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Equine Final Year > Neurology Infectious Diseases > Flashcards

Neurology Infectious Diseases Flashcards

1
Q

What are the 3 potential routes of infection for neurological?

A
  • Direct extension e.g. from otitis interna or sinusitis
  • Bacterial embolization within the brain
  • Bacterial penetration through blood brain barrier.
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2
Q

What are the bacteria types affecing the nervous system?

A

•With the exception of a few neurotropic species (e.g. Listeria), bacteria are opportunistic invaders.

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3
Q

Define meningitis

A

Inflammation of the meninges.

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4
Q

Define encephalitis

A

Inflammation of the brain

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5
Q

Name the 3 causes of patholgoy in the nervous system

A
  • Invasion of the neruon tissue by a pathogenic agent
  • Induction of an immune response
  • Toxin or drug get into and interact with nervous system
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6
Q

Name 2 ways bacteria can invade the neuron tissue by a pathogenic agent (3)

A
  • Direct invasion of peripheral nerves.
  • From adjacent structures such as from the meninges.
  • From the blood Haematogenous.
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7
Q

How can inducing an immune respons cause neurological pathology? (2)

A
  • Inflammation and damage.
  • Potential for auto-immune response.
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8
Q

How can a toxin or drug getting into and interacting with the nervous system cause pathology? (3)

A
  • Block signalling.
  • Damage specific cells.
  • Can get toxicoinfectious delivery which involves infection
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9
Q

What are the 3 routes of spread in the body of a neurological infection?

A
  • Neurotropic - through nervous tissue
  • Neural abscess from a septic focus
  • Haematogenous - disseminated through blood
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10
Q

Why is the incidence of infection in the CNS low?

A

Effective blood brain barrier

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11
Q

What 2 properties are needed of antibiotics for CNS infections?

A

Antibiotics must be able to penetrate the BBB.

Must achieve a high concentration in the CSF.

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12
Q

Name clinical signs of CNS infections

A
  • Depression
  • Pyrexia
  • Cervical pain
  • Hyperaesthesia
  • Photophobia
  • Generalized rigidity
  • Seizures
  • Paralysis local and general
  • Ataxia
  • Papilloedema (optic disc swelling)
  • Possible ophthalmic inflammation.
  • Systemic signs. Septic shock and brachycardia.
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13
Q

What diagnostic indicators do we have/ways of measuring the response to a CNS infection?

A
  • Glucose.
  • Specific Gravity.
  • Intracranial pressure.
  • Immunology.
  1. Measure antibody titres to agents.
  2. Cytology.
  • Microbiology.
  • Enzyme analysis for cell breakdown.
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14
Q

Name 3 microbial tests we have for CNS infections (5)

A
  • Gram-stain on CSF smears
  • Culture and sensitivity assays – although this may not be particularly sensitive if prior antibiotic treatment has been given
  • •Antigen tests on CSF fluid
  • ELISA for pathogen / toxin
  • Molecular tests such as PCR
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15
Q

What is a simultaneous infection of meningitis and encephalitis called?

A

Meningoencephalitis

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16
Q

Name 6 causes of meningitis and encephalitis (8)

A
  • Bacteria
  • Viruses
  • Fungi
  • Protozoa
  • Parasite migrations
  • Chemical agents
  • Immune-mediated
  • Idiopathic cause.
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17
Q

Do the clinical signs of meningitis or encephalitis appear first with meningoencephalitis?

A

Meningitis

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18
Q

What is Meningitis and encephalitis often the result of?

A

Injury to protective barrier or local effects

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19
Q

Name 3 things Meningitis and encephalitis can be secondary to (4)

A
  • Migrating grass awns
  • Other foreign bodies
  • Deep bite wounds
  • Iatrogenic infections
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20
Q

What can Meningitis and encephalitis be a direct extension from? (4)

A
  • Sinusitis
  • Otis media or interna
  • Vertebral osteomyelitis
  • Discospondylitis
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21
Q

Name 4 common AEROBIC bacteria causing Bacterial meningitis and encephalitis (6)

A
  • Pasteurella multicida
  • Staphylococcus spp.
  • Escherichia coli
  • Streptococcus spp.
  • Actinomyces spp.
  • Nocardia spp.
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22
Q

Name 3 common ANAEROBIC bacteria causing Bacterial meningitis and encephalitis (5)

A
  • Bacteroides spp.
  • Peptostreptococcus anaerobius
  • Fusobacterium spp.
  • Eubacterium spp.
  • Propionbacterium spp.
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23
Q

Discuss the therapy of Meningitis and encephalitis.

