5.4 Gram positive spore forming anaerobic rods Flashcards
characteristics of clostridium: morphology, gram, environment, growth, toxins, prevention, etc.
- 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
types of neurotoxic clostridia
C. botulinum
C. tetani
Neurotoxic clostridia: Clostridium tetani characteristics: gram, environment, disease, species, etc
- Gram positive, anaerobe
- Agent of tetanus
- Deep wounds
- Species susceptibility: Horse > human > other species (dogs and cats less)
- All species can develop tetanus
Clostridium tetani spore shape and what we find in infected wounds
tennis-racket shape (terminal spores). There is frequently a mixture of bacteria in the wound.
Clostridium tetani: pathogenesis
- C. tetani produces toxin at infection site.
- Toxin migrates through axon to CNS
- Toxin migrates to inhibitory neuron
- Toxin in inhibitory neuron inhibits release of inhibitory transmitters (GABA and glycin)
- Motor neuron can fire stimulatory signals uninhibited > SPASM
Clostridium tetani: clinical signs
spasms
Clostridium tetani: diagnosis
- clinical signs and history of recent trauma
- detection of toxin or C. tetani DNA by PCR
- direct smear from wound (Gram stain)
Clostridium tetani: treatment and prevention
Treatment: calm, darkness, silence, muscle relaxants, artificial respiration
* Antibiotics: local infection, but cannot act on the toxin
- Prevention: vaccination, wound hygiene, avoid trauma
Neurotoxic clostridia: Clostridium botulinum characteristics: gram, environment, toxins, effects, animals affected
- 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
Clostridium botulinum: pathogenesis: target cells, mechanism, effect
Target cells: cholinergic cells (neuromuscular junction)
Mechanism: blocks presynaptic release of acetylcholine
Effect: flaccid paralysis
Clostridium botulinum: clinical signs
-affects peripheral nerves, flaccid paralysis throughout several body areas
C. botulinum: diagnostic and treatment
- 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)
categories of diseases caused by claustridia
- Enterotoxic, Histotoxic, Neurotoxic
Histotoxic clostridia: Clostridium chauvoei
- what diseases does it cause? how does it do it? where is it found?
- 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)
Clostridium chauvoei toxin results in:
results in muscle necrosis and hemorrhage
Clostridium chauvoei: pathological findings
**histotoxic
Necrotizing myositis
C. chauvoei multiplies in the muscle and produce gas from fermentation of glycogen in the muscle => creptitation
Clostridium chauvoei: clinical signs and diagnosis
- 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
Clostridium chauvoei: prevention
- Prevention: multivalent vaccine C. chauvoei, C. septicum, and where needed, C. novyi (only in endemic areas)
what is malignant oedema caused by? pathogens and route of contamination? how to cure?
- 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
Histotoxic clostridia: malignant oedema clinical signs
- Clinical signs develop within 2 days: fever and localized swellings in muscles and intermuscular connective tissues
- A fatal toxemia often results
Enteric clostridia: C. perfringens characteristics: gram, environment, where found, growth, toxins, etc
- Gram positive rods, large, anaerobe
- Widespread intestine, fecal contamination
- Fastest growing bacterium known
- Variety of pore-forming toxins
> (PCR) divides into 7 types (new!)
C. perfringens Type A: where are they found? what do they produce? when are they significant? what can they cause and in what species?
- 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
C. perfringens Type D: causes what diseases and in what animals? what toxin?
“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
how can C. perfringens be histocytic?
- Wound infections (“gas gangrene”)
- Severe, often fatal, necrotizing mastitis
C. perfringens: dx, prevention, treatment
Diagnosis: Gram, culture, PCR on cultures for toxin type determination
Prevention: Vaccine (toxoid; pulpy kidney disease)
Treatment: antibiotics, debriding (if wound)
Enteric Clostridia: Clostridioides difficile characteristics: morphology, environment, species, growth, survival, toxins, etc.
- 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
Enteric clostridia: Clostridioides difficile diseases
- 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
Enteric clostridia: Clostridioides difficile diagnosis and treatment
- Dx:ELISA toxins,RT-qPCR (but may detect non-diseased animals)
- Treatment: antibiotics, probiotics, fecal flora transplant (?)
