Intestinal Infection and Toxin Production by Clostridium Botulinum as One Cause of Sudden Infant Death Syndrome

Arnon, S. S.; Midura, Thaddeus F.; Damus, Karla; Wood, R. M.; Chin, James

doi:10.1016/s0140-6736(78)91264-3

Cited by 175 publications

(47 citation statements)

References 28 publications

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“…There is, however, a broad clinical spectrum of IB. The mild end of the spectrum appears to be represented by infants who never require hospitalization but who have feeding difficulties, mild hypotonia and floppy neck, and failure to thrive, whereas the severe end of the spectrum may be characterized by a presentation resembling sudden infant death syndrome (SIDS), 28 and these patients require hospitalization for treatment of their respiratory and feeding difficulties.…”

Section: Clinical Manifestationmentioning

confidence: 99%

“…[36][37][38] The mouse neutralization assay is used to test for the presence of toxin in feces or the serum. Therefore, serum and fecal specimens should be collected as soon as the diagnosis of botulism is suspected.…”

Section: Diagnosismentioning

confidence: 99%

“…Although an association between infants with botulism and SIDS was suspected, 28 a prospective study failed to confirm the presence of C. botulinum in 248 cases of SIDS. 51 Because the disease may mimic many other disorders, it is possible that more cases of IB may be recognized.…”

Section: Preventionmentioning

confidence: 99%

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Infant botulism

Brook

2007

J Perinatol

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Infant botulism results from the absorption of heat-labile neurotoxin produced in situ by ingested Clostridium botulinum. Honey and environmental exposure are the main sources of acquisition of the organism. Clinical manifestations are owing to progressive neuromuscular blockade, initially of muscles innervated by cranial nerves and later of the trunk, extremities and diaphragm. Presynaptic autonomic nerves are also affected. The diagnosis is made on clinical grounds and is confirmed by recovery of the organism or by detection of toxin in the stool. Management includes meticulous supportive intensive care that may include mechanical ventilation and administration of human botulinum immunoglobulin in severe cases.

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Section: Clinical Manifestationmentioning

confidence: 99%

Section: Diagnosismentioning

confidence: 99%

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Infant botulism

Brook

2007

J Perinatol

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“…There are conflicting results on the role of viruses [9,10] and toxigenic intestinal bacteria in SIDS [11][12][13][14][15]. Recently, it has been suggested that nasopharyngeal colonization by toxigenic strains of Staphylococcus aureus, particularly those producing the toxic shock syndrome toxin 1 (TSST-1), might be involved in some of these infant deaths [16].…”

Section: Introductionmentioning

confidence: 99%

Factors enhancing adherence of toxigenicStaphylococcus aureusto epithelial cells and their possible role in sudden infant death syndrome

et al. 1993

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SUMMARYToxigenic strains of Staphylococcus aureus have been suggested to play a role in sudden infant death syndrome (SIDS). In this study we examined two factors that might enhance binding of toxigenic staphylococci to epithelial cells of infants in the age range in which cot deaths are prevalent: expression of the Lewisa antigen and infection with respiratory syncytial virus (RSVT). By flow cytometry we demonstrated that binding of three toxigenic strains of S. aureus to cells from nonsecretors was significantly greater than to cells of secretors. Pre-treatment of epithelial cells with monoclonal anti-Lewisa or anti-type-I precursor significantly reduced bacterial binding (P < 0 01); however, attachment of the bacteria correlated only with the amount of Lewisa antigen detected on the cells (P < 0 01). HEp-2 cells infected with RSV bound significantly more bacteria than uninfected cells. These findings are discussed in context, of factors previously associated with SIDS (mother's smoking, bottle feeding and the prone sleeping position) and a hypothesis proposed to explain some cases of SIDS.

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“…Wound botulism, the rarest form, results from infection at the wound site with subsequent toxin production and absorption. Infant botulism occurs during intraintestinal growth of the bacterium and may be a factor related to sudden infant death syndrome (3).…”

Section: I1mentioning

confidence: 99%

The Action of Botulinum Toxin at the Neuromuscular Junction

Sellin¹

1980

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Intestinal Infection and Toxin Production by Clostridium Botulinum as One Cause of Sudden Infant Death Syndrome

Cited by 175 publications

References 28 publications

Infant botulism

Infant botulism

Factors enhancing adherence of toxigenicStaphylococcus aureusto epithelial cells and their possible role in sudden infant death syndrome

The Action of Botulinum Toxin at the Neuromuscular Junction

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