A
  • Other than certain bacteria prognosis is guarded and treatment of little benefit
  • Relapse is common prolonged therapy may be required
  • Appropriate use of antibiotics according to culture serology results
  • Selection of broad spectrum antibiotics that can penetrate the blood brain barrier
  • Bacteriocidal drugs preferred to bacteriostatic drugs
  • Higher than normal dosage may be required
  • In farm animal must consider food animal status
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24
Q

Name 4 recommended drugs for the use with meningitis and encephalitis (6)

A
  • Ampicillin
  • Metronidazole
  • Tetracycline’s
  • Trimethoprim-sulfates,
  • Fluoroquinolones
  • 3rd generation cephalosporin’s
  • Do not forget other supportive care may be needed.
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25
Q

Streptococcus suis:

A) Which industry is affected?

B) What is it associated with?

C) Where are outbreaks common?

D) What is meningitis often characterised by?

E) What Lancefield group?

A

A) Pig

B) Meningitis, arthritis, septicaemia and bronchopneumonia.

C) Intense rear

D) Fever

E) D

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26
Q

How does Streptococcus equi lead to abbscesses in many organs?

A

Extension of the URT infection and lymphatic infection

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27
Q

What is Discospondylitis?

A

An infection of the spinal vertebrae and intervertebral discs

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28
Q

A) What is a common route for infection for discospondylits?

B) What can A be from in other systems?

A

A) Bacteraemia

B) From septic foci

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29
Q

How does the vertebral localization of the pathogens occur in discospondylitis?

A

Through septic metastasis (spread from other adjacent tissues)

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30
Q

A) What is the most common microbiological cause of discospondylitis?

B) What fungi is rarely isolated?

C) What impacts the outcome of infection to create conidtions allowing bacterial colonisation?

A

A) Bacteria

B) Aspergillus

C) Local and systemic factors

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31
Q

What forms a narrow loop with the concavity directed to the feeding artery?

A

In the metaphysis (young animal), and epiphysis ( adult animal) arterial capillaries

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32
Q

How does discospondylosis come about?

A

In the metaphysis (young animal), and epiphysis ( adult animal) arterial capillaries form a narrow loop with the concavity directed to the feeding artery.

This narrow loop, and the sudden change in diameter from a fine arterial capillary to a large venous sinus, causes a slowing of blood flow and an increase in turbulence.

As a result, microorganisms tend to accumulate in the efferent loop.

Accumulation is aided by the reduced concentration of phagocytic cells here.

This is followed by an initial inflammatory reaction leading to the formation of a microthrombus.

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33
Q

What is tissue necrosis and bone destruction are perpetuated by in discospondylosis? (3)

A

Multiplication of the pathogen.

The lytic nature that the exudate acquires due to elevated local lysosomal activity.

Ischemic* damage that follows as a consequence of the accumulation of an exudate in a rigid structure.

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34
Q

What abscess can develop in discospondylosis?

A

Subarachnoid abscess

35
Q

What does disease development depend on the balance between in discopondylosis?

A

Host defence and organism virulence

36
Q

What happens if the defence prevails in the balance bwteen host defence and virulence in discospondylosis?

A

The devitalized tissue becomes surrounded by granulation tissue

37
Q

What happens if the pathogen prevails in the balance between host defences and virlulence of an organism in discospondylosis?

A

Infection progresses with invasion of the subchondral bone-tissue and, eventually, the intervertebral disc.

38
Q

What happens if there is an accumulation of exudate in the balance between host defences and virlulence of an organism in discospondylosis?

A

Diffuse to the vertebral canal or to the paravertebral soft tissues, destroying osteocytes and vascular structures

39
Q

How might propagation of infection affect the spinal cord in discospondylosis? (3)

A
  • By the action of the exudate
  • by the growth of granulation tissue.
  • Potential for spinal compression
40
Q

Listeria?

A) What gram?

B) What shape?

C) Where does it grow?

D) How many serotypes?

A

A) Positive

B) Rod

C) Non-enriched media

D) 16

41
Q

Listeria:

A) What respiration?

B) Catalase?

C) Oxidase?

D) What happens on BA?

A

A) Faculative anaerobes

B) Positive

C) Negative

D) Small haemolytic colonies

42
Q

What are listeria outbreaks associated with?

