Activation ofClostridium perfringens cytotoxic enterotoxin(s) in vivo and in vitro: Role in triggers for sudden infant death

Mach, Annette; Lindsay, James

doi:10.1007/bf01573203

Cited by 20 publications

(7 citation statements)

References 20 publications

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“…The actions of C. perfringens cytotoxic endotoxins have been shown to be exacerbated by interferon‐gamma (IFN‐γ), produced by intestinal brush border cells in response to viral and/or bacterial infections. Prior infection in infants might thus sensitise them resulting in a more virulent infection and sudden death 171 …”

Section: Individual Risk Factorsmentioning

confidence: 99%

Review of risk factors for Sudden Infant Death Syndrome

Sullivan

Barlow²

2001

Paediatric Perinatal Epid

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Sudden infant death syndrome (SIDS) accounts for the largest number of deaths during the first year of life in developed countries. The possible causes of SIDS are numerous and, to date, there is no adequate unifying pathological explanation for SIDS. Epidemiological studies have played a key role in identifying risk factors, knowledge of which has underpinned successful preventive programmes. This review critically assesses information on the main risk factors and causal hypotheses put forward for SIDS, focusing on research published since 1994. The overall picture that emerges from this review is that affected infants are not completely normal in development, but possess some inherent weakness, which may only become obvious when the infant is subjected to stress. Initially there may be some minor impairment or delay in development of respiratory, cardiovascular or neuromuscular function. None of these is likely to be sufficient, in isolation, to cause death and, provided the infant survives the first year of life, may no longer be of any significance. However, when a compromised infant is confronted with one or more stressful situations, several of which are now clearly identified as risk factors, and from which the majority of infants would normally escape, the combination may prove fatal.

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Section: Individual Risk Factorsmentioning

confidence: 99%

Review of risk factors for Sudden Infant Death Syndrome

Sullivan

Barlow²

2001

Paediatric Perinatal Epid

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“…1997). Viral and bacterial infections induce the synthesis of interferons, notably interferon gamma, which can sensitise cells by enhancing permeability, allowing rapid uptake of toxins and reducing the amount required for a lethal dose (Mach and Lindsay 1994). Given that a mild viral infection is a risk factor for SIDS, intraintestinal production of Cl.…”

Section: Enteric Bacteriamentioning

confidence: 99%

“…Furthermore, histopathological change to the SIDS infants' ileal tissue showed remarkable similarity to animal models of CTE damage (Lindsay et al 1993), and in rabbit models, CTE has been shown to contribute to intrathoracic petechiae, a pathological hallmark of SIDS (Siarakas et al 1997). Viral and bacterial infections induce the synthesis of interferons, notably interferon gamma, which can sensitise cells by enhancing permeability, allowing rapid uptake of toxins and reducing the amount required for a lethal dose (Mach and Lindsay 1994). Given that a mild viral infection is a risk factor for SIDS, intraintestinal production of Cl.…”

Section: Clostridium Perfringensmentioning

confidence: 99%

An infectious aetiology of sudden infant death syndrome

Highet

2008

Journal of Applied Microbiology

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Summary Due attention has been given to infectious agents and immune responses to infection in sudden infant death syndrome (SIDS). It has been acknowledged that the pathological, epidemiological and genotypic findings in SIDS infants suggest an infectious aetiology possibly being potentiated by immunoregulatory polymorphisms, however, the cause of SIDS is a mystery and remains open to debate. Consistent pathological findings are seen which display similarities to the pathogenesis of toxaemic shock and/or sepsis. The major risk factors for SIDS parallel those for increased colonization and serious bacterial infections and the natural variation in the incidence of SIDS cases is typical of an infectious disease. The roles played by viral infection, immunoregulatory genes and suspected bacterial species are discussed herein.

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“…Factors that can enhance inflammatory responses include respiratory virus infections [76][77][78][79][80], additive or synergistic effects between bacterial toxins [81], interactions between bacterial toxins and products of cigarette smoke [82,83] and hyperthermia [84].…”

Section: Risk Factors Affecting Induction or Control Of Inflammationmentioning

confidence: 99%

“…Most of the studies on mechanisms involved in interactions between virus infection and bacterial toxins have been carried out in animal models. Induction of pro-inflammatory cytokines that contribute to severity of the host's responses to infectious agents or their products such as endotoxin can be enhanced by co-existing virus infection [76][77][78][79][80].…”

Section: Respiratory Virus Infectionmentioning

confidence: 99%

Ethnicity, infection and sudden infant death syndrome

Blackwell

2004

FEMS Immunology and Medical Microbiology

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Epidemiological studies found the incidence of SIDS among Indigenous groups such as Aboriginal Australians, New Zealand Maoris and Native Americans were significantly higher than those for non-Indigenous groups within the same countries. Among other groups such as Asian families in Britain, the incidence of SIDS has been lower than among groups of European origin. Cultural and childrearing practices as well as socio-economic factors have been proposed to explain the greater risk of SIDS among Indigenous peoples; however, there are no definitive data to account for the differences observed. We addressed the differences among ethnic groups in relation to susceptibility to infection because there is evidence from studies of populations of European origin that infectious agents, particularly toxigenic bacteria might trigger the events leading to SIDS. The risk factors for SIDS parallel those for susceptibility to infections in infants, particularly respiratory tract infections which are also major health problems among Indigenous groups. Many of the risk factors identified in epidemiological studies of SIDS could affect three stages in the infectious process: (1) frequency or density of colonisation by the toxigenic species implicated in SIDS; (2) induction of temperature-sensitive toxins; (3) modulation of the inflammatory responses to infection or toxins. In this review we compare genetic, developmental and environmental risk factors for SIDS in ethnic groups with different incidences of SIDS: low (Asians in Britain); moderate (European/Caucasian); high (Aboriginal Australian). Our findings indicate: (1) the major difference was high levels of exposure to cigarette smoke among infants in the high risk groups; (2) cigarette smoke significantly reduced the anti-inflammatory cytokine interleukin-10 responses which control pro-inflammatory responses implicated in SIDS; (3) the most significant effect of cigarette smoke on reduction of IL-10 responses was observed for donors with a single nucleotide polymorphism for the IL-10 gene that is predominant among both Asian and Aboriginal populations. If genetic makeup were a major factor for susceptibility to SIDS, the incidence of these deaths should be similar for both populations. They are, however, significantly different and most likely reflect differences in maternal smoking which could affect frequency and density of colonisation of infants by potentially pathogenic bacteria and induction and control of inflammatory responses.

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Activation ofClostridium perfringens cytotoxic enterotoxin(s) in vivo and in vitro: Role in triggers for sudden infant death

Cited by 20 publications

References 20 publications

Review of risk factors for Sudden Infant Death Syndrome

Review of risk factors for Sudden Infant Death Syndrome

An infectious aetiology of sudden infant death syndrome

Ethnicity, infection and sudden infant death syndrome

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