Pertussis encephalopathy

Introduction
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By Ravindra Kumar Garg MD

Pertussis encephalopathy is also known as or subsumes Whooping cough encephalopathy. -ed.

Pertussis or whooping cough is an important cause of infant death worldwide. Pertussis is caused by the organism Bordetella pertussis, a gram-negative bacillus. Severe complications of pertussis include pneumonia, encephalopathy, and meningoencephalitis. Central hypoventilation secondary to pertussis encephalopathy occurring during childhood has been described in an isolated case. Several neurologic complications have also been associated with the pertussis vaccines. The whole-cell vaccines may lead to acute encephalopathy, seizures, hypotonic-hyporeactive episodes, inconsolable crying, or anaphylactic reactions. Whole-cell pertussis vaccines are more frequently associated with neurologic complications in comparison to more recent acellular vaccine. However, experts now believe that there is no convincing evidence proving an association between vaccine and persistent brain damage. Vaccine encephalopathy is, in fact, an inherited genetic defect of the SCN1Agene that codes for the voltage-gated neuronal sodium channel. Pertussis vaccination might trigger earlier onset of Dravet syndrome because of an SCN1A mutation. In fact, children who presented with earlier diagnoses of alleged vaccine encephalopathy in infancy were diagnosed years later with Dravet syndrome. Based on review of current literature, the author presents an overview focusing on pertussis encephalopathy and vaccine encephalopathy; in addition, he also discusses epidemiology, pathogenesis, pathology, diagnosis, and treatment of pertussis.

Key Points

  • Encephalopathy is a rare complication of pertussis.
  • Several neurologic complications have been described with the pertussis vaccines, particularly with whole-cell vaccines.
  • There is no convincing evidence proving an association between vaccine and persistent brain damage.
  • Vaccine encephalopathy is, in fact, an inherited genetic defect of the voltage-gated neuronal sodium channel gene.

In This Article

Introduction
Historical note and nomenclature
Clinical manifestations
Etiology
Pathogenesis and pathophysiology
Epidemiology
Prevention
Differential diagnosis
Diagnostic workup
Prognosis and complications
Management
References cited
Contributors