Pediatric Neurology 52 (2015) 487e492

Contents lists available at ScienceDirect

Pediatric Neurology
journal homepage: www.elsevier.com/locate/pnu

Topical Review

Infant Botulism: Review and Clinical Update

Laura K. Rosow MD a, *,1, Jonathan B. Strober MD b
a
Department of Neurology, University of California San Francisco, San Francisco, California
b
Department of Pediatric Neurology, University of California San Francisco, San Francisco, California

abstract

Botulism is a rare neuromuscular condition, and multiple clinical forms are recognized. Infant botulism was first
identified in the 1970s, and it typically occurs in infants younger than 1 year of age who ingest Clostridium botulinum
spores. A specific treatment for infant botulism, intravenous botulism immunoglobulin (BIG-IV or BabyBIGÒ), was
developed in 2003, and this treatment has substantially decreased both morbidity and hospital costs associated
with this illness. This article will review the pathogenesis of infant botulism as well as the epidemiology, clinical
manifestations, diagnosis, and treatment of this condition.

Keywords: botulism, infant, review, Clostridium, botulinum, infantile, paralysis

Pediatr Neurol 2015; 52: 487-492
Ó 2015 Elsevier Inc. All rights reserved.

Introduction by subtypes A and B.3-5 Botulinum-like toxins E and F are

Botulism is a rare neuromuscular disorder resulting from
toxins produced by Clostridium botulinum bacteria. Infant
botulism, first recognized in 1976, typically affects children
younger than 1 year of age.1 It is the most common clinical
form of botulism in the United States, with between 70 and
100 cases recognized annually.2 Infant botulism usually
presents as a combination of hypotonia, bulbar weakness,
and flaccid paralysis of the skeletal muscles, although a
broad range of clinical presentations is possible.
Etiology and pathogenesis
C. botulinum is a sporulating, obligate anaerobic, gram-
positive bacillus present in soil and aquatic sediment.
Seven distinct subtypes exist, depending upon the neuro-
toxin produced, and these are arbitrarily named A-G. Only
subtypes A, B, E, and F cause disease in humans, and almost
all cases of infant botulism in the United States are caused
Article History:
Received October 6, 2014; Accepted in final form January 13, 2015
* Communications should be addressed to: Dr. Rosow; Brigham and
Women’s Department of Neurology; 75 Francis St; Boston, MA 02115.
E-mail address: laura.rosow@gmail.com
1
Present address: Brigham and Women’s Department of Neurology,
Boston, Massachusetts
produced by Clostridium baratii and Clostridium butyricum
and are only rarely implicated in infant botulism.4,6,7
Infant botulism occurs when the clostridial spores of
C. botulinum are ingested, then germinate and multiply in
the gastrointestinal tract, allowing the release of botuli-
num neurotoxin (BoNT) into the bloodstream. BoNT then
irreversibly binds cholinergic receptors in the presynaptic
cell membrane of voluntary motor and autonomic neuro-
muscular junctions. Normally, neuromuscular trans-
mission occurs when vesicles containing acetylcholine
fuse with the presynaptic terminal membrane via
formation of a fusion complex, releasing acetylcholine into
the synaptic cleft. This fusion complex is made up of
three soluble N-ethylmaleimide-sensitive factor attachment
protein receptor (SNARE) proteins: vesicle-associated
membrane protein (VAMP, also known as synaptobrevin);
syntaxin; and synaptosomal-associated protein 25 (SNAP-
25). After BoNT is taken up into the presynaptic terminal, it
cleaves one of these SNARE proteins, thereby disrupting
formation of the fusion complex and preventing acetylcho-
line release into the cleft. This causes failed neuromuscular
transmission and flaccid paralysis. The particular compo-
nents of the SNARE complex that are targeted vary
depending on BoNT subtype: BoNT subtypes A, C, and E
target SNAP-25; subtypes B, D, F, and G target VAMP/
synaptobrevin; and subtype C additionally targets syntaxin
(Fig 1).8 Botulism is the most potent poison known, with a

