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Neurology > Infectious and inflammatory myelopathies > Flashcards

Infectious and inflammatory myelopathies Flashcards

1
Q

Discospondylitis definition

A
  • Infection of the IVD and adjacent vertebral end plates
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2
Q

What is most common etiology of discospondylitis?

A
  • bacterial infection

- Fungal organisms possible as well as algal, but less likely

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3
Q

Which bacteria are most common with discospondylitis?

A
  • Staphylococcus spp most common***
  • E. coli
  • Brucella* (don’t forget!)
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4
Q

Which fungal organisms could cause discospondylitis?

A
  • Aspergillus
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5
Q

Routes of infection for discospondylitis?

A
  • Hematogenous spread
  • Foreign body migration (e.g. grass awn)
  • Iatrogenic (post op or post-injection)
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6
Q

What is most common route of infection for discospondylitis?

A
  • Hematogenous
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7
Q

Source for hematogenous discospondylitis

A
  • UTI thought to be the source
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8
Q

Signalment of discospondylitis

A
  • Often seen in older patients, medium to large breed dogs

- Often hunting dogs

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9
Q

Most common sites and number of sites for discosponydlitis

A
  • L7-S1 most common site
  • Single site more common than multiple sites
  • 40% per one study have multiple sites affected
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10
Q

Presenting complaint for discospondylitis

A
  • Painful
  • Febrile
  • ADR
  • Neuro deficits depend on localization
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11
Q

Diagnosis of discospondylitis

A
  • CBC/Chem/UA (leukocytosis, hyperglobulinemia, UTI )
  • Radiographs**
  • CT
    scan
  • MRI
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12
Q

Appearance of discospondylitis on radiograph

A
  • Jagged

- Evidence of lysis around the vertebral end plate

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13
Q

How to diagnose the organism in discospondylitis?

A
  • Blood cultures (important to make sure it’s not fungal and make sure we are better antibiotic stewards)
  • Urine cultures
  • Disc culture (percutaneous)
  • Surgical cultures ($$$$)
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14
Q

Treatment of discospondylitis

A
  • Antibiotics based on culture and sensitivity for bacterial infection (1st gen cephalosporins, penicillin or amoxicillin to start)
  • Aspergillus (itraconazole or flucaonazole)
  • Brucella (tetracyclines and aminoglycosides)
  • May need to start with a few IV doses
  • Tx lasts for a months
  • Should see improvement within the first week
  • Can do surgery to consider decompression and/or stabilization
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15
Q

When should you see improvement with discospondylitis?

A
  • Within the first week
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16
Q

How long does treatment last for discospondylitis?

A
  • 6-12 months
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17
Q

Which breeds are predisposed to Aspergillus?

A
  • German Shepherds are predisposed likely due to T cell immunodeficiency
  • Poor prognosis
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18
Q

General signalment for non-infectious myelopathies

A
  • Think of younger patients, but never rule out in older patients
  • Can be acute onset, or several week history
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19
Q

Clinical sign classic with meningitis

A
  • Pain
20
Q

Clinical signs classic with myelitis

A
  • Neurological deficits
21
Q

CSF in non-infectious myelopathies in general

A
  • pleocytosis (increased WBC in general)
  • > 5/µL
  • Also should have negative infectious disease titers
22
Q

Steroid responsive meningitis/arteritis underlying pathophysiology

A
  • Immune mediated disease - attacks leptomeninges and blood vessels
23
Q

Who gets steroid responsive meningitis/arteritis?

