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Suspect infantile botulism in a previously healthy infant, typically aged 2-4 months, presenting with symptoms such as difficulty in sucking, swallowing, weak cry, and breathing difficulties, especially if these symptoms are accompanied by constipation and generalized weakness.[1-2]
Early signs include constipation, poor feeding with a weak suck, and a weak cry, progressing to more severe symptoms like difficulty in breathing due to respiratory muscle weakness.[2]
Clinical examination may reveal diminished gag, suck, and corneal reflexes, oculomotor palsies, and a loss of head control.[1]
The condition can rapidly progress to severe complications such as respiratory failure, necessitating immediate medical intervention.[3]
Diagnosis often starts with ruling out other conditions such as sepsis, and a detailed cranial nerve examination can be crucial.[1]
Treatment involves supportive care and administration of Human Botulism Immune Globulin Intravenous (BIG-IV) as early as possible.[3]
Additional info
Infant botulism is a serious condition that requires a high index of suspicion for early diagnosis and prompt treatment. The initial symptoms can be subtle and easily overlooked, which can delay diagnosis and treatment. The condition is caused by ingestion of spores of Clostridium botulinum, which then produce botulinum neurotoxin in the infant's intestines. This toxin leads to neuroparalytic symptoms, starting typically with constipation and followed by a series of bulbar and motor symptoms. Due to the potential for rapid progression to respiratory failure, immediate intervention with BIG-IV is recommended to neutralize circulating toxin. Ongoing research aims to improve treatment options and outcomes for affected infants. Awareness and early recognition of the clinical signs of infant botulism are crucial for timely and effective management.
References
Reference 1
1.
Schleiss, Mark R. (2025). Botulism
(Clostridium botulinum). In Nelson Textbook of Pediatrics (pp. 1817). DOI: 10.1016/B978-0-323-88305-4.00256-X
Infant botulism requires a high index of suspicion for early diagnosis (Table 256.1). “Rule-out sepsis” remains the most common admission diagnosis. If a previously healthy infant (usually 2-4 months of age) demonstrates weakness with difficulty in sucking, swallowing, crying, or breathing, infant botulism should be considered a likely diagnosis. A careful cranial nerve examination is then quite helpful. Rare instances of co-infection withClostridioides difficile,respiratory syncytial virus, or influenza virus have occurred.
Paradoxically, the pupillary light reflex may be unaffected until the child is severely paralyzed, or it may be initially sluggish. Loss of head control is typically a prominent sign. Opisthotonos may be observed. Respiratory arrest may occur suddenly from airway occlusion by unswallowed secretions or from obstructive flaccid pharyngeal musculature. Death from botulism results either from airway obstruction or paralysis of the respiratory muscles. Occasionally, the diagnosis of infant botulism is suggested by a respiratory arrest that occurs after the infant is curled into position for lumbar puncture or after the administration of an aminoglycoside antibiotic administered for suspected sepsis (see later).
In mild cases or in the early stages of illness, the physical signs of infant botulism may be subtle and easily missed. Eliciting cranial nerve palsies and fatigability of muscular function requires careful examination. Ptosis may not be seen unless the head of the child is kept erect.
These symptoms are thought to result from metabolic by-products of growth ofC. botulinumor from the presence of other toxic contaminants in the food, because GI distress is rarely observed in wound botulism. Constipation may occur in food-borne botulism once flaccid paralysis becomes evident. Illness usually begins 12-36 hours after ingestion ofthe contaminated food but can range from as short as 2 hours to as long as 8 days. The incubation period inwound botulismis 4-14 days. Fever may be present in wound botulism but is absent in food-borne botulism unless a secondary infection (often pneumonia) is present. All forms of botulism display a wide spectrum of clinical severity, from the very mild, with minimal ptosis, flattened facial expression, minor dysphagia, and dysphonia, to the fulminant, with rapid onset of extensive paralysis, frank apnea, and fixed, dilated pupils.Fatigability with repetitive muscle activityis the clinical hallmark of botulism.
