Please enable JavaScript.
Coggle requires JavaScript to display documents.
CNS Parasites - Coggle Diagram
CNS Parasites
Parelaphostrongylus tenuis
same order as HOT complex
aka meningeal worm
hosts
A/dead-end H
camelids
sheep
goats
moose
caribou
black tailed deer
red deer
devasting neurological consequences
larvae never reach adulthood, no eggs produced
DH white tailed deer
no symptoms
IH
snails
slugs
tropism
subdural space
meningeal sinuses
PPP 82-92d (7w)
common in MN
life cycle
L1 from deer feces penetrate into foot of gastropod
deer accidentally ingest gastropod IH, larvae release into abomasum
abomasum and SI penetrated, larvae migrate to lumbar spinal nerves 10d post-infection
40 post-infection, immature adults can be found in subdural space
F worms lay eggs in meningeal blood vessels, which hatch in pulmonary artieres
hatched larvae migrate to bronchial tree, reconsumed
clinical signs
appear 45-53d after L3 ingestion
larvae in Baermann exam
assymetric, spinal cord lesions
hypermetria
ataxia
stiffness
muscular weakness
paralysis
head tilt
seizures
blindness
CSF exam
eosinophilic pleocytosis
only suggestive
necropsy
parasite on section
linear tracts in NS parenchyma
meningitis
presence of
gitter cells
eosinophils
lymphocytes
plasma cells
macrophages
prevention/control
:forbidden: pasturing at edge of woods
:forbidden: poorly drained fields
fence off deer watering spots
eliminate organic matter that attracts snails/slugs
use snail/slug-eating fowl
equine protozoal myeloencephalitis (EPM)
causative agents
Sarcocytis neurona
Neospora hughesi
hosts
DH oppossum
infected by oocytes
IHs
skunks
armadillos
fishers
sea otters
raccons
cats
AH horse
neurological dz
oocytes are very fragile in environment
about the size of RBC, v difficult to find on fecal float
epidemiology
61.8% of horses affected are <4yo
breed affects
thoroughbred
standardbred
QH
seroprevalence is 15-89% depending on geography
higher risk times
3x spring and summer
6x autumn
most likely due to food-seeking opposums
signs
usually diagnosis of exclusion
multicentric neurologic signs
dependent on encystment location in white/grey matter
diagnosis
definitive diagnosis is post-mortem
antemortem
consistent clinical signs
immunodiagnostic testing of serum and CSF
looking for exposure
prevention
decrese wildlife interactions
decrease access to creek or water sources
seal food in bins
reduce bird feeders
reduce exposed garbage
Toxoplasma gondii
hosts
DH cats
1% of cats are shedding oocysts
millions shed at a time
very small
diagnostics are challenging
sexual stage takes place in intestine
IH all mammals
zoonotic
immunocompromised
pregnant women
clinical dz seen
prey animals
tissue cysts
consumed by cats, :musical_note: circle of life :drum_with_drumsticks:
mechanical vectors
earthworms
beetles
cockroaches
life cycle
clinical signs
healthy cats
asymptomatic
self-limiting SI diarrhea
shed oocytes for 1-3w
24h-5d later - infective
develop protective strong immuno respsonse
act as DH
diagnosis
difficult
serology
fecal float
unhealthy cats
pregnant cats
vertical transmission
lethargy
depression
sudden death
chorioenteritis
still births
neurological
act as IH
diagnosis
CSF cytology fo tachyzoites
IHC stains
sheep n goats
abortion
white foci in placenta
ewes rarely show signs
prevention
prevent hunting
:forbidden: raw/undercooked meat
clean litterboxes regularly
feed commercially prepared diets
disinfect litterboxes
most oocysts rare resistat
difficult
