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Module 20: Global Vet Med > Rabies & Other Neurological Diseases of Equids > Flashcards

Rabies & Other Neurological Diseases of Equids Flashcards

1
Q

what are equine notifiable diseases (7)

A

rabies

equine infectious anemia

dourine

west nile virus

african horse sickness

equine viral arteritis

glanders

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2
Q

what are non notifiable diseases of importance (3)

A

equine influenza

piroplasmosis

equine protozoal myeloencephalitis

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3
Q

what are diseases of zoonotic potential

A

rabies

WNV

glanders

hendra virus

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4
Q

what diesease can have a quiescent carrier stage (3)

A

equine infectious anemia

piroplasmosis

equine viral arteritis

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5
Q

what viruses cause myeloencephalitis or encephalitis (5)

A

equine herpes virus myeloencephalopathy (EHM)

rabies

arboviruses (WNV, JE, WEE, EEE, VEE)

borna virus

hendra virus

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6
Q

what do arboviruses have in common (3)

A

most OIE list B diseases

most spread between mosquitos and birds

most are SERIOUS zoonosis

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7
Q

what are the mentation clinical signs of viral encephalitides

A

many infections are subclinical – except rabies

mentation: hyperexcitibility or lethargy (profound), comatose

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8
Q

what are the behavioural clinical signs of viral encephalitides (3)

A

head pressing, self-mutation, compulsive walking

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9
Q

what are the gait derangements of viral encephalitides

A

ataxia, paresis and paralysis, muscle fasciculations in WNV

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10
Q

what are cerebral and brainstem signs of viral encephalitides

A

other cerebral/brainstem signs: circling, blindness, deafness

recumbency

fever

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11
Q

what is the epidemiology of equine rabies infection

A

skunks, racoons, red fox most common in US

dogs cats and other horses can spread

small carnivoces (opossum, pole cat) and bats

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12
Q

what is the etiopathogenesis of equine rabies infection

A

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

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13
Q

what is the rabies virus

A

neutropic rhabdovirus (lyssavirus, rhabdoviridae)

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14
Q

what is the pathogenesis of equine rabies infection (4)

A
  1. no spread within blood or lymph fluid
  2. multiplies neurones, perikaryons of neurons
  3. accumulation of nucleocapsid, negri body formation
  4. increase in cellularity in CSF once reaches – may then be detectable by PCR
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15
Q

what is the incubation period of rabies

A

9 days to 1 year

depends on bite site

direct entry of virus to neural tissue allows short IP

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16
Q

what are the clinical signs of rabies

A

very variable in the horse

must be considered DDX for all neurological cases

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17
Q

what are the early signs of rabies

A

hyperasthesia (an increase in the sensitivity of any of your senses)

ataxia

behaviour change

anorexia

paresis

colic

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18
Q

what are the later signs of rabies infection

A

cerebral signs with rapid progression and deterioration ususal over 48 h

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19
Q

what are the furious form signs in rabies

A

aggression

self mutilation

photophobia

hyperasthesia

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20
Q

what are further clinical progression signs of rabies infection

A

progression to recumbency

often with multiple buckling attempts to stand

aggression may remain present

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21
Q

how is rabies infection diagnosed (4)

A
  1. clinical signs (self mutilation)
  2. immunofluorescent antibody test on fresh brain tissue
  3. histopathology (non-suppurative encephalomyelitis)
  4. negri bodies pathognomonic for rabies
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22
Q

