Infantile Botulism


Article Author:
Ngoc Van Horn


Article Editor:
Megan Street


Editors In Chief:
Chaddie Doerr


Managing Editors:
Avais Raja
Orawan Chaigasame
Carrie Smith
Abdul Waheed
Khalid Alsayouri
Kyle Blair
Trevor Nezwek
Radia Jamil
Erin Hughes
Patrick Le
Anoosh Zafar Gondal
Saad Nazir
William Gossman
Hassam Zulfiqar
Navid Mahabadi
Hussain Sajjad
Steve Bhimji
Muhammad Hashmi
John Shell
Matthew Varacallo
Heba Mahdy
Ahmad Malik
Sarosh Vaqar
Mark Pellegrini
James Hughes
Beata Beatty
Daniyal Ameen
Altif Muneeb
Beenish Sohail
Nazia Sadiq
Hajira Basit
Phillip Hynes
Komal Shaheen
Sandeep Sekhon


Updated:
2/17/2019 9:06:50 AM

Introduction

Infantile botulism is caused by Clostridium botulinum, which is an anaerobic spore-forming, gram-positive bacillus. [1][2][3][4]It can be found in the soil, water, and air with a lethal toxin dosage as low as 1mcg/kg. Botulism infection can occur in five different ways:

  • Foodborne botulism: When a person ingests the preformed toxin.
  • Infant botulism: This has occurred in a small population of infants (children under the age of 1 year) who have C. botulinum colonization in their gastrointestinal tract.
  • Wound botulism: When infected wounds contain C. botulinum, and they secrete the toxin.
  • Iatrogenic botulism: This occurs when cosmetic or therapeutic procedures that use the C. botulinum toxin cause systemic intoxication.
  • Intestinal colonization: When a person over the age of 1 year harbors the C. botulinum toxin within the gastrointestinal tract (infantile botulism in children and adults).

Even though there are multiple ways to contact botulism, only three main serotypes are responsible for all of these infections:

  • Type A: predominantly found west of the Mississippi River
  • Type B: predominantly found east of the Mississippi River
  • Type E: found in the Pacific Northwest with a preponderance in Alaska

Etiology

Infantile botulism, ithe most common form of botulism infection, predominates 70% of all new cases of botulism annually. Infants will ingest contaminated milk or food, and the neurotoxin will colonize and replicate in the large intestine. Infantile botulism is caused equally by Type A and Type B serotypes. Foodborne botulism is rarely a childhood illness and is often seen in clusters.[5][6][7][8]

Epidemiology

Infantile botulism infection is responsible for approximately 70% of all new botulism cases a year. In the United States (US) alone, 1.9/100,000 live births yield approximately 77 new cases annually. There is an equal distribution of males and females. Risk factors for infantile botulism include higher birth weights, infants of mothers of advanced maternal age, and breastfed infants. Over 50% of the new cases of infantile botulism in the past 30 years have occurred in California.

The C. botulism toxin is the been most implicated in infected food and dust particles. There is a strong association with foods that have been canned and preserved at home or with incorrect sterilization technique or poor refrigeration. Approximately 20% of cases involve honey or corn syrup. How the spores are transported in these foods is still unclear. Also, living near construction sites with excessive dust particles and vacuum cleaner debris has also been implicated in infections.

Pathophysiology

The active form of the C. botulinum spore produces a neurotoxin that causes descending paralysis. This active form is made of polypeptide chains connected with disulfide bonds. The toxin will enter the presynaptic nerve terminals where it prevents the release of acetylcholine by blocking calcium channels. The resulting action causes an overall decrease of acetylcholine at the neuromuscular junction and leads to flaccid paralysis. Traditionally, the toxin will first affect bulbar musculature than somatic musculature.

Histopathology

Clostridium botulinum is a gram-positive anaerobic bacillus that is spore forming. The inactive state is also heat-resistant.

History and Physical

Parents often describe their infant as having poor feeding, lethargy, a weak cry, and constipation. Babies can present with ptosis in the face and eyes, excessive drooling due to weak suck reflex, and shallow breathing due to respiratory suppression. The classic presentation is characterized by a “floppy baby.”

Progression of the infection shows advanced symptoms of toxin infestation including descending bilateral, symmetric paralysis and bulbar palsies (diplopia, dysarthria, dysphonia, and dysphagia). Many breastfed mothers notice breast engorgement due to their infant’s poor feeding and poor suck. These symptoms can be subtle, especially since constipation, poor feeding, and drooling are all symptoms commonly brought up. Anal sphincter tone will be relaxed and decreased. Deep tenor reflexes can be either diminished or normal. Sensation will be intact but can be hard to distinguish due to weakened muscular tone. Usually, the mental status will be preserved.

