Bacteriology 1 Flashcards
Non-immunological defenses
Protective bones
Blood brain barrier
- carrier mediated, lipid soluble substances, astrocyte processes surround capillaries
Factors that increase risk of infection
Age
Immunosuppression/FPT
Trauma concurrent infections
Risk factors with specific infections of NS
Routes of entry
Hematogenous
Retrograde
Extension of infection from site or direct penetration
Hematogenous
Most common route of entry
Often involves infections in other organ systems
Retrograde movement
Can be organism or toxin (rabies or tetanus)
Direct penetration or extension
Infections of paranasal sinuses, middle ear infection
Extensions of discospondylitis into spinal cord
Trauma from bite wounds, blunt trauma, penetrating objects
Mechanisms of damage
Vascular damage
Injury to parenchyma or meninges
Intoxication
Vascular damage
Vasculitis - leads to endothelial damage & leakage with resultant hemorrhage & parechymal injury (rickettsia)
Septic emboli or thrombus (histophilus somni)
Injury to parenchyma
Direct damage
Indirect damage through induction of inflammatory response
- suppurative
- Pyogranulomatous
- granulomatous
Intoxication
Vasogenic cerebral edema through action of toxin
Inhibition of neurotransmitter function
- botulinum of toxin C. Botulinum
Tetanospasmin of C. Tetani
Most common bacteria causing infection in EQ
Strep equi zooepidemicus
Common causes for bacterial infection in EQ and rum?
FPT
Common in neonates
Brain abscesses more common in EQ and rum than cats and dogs
S. Equi ss equi (horses)
Trueperella pyogenes (cattle)
Trauma
Spread from contigous site
Brain and epidural spinal asbcesses in pigs
Trauma
Spread from contiguous site
Trueperella pyogenes
Clostridia
Gram positive rods
STRICT anaerobes
Motile
Gas producing
Endospore forming
Survival of clostridia
Can survive as spores (long time) or vegetative bacteria
- GIT of animals and humans (C. Tetani)
- soil and vegetation (C. Botulinum)
LOW OXYGEN
C. Tetani transmission
Inoculation into wound (anaerobic with low redox potential) necrotic tissue
C. Botulinum transmission
3 methods
- ingestion
In soil, silage, dead animals, aquatic environments
Spores germinate & veg bacteria produce inactive pro toxin = released upon bacterial cell lysis
- colonization of intestines (Young/foals)
- inoculation of wounds
Mechanisms of c. Tetani
Inside the spinal cord/brain tetanospasmin inhibits release of the neurotransmitters (glycine and GABA) from the inhibitory interneurons of this site.
Lack of inhibition leads to over (continuous) excitation of motor neurons that manifests as á muscle tone, rigidity and spasm
= SPASTIC PARALYSIS
How c. Tetani cause disease
Binding of toxin is irreversible
Once the toxin is within the nerves and axons antibodies /antitoxins can’t reach it
Mechanisms of c. Botulinum
Botulinum toxin is one of the most powerful toxins known; tiny amounts can cause death Ø Inside the GIT (more rarely in a wound) toxin is absorbed and transported to neurones via the blood stream
Ø Toxin ONLY binds to cholinergic
junctions (1°neuro-muscular
junction of peripheral nerves,
also nerve-nerve junctions)
Ø Toxin binds to presynaptic cell
membrane via a receptor
Ø Then passes through cell
membrane by receptor-
mediated endocytosis
How does c. Botulinum cause disease
Blocks release of acetylcholine = cannot contract
Flaccidity paralysis
Respiratory failure is usually cause of death
C. Tetani clinically
Effect is the same no matter the species (muscle rigidity is always seen)
Extent of clinical signs vary
Resistance is related to inability of toxin to penetrate & bind in different species