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Equine II > Infectious neurological disease > Flashcards

Infectious neurological disease Flashcards

1
Q

Vector borne neurological diseases

A

West nile virus

Eastern equine encephalitis (EEE)

Western equine encephalitis (WEE)

Venezualan equine encephalitis (VEE)

Japanses encephalitis

Equine encephalosis virus (EEV)

Tick borne encephalitis

Neuroborreliosis/lyme

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2
Q

Parasitic neurological diseases

A

Equine protozoal myelitis (EPM)

Halicephalobus gingivalis

S. vulgaris (migration)

Trypanosomiasis

Draschia megastoma

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3
Q

Viral neurological diseases

A

EHV-1

Rabies

Hendra/Nipah

Borna disease

Aujesky’s (rare/unlikely)

Equine infectious anaemia (EIA)

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4
Q

Toxic neurological infections

A

Tetanus

Botulism

? Equine Grass sickness

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5
Q

Bacterial neurological diseases

A

Bacterial meningitis

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6
Q

Clostidial disease in horses

A

Tetanus and botulism

Clostridial neurotoxins inhibit neurotransmitter release

Bind to negatively charged molecules on nerve terminal

This complex binds to a protein on nerve terminal surface

Then it is internalised:
○ Tetanus toxin migrates retrograde (motor neuron -> spinal cord -> brainstem)
○ Botulinum toxin stays at NMJ

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7
Q

Tetanus in horses

A

Clostridium tetani

Gram positive, obligate anaerobe

Spore forming

Ubiquitous in soil/faeces

Forms three toxins: tetanospasmin and tetanolysin most important

Antibodies to tetanospasmin are protective

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8
Q

Clinical signs of tetanus in horses

A

Third eyelid protrusion

‘Saw horse’ rigid stance

Raised tailhead

‘Lock jaw’

Dysphagia

Hyperaesthesia

Autonomic signs
§ Tachy/bradydysrhythmias
§ Miosis

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9
Q

Prognosis of tetanus in horses

A

very guarded

Better if identified and treatment started early in course of disease

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10
Q

Treatment of tetanus in horses

A

Eliminate C. tetani organism

Antimicrobials

Neutralise toxin

Give tetanus vaccine (toxoid) at distant site

Control muscle spasm

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11
Q

How to eliminate C.tetani organism from a horse

A

§ Clean and debride wound (if you can find one)
§ Aiming to create an aerobic environment

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12
Q

Antimicrobials for tetanus infection

A

§ Penicillin vs. metronidazole

§ Penicillin may act as a competitive inhibitory neurotransmitter as is similar in structure to GABA -> may worsen disease by blocking GABA

§ Metronidazole is superior in human studies

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13
Q

Tetanus antitoxin

A

§ Antitoxin: does not neutralise toxin that is already bound

§ Give antitoxin BEFORE wound debridement

§ Consider intrathecal antitoxin early on

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14
Q

How do you control muscle spasm in tetanus infection

A

§ Drugs like methocarbamol and diazepam can be used

§ ACP (not hugely effective), alpha 2 agonists

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15
Q

Nursing for tetanus infection

A

Padded stable ideal or anaesthetic induction box
§ May need slinging so consider winch access

Minimise stimulation
§ Cotton wool in ears
§ Low light/noise

Nutritional support and hydration

Manual evacuation of rectum and bladder

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16
Q

Tetanus vaccination

A

Tetanus toxoid

Start at 6mo of age
§ Vaccinate mare in last trimester to confer immunity via colostrum

Two vaccines four weeks apart, then varies according to product license

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17
Q

Tetanus antitoxin

A

Used to provide protection during risk period

Any unvaccinated horse with wound/castration/abscess

Combination of toxoid and antitoxin often given to at-risk/naïve

Often given to foals at first examination
§ Consider maternal antibodies/whether mare vaccinated

Comes in big bottles, is expensive… and needs to be discarded soon after opening despite containing several doses

Therefore, in reality fewer people using at all/often used inappropriately

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18
Q

Botulism in horses

A

Rare in the UK, USA has a higher prevalence

8 different serotypes based on toxin produced (A to G)
○ Different geographic regions associated with different serotypes
○ Affects treatment

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19
Q

Clinical signs of botulism in horses

A

Weakness, flaccidity

Ptyalism, loss of tongue tone

Cranial nerve deficits – dysphagia, ptosis

Trembling, sweating, increased respiratory effort

Reduced parasympathetic activity -> decreased GIT motility

Progress to recumbency

Death may occur due to paralysis of respiratory muscles

20
Q

Three mechanisms of botulism infection in horses

A

Ingestion of preformed toxin

Bacterial infection of wound/umbilicus in foals

Ingestion of spores

21
Q

Botulism- ingestion of preformed toxin

A

Poorly preserved hay/haylage/silage

Animal remains in feed often implicated

22
Q

Botulism - infection of wound/umbilicus in foals

A

Serotype B, toxin produced in wound

23
Q

Botulism - ingestion of spores

A

go on to produce toxin in the GI tract

Causes ‘shaker foal syndrome’

Serotype B, affects foals 2 weeks – 8 months old

24
Q

Pathogenesis of botulism

A

three mechanisms of initial infection

-> haematogenous spread of toxin

-> Toxin binds to nerve terminal

-> block ACh release at NMJ

-> flaccid paralysis

25
Q

Diagnosis of botulism

A

History spoiled feed

Clinical signs

Laboratory tests challenging/unreliable

26
Q

Treatment of botulism

A

Nursing

Supportive/symptomatic treatment

Botulinum antitoxin – need the correct serotype
- Significant association with survival

