoxication characterized by?

A

C. botulinum

FLACID paralysis

38
Q

Neuroparalytic intoxication from C. botulinum is most commonly caused by what 2 neurotoxins in domestic animals?

A

C and D

(G has been renamed C. argentinense)

39
Q

How do the different neurotoxins causing botulism compare?

A

identical in action, but differ in potency, antigenic properties, and distribution

40
Q

What animals are most affected by botulism?

A

ruminants, horses, mink, and waterfowl
- swine, carnivores, and fish are rarely affected

41
Q

What toxin causes botulism? How?

A

botulinum neurotoxins (BoNT)

zinc endopeptidases bind to cholinergic nerve cells and decrease the release of acetylcholine

42
Q

What are BoNTs typically secreted with? Why?

A

accessory proteins to aid in the survival in the GI tract

43
Q

What are the 2 common reservoirs of C. botulinum?

A
  1. soil/aquatic sediments - vehicles of intoxication are contaminated animal and plant material from when animals die and allow spores to germinate and generate toxin, which can be ingested by carrion eaters and contaminate the surrounding environment
  2. contaminated cans of meats and vegetables
44
Q

What are the 3 main ways that C. botulinum is transmitted?

A
  1. toxin ingestion
  2. spore ingestion (human infants)
  3. wound contamination (rare in humans and horses)
45
Q

What are the 5 steps of botulism pathogenesis?

A
  1. BoNT are ingested and absorbed in the GI tract
  2. circulates in the bloodstream
  3. neuromuscular junction of cholinergic nerves
  4. hydrolyzes docking protein (synaptobrevins, SNARE)
  5. synapses degenerate and FLACCID PARALYSIS results due to a lack of acetylcholine
46
Q

When does botulism result in death?

A

when it affects the muscles of respiration and causes respiratory failure

47
Q

What are the 3 common clinical signs of botulism?

A
  1. muscular incoordination leading to recumbency, extrusion of the tongue, and disturbances in chewing and swallowing food
  2. no changes in consciousness
  3. normal temperature unless a secondary infection is occurring (pneumonia)
48
Q

If a whole group of animals is affected by paralysis is tetanus or botulism suspected?

A

botulism
- common in groups bc it is usually caused by feed being contaminated
- tetanus is more individual because it is linked to spores infecting wounds

49
Q

How is the neck typically affected by botulism? Are any gross lesions seen?

A

flaccid neck paralysis

no gross lesions in the brain or muscle

50
Q

What is the initial clinical sign of botulism?

A

limberneck

51
Q

What is required for laboratory diagnosis of botulism?

A

demonstration of the toxin in plasma or tissue before death or from a fresh carcass and presence of toxins in feedstuffs, fresh stomach contents, or vomit
- isolation of organism is not definitive

52
Q

What is the only accepted method of proving the presence of C. botulinum toxin from an animal?

A

toxin is extracted and injected into Guinea pigs or mice —> death occurs within 10 hrs to 3 weeks, preceded by muscle weakness, limb paralysis, and respiratory difficulties

53
Q

How can C. botulinum be isolated?

A

heat samples 65-80 degrees C for 30 mins to induce germination and culture anaerobically on blood agar

54
Q

What does C. botulinum growth on egg yolk agar show?

A

lipase activity

55
Q

How can botulism be treated in an animal that recently ate contaminated food? What can be done following onset of clinical signs?

A

evacuation of the stomach with laxative and purging

antitoxin treatment (mainly in mink and ducks)

56
Q

What toxoids should animals at risk for botulism be treated with?

A

A-D

57
Q

How can waterfowl contamination be limited in botulism outbreaks?

A
  • removal of affected waterfowl to dry land to save healthy birds from exposure and drowning
  • place feed on dry land to attract birds out of contaminated areas
58
Q

What 2 drugs can be used to treat botulism? What do they do?

A
  1. guanidine
  2. tetraethylamide

stimulates ACh release

59
Q

What commercial use is BoNT used for in humans?

A

Botox

Veterinary Bacteriology & Mycology (47 decks)

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