Some symptoms may not be obvious until neuromuscular fatigue sets in. Muscular fatigue tests include the following:

  • Place the patient in a dark room and note the rapidity of the pupillary constriction with a light. Do this multiple times and note if there is sluggishness to the pupil constriction over two to three minutes.
  • With a clean-gloved finger, note the infant’s suck reflex over time. If the patient is infected, the suck reflex will diminish over time.

Evaluation

The diagnosis should always be suspected with a clinically floppy infant or a history and physical with consistent findings. The reasoning is that routine lab tests are often normal. There may be secondary lab findings due to associated sequela from the botulism infection.[9][10][11]

To confirm the diagnosis, both a stool culture and direct toxin assay are required. Toxin assay can be obtained from the stool, serum, or gastric contents. A stool culture can be obtained with an enema but not glycerin suppositories. Stool samples can be put into a sterile urine container. Do not put stool samples in containers with preservatives. They can be stored in a refrigerator prior to being sent but should not be frozen. Results for the direct toxin specimen are often available the morning after the specimen has been received. Stool culture results can vary from one week to one month. 

No imaging is required to make the diagnosis. Testing of the infected food can be done, however, results are often inconclusive and or delayed.

Treatment / Management

Until the diagnosis is confirmed, continue supportive care for the patient. With any patient, first assess and stabilize airway, breathing, and circulation. Approximately 50% of infantile botulism cases will require intubation and an advanced airway regardless of whether they are treated with Botulism Immune Globulin Intravenous (Human); however, those who are not treated may require mechanical ventilation longer. As a result, a clinician should have a very low threshold to intubate a patient. This will require careful monitoring and admission to the intensive care unit.

If trying to decide if the patient requires an advanced airway, the best way to measure respiratory depression at the bedside is with the use of a continuous end-tidal carbon dioxide monitor. To help combat the respiratory distress, patients should be placed in Trendelenburg position at a 20-degree angle with a neck roll to stabilize the neck, cervical spine, and prevent sliding. If the patient has a decreased gag reflex, he or she is at increased risk for aspiration.

Human botulinum neurotoxin a/b immune globulin has shown to decrease the length of hospital stay and length of mechanical ventilation. It is a single dose treatment that is infused intravenously over 30 minutes.

There is no indication for the use of antibiotics in infantile botulism. Further supportive care involving ventilation, nutrition, and position are also essential in the patient’s care.

Differential Diagnosis

  • Sepsis
  • Electrolyte imbalance/dehydration (hypoglycemia, hyponatremia, hyperkalemia)
  • Metabolic disorder and encephalopathy
  • Congenital myopathy
  • Leigh disease
  • Myasthenia gravis
  • Guillain-Barre Syndrome

Prognosis

Prognosis is good with recognition and administration of Human Botulism Immune Globulin Intravenous. After hospitalization, patients need to follow up with neurology and physical therapy. Most cases of infantile botulism result in complete recovery within several months to a year.

Pearls and Other Issues

  • Following resolution of the illness, all live-virus vaccinations should be delayed by 5 months.
  • There have been no cases in which infected babies with resolved cases of infantile botulism have had a recurrence.
  • If the baby was treated with BabyBIG, they have a protective level of toxin-neutralizing antibody 6 months following administration.
  • Any subsequent siblings of infected babies do not have an increased chance of contracting infantile botulism.
  • Following discharge from the hospital, strict hand washing and special handling of soiled diapers of these babies should be practiced because they can continue to shed the toxin for weeks to months.

Enhancing Healthcare Team Outcomes

The diagnosis and management of infantile botulism is done with a multidisciplinary team that consists of a pediatrician, nurse practitioner, primary care provider, anesthesiologist, and an infectious disease specialist. Until the diagnosis is confirmed, continue supportive care for the patient. With any patient, first assess and stabilize airway, breathing, and circulation. Approximately 50% of infantile botulism cases will require intubation and an advanced airway regardless of whether they are treated with Botulism Immune Globulin Intravenous (Human); however, those who are not treated may require mechanical ventilation longer. As a result, a clinician should have a very low threshold to intubate a patient. This will require careful monitoring and admission to the intensive care unit.