A
  • Young dogs around 1 year of age

- Boxers, Beagles, GSP, Goldens, Burnese Mountain Dogs

24
Q

Clinical signs of steroid responsive meningitis/arteritis

A
  • Fever and cervical pain
25
Q

Exam findings of steroid responsive meningitis/arteritis

A
  • Cervical pain only
  • Neck guarding
  • Pain on palpation (EXTREME PAIN)
26
Q

Blood work with steroid responsive meningitis/arteritis

A
  • Leukocytosis (neutrophilia)
27
Q

Major dfdx for meningitis/arteritis

A
  • Polyarthropathy
  • Discospondylitis
  • meningomyelitis, bacterial meningitis
28
Q

Diagnosis of steroid responsive meningitis/arteritis

A
  • Based on CSF analysis
  • Cervical MRI
  • +/- joint taps
  • Infectious disease titers neg
29
Q

CSF with steroid responsive meningitis/arteritis

A
  • Neutrophilic pleocytosis (from IL-8)

- IgA levels increased also

30
Q

Treatment of steroid responsive meningitis/arteritis

A
  • Immunosuppression (steroids, cyclosporine, mycophenolate, etc.)
  • may have concurrent IMPA
31
Q

Granulomatous meningomyelitis

A
  • Similar to disease that we learned about in the brain with granulomatous meningoencephalitis
32
Q

Infectious causes of granulomatous meningomyelitis?

A
  • Bacteria (Straph, Strep, coliforms)
  • Fungal (Cryptococcus, Coccidiomycosis, Blastomycoses)
  • Rickettsial
  • Protozoal (toxoplasmosis and neospora you have to do electron microscopy to differentiate)
33
Q

Etiology of tetanus

A
  • Clostridium tetani

- Anaerobic, spore forming bacterium (very hard to get rid of)

34
Q

Where are Clostridium tetani spores?

A
  • Ubiquitous in the environment
35
Q

How common is tetanus in dogs and cats?

A
  • Uncommon overall

- Cats are 10x more resistant

36
Q

What causes tetanus infection?

A
  • Spore being introduced in a wound
  • Penetrating wounds, contaminated body cavity surgeries (like OVH or castration)
  • Must germinate to produce the toxin
37
Q

WHat is the primary toxin in tetanus**?

A
  • Tetanospasmin
38
Q

Tetanospasmin toxin travel

A
  • Enters nerve via telodenra (nerve endings) at motor end plate either locally or hematogenously
  • Toxin is transported retrograde to the CNS
  • Primary target is the Renshaw cell = inhibitory interneuron in the spinal cord
  • Interferes with release of glycine and GABA (inhibitory neurotransmitters) resulting in extensor tone
  • Causes uncontrolled contraction of extensor muscles
39
Q

What is the primary target of tetanospasmin?

A
  • Renshaw cell (inhibitory interneuron in the spinal cord)

- Interferes with release of glycine and GABA

40
Q

Clinical signs of tetanus

A
  • Focal or generalized (often progresses to generalized ultimately)
  • Muscle stiffness
  • Sardonic grin, lock-jaw, sawhorse posture
41
Q

When do signs of tetanus start?

A
  • 5-10 days after infection
42
Q

Hallmark of tetanus

A
  • Muscle stiffness
43
Q

Diagnosis of tetanus

A
  • Clinical features and history of a previous wound/surgery
  • May be quite difficult to find a wound
  • Look for signs of an infection on blood work (high white cell count, hyperglobulinemia)
  • May see systemic effects - respiratory difficulties, cardiac arrhythmias, hyperthermia (PNS or SNS signs suggest worse prognosis)
44
Q

Treatment goals for tetanus

A
  • Halt toxin production (need to find the source)

- Supportive care

45
Q

Treatment of tetanus

A
  • Supportive care (nursing care, recumbency, bladder management, feeding tubes, sedation as auditory and tactile stimuli will worsen signs)
  • Antibiotic therapy with Penicillin G (metronidazole, clindamycin, and tetracyclines are helpful)
  • If wound is found, clean/debride and can use H2O2 to generate O2
  • Can also locally infuse Abx
  • Antitoxin will prevent further binding of toxin (but may lead to anaphylaxis)
46
Q

Antibiotics for tetanus?

A
  • Penicillin G is abx of choice

- Metronidazole is also effective

Neurology (14 decks)

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