A

Silage

43
Q

Where does listeria infect? (2)

A
  • Mucosal tissues
  • Peripheral nerves
44
Q

What is the pathogenesis of Listeria?

A
  • Infection with L. monocytogenes from ingestion of contaminated feed
  • Possible septicaemia, encephalitis or abortion.
  • sepsis and meningitis.
  • Meningitis is often complicated by encephalitis - a pathology that is unusual for bacterial infections
45
Q

What is the zoonoses of listeria?

A
  • The disease can affect pregnant women, newborns, and adults with weakened immune systems.
  • Source eating contaminated food soft cheeses.
46
Q

Neurotopic spread of listeria:

A) Where does it enter?

B) How are the bacteeria taken up?

C) Where can it ascend nervous tissue to CNS from?

A

A) Mammalian cells

B) Induced phagocytosis

C) Oral cavity

47
Q

How may you diagnose listeria?

A
  • Neurological-signs: CSF fluid from medulla or pons
  • Abortion: cotyledons, foetal aboasal uterine discharge
  • Septicaemia: fresh liver, spleen or blood
  • Smears may reveal Gram +ve rods
  • Immunofluorescence may speed diagnosis
  • Histological: micro abscesses and heavy perivascular-mononuclear cuffing.
  • White cell numbers exceeding 1.2x107
48
Q

How may you culture blood for listeria?

A

•Culture blood, selective agars 37ºC for 24-48 hours.

49
Q

What is this and what may cause it?

A

Perivascular cuffing caused by listeria

50
Q

Name clinical signs of listeria

A
  • Incubation period of neural Listeriosis ranges from 14 to 40 days.
  • Dullness, circling and tilting of head facial paralysis
  • Unilateral facial paralysis can result in drooling and dropping of eyelids and ears.
  • In ruminants may present as encephalitis, abortion, septicaemia, or endophthalmitis.
  • One source of susceptibility is decreased cell- mediated immunity associated with advanced pregnancy
51
Q

How can we treat listeria?

A

In early stages with antibiotics (prolonged high doses of ampicillin or amoxicillin combined with aminoglycoside).

52
Q

Whta do oubreaks in cattle tend to be?

A

Seasonal

53
Q

A) What conditions does listeria replicae in?

B) How can we prevent?

A

A) In the surface layers of poor quality silages pH above 5.5.

B) In good quality silage multiplication is inhibited by acid pH

54
Q

A) How can we prevent listeria in cattle?

B) Why don’t vaccines work?

A

A)

  • Do Not feed poor silage to pregnant ruminants.
  • Do not feed poor quality silage at all?!
  • Ensure feed method used reduces ocular contact.

B)

  • Vaccines do not work as pathogen intracellular!!!
55
Q

How can ingestionbe toxic to the CNS?

A

Toxins can be produced in feed and pasture and by microorganisms.

56
Q

How can infections of the CNS have toxins? (2)

A
  • Toxins can be produced during infections
  • Toxins can be produced by colonisation of young animals by toxin producing bacteria normally excluded from the intestine
57
Q

Name 2 toxin producing bacteria (3)

A
  • Tetanus (Clostridium tetani).
  • Botulism (Clostridium botulinum)
  • Oedema disease (E. coli).
58
Q

Name the toxin produced in symbiotic on pasture.

A

Rye grass staggers (Acremonium loliae fungal endophyte New Zealand)

59
Q

Name the toxin prouced by plants

A

Algae

60
Q

Botulism:

A) What is the organism?

B) What is the toxin effect?

C) What species?

A

A) Clostridium botulinum

B) Block acetylcholine release

C) Many

61
Q

Foal symmetrcil encephalomalacia:

A) What is the organism?

B) What is the toxin effect?

C) What species? (2)

A

A) Clostridium Perfringens Type D

B) Vasculopathy, encephalomalacia

C) Sheep/lambs and goats

62
Q

Oedema disease:

A) What is the organism?

B) What is the toxin effect?

C) What species?

A

A) Echerichi Coli

B) Vasculopathy, necrosis of arteriolar wall

C) Pigs

63
Q

Tetanus:

A) What is the organism?

B) What is the toxin effect?

C) What species?

A

A) Clostridium Tetani

B) Block presynaptic transmission

C) Most (horses and sheep)

64
Q

Clostridium:

A) Gram?

B) Shape?

C) What do all species form?

A

A) Positive

B) Rod

C) Endospore

65
Q

A) Wha conditions do most clostridia grow under?

