CNS Infectious Diseases

Question 1

describe feline ischemic encephalopathy

Answer 1

1. acute cerebral infarction in cats
2. signalment/history:
   -any age, breed, sex
   -summer-fall months
   -acute onset
   -behavioral changes
   -seizures
   -visual deficits, motor deficits
   -sneezing (signs consistent with URI)
3. pathology:
   -ischemic- subsequent atrophy
   -asymmetrical infarction (MCA)
4. likely/commonly caused by cuterebriasis (fly wormy guy)
   -normal intradermal migration but can do aberrant CNS migration and cause clinical signs similar to FIE
   -enters via nasal passages and releases a vasospastic toxin
5. diagnosis:
6. clinical suspicion
7. CSF eval
8. imaging: edema
9. treatment:
   -supportive care
   -anti-convulsants
   -+/- glucocorticoids or ivermectin

prognosis: fair to guarded

Question 2

what are the hallmarks of infectious CNS disease?

Answer 2

1. multifocal disease
2. asymmetric signs!
   -intracranial/spinal cord

Question 3

describe canine distemper pathogenesis (6)

Answer 3

1. likely spread through aerosolized droplets
2. viral protein binds to signaling lymphocytic activation molecules
   -on lymphocytes, macrophages, and dendritic cells
3. local spread to upper resp tract/tonsils
   -spread to entire reticuloendothelial system
4. results in an initial toxicity to lymphocytes: lymphopenia and fever
5. spreads to local lymph nodes (retropharyngeal, tracheal, bronchial)
6. epithelial trophic stage:
   -resp tract: oculonasal discharge
   -GI epithelium: vomiting/diarrhea
   -urinary epithelium
   -persistence in tissues: basal layer of epithelium (hard pad disease/hyperkeratosis)

Question 4

describe how the immune response influences the pathogenesis of canine distemper

Answer 4

1. if strong immune response: humoral and cell mediated: clear virus with no clinical signs
2. if intermediate immune response: cell mediated but slowly developing humoral, clinical signs depend on how quickly virus is cleared, but usually respond and clear virus
3. if poor/weak immune response: severe clinical signs, infects all tissues, persists in tissues lifelong, can have old dog encephalitis

Question 5

describe how canine distemper virus accesses the CNS

Answer 5

if poor immune response:
-get significant viremia: virus infects monocytes and lymphocytes and can enter the choroid plexus and CSF
-then spread via CSF/ventricular system

Question 6

describe canine distemper virus neurological and ocular signs; include treatment

Answer 6

neurological signs:
1. timing:
-either concurrent with clinical signs, within days to weeks of resolved systemic signs, or weeks to month following systemic infection

2. multifocal:
   -seizures
   -vestibular dysfunction
   -other cranial nerves
   -varying GP/UMN tetra to paraparesis
   -any variation of neurological signs
3. ocular signs during epithelial trophic phase:
   -KCS/conjunctivitis
   -chorioretinitis

treatment:
1. anticonvulsants if seizures present
2. treat any concurrent or secondary bacterial infections
3. supportive care

Question 7

describe canine distemper myoclonus

Answer 7

1. rhythmic jerking movements, present at all times, even in sleep
   -contraction-relaxation cycles; LMN phenomenon
2. concurrent with other neurological signs or a sole manifestation

Question 8

describe diagnosis of canine distemper virus

Answer 8

1. clinical suspicion: young dog with GI/respiratory/neurological signs
2. PCR: high sensitivity but
   -false negative: if missing nucleic acids
   -false positive: from vaccination
   -persistence in tissues makes it hard to know if current disease
3. serology:
   -initial signs + titer, but don’t know if current or past infection
   -can also be confounded with vaccination

basicially it’s hard and use clinical suspicion

Question 9

describe feline infectious peritonitis virus (FIP)

Answer 9

1. genetic mutation of feline enteric corona virus (FCoV)
   -high mutation rate but occurs in the individual cat
   -increased risk with increased exposure to FCoV and with factors that negatively impact the immune system
2. common in young kittens or in areas with high density of kittens
   -catteries, shelters, high populations
   -3 months to 18 months of age

