Rabies in Equids + Other Neuro Diseases

Module 23, Week 1

What is myeloencephaitis and encephalitis

Encephalitis is inflammation only of the brain, while myeloencephalitis (or more commonly encephalomyelitis) means inflammation of both the brain (encephalo-) and spinal cord

List some of the viral causes of myeloencephalitis or encephalitis

• EHV1 (MOST LIKELY IN THE UK)

• Rabies

• Arboviruses :

  • Flaviviruses (WNV, JE)

  • Togaviruses (alphaviruses); WEE, EEE, VEE

• Borna virus

• Hendra virus

Arboviruses (most commonly WNV and WEE/EEE/VEE)

How do most of them spread? Are they typically zoonotic?

most spread between mosquitos and birds, with horses (and humans) typically “dead end” hosts

most are SERIOUS zoonoses

Viral Encephalitides

Typical clinical signs?

• Many can be subclinical

• Mentation: hyper-excitability or lethargy (profound), comatose

• Behavior : head pressing, self mutilation, compulsive walking

• Gait derangements : ataxia, paresis, paralysis, muscle fasiculations (twitching) in WNV

• Other: circling, blindness, deafness, recumbency, fever

Equine Rabies

What are 3 ways of spread (epidemiology)

1. skunks, raccoons, and red fox most common in USA

2. dogs, cats, and other horses may also spread to horse via infected saliva in bite wounds

3. small carnivores (opossum, or pole cat) and bats may be more important cause of sprfead to equids in other counties. mules/donkeys naturally inquisitive = get bit

Equine Rabies

What kind of virus is it?

Neurotropic rhabdovirus (Lyssavirus)

Equine Rabies

Describe the pathogenesis

• Virus multiplies in myocytes at bite site and infects peripheral nerces via nerve endings/NMJs

• Progresses along PN via axoplasmic flow to spinal and dorsal root ganglia

• rapid multiplication in CNS (brain and spinal cord, sympathetic trunk): spreads in CSF and subsequent spread to blood

Equine Rabies

Does rabies initially spread within the blood or lymph node?

No! theres no initial spread within the blood or lymph node. it multiplies in neurones, perikaryons of neurons and accumulates in nucleocapsid (negri body formation). there is then an increase in cellularity in CSF ocne reaches (now detectable by PCR). THEN it spreads to salivary glands, secretions, bloood

What are these? Why are they important

Negri bodies

They are pathognomic (specifically diagnostic) for rabies virus infections

Equine Rabies

What is the incubation period?

Depends on site of bite, viral strain, and inoculum dose, ranging from 9 days to 1 year

There is also variable retention time of virus in myocytes, direct entry of virus to neural tissue allows for short IP

Equine Rabies

Clinical signs? Early vs Late

• Very variable in horse!!

• Early signs: hyperesthesia (physical sensitivity, especially of skin), ataxia, behavior change, anorexia, paresis, colic

• Late signs: cerebral signs, with rapid progression and deterioration usual over 48 hr

  • furious form = aggression, self mutilation, photophobia, hyperesthesia

Equine Rabies

Summary to describe the clinical progression

Range of Clinical signs:

• Change in behavior, dysphagia, ataxia

• Apparent colic pain or limb pain

Later clinical progression:

• Usually rapid increase in ataxia/paresis

• Self mutilation and aggression common

Further clinical progression

• Progress progression to recompense, often with multiple' ‘bucking’ attempts to stand

• Aggression may remain present

Equine Rabies

How do we diagnose?

1. Often on clinical signs, especially self mutilation

2. Recumbent paralytic form animals may continue to eat, drink with slower progression

3. Usual progression to death within 48 hours of initial onset

Lab diagnosis

• Immuno fluorescent antibody test on fresh brain tissue very quick

• Make sure you use the correct PPE

• Histopathology would reveal non-suppurative encephalomyelitis

• Negri bodies pathognomic for rabies

Equine Rabies

Treatment

• No progressive treatment, euthanize with appropriate PPE

Equine Rabies

How should we prevent?

• Vaccinate in high risk areas

• Inactivated vaccine given IM annually and high risk areas

• Stray, dog control, minimize exposure to bats

• Do not vaccinate horses that have had immediate contact with suspect case!

EHV-1

What is it? What can it cause?

EHV-1 (Equine Herpes Virus) is a ubiquitous disease (80% of ALL horses latently infected): causes mild respiratory disease in young horses, abortion storms, chorioretinopathy and myeloencephalopathy (EHM = Equine Herpes Myeloencephalopathy)

EHV-1 Myeloencephalopathy (EHM)

What is EHM?

