Myopathic changes associated with severe acute respiratory syndrome: a postmortem case series

Arch Neurol. 2005 Jul;62(7):1113-7. doi: 10.1001/archneur.62.7.1113.

Abstract

Background: The March 2003 outbreak of the severe acute respiratory syndrome (SARS) resulted in significant morbidity and mortality. Muscle weakness and elevated serum creatine kinase levels are commonly encountered in patients with SARS. However, the nature and cause of myopathy associated with a SARS infection are unknown because, to our knowledge, there has been no report of histological or postmortem examination of the skeletal muscle from SARS-infected patients.

Objective: To determine the exact nature of the myopathy associated with SARS.

Method: Postmortem skeletal muscles from 8 consecutive patients who died of SARS in March 2003 were studied under light and electron microscopy as well as immunohistochemistry.

Results: Focal myofiber necrosis was identified in 4 of 8 cases. Macrophage infiltration and regenerative fiber were scanty. All 4 patients treated with a steroid had significant myofiber atrophy. In situ hybridization for coronavirus was negative in all subjects. Viral cultures for coronavirus and examination for viral particles under electron microscopy were performed in 2 patients. The viral culture yielded no organisms and there were no viral particles seen on electron microscopic examination.

Conclusions: There is a spectrum of myopathic changes associated with a SARS infection. Focal myofiber necrosis is common and possibly is immune mediated. Critical illness myopathy and superimposed steroid myopathy may also play an important role in SARS.

Publication types

  • Case Reports

MeSH terms

  • Adult
  • Aged
  • Autopsy
  • Creatine Kinase / blood
  • Female
  • Humans
  • Macrophages
  • Male
  • Microscopy, Electron
  • Middle Aged
  • Muscle Weakness / etiology*
  • Muscle, Skeletal / pathology*
  • Myositis / etiology
  • Necrosis
  • Severe Acute Respiratory Syndrome / complications*

Substances

  • Creatine Kinase