Neuro Pathogens Flashcards
What are the bacterial characteristics of C. botulinum
- Anaerobic gram + rod
- Form endospores (oval and at the end of mother cells)
o Resistant to enviro
o Protective - In soil and aquatic enviro
What are the subtypes of C. botulinum? What are notable features
- 7 types (A-G)
o C and D most common in animals
o Cats resistant to neurotoxins
Where can C. botulinum neurotoxin be found
o Produced by organisms replicating in decaying matter/anaerobic enviro
Canned goods/spoiled forage or silage/dead animals/wounds/GI of neonates
How is C. botulinum neurotoxin acquired? Which is more common
o Transmit
Ingestion of pre-formed toxin (food borne)
* Way more common route
Toxico-infectious botulism (spores germinate in wounds of GI)
What is the pathogenesis of C. botulinum
- Pathogenesis: irreversible
o Botulinum toxin
o Absorbed in GI
o Enter bloodstream
o Neuromuscular junction of cholinergic neurons
o Internalized by motor neurons
o Cleave SNARE proteins (facilitate release of Ach)
o Block release of neurotransmitters
What are the clinical signs of C. botulinum? When do they occur?
- Clinical signs
o 3-17d post ingestions
o Mydriasis
o Dry MM
o Reduced salivation
o Tongue flaccidity and flaccid paralysis/recumbency
o Dysphagia
o Paralysis of resp muscles/death
How is C. botulinum diagnosed? What is one thing to be aware of
- Dx: be aware the samples may contain neurotoxin
o Clinical signs + history of contaminated feed
o Show toxin in serum: mouse inoculation or ELIS
o Show toxin genes: PCR
How is C. botulinum treated?
o polyvalent antiserum = bind/neutralize toxin
o tetraethylamide and guanidine hydrochloride: increase NT at synapse
o if mildly affected = recover without tx
How is C. botulinum controlled?
- Control: vx (in south Africa and Australia where its endemic)
o Don’t feed bad/spoiled food to domestic animals
o Give balanced diet to herbivores
How does C. botulinum affect humans?
o Food: canned food
o Toxico-infectious: illicit drug use/contaminated needles or infant botulism (from honey)
o Use: strabismus/post stroke spasticity/spinal cord injury spasticity/muscle spasms/migraine/cosmetic
What are the bacterial features of C. tetani
- Anaerobic gram + rod
- Form endospores
o Located at the tip of the mother cell
o Drumstick appearance
o Resistant too chemicals - Found in soil
Where is C. tetani produced
- Toxin: cause tetanus (susceptibility varies by species)
o Tetanospasmin – made by organisms replicating in damaged tissue (anaerobic)
What is the pathogenesis of C. tetani
- Pathogenesis: irreversible
o Tetanospasmin
o Motor neuron terminal
o Retrograde movement
o Synapse
o Inhibitory neurons – inhibit SNARE protein
o Blocks release of neurotransmitter = prevent modulation of motor neurons (excess excitatory input with no inhibitory regulation
What are the clinical signs of C. tetani and when do they occur?
- Clinically: 5 – 14d after infection
o Stiff/localized spasms = ‘lock jaw’ and sawhorse stance
o Altered heart and resp rates
o Dysphagia
o Altered facial expression
o Prolapse of third eyelid
o Depends on anatomy/amount of toxin/species susceptibility
How is C. tetani diagnosed?
- Dx: clinical sings
o History of recent trauma + unvaccinated
o Culture and PCR
What is a common differential for C. tetani? How to differentiate them?
