Felis ISSN 2398-2950

Cerebellum: hypoplasia (feline panleukopenia related)

Contributor(s): Peter Dickinson, Simon Platt

Introduction

  • Rare condition.
  • Cause: in-utero infection with feline panleukopenia virus.
  • Signs: onset of generalized ataxia with hypermetric gait and intention tremors usually from approximately 4 weeks of age.
  • Diagnosis: history, signs, brain imaging.
  • Treatment: none.
  • Prognosis: guarded for normal life although many kittens survive with good quality of life.

Pathogenesis

Etiology

Pathophysiology

  • The parvovirus   Feline panleucopenia (parvo)  has a predilection for cells with active DNA synthesis.
  • Such cells include the external germinal cell layer, which normally gives rise to the cerebellar granule cells.
  • The virus also has a separate cytopathogenic effect on Purkinje cells.
  • Destruction of the external germinal layer produces hypoplasia of the granule cell layer.
  • The virus also very occasionally causes more diffuse CNS germinal cell necrosis by unknown mechanisms resulting in cerebrocortical, diencephalic and brain stem lesions.
  • The cerebrum is particularly susceptible to the cytopathogenic effects of feline parvovirus in the early second trimester.
  • Persistence of the virus in mitotically active cells, such as endothelial cells and macrophages, accounts for the severe dysplasia of the cerebellum as it develops later in gestation and during the immediate post-natal period.

Timecourse

  • Abnormality usually recognized from 4 weeks.

Diagnosis

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Treatment

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Outcomes

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Further Reading

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