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Neurology: Borna disease

ISSN 2398-2977

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Synonym(s): Near Eastern Equine Encephalitis (NEEE)

Introduction

  • A rare, sporadic, severe neurological disease occurring in spring and early summer.
  • Cause: Borna disease virus (BDV) - classified by itself in theBornaviridaefamily.
  • Signs: abnormal mentation; compulsive behavior; circling; head pressing; depression; tremors; hyperesthesia; often progresses to convulsions or coma. 
  • Diagnosis: neurological examination; antibody testing of CSF and serum.
  • Treatment: symptomatic care.
  • Prognosis: grave high mortality; residual neurological deficits are common, necessitating euthanasia.

Presenting signs

  • Subclinical encephalitis, peracute encephalitis through transient ataxia and fever all occur.
  • Abnormal behavior.
  • Neurological signs.
  • Depression.

Acute presentation

  • Behavioral and mentation changes.
  • Signs of forebrain disease such as circlng, head-pressing, constant yawning, aggressiveness.
  • Asymmetric vestibular signs and various cranial nerve functional deficits.
  • Ataxia.
  • Dysphagia.
  • Hyperesthesia.
  • Seizures.
  • Coma.

Geographic incidence

  • Europe and the Middle East.
  • BDV-antibodies have been isolated from otherwise healthy horses in Israel, Japan and the USA, although the disease has not been recorded there.

Public health considerations

  • Cases in humans, sheep, cattle, goats, ostriches, rabbits and cats have been documented.

Cost considerations

  • Treatment is often unsuccessful.
  • Successful treatment is often prolonged and residual deficiencies are common, resulting in euthanasia several months down the line.

Pathogenesis

Etiology

  • Caused by Borna disease virus (BDV).
  • Cell-free virus has still to be isolated for full virology to be possible.
  • Route of infection is unknown - ? inhalation, ingestion, tick-borne.

Pathophysiology

  • Low morbidity.
  • The specific etiology of the development of the clinical disease is unknown, but thought to be the result of a virus-induced, cell-mediated, immunopathological reaction.
  • The virus can produce latent or persistent infections, or asymptomatic carrier states which may excrete the virus and be a potential risk to others.
  • High mortality around 80%.

Timecourse

  • A long incubation period of 4 weeks to 6 months before clinical signs.
  • Acute encephalitis phase usually lasts 1-3 weeks.
  • Full recovery is rare.

Epidemiology

  • Route of infection is unknown - ? inhalation, ingestion or tick-borne.
  • Cases are usually sporadic.
  • In-contacts or recovered animals may become asymptomatic carriers which can excrete the virus indefinitely.
  • ? Wild birds are implicated in transmission of the disease between populations.

Diagnosis

Presenting problems

  • Ataxia.
  • Abnormal behavior.

Client history

  • In-contact with disease.
  • Abnormal behavior.
  • Depression.
  • Dysuria.
  • Colic.

Clinical signs

  • Any combination of:
    • Abnormal mentation. 
    • Depression.
    • Head pressing.
    • Tremors.
    • Circling.
    • Maniacal or compulsive behavior, eg:
      • Chewing.
      • Biting the air.
      • Marching gait.
    • Hyperesthesia.
    • Forelimb/hindlimb ataxia.
  • Often progresses to convulsions or coma.

Diagnostic investigation

Confirmation of diagnosis

Discriminatory diagnostic features

  • History and clinical signs.
  • Neurological examination.

Definitive diagnostic features

  • Antibody testing: demonstration of specific antibodies for Borna virus in CSF and serum.
  • Post mortem: demonstration of specific intranuclear inclusion bodies on histology.

Gross autopsy findings

  • Usually unremarkable.

Histopathology findings

  • A diffuse, non-suppurative encephalitis most prominent in the gray matter of the brainstem.
  • Characteristic Joest-Degen inclusion body in the nucleus of nerve cells of the hippocampus and olfactory lobes of the cerebral cortex.

Differential diagnosis

Treatment

Initial symptomatic treatment

  • Symptomatic care:
  • Confine to a padded box or stall with a deep bed if recumbent, compulsive behavior, or convulsions are exhibited. 
  • Create a darkened, quiet environment if hyperesthesia.
  • The acute encephalitis phase may last up to 3 weeks and prolonged, intensive supportive care will be required to assist recovery.

Standard treatment

  • To reducing cerebral inflammation and swelling:
    • Dimethyl sulfoxide   Dimethyl sulfoxide  as a 10% solution: 1-4 g/kg IV SID for 3-5 days.
    • Dexamethasone   Dexamethasone  : 0.04-0.3 mg/kg IV SID for 3-5 days; followed by a gradually decreasing dose over the next 7 days.
  • To treat hyperesthesia or convulsions:
    • Diazepam   Diazepam  : 20-40 mg/500 kg IV horse to effect.
    • Phenobarbital   Phenobarbital  : loading dose of 8-15 mg/kg IV to effect; followed by maintenance dose IV or PO of 2-10 mg/kg SID.

Monitoring

  • If the horse is recumbent for prolonged periods attention must be paid to the prevention of decubital ulcers   Elbow: wound - pressure sore  the horse should be deep-bedded and turned frequently.

Subsequent management

Treatment

  • Decubital ulcers should be treated appropriately.

Monitoring

  • Progress should be monitored closely throughout many cases have residual neurological deficits, eg ataxia, tremors, convulsions, dysphagia, which may necessitate euthanasia   Euthanasia  .
  • Laminitis may occur secondary to prolonged steroid use.
  • Trauma may be self-inflicted during maniacal behavior episodes the stall/box should be padded and the animal protected from self-harm where possible.
  • Repeated seizures can lead to permanent brain damage seizures should be monitored and an attempt made to control them if they become frequent.

Prevention

Control

  • Isolate infected animals.
  • Antibody test in-contact animals for latent state.

Prophylaxis

  • A vaccine is available which appears to confer immunity in the horse, but it is not usually used because of the low incidence of the disease.
  • Avoid contact with infected animals.

Outcomes

Prognosis

  • Grave around 80% mortality.

Expected response to treatment

  • Residual neurological deficits are common, eg ataxia, tremors, convulsions, dysphagia, which may preclude safe use of the animal and necessitate euthanasia   Euthanasia  .
  • A persistent carrier state is common following recovery from the initial encephalitis episode.

Reasons for treatment failure

  • Residual neurological deficits or repeated seizure activity necessitating euthanasia.
  • Persistent carrier state resulting in a continued risk of contagion to in-contacts, including humans, resulting in euthanasia.

Further Reading

Publications

Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Priestnall S L et al (2011) Borna disease virus infection of a horse in Great Britain. Vet Rec 168 (14), 380 PubMed.