Infection and sudden unexpected death in infancy: a systematic retrospective case review

Weber, MA; Klein, Nigel; Hartley, Jeanne; Lock, PE; Malone, Marian; Sebire, Neil J.

doi:10.1016/s0140-6736(08)60798-9

Cited by 133 publications

(126 citation statements)

References 16 publications

Supporting

Mentioning

118

Contrasting

Order By: Relevance

“…Myocarditis may present clinically with a range of symptoms and is increasingly implicated as a cause of sudden death in infancy and childhood. A recent study of autopsies in a United Kingdom hospital reported myocarditis as the cause of death in approximately 2% of the deaths of children Ͻ18 years old, 57% of which were sudden deaths (16,17).…”

Section: Case Reportmentioning

confidence: 99%

First Report of Sudden Death Due to Myocarditis Caused by Adenovirus Serotype 3

et al. 2010

View full text Add to dashboard Cite

Myocarditis is a rare cause of sudden death in childhood. We describe the sudden death of a child from viral myocarditis, which we demonstrate was likely caused by an uncontrolled inflammatory response to a disseminated adenovirus serotype 3 infection originating in the tonsil. CASE REPORTAn 11-year old boy collapsed suddenly at home. He was transferred to a hospital by ambulance. Cardiopulmonary resuscitation was unsuccessful, and he was pronounced dead. He had visited his general practitioner (GP) 1 day earlier with a sore throat and was treated with antibiotics for tonsillitis. No investigations were carried out by his GP or on arrival at the hospital due to his sudden death. He had no past medical history of note, and there was no family history of cardiac illness or sudden death. No recent foreign travel was reported, nor was there contact with persons from abroad. A postmortem was carried out at the direction of the coroner.Much of the postmortem examination was normal. His tonsils were mildly enlarged and showed a surface purulent exudate. However, on postmortem examination, his heart was enlarged (weight, 214.2 g; expected weight, 124 g). On sectioning, the myocardium appeared diffusely abnormal with areas of petechiae and pallor. There was no evidence of myocardial hypertrophy. Microscopically, there was a severe myocardial infiltrate diffusely present composed of lymphocytes, histiocytes, and plasma cells with occasional eosinophils and neutrophils (Fig. 1). There were admixed areas of necrosis and hemorrhage. There was no evidence of fibrosis or myofiber hypertrophy. Immunohistochemical staining revealed that the infiltrate was predominantly lymphohistiocytic (CD45 positive). CD3 staining confirmed that this was a T-lymphocytemediated response (Fig. 2).All routine investigations, including swabs for bacterial culture, blood cultures, meningococcal PCR, and pneumococcal PCR, were negative. Toxicology testing for alcohol and drugs was negative. Target-specific immunoglobulin M assays were performed for Mycoplasma pneumoniae, cytomegalovirus, Epstein-Barr virus, parvovirus B19, and rubella virus, along with complement fixation testing for total antibodies to Mycoplasma pneumoniae, Chlamydia group, and adenovirus and latex agglutination testing for Toxoplasma gondii. All serological investigations were negative. In addition, no viruses were observed in the lung or myocardial tissue by electron microscopy. Cerebrospinal fluid Gram staining and culture were negative.The most common viral etiologies of myocarditis are Coxsackie group B viruses and members of the adenovirus genus (3, 5). Therefore, molecular methods were employed to investigate the presence of these viruses. Total viral RNA/DNA was extracted from serum using the Qiagen QIAmp viral RNA mini kit, and total viral DNA was extracted from myocardial and pulmonary tissue using the QIAamp DNA mini kit (Qiagen) in accordance with the manufacturer's instructions. Enterovirus RNA was not detected in lung or myocardial tissue using a nested reverse trans...

show abstract

Section: Case Reportmentioning

confidence: 99%

First Report of Sudden Death Due to Myocarditis Caused by Adenovirus Serotype 3

et al. 2010

View full text Add to dashboard Cite

show abstract

“…Infection of normally sterile sites with major bacterial pathogens in SIDS has been independently described by two research groups. (Weber et al 2008, Goldwater 2008 mechanism of which is not fully understood, however, the cytokine storm almost certainly plays a major role (Hotchkiss & Karl 2003) and the hypoxaemia the storm produces seems to precede the final demise in monitored SIDS cases. In addition, it is plausible that the findings of Vargas et al(2013) in relation to Pneumocystis lung colonization/infection, with increased mucus production, could contribute to hypoxaemia but not necessarily be a direct cause of SIDS given that the fungus was found in a similar proportion of dead control babies (Vargas et al 2007).…”

