Infectious neurological disease Flashcards

(46 cards)

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
Diagnosis of botulism
History spoiled feed Clinical signs Laboratory tests challenging/unreliable
26
Treatment of botulism
Nursing Supportive/symptomatic treatment Botulinum antitoxin – need the correct serotype - Significant association with survival
27
Prognosis of botulism
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
Equine Herpesvirus myeloencephalitis (EHM)
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
Signs of Equine Herpesvirus myeloencephalitis (EHM)
(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
Diagnosis of Equine herpesvirus myoencephalitis (EHM)
Clinical signs Nasopharyngeal swab PCR Serology (paired) Virus isolation CSF xanthochromic/yellow
31
Treatment of Equine herpesvirus myeloencephalitis
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
Vaccination for Equine herpes virus myeloencephalitis
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
Biosecurity in EHV-1 outbreak
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
West Nile Virus
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
Clinical signs of West Nile virus
Dull/lethargic Facial paralysis, dysphagia Muscle fasciculations Hyperexcitability Ataxia Recumbency
36
Diagnosis of West Nile Virus
IgM capture ELISA
37
Treatment of West Nile Virus
No specific treatment
38
Vaccination for West Nile Virus
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
Neuroborreliosis
Zoonotic Lyme disease Borrelia burgdorferi – spirochete bacteria Transmitted by ixodes ticks Seropositive horses high in healthy population so caution with diagnosis
40
Clinical signs of Neuroborreliosis
Muscle atrophy/weight loss, cranial nerve dysfunction, ataxia, behavioural change, uveitis, pyrexia, joint effusion/shifting lameness
41
Diagnosis of neuroborreliosis
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
Treatment of Neuroborreliosis
Prolonged (months) tetracyclines Typically start with intravenous oxytetracycline then move to oral doxycycline (unlicensed)
43
Equine protozoal myeloencaphalitis
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
Rabies in horses
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
Western/Easter/Venezuelan Equine encephalitis
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
Clinical signs of Western/Eastern/Venezuelan Equine Encephalitis
Pyrexia, dull, circling/head pressing, dysphagia, paralysis… Death