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1.22.2.10 - Circulation, Blood Brain Barrier and Infection - Coggle Diagram
1.22.2.10 - Circulation, Blood Brain Barrier and Infection
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Listeriosis
Features
Gram positive, rod, facultative anaerobes, small haemolytic colonies
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Zoonoses
The disease can affect pregnant women, newborns and adults with weakened immune systems
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In ruminants
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They can replicate in poor quality silage pH above 5.5 - in quality silage multiplication is inhibited by acid pH-> outbreaks tend to be seasonal
In ruminants may present as encephalitis, abortion, septicaemia or endophthalmitis
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Clinical signs
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Dullness, cirlcing and tilting of head facial paralysis
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Rabies
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General features
Present in saliva-> transmitted by biting carnivores: In europe the principle reservoir is red fox, in north america the principle reservoir is raccoons, skunks and fox
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Incubation period time between bite and development of signs of neurological involvement is between 14-90 days
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A number of other neurotropic Lyssaviruses closely related to rabies virus and indistinguishable from rabies
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Treatment
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Should there have been a person bitten or scratched by the potentially infected animal, the Veterinary Inspector (VI) would require the destruction of the animal in order to confirm or rule out a diagnosis of rabies by post mortem
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Vaccination
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Not required in UK for domestic animals - Necessary if travelling abroad, to obtain the Animal Health Certificate (replace the pet passport since 1st Jan 2021) to enter/re-enter UK without mandatory quarantine.
Active vaccination available for human exposure, needs to be administered rapidly as ineffective once neurological signs
Toxin of the CNS
Ingestion
Toxins can be produced by fungi, plants and microorgnisms and ingested via contaminated pasture and feed
Infection
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Toxins can be produced by colonisation of young animals by toxin producing bacteria normally excluded from the intestine
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Clostridia
Relatively large, Gram-positive, rods, form endospores.
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Tetanus
C. tetani toxins produced by organisms replicating locally in tissues (eg GI tract) or wounds. Toxicoinfectious.
Causes muscular spasms spastic paralysis.
Descending tetanus: toxin disseminated in bloodstream → remote areas → toxin enters CNS at many levels → generalized tetanus, often beginning cranially horses.
Ascending tetanus: toxin travels along the peripheral nerves → binds to specific gangliosides of the motor nerve terminals → suppresses release of afferent inhibitory neurotransmitters eg, glycine → spastic paralysis and characteristic spasms carnivores.
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Treatment
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Early intervention, including wound cleaning, boosting immunity, parenteral antitoxin administration, and muscle relaxants.
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Antitoxins that neutralize circulating toxin are only effective before the toxin has entered the nerve terminals.
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Botulism
C. botulinum toxin produced in decaying organic matter (bodies) and problem is from ingestion Intoxication.
Sources: carrion or C. botulinum colonised, feed rotting hay or silage Multiple animals may be affected.
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Botulinum toxin passes into the nerve terminal and inhibition of acetylcholine release (Irreversible stops vesicle fusion in nerve end).
Treatment
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In ruminants, clinical signs will not resolve until the neurotoxin has decayed; this will take a number of weeks/months. usually impractical to attempt nursing for this period of time and consideration must be given to the welfare implications for the affected animal.