o Ddx: strychnine
To differentiate = identify the gram stain and drumstick forms
What are the 3 steps to treat C. tetani
- Tx:
o Neutralized unbound toxin: IV antitoxin (3d) + stimulate immune (toxoid inj)
o Kill/inhibit: penicillin/flush lesion with hydrogen peroxide
o Remove bacteria: debride and remove foreign bodies
How to control C. tetani
- Control: vaccinate (last up to 5 years) = best way to control
o Horse: surgical debridement of wounds
o Antitoxin to at risk animals
Horse post surgery/wound – theilers disease risk
List the susceptibility of common species to C. tetani
o Susceptibility
Horse and humans most susceptible
Ruminant/pig
Dog/cat
Chickens resistant
Compare the location at which C. tetani vs C. botulinum works
o tetani: Inhibition occurs in the synapse between inhibitory neuron and motor neuron (not neuromuscular junction - botulnium_
What are the bacterial features of L. monocytogenes
Listeria monocytogenes
* Gram + rod
* No spores
* Psychrophile: grow from 4-45C and pH of 5.5 – 9.6
o Food and poor quality silage
* Found in the environment
* Zoonotic
What are the 2 main virulence factors of L. monocytogenes? What do they help facilitate
Virulence factors
o Internalins: adhere to epithelial cells
o Listeriolysins: protect from phagocytosis
o Facilitate
Intracellular replication
Evade humoral defenses
What is the pathogenesis of L. monocytogenes
- Pathogenesis
o Ingest contaminated feed
o Enter either
GI = blood
* Infect fetus = abortion
* Septicemia
* migrate to brain/brainstem = microabscess = encephalitis
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Oral cavity = migrte to cranial nerves = migrate to brain/brainstem = microabscess = encephalitis
What are the clinical signs of L. monocytogenes and when do they occur
- Clinically: 14 – 40d post ingestion
o Encephalitis: impair CN 5, 7, 8, 9
Unilateral facial paralysis (head tilt/drooling/drooping eyelid and ear)
o Ataxia
o Recumbency
o Death
o Abortion (12d post infection)
o Septicemia
o Less common: mastitis/ophthalmitis
How is L. monocytogenes diagnosed and what samples do you take
- Dx: clinical signs + feeding silage
o Culture + PCR
o Sample: CSF/uterine discharge/placenta/blood sample
o Immunofluorescence
How is L. monocytogenes treated?
- Tx:
o Septicemia: systemic abx (ampicillin/amoxicillin)
o Neurologic: high dose ampicillin/amoxicillin and aminoglycoside
o Conjunctival abx
How is L. monocytogenes controlled?
- Control: avoid poor quality silage (especially with pregnant) – should be <4.2 pH
o Vaccine – not in CA
How does L. monocytogenes appear in humans?
o Transmit: indirectly via milk/cheese/vegetables
o Clinically: mild in healthy and non-pregnant
Popular lesions of hands and arms
Abortion if pregnant
Life threatening in newborns
What animals are commonly affected by otitis media/interna
- Target: all animals of any ages
o Uni or bilateral
How is otitis media/interna transmitted
o Mites
o Foreign body
What are the main causative agents of otitis media/interna
o Mycoplasma bovis
o P. multicida
o Truperella pyogenes
o Staph intermedius and pseudointermedius
o Pseudomonas aeruginosa
o Proteus
What is the pathogenesis of otitis media/interna?
2 ways
o External ear infection = tympanic membrane = middle ear = internal ear
o Pharyngeal bacteria = auditory tube = middle ear = internal ear
What are the clinical signs of otitis media/interna?
- Clinically: varied
o Reduced hearing
o Ead shaking
o Ear discharge
o Scratching
o Signs depend on cranial nerves affected
Facial paralysis
Head tilt and circling
Nystagmus keratoconjunctivitis
How is otitis media/interna diagnosed?
- Dx: otoscopic exam (ruptured or discoloured tympanic membrane + mucoid discharge)
o CT or MRI because 70% otitis media in dogs have intact tympanic membrane
How is otitis media/interna treated?
- Tx: abx with C/S
o Otitis media = for 6-8 weeks
o Otitis interna (intracranial) = for 3 months
What are the 3 main differences between C. botulinum and tetani toxins
- site of production
tetani: wound
botulinum: in carcass/decaying veg/canned food/wound/GI - Mode of toxin action
tetani: synaptic inhibition
botulinum: inhibition of neuromuscular junction - Clinical effect
tetani: synaptic inhibition
botulinum: flaccid paralysis