Infant botulismdiffers in apparent initial symptoms of illness only because the infant cannot verbalize them. Clinical progression can be more rapid and more severe in very young infants. The incubation period in infant botulism is estimated to be 3-30 days. Usually, the first indication of illness is a decreased frequency or even absence of defecation, and indeed, constipation may be the chief complaint (although this sign is also frequently overlooked). Parents typically notice inability to feed, lethargy, weak cry, and diminished spontaneous movement. Dysphagia may be evident, and an increase in secretions drooling from the mouth may be noted. Gag, suck, and corneal reflexes all diminish as the paralysis advances. Oculomotor palsies may be evident. Paradoxically, the pupillary light reflex may be unaffected until the child is severely paralyzed, or it may be initially sluggish. Loss of head control is typically a prominent sign. Opisthotonos may be observed.
Reference 2
2.
Elsevier ClinicalKey Clinical Overview
Diagnosis
Infant botulism cases are usually reported as isolated cases
Most cases occur between ages 2 and 8 months
Historical symptoms of infant botulism include the following:
Constipation
Difficulty feeding with poor suck
Weak cry
Irritability
Loss of control of neck muscles
Classic historical symptoms of botulism in children (beyond infancy) and adults
Diplopia
Blurred vision
Symptoms of bulbar palsy
Dysarthria
Dysphonia
Dysphagia
Respiratory
Dyspnea
Cough
Genitourinary
Urinary retention secondary to smooth muscle paralysis
Gastrointestinal
Gastrointestinal symptoms are absent in wound botulism
In other types of botulism, symptoms are as follows:
Nausea
Dry mouth
Dysphagia
Constipation caused by toxin effect on parasympathetic autonomic ganglia
If diarrhea occurs together with foodborne botulism, it is most likely secondary to another agent in the food causing loose, watery stools
Foodborne botulism has been reported in outbreaks involving more than 1 person
Symptoms typically begin 12 to 36 hours after ingestion of the preformed toxin
Wound botulism is usually reported as an isolated case
Symptoms typically begin 4 to 14 days after exposure to the toxin
Inhalational botulism
Symptoms typically begin 12 to 72 hours after inhalation of the preformed toxin
Diagnosis
Classic signs of infant botulism
Generalized weakness and descending (global) hypotonia
Weak cry
Weak suck-swallow reflex
Hypoxia and respiratory distress attributable to respiratory muscle weakness
Classic signs of all forms of botulism in children (beyond infancy) and adults
Neurologic
Acute, symmetric, descending flaccid paralysis
Bulbar palsy
Ptosis (bilateral)
Mydriatic, sluggishly reactive pupils
Clear sensorium
Preservation of sensation
Cardiac
Bradycardia in the setting of hypotension
Respiratory
Respiratory thoracic muscle and diaphragmatic dysfunction progressing to hypoventilation and apnea
Absence of fever (unless concomitant infection present, as in the case of cellulitis and wound botulism)
Terminology
Botulism is a paralytic neuromuscular disease caused by the botulinum toxin, one of the most potent neurotoxins in the world
Clostridium botulinum , a gram-positive anaerobe, is the most common source of the neurotoxin
In adults, presents with initial onset of bilateral cranial neuropathies followed by symmetric descending weakness
In infants, presents with difficulty feeding, weak cry, irritability, and hypotonia
Infant botulism (IB) is defined as a potentially life-threatening neuroparalytic disorder affecting children younger than 12 months. It is caused by ingestion of food or dust contaminated by spores, which germinate in the infant's large bowel and produce botulinum neurotoxin. Although the real impact of IB is likely underestimated worldwide, the USA has the highest number of cases. The limited reporting of IB in many countries is probably due to diagnostic difficulties and nonspecific presentation. The onset is usually heralded by constipation, followed by bulbar palsy, and then by a descending bilateral symmetric paralysis; ultimately, palsy can involve respiratory and diaphragmatic muscles, leading to respiratory failure. The treatment is based on supportive care and specific therapy with Human Botulism Immune Globulin Intravenous (BIG-IV), and should be started as early as possible. The search for new human-like antibody preparations that are both highly effective and well tolerated has led to the creation of a mixture of oligoclonal antibodies that are highly protective and can be produced in large quantities without the use of animals. Ongoing research for future treatment of IB involves the search for new molecular targets to produce a new generation of laboratory-produced antitoxins, and the development of new vaccines with safety and efficacy profiles that can be scaled up for clinical use. This narrative literature review aims to provide a readable synthesis of the best current literature on microbiological, epidemiological and clinical features of IB, and a practical guide for its treatment.