Section: ) Evidence For Infection and Inflammation In Sids Pathogenesismentioning

confidence: 99%

SIDS Risk Factors: Time for New Interpretations. The Role of Bacteria

Goldwater¹,

Bettelheim²

2013

PRIJ

View full text Add to dashboard Cite

The aim of this paper is to help draw attention to perceived ideas regarding the risk factors and the implied pathogenesis of Sudden Infant Death Syndrome (SIDS), and SIDS research in general. Our paper shows there is little if any evidence to support the broadly held notion of an association between respiratory function and sudden infant death syndrome. Researchers who hold to this approach to explain the risk factors of bed-sharing and prone sleep position, etc. have failed to meet the standards of scientific endeavour that we would expect of good research. To counter this imbalance we have proposed an evidence-based explanation for SIDS risk factors showing that microbiological studies of SIDS corroborate epidemiologic and pathological data in establishing a plausible pathogenetic mechanism. We reviewed recent publications on current research and the epidemiology of SIDS and publications on the microbiology of SIDS. Conclusion: Comparison of the data presented, suggest that the risk factors of bed-sharing, and smoke exposure, prone sleep position and alcohol can be explained by the theories of a microbiological infection model of SIDS pathogenesis.

show abstract

“…DeSa (8) identified 20 cases, 17 of which were infants, with isolated myocarditis among 3086 necropsies. In a study of 1516 autopsies of children between birth and 18 y of age, myocarditis was present in 28 (1.8%); half occurred in infants and represented 2% of infant deaths referred for autopsy (1). Conversely, in a Swedish study, myocarditis was identified in 16.8% of 410 infants who died naturally and in 7.4% of 27 violent deaths (9).…”

mentioning

confidence: 97%

“…Confusion can result from lack of clinically verified classification schemes that establish minimum severity of inflammation and cellular destruction in vital organs necessary to cause death. There is a lack of consensus regarding the significance of organisms isolated from normally sterile body sites at autopsy in the absence of inflammation (1)(2)(3).…”

mentioning

confidence: 99%

Myocardial Inflammation, Cellular Death, and Viral Detection in Sudden Infant Death Caused by SIDS, Suffocation, or Myocarditis

et al. 2009

View full text Add to dashboard Cite

ABSTRACT:The significance of minor myocardial inflammatory infiltrates and viral detection in SIDS is controversial. We retrospectively compared the demographic profiles, myocardial inflammation, cardiomyocyte necrosis, and myocardial virus detection in infants who died of SIDS in a safe sleep environment, accidental suffocation, or myocarditis. Formalin-fixed, paraffin-embedded myocardial sections were semiquantitatively assessed for CD3 lymphocytes and CD68 macrophages using immunohistochemistry and for cardiomyocyte cell death in H&E-stained sections. Enteroviruses and adenoviruses were searched for using PCR technology. The means of lymphocytes, macrophages, and necrotic cardiomyocytes were not statistically different in SIDS and suffocation cases. Enterovirus, not otherwise specified, was detected in one suffocation case and was the only virus detected in the three groups. Very mild myocardial lymphocyte and macrophage infiltration and scattered necrotic cardiomyocytes in SIDS are not pathologic, but may occur after the developing heart is exposed to environmental pathogens, including viruses. (Pediatr Res 66: 17-21, 2009)

show abstract

Infection and sudden unexpected death in infancy: a systematic retrospective case review

Cited by 133 publications

References 16 publications

First Report of Sudden Death Due to Myocarditis Caused by Adenovirus Serotype 3

First Report of Sudden Death Due to Myocarditis Caused by Adenovirus Serotype 3

SIDS Risk Factors: Time for New Interpretations. The Role of Bacteria

Myocardial Inflammation, Cellular Death, and Viral Detection in Sudden Infant Death Caused by SIDS, Suffocation, or Myocarditis

Contact Info

Product

Resources

About