0887-8994/$ e see front matter Ó 2015 Elsevier Inc. All rights reserved.
http://dx.doi.org/10.1016/j.pediatrneurol.2015.01.006
488 L.K. Rosow, J.B. Strober / Pediatric Neurology 52 (2015) 487e492

FIGURE 1.
(A) Healthy neuromuscular transmission. Acetylcholine (ACh)-containing vesicles bind to the presynaptic terminal membrane via formation of the soluble
N-ethylmaleimide-sensitive factor attachment protein receptors (SNARE) complex, leading to membrane fusion and release of ACh into the synaptic cleft.
ACh molecules then bind to receptors on the muscle cell, allowing influx of sodium and muscle contraction. (B) Effect of botulinum neurotoxin (BoNT). BoNT
binds receptors on the presynaptic terminal and is endocytosed. The light chain is dissociated from the heavy chain and translocates into the cytoplasm,
where it cleaves specific SNARE proteins according to BoNT subtype. Subtypes A, C, and E target SNAP-25; subtypes B, D, F, and G target vesicle-associated
membrane protein (VAMP); and subtype C further targets syntaxin. (The color version of this figure is available in the online edition.)

lethal dose of only 10 9 mg/kg of body weight. The incu-
bation period of botulism is hypothesized to range between
3 and 30 days.9
There are multiple other recognized clinical forms of
botulism, including wound botulism, in which wounds
become contaminated with C. botulinum spores, and food-
borne botulism, in which preformed toxin is ingested
from contaminated food sources. Adult intestinal toxemia is
an uncommon presentation of botulism that is similar in
pathogenesis to infant botulism, occurring via ingestion of
clostridial spores. Rarely, cases of botulism have also been
reported from inhalational or iatrogenic exposure.10,11 In
the United States, infant botulism is by far the most com-
mon form, constituting approximately 65% of reported
botulism cases per year.12 Outside the United States, infant
botulism is less common.3
Epidemiology and risk factors
The first diagnosis of infant botulism was made in 1976,
although the first known case (diagnosed retrospectively) is
believed to have occurred in California as far back as
1931.1,13 Botulism affects infants ranging from less than
1 week to 1 year of age, with a median age of 10 weeks. Up
to 95% of infant botulism cases occur in children younger
than 6 months of age.14,15 Geographically, the prevalence of
infant botulism in the United States is highest in California,
Utah, and the eastern Pennsylvania-New Jersey-Delaware
area.16,17 Type A disease tends to be more prevalent in the
Western United States, whereas type B disease is more
prevalent in the Eastern United States.5,16 Infants living in
rural/farm environments appear to be at higher risk for
contracting botulism than those living in more urban en-
vironments, presumably because of higher exposure to dust
particles.18 It has been suggested that exposure to soil from
active construction sites may also increase the risk of con-
tracting botulism, whether by living near a construction site
or by having a parent who works in construction; however,
this link has not been conclusively established.19-21
Infants are felt to be particularly susceptible to intestinal
colonization by C. botulinum because of the immaturity of
their gut flora. This concept is supported by animal studies
demonstrating that infant mice experience age-related
susceptibility to botulism colonization of the gastrointes-
tinal tract. Additionally, human infants that experience
transient perturbations in gut flora, such as after weaning
from breast milk, appear to have further increased risk of
intestinal colonization by C. botulinum.16 The risks and
benefits conferred by breastfeeding itself are less clear:
although infants hospitalized for botulism are more likely to
have been breastfed than formula-fed, some studies suggest
that breastfeeding delays the progression of botulism and is
therefore protective.18,22 Formula-fed infants, on the other
hand, tend to develop botulism at earlier ages and may have
a more fulminant presentation.22 Given the relatively rare
occurrence of botulism, current recommendations support