Question 10

describe pathogenesis of FIP

Answer 10

1. incubation for 2-3 weeks
2. if strong delayed hypersensitivity (cell mediated) and a WEAK humoral response: dry form
   -delayed hypersensitivity = granulomatous lesions
3. if strong humoral response but WEAK delayed hypersensitivity (cell mediated)l wet form
   -antibody-antigen complexes (arthrus type III) = vasculitis = leakage of serum and protein

Question 11

describe the dry form of FIP

Answer 11

granulomatous/nonexudative and involves the brain, eye, or abdominal and thoracic viscera; more commonly results in neuro signs!

specifically:
1. pyogranulomatous inflammation causes:
-uveitis, keratoprecipitates, hypopion, and/or chorioretinitis

Question 12

describe the wet form of FIP

Answer 12

chronic serofibrinous peritonitis or pleuritis, ascites, and gradual abdominal enlargement

specifically:
1. vasculitis causes:
-vestibular signs
2. seizures
3. changes in mentation

Question 13

describe diagnosis of FIP

Answer 13

1. intermittent fatigue signs
2. fever, lethargy, poor appetite
3. hematology: nonregenerative anemia
4. chemistry: hypergammaglobulinemia
   -polyclonal, reduced albumin to globulin ratio, increased liver enzymes, azotemia
5. no test is 100%
   -can just support clinical diagnosis with:
   -albumin: globulin ratio <0.6
   -serum protein electrophoresis
   -effusion cytology
6. MRI: ependymitis/vasculitis

Question 14

describe FIP treatment

Answer 14

1. remdesivir: antiviral, more widely available now
2. supportive care

Question 15

what signs are commonly observed in fungal diseases; why?

Answer 15

systemic signs anywhere: bone, brain, eyes, skin common but all have pulmonary signs bc the spores are inhaled!

Question 16

describe cryptococcus neoformans/gatii

Answer 16

1. worldwide distribution
2. most common fungal disease in CATS
3. any aged cat, but younger more common
4. any aged dog but media around 4 years

Question 17

describe pathogenesis of cryptococcus

Answer 17

1. acquired via inhalation; colonizes nose
   -can cause rhinitis, may be self limiting
2. or can cross cribriform plate (hematogenous spread via macrophages to enter CNS)

Question 18

describe diagnosis of cryptococcus (4)

Answer 18

1. clinical suspicion
2. cytology
3. serum latex capsular antigen test; sheds in CNS so we will find it in CSF!
4. MRI

Question 19

describe treatment and prognosis of cryptococcus

Answer 19

1. fluconazole:
   -azole = cell membrane inhibitor
   -intraconazole (liver toxicity)

cats: goodish prognosis with longterm treatment

dogs: more guarded

Question 20

describe neospora caninum transmission

Answer 20

1. dog is definitive host
2. can do vertical transmission through transplacental
   -will see in litters with variable numbers affected in dogs <2 years
3. or acquired via ingestion of dead host

Question 21

describe clinical signs of congenital neospora caninum

Answer 21

1. predilection for lumbar intumescence and roots so causes rigid hyperextension of pelvic limbs in puppies
   -arthrogryposis/striffness
2. generalized myopathy

Question 22

describe clinical signs of acquired neospora caninum

Answer 22

predilection for cerebellum in adult dogs, so cerebellar ataxia

Question 23

describe diagnosis of neospora caninum (3)

Answer 23

1. clinical suspicion
2. serology: but hard to rule out active disease versus exposure
3. muscle biopsy for organism ID

Question 24

describe treatment of neospora caninum

Answer 24

1. tachyzoites: clindamycin or sulfonamide trimethoprim for 4 weeks, static effect
2. bradyzoites (encysted): ponazuril for cidal effect for 4 weeks
3. severe clinical signs may not improve
4. treat the entire litter if notice one congenital?