Evidence for infection, inflammation and shock in sudden infant death: parallels between a neonatal rat model of sudden death and infants who died of sudden infant death syndrome

Author:

Blood-Siegfried Jane1,Rambaud Caroline2,Nyska Abraham3,Germolec Dori R.4

Affiliation:

1. Duke University Medical Center, Durham, North Carolina, USA, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, USA,

2. Service de Medecine Legale, Hôpital Raymond Poincare, Garches, France

3. Haharuv 18, Timrat, Israel, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, USA

4. National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, USA

Abstract

This study compared pathological findings from a neonatal rat model of sudden death with those from 40 sudden infant death syndrome (SIDS) infants collected at autopsy. In the rat model, influenza A virus was administered intranasally on postnatal day 10, and on day 12 a sublethal, intraperitoneal dose of Escherichia coli endotoxin; mortality was 80%. Tissue samples from the animals and infants were fixed in formaldehyde, embedded in paraffin, and sections stained with hematoxylin and eosin. Tissues from the SIDS specimens were additionally cultured for bacteria and viruses; post-mortem blood samples were evaluated for signs of inflammation. All sections were examined by a pediatric forensic pathologist familiar with SIDS pathology. Comparisons between the rat model and the human SIDS cases revealed that both exhibited gross and microscopic pathology related to organ shock, possibly associated with the presence of endotoxin. Uncompensated shock appeared to be a likely factor that caused death in both infants and rat pups. Response to a shock-inducing event might have played an important role in the events leading to death. The similarities between the neonatal rats and the human cases indicate that further research with the model might elucidate additional aspects of SIDS pathology.

Publisher

SAGE Publications

Subject

Infectious Diseases,Cell Biology,Molecular Biology,Immunology,Microbiology

Reference32 articles.

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