breastfeeding, even in patients who have developed
botulism.23
Ingestion of contaminated honey has been implicated in
a number of cases of infant botulism; however, it is worth
noting that in the majority of cases, a definitive source of
C. botulinum spores is never identified.1,24 In many patients
in whom no source is found, infection is presumed to result
from swallowing spores that adhere to microscopic dust
particles in the air.4 Corn syrup was previously found to
contain C. botulinum spores, but changes in production
practices have apparently eliminated this problem, and no
cases of infant botulism to date have been definitively
attributed to contaminated corn syrup.16,24 Nonetheless, the
American Academy of Pediatrics continues to recommend
 L.K. Rosow, J.B. Strober / Pediatric Neurology 52 (2015) 487e492
against feeding unpasteurized corn syrup to infants
younger than 12 months of age.14
In addition to being a common presenting symptom of
botulism, constipation has been shown to represent an in-
dependent risk factor for botulism in infants older than
2 months of age.18 This is presumably because decreased
colonic motility allows C. botulinum spores further time to
germinate in the gastrointestinal tract and produce toxin.
Clinical manifestations
Clinically, botulism infection can cause a wide spectrum
of presentations in infants, ranging from mild hypotonia to
a combination of bilateral cranial nerve palsies, flaccid pa-
ralysis, and diaphragmatic weakness necessitating me-
chanical ventilation. In some patients, this presentation can
be quite rapid and severe.25,26 Clinical presentations are
often more severe in patients with type A botulism than in
patients with type B botulism, and these patients have a
longer mean hospital stay.27
Typically, the first symptom noted in infant botulism is
constipation (characterized by 3 or more days without
defecation), which is then followed by some combination of
lethargy, decreased spontaneous activity, and diminished
appetite. Infants then go on to experience loss of head
control (from weakness of the neck muscles), followed by
symmetric descending hypotonia and weakness, ultimately
progressing to involve diaphragmatic muscles.27 Approxi-
mately half of patients will require mechanical ventilation
at some point during their hospital course.17 Symmetric
cranial nerve palsies (ptosis, sluggishly reactive pupils,
diminished gag reflex, and bifacial weakness) are often
particularly notable. Muscle stretch reflexes are typically
preserved.17 In advanced illness, autonomic disturbances
may be present, such as decreased heart rate variability.28
The differential diagnosis for infant botulism is broad
and includes various genetic, metabolic, neuromuscular,
and infectious etiologies. Patients may be admitted for “rule
out sepsis” or “failure to thrive.”4 In a study of 681 patients
with strongly suspected botulism, 23 were ultimately found
to have alternate diagnoses. Eight of these patients were
diagnosed with a metabolic disorder, such as mitochondrial
FIGURE 2.
Incremental compound muscle action potential response with 50 Hz repetitive stimulation in a 4-month-old boy with confirmed botulism.
489
disease, maple syrup urine disease, or glutaric aciduria type
I. Spinal muscular atrophy type I was diagnosed in five pa-
tients. Alternate infectious etiologies were found in three
patients (e.g., enterovirus encephalitis, respiratory syncytial
virus bronchiolitis). Additional diagnoses included Miller-
Fisher variant Guillain-Barré syndrome and presumptive
Lambert Eaton syndrome secondary to neuroblastoma.15
Diagnosis
Botulinum toxin is readily detected in stool using a toxin
neutralization bioassay. Following the initial exposure,
toxin may continue to be present in stool for up to several
months.29 If stool is not passed readily because of con-
stipation, gentle manual disimpaction may be attempted, or
a small enema of sterile, nonbacteriostatic water (up to
30 mL) can be used to obtain a specimen.30 Toxin is less
commonly found in serum than in stool and has been
detected in only 1% of US infants with botulism.24
On initial presentation, basic serum studies in the infant
