Zusammenfassung
Der Säuglingsbotulismus stellt eine eigenständige Form des Botulismus dar, bei der es nach Ingestion der ubiquitär verbreiteten Clostridium botulinum-Sporen und Keimen der Erreger im Darm zur intestinalen Neurotoxinproduktion kommt. Entsprechend entwickeln sich die Symptome im Unterschied zum klassischen Nahrungsmittelbotulismus, bei dem es kurz nach Ingestion des in der Nahrung gebildeten Toxins zum abrupten Krankheitsbeginn kommt, bei Säuglingsbotulismus meist eher langsam. Die mikrobiologische Diagnose erfolgt durch Erreger- und Toxinnachweis im Stuhl. Positive Befunde ergeben allerdings nur einen indirekten Anhalt für eine klinisch relevante Toxinwirkung, da auch asymptomatische Träger vorkommen. Das Toxin führt durch irreversible Blockade der Acetylcholinfreisetzung zu Lähmungen, wobei sich in Abhängigkeit von der produzierten Toxinmenge ein breites klinisches Spektrum findet, das von oligosymtomatischen Formen bis zu fulminante Verläufen reicht, die innerhalb weniger Stunden zur Ateminsuffizienz führen und eine mögliche Ursache plötzlicher Todesfälle im Säuglingsalter darstellen. Außerdem können unerkannte leichte Verlaufsformen oder beginnende Lähmungen als Cofaktor für andere SIDS-Risikofaktoren wirken, und in Studien bei an SIDS verstorbenen Kindern gelang ein Botulismunachweis in bis zu 20 % der Fälle. Daher ist es wichtig, bei einer unklaren muskulären Hypotonie im ersten Lebensjahr an die Möglichkeit einer Botulismusinfektion zu denken.
Abstract
Infant botulism represents a distinct entity of botulism. Ingestion of the ubiquitously present spores of Clostridium botulinum leads to germination of the organisin and neurotoxin production in the infantil intestine. Symptoms typically develop gradually in contrast to classical food botulism in which an acute onset of symptoms shortly after the ingestion ofpreformed toxin in a food is characteristic. Microbiologically, the diagnosis is established by identification of Clostridium botulinum organism and toxin in stool specimen. However, positive results in these tests provide only indirect evidence for the clinical relevance of the neurotoxin since asymptomatic carriers have been found. The toxin irreversibly blocks the release of acetylcholin from the motoric end plate which results in muscle weakness and paralysis. Depending on the amount of toxin produced, infant botulism exhibits a broad clinical spectrum ranging from oligosymptomatic forms to a fulminant course with acute respiratory failure within hours leading to sudden death. Unrecognized mild forrns or beginning muscle weakness can be a co-factor for other risk factors of sudden infant death (SIDS). In studies analyzing infants who died from SIDS, botulism bacteria or toxin were found in up to 20 % of cases. Infant botulism therefore represents an important differential diagnosis of unexplained and inconclusive muscular hypotonia in the first year of life.
Schlüsselwörter
Säuglingsbotulismus - Botulismus - plötzlicher Kindstod - SIDS
Key words
Infant botulism - Botulism - sudden infant death - crib death
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Dr. Ulrike Bartram
Universitäts-Kinderklinik Würzburg
Josef-Schneider-Straße 2
97080 Würzburg
