Infectious neurological disease Flashcards
Vector borne neurological diseases
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
Parasitic neurological diseases
Equine protozoal myelitis (EPM)
Halicephalobus gingivalis
S. vulgaris (migration)
Trypanosomiasis
Draschia megastoma
Viral neurological diseases
EHV-1
Rabies
Hendra/Nipah
Borna disease
Aujesky’s (rare/unlikely)
Equine infectious anaemia (EIA)
Toxic neurological infections
Tetanus
Botulism
? Equine Grass sickness
Bacterial neurological diseases
Bacterial meningitis
Clostidial disease in horses
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
Tetanus in horses
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
Clinical signs of tetanus in horses
Third eyelid protrusion
‘Saw horse’ rigid stance
Raised tailhead
‘Lock jaw’
Dysphagia
Hyperaesthesia
Autonomic signs
§ Tachy/bradydysrhythmias
§ Miosis
Prognosis of tetanus in horses
very guarded
Better if identified and treatment started early in course of disease
Treatment of tetanus in horses
Eliminate C. tetani organism
Antimicrobials
Neutralise toxin
Give tetanus vaccine (toxoid) at distant site
Control muscle spasm
How to eliminate C.tetani organism from a horse
§ Clean and debride wound (if you can find one)
§ Aiming to create an aerobic environment
Antimicrobials for tetanus infection
§ 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
Tetanus antitoxin
§ Antitoxin: does not neutralise toxin that is already bound
§ Give antitoxin BEFORE wound debridement
§ Consider intrathecal antitoxin early on
How do you control muscle spasm in tetanus infection
§ Drugs like methocarbamol and diazepam can be used
§ ACP (not hugely effective), alpha 2 agonists
Nursing for tetanus infection
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
Tetanus vaccination
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
Tetanus antitoxin
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
Botulism in horses
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
Clinical signs of botulism in horses
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
Three mechanisms of botulism infection in horses
Ingestion of preformed toxin
Bacterial infection of wound/umbilicus in foals
Ingestion of spores
Botulism- ingestion of preformed toxin
Poorly preserved hay/haylage/silage
Animal remains in feed often implicated
Botulism - infection of wound/umbilicus in foals
Serotype B, toxin produced in wound
Botulism - ingestion of spores
go on to produce toxin in the GI tract
Causes ‘shaker foal syndrome’
Serotype B, affects foals 2 weeks – 8 months old
Pathogenesis of botulism
three mechanisms of initial infection
-> haematogenous spread of toxin
-> Toxin binds to nerve terminal
-> block ACh release at NMJ
-> flaccid paralysis
Diagnosis of botulism
History spoiled feed
Clinical signs
Laboratory tests challenging/unreliable
Treatment of botulism
Nursing
Supportive/symptomatic treatment
Botulinum antitoxin – need the correct serotype
- Significant association with survival
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
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
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
Diagnosis of Equine herpesvirus myoencephalitis (EHM)
Clinical signs
Nasopharyngeal swab PCR
Serology (paired)
Virus isolation
CSF xanthochromic/yellow
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
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
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
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
Clinical signs of West Nile virus
Dull/lethargic
Facial paralysis, dysphagia
Muscle fasciculations
Hyperexcitability
Ataxia
Recumbency
Diagnosis of West Nile Virus
IgM capture ELISA
Treatment of West Nile Virus
No specific treatment
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)
Neuroborreliosis
Zoonotic
Lyme disease
Borrelia burgdorferi – spirochete bacteria
Transmitted by ixodes ticks
Seropositive horses high in healthy population so caution with diagnosis
Clinical signs of Neuroborreliosis
Muscle atrophy/weight loss,
cranial nerve dysfunction,
ataxia,
behavioural change,
uveitis,
pyrexia,
joint effusion/shifting lameness
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
Treatment of Neuroborreliosis
Prolonged (months) tetracyclines
Typically start with intravenous oxytetracycline then move to oral doxycycline (unlicensed)
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
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
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
Clinical signs of Western/Eastern/Venezuelan Equine Encephalitis
Pyrexia,
dull,
circling/head pressing,
dysphagia,
paralysis…
Death