with botulism (complete blood count, chemistry panel) will
typically be normal, or they may demonstrate mild per-
turbations related to dehydration. Cerebrospinal fluid may
show mildly elevated protein, again related to dehydration.4
Magnetic resonance imaging and electroencephalography
are generally not indicated, but if obtained, they will usually
be unremarkable.
Nerve conduction studies and electromyography can be
used to help confirm the botulism diagnosis and to exclude
alternate diagnoses. The following findings on nerve con-
duction studies, taken together, are felt to be highly sug-
gestive of a diagnosis of botulism: decreased amplitude of
compound motor unit action potentials in at least two
muscle groups; tetanic and posttetanic facilitation, defined
by an amplitude of more than 120% of baseline; and pro-
longed posttetanic facilitation longer than 120 seconds,
with absence of posttetanic exhaustion (Fig 2).31 In addi-
tion, there may be a characteristic pattern of brief, small-
amplitude, overly abundant motor action potentials
following stimulation of a muscle.17 Absence of this pattern,
however, does not exclude the diagnosis of botulism.24 On
needle electromyography, one might see fibrillation
490 L.K. Rosow, J.B. Strober / Pediatric Neurology 52 (2015) 487e492
potentials and positive sharp waves as well as low-
amplitude, short-duration motor unit potentials.31
Treatment
Historically, treatment of infant botulism focused on
supportive care because no definitive treatment was
approved for use in infants until relatively recently. In 2003,
the US Food and Drug Administration approved a human-
derived antitoxin for treatment of infant botulism,
dramatically changing the course for patients with this
illness. Intravenous botulism immunoglobulin (BIG-IV or
BabyBIGÒ) consists of immunoglobulin derived from
pooled plasma of donors immunized with pentavalent
botulinum toxoid, and it acts by neutralizing free botulinum
toxin. It has a prolonged half-life of around 28 days. BIG-IV
is administered as a one-time 50-mg intravenous dose, and
each dose is formulated to contain at least 15 IU of
neutralizing antibodies against toxin type A and 4 IU of
neutralizing antibodies against toxin type B. BIG-IV was
developed by the California Department of Health Services
under the Federal Orphan Drug Act, and it is now distrib-
uted on a case-by-case basis by the Infant Botulism Treat-
ment and Prevention Program (www.infantbotulism.org).32
BIG-IV was originally studied in a randomized, placebo-
controlled trial from 1992 to 1997 and then in an open-
label study from 1997 until 2003, after which time the
agent was approved for use.33 Infants were included if they
presented with an acute-onset flaccid paralysis consistent
with botulism and were able to be randomized within
3 days of hospitalization. Confirmatory testing was not
required before initiation of treatment, though all patients
had fecal/enema samples sent for C. botulinum identifica-
tion and typing. Unconfirmed cases and clinical mimics
were excluded from final efficacy analyses, but were still
included in the safety analysis. In all, 129 patients were
randomized for treatment with study drug versus placebo,
and 122 had laboratory-confirmed botulism and were
included in the efficacy analysis. This study found that
treatment with BIG-IV significantly reduced the length of
hospital stay from a mean of 5.7 weeks to 2.6 weeks
(P < 0.001). In addition, duration of intensive care, me-
chanical ventilation, and tube or intravenous feeding were
all significantly reduced in patients treated with BIG-IV. All
of these benefits were present whether patients had botu-
lism subtype A or B. In general, infants who were given
treatment earlier in their illness fared better than those in
whom treatment was delayed. There was no significant
difference in adverse effects found between the BIG-IV and
placebo groups. The only adverse reaction attributed to BIG-
IV was a transient, blush-like rash, which also occurred in
untreated infants, albeit to a lesser extent. Total charges for
hospital stays were significantly decreased in patients
