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Bacteriology > 5.4 Gram positive spore forming anaerobic rods > Flashcards

5.4 Gram positive spore forming anaerobic rods Flashcards

1
Q

characteristics of clostridium: morphology, gram, environment, growth, toxins, prevention, etc.

A
  • Large spore-forming rods
  • Gram positive
  • Widespread in environment (soil), large bowel
  • Rapid multiplication, simple growth requirements
  • Powerful toxin producers
  • Often prevented by toxoid immunization
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2
Q

types of neurotoxic clostridia

A

C. botulinum
C. tetani

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3
Q

Neurotoxic clostridia: Clostridium tetani characteristics: gram, environment, disease, species, etc

A
  • Gram positive, anaerobe
  • Agent of tetanus
  • Deep wounds
  • Species susceptibility: Horse > human > other species (dogs and cats less)
  • All species can develop tetanus
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4
Q

Clostridium tetani spore shape and what we find in infected wounds

A

tennis-racket shape (terminal spores). There is frequently a mixture of bacteria in the wound.

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5
Q

Clostridium tetani: pathogenesis

A
  1. C. tetani produces toxin at infection site.
  2. Toxin migrates through axon to CNS
  3. Toxin migrates to inhibitory neuron
  4. Toxin in inhibitory neuron inhibits release of inhibitory transmitters (GABA and glycin)
  5. Motor neuron can fire stimulatory signals uninhibited > SPASM
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6
Q

Clostridium tetani: clinical signs

A

spasms

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7
Q

Clostridium tetani: diagnosis

A
  • clinical signs and history of recent trauma
  • detection of toxin or C. tetani DNA by PCR
  • direct smear from wound (Gram stain)
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8
Q

Clostridium tetani: treatment and prevention

A

Treatment: calm, darkness, silence, muscle relaxants, artificial respiration
* Antibiotics: local infection, but cannot act on the toxin

  • Prevention: vaccination, wound hygiene, avoid trauma
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9
Q

Neurotoxic clostridia: Clostridium botulinum characteristics: gram, environment, toxins, effects, animals affected

A
  • Gram positive, anaerobe
  • Ubiquitous environment
  • Most potent toxin known
  • Causes flaccid paralysis if toxin ingested
  • “Intoxication” (ingest preformed toxin) mostly
  • Animals affected: wildfowl, poultry, cattle, sheep, horses (occasionally dogs and pigs)
  • Humans: improperly home-canned, preserved, or fermented foods can provide the right conditions for spores to grow and make botulinum toxin
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10
Q

Clostridium botulinum: pathogenesis: target cells, mechanism, effect

A

Target cells: cholinergic cells (neuromuscular junction)
Mechanism: blocks presynaptic release of acetylcholine
Effect: flaccid paralysis

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11
Q

Clostridium botulinum: clinical signs

A

-affects peripheral nerves, flaccid paralysis throughout several body areas

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12
Q

C. botulinum: diagnostic and treatment

A
  • Clinical suspicion: flaccid paralysis
  • Toxin test (mouse > ELISA)
  • PCR for toxin-genes in enrichment cultures
    ==> Only suggestive (can be false positive)

Botulinum toxin causes a “wasp-waist” (diaphragmatic paralysis) in mice (highly sensitive test)

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13
Q

categories of diseases caused by claustridia

A
  • Enterotoxic, Histotoxic, Neurotoxic
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14
Q

Histotoxic clostridia: Clostridium chauvoei
- what diseases does it cause? how does it do it? where is it found?

A
  • Agent of “blackleg”
  • Acute, infectious, necrotizing myositis in young calves at pasture in summer
  • Germination latent spores in the muscle
  • Locally necrotizing myositis=>systemic toxemia=> death
  • Infectious (farm problem)
  • Endemic areas (western Canada, northern Ontario; globally)
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15
Q

Clostridium chauvoei toxin results in:

A

results in muscle necrosis and hemorrhage

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16
Q

Clostridium chauvoei: pathological findings

A

**histotoxic
Necrotizing myositis

C. chauvoei multiplies in the muscle and produce gas from fermentation of glycogen in the muscle => creptitation

17
Q

Clostridium chauvoei: clinical signs and diagnosis

A
  • Clinically: a rapidly fatal, febrile disease in well-nourished young cattle, particularly in beef breeds, with crepitant swellings of the large muscles
  • Gram stain and culture (differential diagnosis PM overgrowth clostridia)
  • Ultrasonographic examination of affected areas
  • PCR
18
Q

Clostridium chauvoei: prevention

A
  • Prevention: multivalent vaccine C. chauvoei, C. septicum, and where needed, C. novyi (only in endemic areas)
19
Q

what is malignant oedema caused by? pathogens and route of contamination? how to cure?

