CNS Infectious Diseases Flashcards
describe feline ischemic encephalopathy
- acute cerebral infarction in cats
- signalment/history:
-any age, breed, sex
-summer-fall months
-acute onset
-behavioral changes
-seizures
-visual deficits, motor deficits
-sneezing (signs consistent with URI) - pathology:
-ischemic- subsequent atrophy
-asymmetrical infarction (MCA) - 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 - diagnosis:
- clinical suspicion
- CSF eval
- imaging: edema
- treatment:
-supportive care
-anti-convulsants
-+/- glucocorticoids or ivermectin
prognosis: fair to guarded
what are the hallmarks of infectious CNS disease?
- multifocal disease
- asymmetric signs!
-intracranial/spinal cord
describe canine distemper pathogenesis (6)
- likely spread through aerosolized droplets
- viral protein binds to signaling lymphocytic activation molecules
-on lymphocytes, macrophages, and dendritic cells - local spread to upper resp tract/tonsils
-spread to entire reticuloendothelial system - results in an initial toxicity to lymphocytes: lymphopenia and fever
- spreads to local lymph nodes (retropharyngeal, tracheal, bronchial)
- epithelial trophic stage:
-resp tract: oculonasal discharge
-GI epithelium: vomiting/diarrhea
-urinary epithelium
-persistence in tissues: basal layer of epithelium (hard pad disease/hyperkeratosis)
describe how the immune response influences the pathogenesis of canine distemper
- if strong immune response: humoral and cell mediated: clear virus with no clinical signs
- 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
- if poor/weak immune response: severe clinical signs, infects all tissues, persists in tissues lifelong, can have old dog encephalitis
describe how canine distemper virus accesses the CNS
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
describe canine distemper virus neurological and ocular signs; include treatment
neurological signs:
1. timing:
-either concurrent with clinical signs, within days to weeks of resolved systemic signs, or weeks to month following systemic infection
- multifocal:
-seizures
-vestibular dysfunction
-other cranial nerves
-varying GP/UMN tetra to paraparesis
-any variation of neurological signs - 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
describe canine distemper myoclonus
- rhythmic jerking movements, present at all times, even in sleep
-contraction-relaxation cycles; LMN phenomenon - concurrent with other neurological signs or a sole manifestation
describe diagnosis of canine distemper virus
- clinical suspicion: young dog with GI/respiratory/neurological signs
- 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 - 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
describe feline infectious peritonitis virus (FIP)
- 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 - common in young kittens or in areas with high density of kittens
-catteries, shelters, high populations
-3 months to 18 months of age
describe pathogenesis of FIP
- incubation for 2-3 weeks
- if strong delayed hypersensitivity (cell mediated) and a WEAK humoral response: dry form
-delayed hypersensitivity = granulomatous lesions - 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
describe the dry form of FIP
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
describe the wet form of FIP
chronic serofibrinous peritonitis or pleuritis, ascites, and gradual abdominal enlargement
specifically:
1. vasculitis causes:
-vestibular signs
2. seizures
3. changes in mentation
describe diagnosis of FIP
- intermittent fatigue signs
- fever, lethargy, poor appetite
- hematology: nonregenerative anemia
- chemistry: hypergammaglobulinemia
-polyclonal, reduced albumin to globulin ratio, increased liver enzymes, azotemia - no test is 100%
-can just support clinical diagnosis with:
-albumin: globulin ratio <0.6
-serum protein electrophoresis
-effusion cytology - MRI: ependymitis/vasculitis
describe FIP treatment
- remdesivir: antiviral, more widely available now
- supportive care
what signs are commonly observed in fungal diseases; why?
systemic signs anywhere: bone, brain, eyes, skin common but all have pulmonary signs bc the spores are inhaled!
describe cryptococcus neoformans/gatii
- worldwide distribution
- most common fungal disease in CATS
- any aged cat, but younger more common
- any aged dog but media around 4 years
describe pathogenesis of cryptococcus
- acquired via inhalation; colonizes nose
-can cause rhinitis, may be self limiting - or can cross cribriform plate (hematogenous spread via macrophages to enter CNS)
describe diagnosis of cryptococcus (4)
- clinical suspicion
- cytology
- serum latex capsular antigen test; sheds in CNS so we will find it in CSF!
- MRI
describe treatment and prognosis of cryptococcus
- fluconazole:
-azole = cell membrane inhibitor
-intraconazole (liver toxicity)
cats: goodish prognosis with longterm treatment
dogs: more guarded
describe neospora caninum transmission
- dog is definitive host
- can do vertical transmission through transplacental
-will see in litters with variable numbers affected in dogs <2 years - or acquired via ingestion of dead host
describe clinical signs of congenital neospora caninum
- predilection for lumbar intumescence and roots so causes rigid hyperextension of pelvic limbs in puppies
-arthrogryposis/striffness - generalized myopathy
describe clinical signs of acquired neospora caninum
predilection for cerebellum in adult dogs, so cerebellar ataxia
describe diagnosis of neospora caninum (3)
- clinical suspicion
- serology: but hard to rule out active disease versus exposure
- muscle biopsy for organism ID
describe treatment of neospora caninum
- tachyzoites: clindamycin or sulfonamide trimethoprim for 4 weeks, static effect
- bradyzoites (encysted): ponazuril for cidal effect for 4 weeks
- severe clinical signs may not improve
- treat the entire litter if notice one congenital?