treated with BIG-IV, from $163,400 to $73,800 (USD). BIG-IV
costs a flat fee of $45,300 per patient for a one-time dose;
nonetheless, economic analyses indicate that use of this
agent is quite cost-effective because of the savings incurred
during hospitalization.33-35 In fact, through open-label use
of BIG-IV in California during the study period, it was
calculated that a total of 20.3 years of hospital stay and
$34.2 million of hospital charges were avoided.33 Based on
the results of this study and the low rate of adverse
reactions to BIG-IV, it is generally recommended that all
infants with suspected botulism undergo prompt treatment
with BIG-IV as soon as possible, before confirmatory testing
is obtained. BIG-IV can be obtained by contacting the Infant
Botulism Treatment and Prevention Program’s on-call
physician at any time at (510) 231-7600.
Trivalent equine botulinal antitoxin is the preferred
method of treatment for botulism in adult patients. Use of
this agent is not routinely recommended in infants, given
concerns regarding adverse reactions and lifelong sensiti-
zation to equine proteins.36,37 One longitudinal, retrospec-
tive study in Argentina suggested that equine antitoxin may
represent a safe alternative treatment when treatment with
BIG-IV is not economically feasible.37 It is worth noting,
however, that no randomized, controlled trials on the use of
equine antitoxin in infants have been performed to date,
and no long-term safety data have been collected on this
agent in infants.
Although BIG-IV has significantly altered the course of
treatment for infant botulism, supportive care remains
critically important for reducing immediate complications
and long-term sequelae of infection. In particular, moni-
toring of respiratory function and appropriate use of
endotracheal intubation (for airway protection and for
mechanical ventilation) are important.4 Nonintubated pa-
tients should be positioned with the head of the bed
elevated to 30 above the level of the feet to minimize risks
of aspiration. Enteral feeding should be initiated promptly
and continued through the course of the illness until pa-
tients are able to take food by mouth safely and adequately.2
Electrolytes should be monitored because venous pooling in
the paralyzed infant may lead to significant hyponatremia
from increased secretion of antidiuretic hormone.16,38,39
Patients with severe disease may develop bladder atony
and should be monitored for urinary retention, which can
be alleviated with gentle manual pressure (the “credé
method”).38 Patients should also be monitored carefully for
evidence of Clostridium difficile colitis, which can occur in
infants with colonic stasis from botulism.40,41
Other common infectious complications of botulism in
infants include otitis media, aspiration pneumonia, and
urinary tract infections.2 Judicious antibiotic use in the
setting of superimposed infections is appropriate, but care
should be taken to avoid clostridiacidal antibiotics, which
can increase toxin release and cause clinical deterioration.9
Aminoglycoside medications should also be avoided
because these can potentiate the paralytic effects of toxin by
decreasing acetylcholine release from diaphragmatic nerve
terminals.24,38,42
Prognosis
Recovery ultimately occurs via regeneration of nerve
terminals and motor endplates, with the diaphragm
recovering before peripheral muscles. Recovery can take
from weeks to months, during which time residual hypo-
tonia may be noted.39 In the absence of significant com-
plications, however, the prognosis for a full recovery is
excellent. Infants who stop improving with treatment or
who experience clinical deterioration should be carefully
evaluated for infectious complications or for evidence of
inadequate respiratory or nutritional support. Parents can
 L.K. Rosow, J.B. Strober / Pediatric Neurology 52 (2015) 487e492
be reassured that their children should not experience
significant cognitive sequelae of botulism infection, unless
severe complications have occurred (e.g., hypoxic brain
injury from respiratory insufficiency).23