A
  • Malignant edema = gas gangrene (mixed infection)
  • C. septicum (most importante)
  • C. novyi type A
  • C. perfringens type A
  • C. sordellii
  • C. chauvoei

> histotoxic claustridia

  • Wound contamination/infection by a histotoxic Clostridium
  • Serious, deep (“anaerobic”), traumatic wound
  • Characterized by rapidity (usually), gas formation, toxemia
  • Requires antimicrobials and surgical debridement
20
Q

Histotoxic clostridia: malignant oedema clinical signs

A
  • Clinical signs develop within 2 days: fever and localized swellings in muscles and intermuscular connective tissues
  • A fatal toxemia often results
21
Q

Enteric clostridia: C. perfringens characteristics: gram, environment, where found, growth, toxins, etc

A
  • Gram positive rods, large, anaerobe
  • Widespread intestine, fecal contamination
  • Fastest growing bacterium known
  • Variety of pore-forming toxins
    > (PCR) divides into 7 types (new!)
22
Q

C. perfringens Type A: where are they found? what do they produce? when are they significant? what can they cause and in what species?

A
  • Most strains are intestinal commensals > finding a C. perfringens in the gut of an animal is perfectly normal!
    > Normal to find Alpha toxin
  • Finding one in the gut of an animal producing a toxin other than the alpha toxin may have a significance.
  • Dogs and foals: hemorrhagic necrotizing enteritis (Alpha + NetF toxin)
  • Calves: abomasitis
23
Q

C. perfringens Type D: causes what diseases and in what animals? what toxin?

A

“Pulpy kidney” disease
Sheep and goats
Over-eating disease: Upsets in gut flora from change to rich diet
“epsilon” toxin=> absorbed into body, produces encephalomalacia
Often no enteritis

> Typical example of toxaemia: toxin in the blood, and acts somewhere else

24
Q

how can C. perfringens be histocytic?

A
  • Wound infections (“gas gangrene”)
  • Severe, often fatal, necrotizing mastitis
25
Q

C. perfringens: dx, prevention, treatment

A

Diagnosis: Gram, culture, PCR on cultures for toxin type determination
Prevention: Vaccine (toxoid; pulpy kidney disease)
Treatment: antibiotics, debriding (if wound)

26
Q

Enteric Clostridia: Clostridioides difficile characteristics: morphology, environment, species, growth, survival, toxins, etc.

A
  • Gram positive rod, anaerobe
  • Isolated from marine, soil, sand, hospitals, feces
  • Camels, horses, donkeys, dogs, cats, birds, cattle, snakes
  • Overgrowth from disruption of bowel flora (antibiotic therapy)
    > Uncontrolled proliferation of C. difficile which survives as a spore
    > Onset several days after start of antibiotic, or after termination of treatment
  • Toxin A: enterotoxin, fluid accumulation in gut, lethal PO
  • Toxin B: cytotoxin
27
Q

Enteric clostridia: Clostridioides difficile diseases

A
  • Pseudomembranous colitis (overgrowth): humans and guinea pigs
  • Hemorrhagic necrotizing enterocolitis: foals
    > first week of life, watery diarrhea, dehydration
    > Death within 24 hours
  • Chronic diarrhea: dogs
    > Shed in feces of normal dogs
28
Q

Enteric clostridia: Clostridioides difficile diagnosis and treatment

A
  • Dx:ELISA toxins,RT-qPCR (but may detect non-diseased animals)
  • Treatment: antibiotics, probiotics, fecal flora transplant (?)

Bacteriology (15 decks)

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