what considerations need to be made when diagnosing rabies

A

full protective equiment when handling any tissue

contact OV lab to move carcass

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23
Q

what is the treatment of rabies

A

fatal

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24
Q

how is rabies prevented

A

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

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25
what does EHV1 cause
equine herpes virus 1 myeloencephalopathy resp disease in young horses, abortion storms, chorioretinopathy, myeloencephalopthy (EHM)
26
what is the shedding period post infection of EHV1
1-3 weeks 80% ALL horses latently infected -- recrudescence and further shedding
27
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
28
what is the neurotropic strain of EHV1
single AA polymorphism in DNA
29
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
30
is the horse protected by prev vaccination against neurotropic strain of EHV1
not protected by prev vaccination
31
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)
32
what are more rare signs of EHV1 myeloencephalopathy
uveitis hypopyon retinal detachment blindness occasional lower limb edema
33
what signs usually stabilize in EHV1 myeloencephalopathy
neurological signs usually stabilize within 24-48hours but variable pathogenicity in different strains
34
what is chorioretinitis
common post infection with EHV1 bullet hole lesions in the chrioretina
35
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
36
how is EHV1 myeloencephalopathy diagnosed (8)
1. history 2. clinical signs 3. evidence in herd members of pyrexia/URT or neuro disease 4. multicentric lesions affecting cauda equina but CN deficits also cna be present 5. CSF: xanthochromia (bilirubin in CSF), PCR 6. serology: CFT for IgM or paired ELISA 7. viral isolation: PCR, culture of nasopharyngeal swab or blood 8. necropsy
37
how is EHM treated
1. 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 3. antiviral? acyclovir poor bioavailability valacyclovir better ($$) 4. quarantine and hygiene measures shed for up to 3 weeks after cessation of c/s
38
how long does shedding occur after cessation of clinical signs of EHM
shed for up to 3 weeks after cessation of c/s
39
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
40
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
41
what type of virus is WNV
flavivirus
42
what are the hosts of WNV
birds humans horses other mammals
43
what are the most important host in WNV
birds dead birds act as a screen humans and horses are dead end hosts
44
what is the zoonotic disease of WNV
encephalitis, myositis, neuralgia
45
what are the vectors of WNV
mosquitos maybe ticks
46
where is WNV endemic
africa southern europe asia middle east
47
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
48
what is the mortality rate of WNV
30-40%
49
how is WNV diagnosed (5)
1. clinical signs - combo of neurological signs +/- fever, muscle fasiculations 2. IgM ELISA 2 weeks 3. IgG species specific ELISA 4. PCR on EDTA blood or brain tissue 5. brain immunohistochemistry
50
how is WNV prevented
1. vector control 2. vaccination
51
how is WNV controlled through vectrol control (6)
1. reduce mosquito breeding sites 2. vector proof meshes on stables 3. mosquito repellent 4. fans/dispersal devices 5. treat still water sources 5. surveillence schemes to check for parasite in dead birds 6. APHA monitoring of suspect cases
52
how is WNV controlled through vaccination
primary course: 2 doses at interval of 4 weeks; then anual booster
53
what type of virus is eastern/western/venezuelan encephalitis virus
alpha virus
54
where is eastern/western/venezuelan encephalitis virus endemic to
americas
55
is eastern/western/venezuelan encephalitis virus zoonotic
yes
56
what is the fatality rate of eastern/western/venezuelan encephalitis virus
EEE: 75-90% VEE: 40-80% WEE: 19-50%
57
what are the reservoirs and vectors of eastern/western/venezuelan encephalitis virus
reservoirs: birds/small mammals vector: mosquits
58
which one of the eastern/western/venezuelan encephalitis virus causes a viremia such that the horse becomes the primary reservoir
VEE
59
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
60
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
61
is eastern/western/venezuelan encephalitis virus notifiable
yes
62
how is eastern/western/venezuelan encephalitis virus diagnosed
clinical signs and epidemiology suggestive virus detection/isolation serology
63
where is the hendra virus
aus
64
what are the risk factors for hendra virus (6)
1. food trees 2. bat birthing season 3. TBs 4. \>8yo 5. pasture housing 6. pregnancy
65
what is the reservoir of hendra virus
fruit bats
66
what are the clincal signs of hendra virus
pyrexia severe pneumonia frothy nasal discharge icterus recumbency death
67
how is hendra virus diagnosed
signs virus isolation serology PCR histopathology/EM
68
is hendra virus zoonotic
yes careful with PM
69
where is the borna virus located
germany austria switzerland
70
what type of virus is borna virus
neurotropic spread to and throughout nervous system
71
what does borna virus cause
immunological response induces disease meningoencephalitis/encephalitis
72
what is borna virus associated with in people
psychological disease
73
what are the clinical signs of borna virus
mentation and behavioural changes ataxia, paresis cranial nerve dysfunction decreased sensation
74
how is borna virus diagnosed
history, clinical signs CSF serology PM -- histopathology, virology, PCR, immunohistochemistry
75
what are the disease outcomes of borna virus
76
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
77
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
78
how is infection prevention
1. reduce exposure to vectors (mosquitos, stable management) 2. vaccination: WNV, EEE/WEE/VEE
79
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)

Module 20: Global Vet Med (21 decks)

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