The mortality rate for infant botulism in the United States
is less than 1%.4 Historically, it has been felt that fulminant,
unrecognized botulism contributes to sudden infant death
syndrome; however, this is an area of controversy. One study
in Germany found that in postmortem analysis, C. botulinum
was isolated in 15 of 72 cases of sudden infant death syn-
drome, suggesting that the cause of death was from undi-
agnosed botulism.43 A 10-year prospective study of sudden
infant death syndrome in Australia, on the other hand, found
no evidence of C. botulinum in stool samples from 248 in-
fants.44 It has been suggested that this variability may be
related to differing regional prevalence of C. botulinum.3
Following hospitalization, parents should be counseled
on meticulous hygiene, particularly with regards to dia-
pering and handwashing, because C. botulinum can be
excreted in the stool for up to several months.23,29 They
should also be advised to defer any live-virus vaccines for
their child (measles, mumps, rubella, varicella) until
5 months after BIG-IV was administered, because the anti-
bodies in BIG-IV will interfere with the effectiveness of the
vaccines. Rotavirus vaccination should also be deferred until
5 months after treatment because of concerns regarding
slowed intestinal motility in botulism patients.23
Conclusion
Infant botulism is a rare, potentially life-threatening
neuromuscular disorder resulting from the ingestion of
C. botulinum spores before 1 year of age. Use of BIG-IV in the
past several years has substantially decreased both
morbidity and hospital costs associated with this illness.
With prompt recognition, timely initiation of treatment,
and meticulous supportive care, infants with botulism
typically go on to make a full recovery.
References
1. Arnon SS, Midura TF, Clay SA, Wood RM, Chin J. Infant botulism.
Epidemiological, clinical, and laboratory aspects. JAMA. 1977;237:
1946-1951.
2. Long SS. Infant Botulism and Treatment With BIG-IV (BabyBIG(r)).
Pediatr Infect Dis J. 2007;26:261-262.
3. Fox CK, Keet CA, Strober JB. Recent advances in infant botulism.
Pediatr Neurol. 2005;32:149-154.
4. Arnon SS. Chapter 159-Infant Botulism. In: Feigin and Cherry’s
Textbook of Pediatric Infectious Diseases. 6th ed. Philadelphia, PA:
Saunders; 2009.
5. Morris Jr JG, Snyder JD, Wilson R, Feldman RA. Infant botulism in the
United States: an epidemiologic study of cases occurring outside of
California. Am J Public Health. 1983;73:1385-1388.
6. Barash JR, Tang TWH, Arnon SS. First case of infant botulism caused
by Clostridium baratii type F in California. J Clin Microbiol. 2005;43:
4280-4282.
7. Lúquez C, Dykes JK, Yu PA, Raphael BH, Maslanka SE. First report
worldwide of an infant botulism case due to Clostridium botulinum
type E. J Clin Microbiol. 2010;48:326-328.
8. Peng Chen Z, Morris J, Rodriguez R, Shukla A, Tapia-Núñez J,
Okun M. Emerging Opportunities for Serotypes of Botulinum Neu-
rotoxins. Toxins. 2012;4:1196-1222.
9. Domingo RM, Haller JS, Gruenthal M. Infant Botulism: Two Recent
Cases and Literature Review. J Child Neurol. 2008;23:1336-1346.
491
10. Roblot F, Popoff M, Carlier JP, et al. Botulism in patients who inhale
cocaine: the first cases in France. Clin Infect Dis. 2006;43:e51-e52.
11. Chertow DS, Tan ET, Maslanka SE, et al. Botulism in 4 adults
following cosmetic injections with an unlicensed, highly concen-
trated botulinum preparation. JAMA. 2006;296:2476-2479.
12. Centers for Disease Control and Prevention. CDC - Botulism, General
Information - NCZVED. 2011. Available at: http://www.cdc.gov/
nczved/divisions/dfbmd/diseases/botulism/#how_common. Accessed
January 12, 2014.
13. Arnon SS, Werner SB, Faber HK, Farr WH. Infant botulism in 1931.
Discovery of a misclassified case. Am J Dis Child. 1979;133:
580-582.
14. Ogle J, Anderson M. Chapter 42. Infections: Bacterial & Spirochetal.
In: CURRENT Diagnosis & Treatment: Pediatrics. 21st ed. New York:
McGraw-Hill; 2012.
15. Francisco AMO, Arnon SS. Clinical Mimics of Infant Botulism. Pedi-
atrics. 2007;119:826-828.
16. Long SS. Infant botulism. Pediatr Infect Dis J. 2001;20:707-709.
17. Thompson JA, Filloux FM, Van Orman CB, et al. Infant botulism in