B) How are vegetative cells killed?

A

A) Anaerobic

B) Exposure to Oxygen

66
Q

Due to clostridia being fastidious anaerobes, name 2 things which need to happen with samples (3)

A
  • Need to be from live recently dead animals
  • Placed in anaerobic transport media
  • Cultured promptly under anaerobic conditions.
67
Q

How can you differentiate between clostridium?

A

Combination of colonial morphology, biochemistry and toxin identification and molecular tests

68
Q

C. Tetani:

A) What is the site of production?

B) What geenes regulate?

C) What antigenic type?

D) What is the mode of action?

A

A) Wound

B) Plasmid

C) 1 type - tetanospasmin

D) Synaptic inhibition

69
Q

C. Botulinium:

A) What is the site of production?

B) What geenes regulate?

C) What antigenic type?

D) What is the mode of action?

A

A) In carcases, decay veg, canned foods

B) Usually genome (C and D in phage)

C) 8

D) Inhibition of neuromuscular junction

70
Q

How can clostridium lead to a toxicoinfection? (2)

A
  • In horses the Clostridium grows in the GI tract with in vivo production of toxin (shaker foal syndrome eastern USA).
  • In wounds of animals It can also develop from wound infection.
71
Q

What is a source of clostridium?

A

Carrion, contaminated or C. botulinum colonised, feed rotting hay or silage

72
Q

Discuss the clostrdial toxin

A

The toxin is a protein

It is activated by cleavage.

Differences in how tetanus and botulinum toxin is due to different sites of action but both interact with SNARE protein in nerves.

Botulinum toxin can be distinguished antigenically eight types of toxin (A, B, Ca, Cb, D, E, F, G).

Types C and D cause most outbreaks in domestic animals.

Botulinum toxin is very potent 10 pg can kill a mouse.

Antitoxins are available that neutralize circulating toxin, but they are not effective after the toxin has entered the nerve terminals.

A vaccine is available for horses and cattle in endemic areas

73
Q

How can the Botulinum toxin Stop stimulation and leads to flaccid paralysis?

A

Preformed toxin absorbed from the GI tract circulates the blood and acts at neuromuscular junctions of the cholinergic nerves and peripheral autonomic nerve synapses. Binds the somatic and autonomic nerve terminals. Inhibits neurotransmitter release. Death from paralysis of respiratory muscles.

74
Q

How does the Tetanus toxin Block inhibitory transmitter release triggering spastic paralysis?

A

Toxin binds ganglioside receptors on motor neurones. It them moves in vesicles via axonal transport to the to nerve body and its dendritic processes. The toxin then transfers trans-synaptically to inhibitory neurones where it interacts with and blocks vesicle docking and inhibitory-neurotransmitter release is blocked leading to spastic paralysis.

75
Q

What are some clinical signs of tetnus?

A

Stiffness , local spasms, effects on heart and respiratory rate, dysphagia, altered facial expression.

76
Q

What is the incubation of tetnus?

A

5-10 days

77
Q

How do you diagnose tetanus?

A
  • Usually presumptive based on clinical signs
  • Need to differentiate from strychnine poisoning
  • Gram smears looking for characteristic drumstick forms of C. tetani
78
Q

How can you treat tetanus?

A
  • Antitoxin administration
  • Large doses of penicillin (I.M.)
  • Debridment of wounds (potential to use Hydrogen peroxide wash)
79
Q

How can you control tetanus?

A
  • Vaccination of at risk animals (Horses common)
  • Debridment of wounds
  • Passive antitoxin in unvaccinated animals
80
Q

How long after ingesstion does botulism develop?

A

3-17 days

81
Q

How do you diagnose botulism?

A
  • Suspect cases handle with care as may be large level of toxin about
  • Clinical signs and food intake history may suggest botulism or ill define neurological disease
  • Confirmation by detection of toxin in serum (not confirmed)
  • Toxin genes can be detected from uncultivable bacteria feed
82
Q

How do you treat botulism?

A
  • If available polyvalent antiserum.
  • Therapeutic use of guanidine hydrochloride to enhance neurotransmitter release.
83
Q

How can you control botulism?

A
  • Vaccination of at risk animals with toxoid
  • Removal of suspect foodstuff
84
Q

What are signs of botulism?

A

Dilated pupils, dry mucous membranes, decreased salivation, tongue flaccidity, dysphagia.

Equine Final Year (102 decks)

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