Infant Botulism

Infants are notoriously good at keeping us guessing in the emergency department (ie, “Never Trust a Neonate.”). They look weird, they act weird, they kind of are weird, but we love them just the same.  Families, for good reason, bring their infants in for all sorts of complaints and concerns.  It’s up to us to decipher whether a sometimes vague complaint represents something benign or something more sinister.  We have all seen a baby who isn’t feeding well, and one who hasn’t pooped in a few days… but when should we be concerned about that?  Let’s take a moment – over this delectable honey-glazed morsel – to refresh our memories about infant botulism!

Infant Botulism: Basics

• Infant botulism is an acute, symmetric, descending flaccid paralysis caused by botulinum neurotoxin.
• The toxin is produced by Clostridium botulinum spores that germinate and colonize in the immature and relatively sterile infant gastrointestinal tract. 
  • Clostridium baratti and Clostridium butyricum are less common bacteria that also cause botulism.
• It primarily affects infants and ~95% of confirmed cases were in patients under 6 months of age.[1]
  • Worldwide cases of infant botulism have been recorded in children ranging from 1 day to 14 months of age. [2]
• The Clostridium botulinum neurotoxin irreversibly binds presynaptic cholinergic receptors and blocks acetylcholine release.
• Honey is the best-known preventable source, but most cases have no honey exposure
  • Honey should be avoided in infants <12 months!!
• Airborne/environmental dust (construction, landscaping, windy/dusty areas) is now the predominant source. [2]

Infant Botulism: Signs & Symptoms

Infant botulism can present with very vague and inconspicuous symptoms…

• Constipation: classical first/sentinel sign (often 3–24 days before presentation) [1-2]
• Poor feeding and poor latching
• Bulbar/cranial nerve palsies: weak suck/swallow, weak cry, pooled oral secretions, drooling, diminished gag, ptosis, sluggish pupils, ocular palsies, loss of facial expression
• Descending symmetric weakness: loss of head control, generalized hypotonia (“floppy baby!”), decreased spontaneous movement
• Autonomic features: fluctuating heart rate/blood pressure, flushing, dry mouth, urinary retention
• Progression to respiratory failure from upper airway collapse and diaphragmatic paralysis is the main life threat

Look for the classic triad: constipation, bulbar palsies, and descending hypotonia with intact mentation!

Infant Botulism: Differential

• Meningitis/Sepsis
  • In your febrile infants with concern for botulism, avoid aminoglycosides when able as they can worsen neuromuscular blockade
• Inborn errors of metabolism (think: organic acidurias, urea cycle abnormalities, fatty acid oxidations disorders)
• Guillain-Barré syndrome (typically areflexic with ascending weakness, compared to botulism’s descending weakness)
• Acute flaccid myelitis: asymmetric motor deficits, typically preceded by URI
• Congenital abnormalities!
  • Neonatal myasthenia gravis: fatiguable weakness improving with rest
  • Congenital hypothyroidism: newborn with hypotonia, lethargy, facial puffiness
  • Congenital adrenal hyperplasia: hyponatremia, hyperkalemia, genital ambiguity (always look in the diaper!)
  • Congenital heart disease
• Spinal Muscular Atrophy (SMA Type 1): Profound symmetric hypotonia and areflexia
  • Usually lacks the prominent bulbar palsies, constipation, and fixed, sluggish pupils seen in botulism
• Tick paralysis: ask about travel and exposure history
• Poliomyelitis: probably not worrisome (for now), but please vaccinate your children…

Botulism: Diagnosis

• Primarily a clinical diagnosis; early recognition is crucial!
• The mouse bioassay (MBA) is the clinical gold standard for detecting botulinum neurotoxin (BoNT) produced by Clostridium botulinum
• How MBA works [3]:
  • Injection: A sample (serum, stool, or food extract) is injected intraperitoneally into mice
  • Observation: Inoculated mice are monitored for signs of botulism over 1 to 4 days
  • Serotype Identification: To find out which of the toxin type (A through G) is present, paired mice receive specific neutralizing antitoxins alongside the sample

Treatment

• Botulism ImmunoGlobulin (“BabyBIG”)
  • Contains human-derived IgG antibodies that bind and neutralize circulating botulinum toxin (types A and B)
  • “BabyBIG” halts the progression of paralysis, allowing infant motor nerves to regenerate naturally [4]
• Supportive care – being mindful of potential respiratory depression
• Notify public health
• Contact the California Department of Public Health Infant Botulism Treatment and Prevention Program (IBTPP) 24-hr line: 510-231-7600 (infantbotulism.org) [1,4]

Moral of the Morsel

• Be vigilant! Early recognition and “BabyBIG” administration is critical! Suspect infant botulism in any afebrile, alert infant with constipation, bulbar palsies, and descending hypotonia.
• Call your friends! Notify public health department and reach out to the California Botulism Team for help!
• Monitor closely! The main threat is respiratory failure from upper airway collapse and diaphragmatic weakness. Monitor your airways!
• Not so sweet! Children under the age of 1 year should avoid honey.

References

1. Red Book: 2024–2027 Report of the Committee on Infectious Diseases (33rd Edition); Book chapter: Botulism and Infant Botulism (Clostridium botulinum)
2. Pediatrics: The Journal of American Academy of Pediatrics; Volume 55, Issue 4 (Apr 2025). Global Occurrence of Infant Botulism: 2007–2021. Dabritz, HA; Chung, CH; Read, JS; Khouri, JM.
3. CDC: US Centers for Disease Control and Prevention. Botulinum Neurotoxin Detection and Differentiation by Mass Spectrometry. Volume 11, Number 10—October 2005
4. CDPH. California Department of Public Health. Infant Botulism Treatment and Prevention Program.