27
Q

Prognosis of botulism

A

Median time of hospitalisation for survivors = two weeks

Pneumonia, decubital ulcers, corneal ulcers…

48% survived
- 67% that arrived at the hospital standing survived
- 95% that remained standing during treatment survived

28
Q

Equine Herpesvirus myeloencephalitis (EHM)

A

EHV-1 (Alphaherpes virus)
○ Usually causes respiratory disease
○ May cause abortion or neurological disease

EHV is ubiquitous
○ Certain strains more neurotropic

Causes vascular infarction/thrombosis

Ischaemic/haemorrhagic degeneration

29
Q

Signs of Equine Herpesvirus myeloencephalitis (EHM)

A

(background respiratory dz)

Pyrexia, dull, inappetent – viraemic phase

Sudden onset neurological signs

Ataxia – hindlimb > forelimb

Caudal spinal cord segments;
§ Bladder distension and urinary incontinence
§ Penile protrusion in males
§ Flaccid tail and anus

30
Q

Diagnosis of Equine herpesvirus myoencephalitis (EHM)

A

Clinical signs

Nasopharyngeal swab PCR

Serology (paired)

Virus isolation

CSF xanthochromic/yellow

31
Q

Treatment of Equine herpesvirus myeloencephalitis

A

If they survive may have neurological deficits for life and prolonged recovery times

Better prognosis if recover quickly and remain able to stand
§ Some take months to improve
§ May have permanent neurological deficits

Mortality rate but may be high (30-50%)

Can be prolonged recovery time

Prognosis worse if they become recumbent

32
Q

Vaccination for Equine herpes virus myeloencephalitis

A

Routine vaccination of at-risk populations helps to minimise outbreaks

Vaccination doesn’t protect against EHM - reduces environmental load

Do not vaccinate at-risk horses in the face of an outbreak

33
Q

Biosecurity in EHV-1 outbreak

A

Keep groups small, separate pregnant animals etc. on premises

Isolate new arrivals for 3 weeks, monitor temperatures

During outbreak:
§ Isolate in contacts
§ Take temperature twice daily, separate staff and shower/change clothes, no through-traffic, separate stable tools
§ No movement on or off premises

34
Q

West Nile Virus

A

Zoonotic and notifiable

Flavivirus

Not in the UK yet, but we have the vectors

Horse is a dead-end host, as are humans

Vector borne via mosquitoes, birds are an amplifier host

Most infected horses won’t display clinical signs

35
Q

Clinical signs of West Nile virus

A

Dull/lethargic

Facial paralysis, dysphagia

Muscle fasciculations

Hyperexcitability

Ataxia

Recumbency

36
Q

Diagnosis of West Nile Virus

A

IgM capture ELISA

37
Q

Treatment of West Nile Virus

A

No specific treatment

38
Q

Vaccination for West Nile Virus

A

From 5mo of age (possibly younger)

Reduces severity of disease and viraemia

May complicate testing (but IgM response after vaccination considered ‘infrequent’ so vaccines are largely compatible with IgM capture ELISA testing)

39
Q

Neuroborreliosis

A

Zoonotic

Lyme disease

Borrelia burgdorferi – spirochete bacteria

Transmitted by ixodes ticks

Seropositive horses high in healthy population so caution with diagnosis

40
Q

Clinical signs of Neuroborreliosis

A

Muscle atrophy/weight loss,

cranial nerve dysfunction,

ataxia,

behavioural change,

uveitis,

pyrexia,

joint effusion/shifting lameness

41
Q

Diagnosis of neuroborreliosis

A

Positive antibody titre (PCR OspA antigen)

If have joint effusion can attempt to test synovial fluid, or stain with silver stains and manually look for spirochetes

42
Q

Treatment of Neuroborreliosis

A

Prolonged (months) tetracyclines

Typically start with intravenous oxytetracycline then move to oral doxycycline (unlicensed)

43
Q

Equine protozoal myeloencaphalitis

A

Not usually a DDx in UK

Protozoal disease - Sarcocystis neurona and Neospora hughesi

Increased risk at times of stress

White and grey matter affected at any site in CNS so signs vary

44
Q

Rabies in horses

A

Zoonotic and notifiable

Not present in the UK, but notifiable so important to be aware of it

Lyssavirus, may affect any mammal

Fatal

Variable incubation period (2 weeks -> several months)

Variable clinical signs, progress rapidly (ataxia, pyrexia, colic, lethargy, self-mutilation, aggression…)

Cannot test pre-mortem

Vaccination programs successful

45
Q

Western/Easter/Venezuelan Equine encephalitis

A

Zoonotic and notifiable

Exotic to the UK but notifiable – need to be aware may be a DDx if there’s a history of travel, but you’re very unlikely to see it

Togaviral encephalitis

Primary reservoir birds/rodents – horses are sentinel hosts

Therefore incidence of equine cases useful to predict human risk

Zoonotic – fatal

46
Q

Clinical signs of Western/Eastern/Venezuelan Equine Encephalitis

A

Pyrexia,

dull,

circling/head pressing,

dysphagia,

paralysis…

Death

Equine II (28 decks)

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