Rabies & Other Neurological Diseases of Equids Flashcards
what are equine notifiable diseases (7)
rabies
equine infectious anemia
dourine
west nile virus
african horse sickness
equine viral arteritis
glanders
what are non notifiable diseases of importance (3)
equine influenza
piroplasmosis
equine protozoal myeloencephalitis
what are diseases of zoonotic potential
rabies
WNV
glanders
hendra virus
what diesease can have a quiescent carrier stage (3)
equine infectious anemia
piroplasmosis
equine viral arteritis
what viruses cause myeloencephalitis or encephalitis (5)
equine herpes virus myeloencephalopathy (EHM)
rabies
arboviruses (WNV, JE, WEE, EEE, VEE)
borna virus
hendra virus
what do arboviruses have in common (3)
most OIE list B diseases
most spread between mosquitos and birds
most are SERIOUS zoonosis
what are the mentation clinical signs of viral encephalitides
many infections are subclinical – except rabies
mentation: hyperexcitibility or lethargy (profound), comatose
what are the behavioural clinical signs of viral encephalitides (3)
head pressing, self-mutation, compulsive walking
what are the gait derangements of viral encephalitides
ataxia, paresis and paralysis, muscle fasciculations in WNV
what are cerebral and brainstem signs of viral encephalitides
other cerebral/brainstem signs: circling, blindness, deafness
recumbency
fever
what is the epidemiology of equine rabies infection
skunks, racoons, red fox most common in US
dogs cats and other horses can spread
small carnivoces (opossum, pole cat) and bats
what is the etiopathogenesis of equine rabies infection
virus multiplies in myocytes at bite site and infects peripheral nerves via nerve endings/NMJs
progresses along PN via axoplasmic flow to spinal and dorsal root ganglia
rapid multiplication in CNS (brain, spinal cord, sympathetic trunk) spread in CSF and blood
what is the rabies virus
neutropic rhabdovirus (lyssavirus, rhabdoviridae)
what is the pathogenesis of equine rabies infection (4)
- no spread within blood or lymph fluid
- multiplies neurones, perikaryons of neurons
- accumulation of nucleocapsid, negri body formation
- increase in cellularity in CSF once reaches – may then be detectable by PCR
what is the incubation period of rabies
9 days to 1 year
depends on bite site
direct entry of virus to neural tissue allows short IP
what are the clinical signs of rabies
very variable in the horse
must be considered DDX for all neurological cases
what are the early signs of rabies
hyperasthesia (an increase in the sensitivity of any of your senses)
ataxia
behaviour change
anorexia
paresis
colic
what are the later signs of rabies infection
cerebral signs with rapid progression and deterioration ususal over 48 h
what are the furious form signs in rabies
aggression
self mutilation
photophobia
hyperasthesia
what are further clinical progression signs of rabies infection
progression to recumbency
often with multiple buckling attempts to stand
aggression may remain present
how is rabies infection diagnosed (4)
- clinical signs (self mutilation)
- immunofluorescent antibody test on fresh brain tissue
- histopathology (non-suppurative encephalomyelitis)
- negri bodies pathognomonic for rabies
what considerations need to be made when diagnosing rabies
full protective equiment when handling any tissue
contact OV lab to move carcass
what is the treatment of rabies
fatal
how is rabies prevented
vaccination in high risk areas
inactivated vaccine IM in high risk regions
stray dog control
do NOT vaccinate horses that have had immediate contact with suspected case – monitor for incubation period
what does EHV1 cause
equine herpes virus 1 myeloencephalopathy
resp disease in young horses, abortion storms, chorioretinopathy, myeloencephalopthy (EHM)
what is the shedding period post infection of EHV1
1-3 weeks
80% ALL horses latently infected – recrudescence and further shedding
what is the rarest manifestation of EHV1 and what are the signs of this manifestation
Equine Herpes Myeloencephalopathy (EHM)
pyrexia and resp signs (rhinopneumonitis) in herd mates or individuals with neuro signs
what is the neurotropic strain of EHV1
single AA polymorphism in DNA
what does the neurotropic strain of EHV1 cause
causes resp spread –> basement memb –> lymph nodes –> leukocyes –> vascular endothelium (9-13d post infection)
causes immune mediated vasculitis
ischemic myeloencephalopathy
outbreaks of ataxia and urinary incontinence in mature horses
is the horse protected by prev vaccination against neurotropic strain of EHV1
not protected by prev vaccination
what are the signs of EHV1 myeloencephalopathy
URT signs
pyrexia
inappetance
lethargy
symmetric hindlimb ataxia and paresis
urinary/fecal retention
recumbency
CN signs (esp CN V, VII, VIII, XII)
what are more rare signs of EHV1 myeloencephalopathy
uveitis
hypopyon
retinal detachment
blindness
occasional lower limb edema
what signs usually stabilize in EHV1 myeloencephalopathy
neurological signs usually stabilize within 24-48hours but variable pathogenicity in different strains
what is chorioretinitis
common post infection with EHV1
bullet hole lesions in the chrioretina
what would clinical signs of a EHV1 myeloencephalopathy look like
clinical signs occur in up to 40% in herd
may be preceeded by second pyrexia bout
edema of limbs, perineum
hind limb ataxia
urinary overflow incontinence
atonic tail
sensory deficits
mares develop neuro signs may abort in last trimester with isolation of same viral strain
may involve forebrain: dull mentation, low head carriage, inability to rise, may be central vision loss
how is EHV1 myeloencephalopathy diagnosed (8)
- history
- clinical signs
- evidence in herd members of pyrexia/URT or neuro disease
- multicentric lesions affecting cauda equina but CN deficits also cna be present
- CSF: xanthochromia (bilirubin in CSF), PCR
- serology: CFT for IgM or paired ELISA
- viral isolation: PCR, culture of nasopharyngeal swab or blood
- necropsy
how is EHM treated
- anti-inflammatories:
NSAIDs: phenylbutazone may decrease endothelial inflammation
corticosteroids: controversial but useful for 2-3 days
2. supportive:
position/slings
antimicrobials
urinary catherization/rectal evacuation
hydration & nutrition
- antiviral?