Rarest manifestation of disease: may be pyrexic, with respiratory signs, and herd mates or individuals with neuro signs

EHV-1 Myeloencephalopathy (EHM)

Clinical signs

• Symmetric ataxia (typically affect Hind limbs first)

• Urinary/fecal retention, recumbency

• CN signs common, especially V, VII, VIII, XII

• Multifocal Neuro signs with variable forebrain disease (dullness, low head carriage, inability to rise, central vision loss)

• May be preceded by URT signs, pyrexia, inappetence, lethargy

• ** typically see symmetric ataxia, reduced tail tone, and struggle to urinate/defecate FIRST

EHV-1 Myeloencephalopathy (EHM)

How to diagnose

• Hx, CS, evidence in herd

• Recent travel, competition, or mixing?

• Multicentric lesions predominantly affecting cauda equina (bundle of nerves at very bottom of spinal cord), but cranial nerve deficits can also be present

  • CSF: xanthochromia, PCR

  • Serology

  • Viral Isolation: PCR,, culture (nasopharyngeal swab or blood)

• necropsy

EHV-1 Myeloencephalopathy (EHM)

Treatment options

• Anti inflammatories: NSAIDS, corticosteroids (controversial, but useful for 2-3 days)

• Supportive tx: position/slings, antimicrobials, urinary cath/rectal evacuation

• Possibly anti-virals

• Quarantine, hygiene measures

EHV-1 Myeloencephalopathy (EHM)

Prognosis and prevention

• Related to disease, severity, and response to treatment

• Recumbent horses = poor/grave

• Prevention and control = difficult

• Vaccination = controversial, does not prevent, but will increase herd immunity and decrease shedding period

• Herd management = keep young stock and older broodmares in separate areas, consider vaccination of all stock

West Nile Virus (WNV)

What type of virus is it? What are the hosts? zoonotic?

• Flavivirus

• Hosts: birds, humans, horses, other mammals

  • humans/horses = dead end hosts

• ZOONOTIC

West Nile Virus (WNV)

What 2 things can amplify the virus and are involved in the virus cycle?

birds and mosquitos

West Nile Virus (WNV)

What is the Transmission cycle (pic)

West Nile Virus (WNV)

Clinical signs

• ataxia, paresis

• Muscle fasciculations - twitching

• Hyperesthesia

• Behavioral changes

• Cranial nerve deficits: CNVII, XII, IX

• Recumbency

West Nile Virus (WNV)

Diagnosis

• Clinical signs

• Laboratory techniques:

  • IgM ELISA after two weeks

  • IgG species- specific ELISA

  • Nested RT-PCR on EDTA blood or brain tissue

  • brain immunohistopchemistry

West Nile Virus (WNV)

How can we prevent?

• Vector control!!! - reduce mosquitos

• Vaccination - most US horses are vaxxed

Alpha Viruses

What are they? Where are they endemic to? Zoonotic?

• Eastern/Western/Venezuelan encephalitis viruses

• endemic to the americas

• zoonotic!!

• high fatality rate in horses

Alpha Viruses (WEE/EEE/VEE)

Main amplifying host? Vector? Dead end hosts?

• amplifying = birds

• vectors = mosquitos

• dead end hosts = horses and humans (with the exception of VEE, cause horses develop marked viremia bc the horse is the primary reservoir and perpetuates infection with horse/mosquito cycle!)

Alpha Viruses (WEE/EEE/VEE)

Clinical signs

• Wide range: asymptomatic or severe CNS signs

• initial viremia = fever, lethargy stiffness

• behavioral changes

• blindness, CN deficits

• ataxia, paresis

• recumbency, seizures, coma

• Death: EEE > VEE > WEE

Alpha Viruses (WEE/EEE/VEE)

Diagnosis

• CS and epidemiology suggestive

• virus detection/isolation

• serology

• main research aim to improve vaccine efficiency so as to require fewer doses to establish effective immune response

• NOTIFIABLE DISEASE

Hendra Virus: Australia

Risk factors?

• Food trees

• Bat birthing season

• Breed (Thoroughbreds)

• >8yo

• Pasture housing

• Pregnancy

Hendra Virus: Australia

Clinical signs? Diagnosis?

• Pyrexia

• severe pneumonia

• Frothy nasal discharge

• icterus

• Recumbency

• Death

Dx: CS, virus isolation, serology, PCR, hisptopathology, zoonotic, caution w necropsy

Borna Virus

• there is a slide on this but its a lot of random shit and not in the UK or the US

Main ways to prevent infection of these viral diseases

1. reduce exposure to vectors

2. vaccination