Human botulinum neurotoxin a/b immune globulin has shown to decrease the length of hospital stay and length of mechanical ventilation. It is a single dose treatment that is infused intravenously over 30 minutes. With treatment, most infants do recover, but many may require physical therapy for months or even years. Fortunately, recurrence is very rare. Mothers should be educated on the importance of hand washing.[12][13][14] (Level V)

 


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Infantile Botulism - Questions

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Which sign is not associated with infant botulism?



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Which of the following is the most common cause of flaccid paralysis in infants?



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What is the best management of infantile botulism?



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Which of the following findings is NOT expected to occur with infantile botulism?



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Ingestion of which of the following causes infant botulism?



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A 4 month old is brought in with weakness and constipation for 6 days. The exam is remarkable for decreased tone, sluggish pupils, drooping eyelids, and decreased reflexes. Select the most likely diagnosis.



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Which of the following is incorrect about infant botulism?



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A 4-week-old previously healthy female infant develops constipation, feeding difficulties, and failure to thrive. The exam shows generalized hypotonia, ptosis, weak cry, and dilated pupils that react poorly to light. What is the most likely diagnosis?



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Which of the following statements about infant botulism is true?



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An infant has had a one-week history of constipation. He then has difficulty feeding and facial diplegia. Because of colic, the mother has been giving the infant weak chamomile tea with honey. Select the most likely diagnosis.



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A 5-month-old male is brought in with lethargy, a weak cry, and poor feeding. There have been no fevers, congestion, vomiting or diarrhea. The infant has not had a bowel movement in 3 days. Normally, the patient takes 6 oz. per feeding but only has been taking 2 oz. The mother is concerned the infant has been unable to hold her head up and has been less active. Exam shows no fever, normal vital signs, and no obvious distress. The child is alert, mucosa is clear, and the anterior fontanelle is flat. Cardiopulmonary exam is normal. Abdomen is soft without masses. Neurologic exam shows reactive pupils, decreased tone, and decreased gag. There is notable head lag and diminished DTRs. What is the most likely diagnosis?



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A 5-month-old female is brought in with lethargy, a weak cry, and poor feeding. There has been no fever, congestion, vomiting, or diarrhea. The infant has not had a bowel movement in 3 days. Normally, the patient takes 6 ounces per feeding but only has been taking 2 ounces. The mother is concerned because the infant has been unable to hold his head up and has been less active. Past medical history is unremarkable. The delivery was uncomplicated and neonatal screening and vaccinations are up to date. Exam shows no fever, normal vital signs, and no obvious distress. The child is alert, the oral mucosa is clear, and the anterior fontanelle is flat. The cardiopulmonary exam is normal. The abdomen is soft without masses. Neurologic exam shows reactive pupils, decreased tone, and decreased gag. There is notable head lag and diminished deep tendon reflexes. What is the most appropriate test?



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An infant is suspected of having botulism. The stool sample for botulinum toxin must be sent to the Centers for Disease Control and Prevention for confirmation. Which of the following tests would be helpful while awaiting the toxin results?



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What are clinical signs of infantile botulism?



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Which of the following causes the symptoms of infantile botulism?



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How do most infants get botulism?



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Which patient has the greatest risk of infant botulism?



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Which of the following is not a potential complication of infant botulism?



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An 8-month old previously healthy male who is fully vaccinated is brought to the emergency department for lethargy. The vital signs are temperature 99.6 F, respiratory rate 9/minute, pulse 106 bpm, blood pressure 95/50 mmHg, and pulse oximetry 75% on room air. His eyes are dilated and his breathing is shallow. There are no rashes or signs of trauma. The parents deny that he could have gotten into anything but do state that they recently gave the child some canned peaches from last year’s harvest. The patient has minimal response to painful stimuli and when he has a weak gag reflex. What should be done initially?



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An 8-month old previously healthy male who is fully vaccinated is brought to the emergency department for lethargy. The vital signs are temperature 99.6 F, respiratory rate 9/minute, pulse 106 bpm, blood pressure 95/50 mmHg, and pulse oximetry 75% on room air. His eyes are dilated and his breathing is shallow. There are no rashes or signs of trauma. The parents deny that he could have gotten into anything but do state that they recently gave the child some canned peaches from last year’s harvest. The patient has minimal response to painful stimuli and when he has a weak gag reflex. While waiting to perform a rapid sequence intubation (RSI) and pre-oxygenating the patient, you notice what other clinical findings?