acyclovir poor bioavailability
valacyclovir better ($$)
- quarantine and hygiene measures
shed for up to 3 weeks after cessation of c/s
how long does shedding occur after cessation of clinical signs of EHM
shed for up to 3 weeks after cessation of c/s
how is EHV1 myeloencephaopathy prevented
difficult
neuro cases may still be infectious – effective isolation needed
vaccination? does not prevent EHM but will increase herd immunity and decrease shedding period if exposed to EHV1
herd management: keep youngstock and older broodmares in separate areas
consider vaccination of all stock – may decrease incidence of abortion
what is the prognosis of EHV1 myeloencephaopathy
related to disease severity and response to treatment
recumbent – poor/grave
less severe –> complete recovery or residual deficits
what type of virus is WNV
flavivirus
what are the hosts of WNV
birds
humans
horses
other mammals
what are the most important host in WNV
birds
dead birds act as a screen
humans and horses are dead end hosts
what is the zoonotic disease of WNV
encephalitis, myositis, neuralgia
what are the vectors of WNV
mosquitos
maybe ticks
where is WNV endemic
africa
southern europe
asia
middle east
what are the clinical signs of WNV
ataxia, paresis
muscle fasiculations
hyperasthesia
behavioural changes
CN deficits: VII, XII, IX
combo of peripheral and central signs suggestive
what is the mortality rate of WNV
30-40%
how is WNV diagnosed (5)
- clinical signs
- combo of neurological signs
+/- fever, muscle fasiculations
- IgM ELISA 2 weeks
- IgG species specific ELISA
- PCR on EDTA blood or brain tissue
- brain immunohistochemistry
how is WNV prevented
- vector control
- vaccination
how is WNV controlled through vectrol control (6)
- reduce mosquito breeding sites
- vector proof meshes on stables
- mosquito repellent
- fans/dispersal devices
- treat still water sources
- surveillence schemes to check for parasite in dead birds
- APHA monitoring of suspect cases
how is WNV controlled through vaccination
primary course: 2 doses at interval of 4 weeks; then anual booster
what type of virus is eastern/western/venezuelan encephalitis virus
alpha virus
where is eastern/western/venezuelan encephalitis virus endemic to
americas
is eastern/western/venezuelan encephalitis virus zoonotic
yes
what is the fatality rate of eastern/western/venezuelan encephalitis virus
EEE: 75-90%
VEE: 40-80%
WEE: 19-50%
what are the reservoirs and vectors of eastern/western/venezuelan encephalitis virus
reservoirs: birds/small mammals
vector: mosquits
which one of the eastern/western/venezuelan encephalitis virus causes a viremia such that the horse becomes the primary reservoir
VEE
what are the clinical signs of eastern/western/venezuelan encephalitis virus
wide range: asymptomatic to severe CNS signs
initial viremia –> fever, lethargy, stiffness
behavioural changes
blindness, cranial nerve deficits
ataxia, paresis
recumbency, seizures, coma
how is eastern/western/venezuelan encephalitis virus prevented
100% preventable through proper vaccination
horses that reside in endemic areas and <4 years old should get alphavirus vaccines 3x per year
combined vaccination protocols
is eastern/western/venezuelan encephalitis virus notifiable
yes
how is eastern/western/venezuelan encephalitis virus diagnosed
clinical signs and epidemiology suggestive
virus detection/isolation
serology
where is the hendra virus
aus
what are the risk factors for hendra virus (6)
- food trees
- bat birthing season
- TBs
- >8yo
- pasture housing
- pregnancy
what is the reservoir of hendra virus
fruit bats
what are the clincal signs of hendra virus
pyrexia
severe pneumonia
frothy nasal discharge
icterus
recumbency
death
how is hendra virus diagnosed
signs
virus isolation
serology
PCR
histopathology/EM
is hendra virus zoonotic
yes
careful with PM
where is the borna virus located
germany
austria
switzerland
what type of virus is borna virus
neurotropic
spread to and throughout nervous system
what does borna virus cause
immunological response induces disease
meningoencephalitis/encephalitis
what is borna virus associated with in people
psychological disease
what are the clinical signs of borna virus
mentation and behavioural changes
ataxia, paresis
cranial nerve dysfunction
decreased sensation
how is borna virus diagnosed
history, clinical signs
CSF
serology
PM – histopathology, virology, PCR, immunohistochemistry
what are the disease outcomes of borna virus
what is the general treatment of viral encephalitides
no specific treatment – anti-viral meds? some known benefit for EHV1/EHM
supportive
- antiinflammatories
nursing
fluids and nutritional support
sligns for recumbent horse
what are the safety percautions for clinical cases
cover cuts with water resistant dressing
PPE
hand cleansers/soap
disinfectants
waste disposal bags
P2 particulate respirators
how is infection prevention
- reduce exposure to vectors (mosquitos, stable management)
- vaccination: WNV, EEE/WEE/VEE
how is the UK industry protected
vet vigilance for unusual field clinical case key –> prompt reporting and isolation (dourine, EIA, WNV and AHSV)
care with imported horses (10 day health certificate)
vigilance for incorrect/absent passports
vaccination for at risk horses (WNV)
updating and attention to disease outbreak status
continued monitoring (senitenel birds, culicoides species, tick populations)
