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SS - Exam 1 > Bacteriology 1 > Flashcards

Bacteriology 1 Flashcards

1
Q

Non-immunological defenses

A

Protective bones
Blood brain barrier
- carrier mediated, lipid soluble substances, astrocyte processes surround capillaries

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2
Q

Factors that increase risk of infection

A

Age
Immunosuppression/FPT
Trauma concurrent infections

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3
Q

Risk factors with specific infections of NS

A
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4
Q

Routes of entry

A

Hematogenous
Retrograde
Extension of infection from site or direct penetration

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5
Q

Hematogenous

A

Most common route of entry
Often involves infections in other organ systems

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6
Q

Retrograde movement

A

Can be organism or toxin (rabies or tetanus)

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7
Q

Direct penetration or extension

A

Infections of paranasal sinuses, middle ear infection
Extensions of discospondylitis into spinal cord
Trauma from bite wounds, blunt trauma, penetrating objects

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8
Q

Mechanisms of damage

A

Vascular damage
Injury to parenchyma or meninges
Intoxication

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9
Q

Vascular damage

A

Vasculitis - leads to endothelial damage & leakage with resultant hemorrhage & parechymal injury (rickettsia)
Septic emboli or thrombus (histophilus somni)

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10
Q

Injury to parenchyma

A

Direct damage
Indirect damage through induction of inflammatory response
- suppurative
- Pyogranulomatous
- granulomatous

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11
Q

Intoxication

A

Vasogenic cerebral edema through action of toxin
Inhibition of neurotransmitter function
- botulinum of toxin C. Botulinum
Tetanospasmin of C. Tetani

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12
Q

Most common bacteria causing infection in EQ

A

Strep equi zooepidemicus

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13
Q

Common causes for bacterial infection in EQ and rum?

A

FPT
Common in neonates

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14
Q

Brain abscesses more common in EQ and rum than cats and dogs

A

S. Equi ss equi (horses)
Trueperella pyogenes (cattle)
Trauma
Spread from contigous site

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15
Q

Brain and epidural spinal asbcesses in pigs

A

Trauma
Spread from contiguous site
Trueperella pyogenes

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16
Q

Clostridia

A

Gram positive rods
STRICT anaerobes
Motile
Gas producing
Endospore forming

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17
Q

Survival of clostridia

A

Can survive as spores (long time) or vegetative bacteria
- GIT of animals and humans (C. Tetani)
- soil and vegetation (C. Botulinum)
LOW OXYGEN

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18
Q

C. Tetani transmission

A

Inoculation into wound (anaerobic with low redox potential) necrotic tissue

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19
Q

C. Botulinum transmission

A

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

20
Q

Mechanisms of c. Tetani

A

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

21
Q

How c. Tetani cause disease

A

Binding of toxin is irreversible
Once the toxin is within the nerves and axons antibodies /antitoxins can’t reach it

22
Q

Mechanisms of c. Botulinum

A

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

23
Q

How does c. Botulinum cause disease

A

Blocks release of acetylcholine = cannot contract
Flaccidity paralysis
Respiratory failure is usually cause of death

24
Q

C. Tetani clinically

A

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

25
Q

Highly susceptible species to tetanus

A

Horses, Guinea pigs, humans, mice, rabbits

26
Q

Less susceptible species to tetanus

A

Dogs, cattle, pigs, sheep, goats, cats

27
Q

Extremely resistant to tetanus

A

Most birds and cold blooded animals

28
Q

Horse presenting clinically

A

Convulsive contractions
Extensor rigidity - stiff gait, tail held erect, protrusion of 3rd eye lid
Death due to spams of respiration
^ temp, ^ HR, ^ RR, ^ salivation, ^ CK

29
Q

Clinical piglets & lambs with tetanus

A

Piglets & lambs - castration, shearing, docking, vaccinating, injections
Adult cattle, sheep, goats - genital tract post parturition, post castration
Neonatal tetanus - umbilical cord

30
Q

Types of botulism - cattle

A

Susceptible to types B, C, D

31
Q

Types of botulism - horses

A

Susceptible to types A, B, C, D

32
Q

Types of botulism - dogs

A

Susceptible to type C (D)

33
Q

Types of botulism - cats

A

Susceptible to only type C

34
Q

Botulism clinically

A

General weakness, muscle fasiculation, buckling
Dyphagia
Paralysis of tongue

35
Q

Botulism in birds

A

Common in water fowl
Known as “limber neck” = neck dragging or hanging

36
Q

Botulism in cattle

A

Associated with eating feed contaminated with dead animals or spoiled silage
Also with cattle grazing pastures that are deficient in phosphorous; cows eat bones (pica) to get phosphorus and ingest preformed toxin

37
Q

Signs in cattle with botulism

A

Signs include recumbency, drooling, dysphagia, rumenal atony, & laboured breathing

38
Q

Botulism in cats

A

CATS are resistant to the effects of botulinum toxin. Thus, botulism is VERY RARE in this species
Has been reported occasionally in lions!

39
Q

Can the host get rid of the infections?

A

Nope
Natural immunity or susceptibility vary
Acquired immunity
- passive: antitoxin to neutralize, horses/humans
- active: toxoid, essential for horses (sheep, cattle, pigs and people)

40
Q

Diagnosing C. Tetani

A

No good methods
Clinical signs, species, recent history !!!**
Can try for wound/fine needle aspirate
Serum tests - rarely used

41
Q

Diagnosing c. Botulinum

A

Rare clinical signs (post mortem lesions or histology)
Typical clinical signs, toxin specific PCR
- food, blood, tissue etc to test

42
Q

Treatment for c. Tetani

A
43
Q

Treatment for c. Botulinum

A

Antibiotics - no value
Antitoxins - maybe help in early stages
Toxoid - vaccine, more preventative
Supportive therapy - most common treatment

44
Q

Control effects

A

Clean wounds
Vaccinate with toxoid in foals + boosters
Pregnant mares often vaccinated with toxoid (4-6 weeks before foaling = pass on antibodies)

45
Q

C. Botulinum vaccine

A

Vaccination is a toxoid not routine for most species (sporadic disease) use correct type based of species susceptibility
- cattle, occasionally hoses
- mink

46
Q

Management of c. Botulinum

A

Prevent access to preformed toxin
Contaminated food or water with dead animals
Spoiled silage /food

SS - Exam 1 (33 decks)

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