• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/35

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

35 Cards in this Set

  • Front
  • Back

Clostridium species

Clostridium tetani


Clostridium botulinum


Clostridium perfringens (type A)

Clostridium Bacterial characteristics


(tetani)

Gram positive


obligate anaerobe


endospore forming

Clostridium Bacterial characteristics


(botulinum & perfringens)

gram positive


obligate anaerobe


endospore forming


fastidious anaerobe

Clostridium tetani


host species

many

Clostridium tetani


where did it come from

soil, feces, sewage, environment

Clostridium tetani


how are animals exposed

spores entering following trauma



Clostridium tetani


how does it cause disease

incubation only days to 2 weeks

Clostridium tetani


how does it cause disease (virulence factors)

tentanolysin (hemolysin) --> promotes anaerobic microenvironment for growth




Tetanospasmin (neurotoxin)


- not present on all strains


inactive protoxin released by lysis of bacterial wall


- proteolyis activates toxin heavy chain - receptor binding and entry into axon. light chain - prevents neurotransmitter release by cleaving synaptobrevin necessary for export of intracellular vesicles

Clostridium tetani


clinical signs

early -> muscle fasciculations and exaggerated responses to stimuli --> impaired muscle function in head and neck




advanced--> total body rigidity --> respiratory failure

Clostridium tetani


how to diagnose

culture


clinical signs

Clostridium tetani


will the infection spread to other animals

no, separate infections!

Clostridium tetani


how to treat

clean and debride wound


antibiotics (penicillin)


antitoxin to neutralize unbound toxin (will not reverse CNS effects)


supportive care

Clostridium tetani


how to prevent

vaccination

Clostridium tetani


in horses...

highly sensitive to toxin compared to other species.


- post partum mares with traumatic deliveries and foal via umbilicus


- guarded prognosis 50% mortality

Clostridium botulinum


host species

many

Clostridium botulinum


where did it come from

soil, invertebrates, nematodes (environment)

Clostridium botulinum


how are animals exposed

toxin C = carcasses


Toxin C & D = affect animals


toxin A, B, C = horses

Clostridium botulinum


how does it cause the disease

same as tetanus but target neuromuscular junction




intoxication - ingestion of toxin in contaminated feeds




toxicoinfectious - foals ingest spores (infection and toxin release). spores gain entry via wound (infection and toxin release)

Clostridium botulinum


clinical signs

- restlessness, incoordination, rear limb weakness




- inability to stand




- head and neck signs (paraylsis of tongue, drooling, poor pupillary light response)




- death

Clostridium botulinum


how to diagnose

culture


clinical signs



Clostridium botulinum


will it spread to other animals

no, separate infections

Clostridium botulinum


how to treat

heptavalent antitoxin to neutralize unbound toxin




supportive care


antibiotics for secondary infection


wound botulism -> surgical debridement/antibiotics

Clostridium botulinum


prognosis

death if not treated early

Clostridium botulinum


how to prevent

prepare food properly

Clostridium botulinum


zoonotic

no

Clostridium perfringens (type A)


common name

Histotoxic Clostridia

Clostridium perfringens (type A)


host species

many

Clostridium perfringens (type A)


where did it come from

environment/normal flora

Clostridium perfringens (type A)


how are animals exposed

predisposing factos


- wound = inoculates clostridia into tissue


- tissue damage = anaerobic conditions


- clostridium secretes necrotizing toxins = progressive necrosis and gas formation


- rapid expansion of pathology muscle sheath = death

Clostridium perfringens (type A)


how does it cause diesease

clostridial spores & tissue trauma - germinate and release toxins - tissue necrosis + edema + hemolysis = death

Clostridium perfringens (type A)


why does it cause disease (virulence factors)

- alpha toxin = phopholipase that damages host cell membranes




- beta toxin = mucosal necrosis, CNS and cardiac signs, lethal




- epsion = secretes as prototoxin by proteolysis -> pore forming toxin -> K & fluid leakage from host cells -> toxin in blood stream --> CNS signs

Clostridium perfringens (type A)


Clinical signs

Type C strain (poor quality feed)


- necrotic enteritis


- neonates


- NO diarrhea




Type D strain (upset GI flora)


- alpha and epsilon toxin --> edema, tissue necrosis, CNS signs, respiratory distress


- brain edema, glucose in urine


- older animals


- sudden death

Clostridium perfringens (type A)


how to diagnose

sample submission of intestinal contents, blood clots, liver, blood , serum, feces.




must find organism and toxin compatible with history

Clostridium perfringens (type A)


how to treat

no effective treatment

Clostridium perfringens (type A)


how to prevent

vaccination (dry cow)


good colostrum feeding


proper food