History and exam
Key diagnostic factors
common
presence of risk factors
Key risk factors include ingestion of contaminated foods, infant age group, and biological terrorism.
blurred vision and diplopia
Paralysis of cranial nerves III, IV, and VI.
impaired accommodation
Paralysis of cranial nerves III, IV, and VI.
ptosis
Paralysis of cranial nerves III, IV, and VI.
oculobulbar weakness
Oculobulbar weakness is an early feature of botulism. Absence indicates an alternative diagnosis.
Presents as blurred vision, diplopia, dysarthria, and dysphagia.
Affected infants develop feeding difficulties and a weakened cry.
hypoglossal weakness
Involvement of cranial nerves IX, X, and XII.
dysarthria
Involvement of cranial nerves IX, X, and XII.
dysphagia
Involvement of cranial nerves IX, X, and XII.
symmetrical descending flaccid paralysis
Affects the voluntary muscles of the neck, shoulders, and upper extremities, followed by the proximal and distal lower extremities.
Deep tendon reflexes, initially present, diminish or disappear within a few days of infection.
Respiratory dysfunction may result from diaphragmatic and accessory muscle weakness.
Other diagnostic factors
common
hypotonia
Sign of bulbar and extremity weakness in infants.
feeding difficulties in infants
Symptom of bulbar and extremity weakness in infants.
weakened cry in infants
Symptom of bulbar and extremity weakness in infants.
hypothermia
May be a presenting manifestation of autonomic dysfunction.
urinary retention
May be a presenting manifestation of autonomic dysfunction.
constipation
dry mouth and throat
May be a presenting manifestation of autonomic dysfunction.
postural hypotension
May be a presenting manifestation of autonomic dysfunction.
gastrointestinal illness
Abdominal cramps, nausea, vomiting, and diarrhoea may also occur within 2 to 36 hours of ingestion of contaminated food, although these symptoms are often attributed to coincidental non-Clostridium pathogens.[47]
diminished or absent deep tendon reflexes
Initially present; diminish or disappear within a few days of infection.
absence of fever
The presence of fever should prompt consideration of an alternative diagnosis or of more than one infectious process.
uncommon
respiratory dysfunction
May result from either upper airway obstruction (pharyngeal collapse due to cranial nerve involvement) or diaphragmatic and accessory muscle weakness.
pupillary dilation
Pupillary dilation occurs in <50% of cases.[47] Its absence does not diminish the likelihood of botulism.
Risk factors
strong
ingestion of contaminated foods
infant age group
Infant botulism occurs with toxin types A, B, or F. It is the most common form of the disease, and in 2017 there were 141 confirmed or probable paediatric cases in the US. CDC: national botulism surveillance Opens in new window In England and Wales between 1975 and 2013, 16 cases of infant botulism were reported.[5]
Infection occurs as a consequence of absorption of toxin produced by Clostridium botulinum in situ. The organism colonises the intestine of infants aged 6 days to 12 months in the absence of competing normal flora found in children and adults.[39]
Due to the micro-environment of the infant intestinal tract, ingested spores are able to germinate and the bacteria is then able to produce the toxin. In adults, spores are not able to germinate.
Infant botulism is often attributed to honey ingestion. Other sources, including contaminated soil, have also emerged.
biological terrorism
A deliberate release of botulinum toxin should be suspected if patients with acute flaccid paralysis and prominent bulbar palsies present in large numbers. An unusual toxin type (i.e., C, D, F, or G) or symptoms among patients with a common geographical location may also suggest an act of bioterrorism.
weak
ingestion of honey in infants
Infant botulism is often attributed to honey ingestion, but since the feeding of honey to infants has been discouraged the number of cases has decreased.
ingestion of soil in infants
Clostridium botulinum spores are found throughout the world in soil samples. Ingestion of soil is a potential cause of botulism in infants.
intravenous drug use
Wound botulism has been associated almost exclusively with injection drug users of 'black tar' heroin, first reported in the US in the 1990s.
Contamination of the heroin during preparation leads to infection, particularly in patients who inject via 'skin popping' (drug injection into tissue rather than the vein).[15][16][17]
Several similar cases have been reported in Europe since 2000.[36][37][38]
crush injury
May predispose patients to wound botulism.
May be caused by either type A or type B toxins, and is the result of wound contamination by Clostridium botulinum spores. Subsequent germination and toxin production lead to abscess formation and a clinical syndrome comparable with foodborne disease.
abnormal bowel anatomy
In rare instances, adults become colonised with, and subsequently infected by, toxin-producing Clostridium botulinum,leading to gastrointestinal disease.
Adults at risk include those with loss of bowel flora due to anatomical abnormalities, functional disorders, or antibiotic use.
In Italy, cases of toxin E production by Clostridium butyricum were discovered in association with Meckel's diverticulum.[40]
therapeutic or cosmetic use of botulinum toxin
Rare cases of iatrogenic botulism have been reported among children after the therapeutic use of toxin type B for spastic quadriparesis or the use of toxin type A to reduce spasticity and dystonia associated with cerebral palsy.[19][41]
In addition, iatrogenic botulism cases have been reported with the unlicensed cosmetic use of botulinum toxin A.[20]
exposure to reptiles
There have been reports of botulism caused by Clostridium butyricum (producing botulinum neurotoxin type E) in young children exposed to pet reptiles, notably terrapins.[42]
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