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An 8-month old previously healthy male who is fully vaccinated is brought to the emergency department for lethargy. The vital signs are temperature 99.6 F, respiratory rate 9/minute, pulse 106 bpm, blood pressure 95/50 mmHg, and pulse oximetry 75% on room air. His eyes are dilated and his breathing is shallow. There are no rashes or signs of trauma. The parents deny that he could have gotten into anything but do state that they recently gave the child some canned peaches from last year’s harvest. The patient has minimal response to painful stimuli and when he has a weak gag reflex. After the patient is stabilized and placed on mechanical ventilation, what tests are required to make the diagnosis?



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An 8-month old previously healthy male who is fully vaccinated is brought to the emergency department for lethargy. The vital signs are temperature 99.6 F, respiratory rate 9/minute, pulse 106 bpm, blood pressure 95/50 mmHg, and pulse oximetry 75% on room air. His eyes are dilated, and his breathing is shallow. There are no rashes or signs of trauma. The parents deny that he could have gotten into anything but do state that they recently gave the child some canned peaches from last year’s harvest. The patient has minimal response to painful stimuli and when he has a weak gag reflex. After the patient is stabilized and placed on mechanical ventilation, what is the definite treatment that can decrease hospital stay and days requiring mechanical ventilation?



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An infant presents with constipation, a diminished gag reflex, lethargy, and weak neck muscles. Which of the following would not be expected?



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Infantile Botulism - References

References

Kuehn B, Wound Botulism Outbreak. JAMA. 2019 Feb 12;     [PubMed]
Fortunato F,Martinelli D,Cappelli MG,Taurisano P,Barbuti G,Quarto M,Prato R, Food-borne botulism in Apulia region, Italy: an expert witness testimony. Annali di igiene : medicina preventiva e di comunita. 2019 Mar-Apr;     [PubMed]
Ibatullin RA,Magjanov RV, Case of iatrogenic botulism after botulinotherapy in clinical practice. Terapevticheskii arkhiv. 2018 Nov 22;     [PubMed]
Karsen H,Ceylan MR,Bayındır H,Akdeniz H, Foodborne botulism in Turkey, 1983 to 2017. Infectious diseases (London, England). 2019 Jan 21;     [PubMed]
Poulain B,Popoff MR, Why Are Botulinum Neurotoxin-Producing Bacteria So Diverse and Botulinum Neurotoxins So Toxic? Toxins. 2019 Jan 11;     [PubMed]
Lyons-Warren AM,Risen SR,Clark G, Infant Botulism With Asymmetric Cranial Nerve Palsies. Pediatric neurology. 2018 Nov 30;     [PubMed]
Peak CM,Rosen H,Kamali A,Poe A,Shahkarami M,Kimura AC,Jain S,McDonald E, Wound Botulism Outbreak Among Persons Who Use Black Tar Heroin - San Diego County, California, 2017-2018. MMWR. Morbidity and mortality weekly report. 2019 Jan 4;     [PubMed]
Ni SA,Brady MF, Botulism Antitoxin 2018 Jan;     [PubMed]
Walsh K, Case reports on dangerous infectious diseases: a review of patient consent. Journal of the Royal Army Medical Corps. 2018 Jun 29;     [PubMed]
Sobel J,Rao AK, Making the Best of the Evidence: Toward National Clinical Guidelines for Botulism. Clinical infectious diseases : an official publication of the Infectious Diseases Society of America. 2017 Dec 27;     [PubMed]
Wendt S,Eder I,Wölfel R,Braun P,Lippmann N,Rodloff A, [Botulism: Diagnosis and Therapy]. Deutsche medizinische Wochenschrift (1946). 2017 Sep;     [PubMed]
O'Horo JC,Harper EP,El Rafei A,Ali R,DeSimone DC,Sakusic A,Abu Saleh OM,Marcelin JR,Tan EM,Rao AK,Sobel J,Tosh PK, Efficacy of Antitoxin Therapy in Treating Patients With Foodborne Botulism: A Systematic Review and Meta-analysis of Cases, 1923-2016. Clinical infectious diseases : an official publication of the Infectious Diseases Society of America. 2017 Dec 27;     [PubMed]
Griese SE,Kisselburgh HM,Bartenfeld MT,Thomas E,Rao AK,Sobel J,Dziuban EJ, Pediatric Botulism and Use of Equine Botulinum Antitoxin in Children: A Systematic Review. Clinical infectious diseases : an official publication of the Infectious Diseases Society of America. 2017 Dec 27;     [PubMed]
Pirazzini M,Rossetto O, Challenges in searching for therapeutics against Botulinum Neurotoxins. Expert opinion on drug discovery. 2017 May;     [PubMed]

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