Clinical Pearls & Morning Reports
Published January 24, 2024
Signs and symptoms of infant botulism include irritability, constipation, features of bulbar palsies (a weak cry, ptosis in both eyes, and poor feeding), lethargy, weakness, and respiratory difficulties. Bulbar and facial muscle weakness may mask the clinical signs typically associated with respiratory distress, such as facial grimacing or nasal flaring. Read the NEJM Case Records of the Massachusetts General Hospital here.
Q: What are the different ways that Clostridium botulinum may be transmitted to humans?
A: The neurotoxins produced mostly by C. botulinum are the drivers of the clinical illness known as botulism. There are multiple C. botulinum transmission categories: the bacterial spores or toxins can be introduced into the body through food consumption (infant botulism, foodborne botulism, or adult intestinal toxemia), through contamination of an infected wound (wound botulism), or iatrogenically (botulism associated with cosmetics or migraine treatment). Overall, botulism is a rare disease in the United States, and infant botulism is the most common transmission category.
Q: Is infant botulism most often caused by exposure to honey?
A: In patients with infant botulism, the ingestion of spores may result in colonization and germination, followed by toxin production and subsequent toxemia. Clearly defined food exposures, such as exposures to honey or corn syrup, account for only a minority of cases. In fact, multiple factors affect the acquisition of the clinical disease, with infants’ gastrointestinal tracts being particularly susceptible. Often, there is a history involving rural living, dust production, or nearby soil perturbation. The incubation period after exposure to spores may be a few days to a few weeks.
A: After sporulation, the enteric botulinum neurotoxin enters the systemic circulation and interrupts the normal signal transmission at the neuromuscular junction. The enteric botulinum neurotoxin irreversibly binds a specific receptor on the presynaptic peripheral cholinergic nerve terminal and then enters the cell, breaking down a critical protein associated with exocytosis and interrupting the release of the neurotransmitter acetylcholine into the intersynaptic space. Once cleaved, this exocytosis-associated protein complex requires up to 4 weeks to regenerate, which explains the protracted course of the illness.
A: The diagnosis of botulism is typically made with the detection of enteric botulinum neurotoxin in stool. This test is generally available only through local departments of public health, and it may take several days for the results to become available. Therefore, it is not appropriate to delay the administration of the antitoxin while waiting for the diagnosis to be microbiologically confirmed. Early recognition of the illness and prompt administration of medication, preferably within 7 days after symptom onset, are imperative to increase the likelihood of a good outcome. Infant botulism is treated with human-derived anti–botulism toxin antibodies (infant botulism immune globulin, known as BabyBIG). BabyBIG antibodies do not penetrate the neuron, so it is critical to administer the antitoxin as soon as possible, before enteric botulinum neurotoxin enters the cell.