the age of botulism immune globulin. Neurology. 2005;64:
2029-2032.
18. Spika JS, Shaffer N, Hargrett-Bean N, Collin S, MacDonald KL,
Blake PA. Risk factors for infant botulism in the United States. Arch
Pediatr Adolesc Med. 1989;143:828.
19. Thompson JA, Glasgow LA, Warpinski JR, Olson C. Infant botulism:
clinical spectrum and epidemiology. Pediatrics. 1980;66:936-942.
20. Long SS. Epidemiologic study of infant botulism in Pennsylvania:
Report of the Infant Botulism Study group. Pediatrics. 1985;75:
928-934.
21. Arnon SS, Damus K, Chin J. Infant botulism: epidemiology and
relation to sudden infant death syndrome. Epidemiol Rev. 1981;3:
45-66.
22. Arnon SS, Damus K, Thompson B, Midura TF, Chin J. Protective role
of human milk against sudden death from infant botulism. J Pediatr.
1982;100:568-573.
23. State of California - Health and Human Services Agency. Patient
Management. Infant Botulism Treat. Prev. Program 2010. Available
at: http://www.infantbotulism.org/physician/patient.php. Accessed
January 14, 2014.
24. American Academy of Pediatrics. Botulism and infant botulism
(Clostridium botulinum). In: Red Book Atlas of Pediatric Infectious
Diseases. 28th ed. Elk Grove Village, IL: Pickering LK; 2009.
25. Tsai H-J, Liang W-C, Wang C-H, et al. Botulism with Unusual Rapid
Progression to Complete Paralysis in a Child. Pediatr Neonatol; 2013.
26. Mitchell WG. Catastrophic Presentation of Infant Botulism May
Obscure or Delay Diagnosis. Pediatrics. 2005;116:e436-e438.
27. Arnon SS. Infant botulism. Annu Rev Med. 1980;31:541-560.
28. Patural H, Goffaux P, Paricio C, et al. Infant botulism intoxication
and autonomic nervous system dysfunction. Anaerobe. 2009;15:
197-200.
29. Derman Y, Korkeala H, Salo E, LöNnqvist T, Saxen H, Lindströ MM.
Infant botulism with prolonged faecal excretion of botulinum
neurotoxin and Clostridium botulinum for 7 months. Epidemiol
Infect. 2013;142:335-339.
30. State of California - Health and Human Services Agency. Specimen
Collection. Infant Botulism Treat. Prev. Program 2010. Available at:
http://www.infantbotulism.org/laboratorian/collection.php. Accessed
January 13, 2014.
31. Gutierrez AR, Bodensteiner J, Gutmann L. Topical Review: Electro-
diagnosis of Infantile Botulism. J Child Neurol. 1994;9:362-366.
32. Arnon SS. Creation and Development of the Public Service Orphan
Drug Human Botulism Immune Globulin. Pediatrics. 2007;119:
785-789.
33. Arnon SS, Schechter R, Maslanka SE, Jewell NP, Hatheway CL. Hu-
man botulism immune globulin for the treatment of infant botu-
lism. N Engl J Med. 2006;354:462-471.
34. State of California - Health and Human Services Agency. Invoice and
purchase agreement for BabyBIG(r). Infant Botulism Treat. Prev.
Program 2011. Available at: http://www.infantbotulism.org/
physician/IPA-2013.pdf. Accessed January 11, 2014.
35. May MLA, Corkeron MA, Stretton M. Infant botulism in Australia:
availability of human botulinum antitoxin for treatment. Med J Aust.
2010;193:614-615.
36. Black RE, Gunn RA. Hypersensitivity reactions associated with
botulinal antitoxin. Am J Med. 1980;69:567-570.
492 L.K. Rosow, J.B. Strober / Pediatric Neurology 52 (2015) 487e492

37. Vanella de Cuetos EE, Fernandez RA, Bianco MI, et al. Equine Bot-
ulinum Antitoxin for the Treatment of Infant Botulism. Clin Vaccine
Immunol. 2011;18:1845-1849.
38. Brook I. Infant botulism. J Perinatol. 2007;27:175-180.
39. Cox N, Hinkle R. Infant botulism. Am Fam Physician. 2002;65:
1388-1392.
40. Schechter R, Peterson B, McGee J, Idowu O, Bradley B. Clostridium
difficile colitis associated with infant botulism: near-fatal case analo-
gous to Hirschsprung’s enterocolitis. Clin Infect Dis. 1999;29:367-374.
41. Fenicia L, Da Dalt L, Anniballi F, Franciosa G, Zanconato S, Aureli P.
A case of infant botulism due to neurotoxigenic Clostridium
butyricum type E associated with Clostridium difficile colitis. Eur J
Clin Microbiol Infect Dis. 2002;21:736-738.
42. Goonetilleke A. Clostridial neurotoxins. J Neurol Neurosurg Psychi-
atry. 2004;75(suppl_3):iii35-iii39.
43. Bohnel H, Behrens S, Loch P, Lube K, Gessler F. Is there a link be-
tween infant botulism and sudden infant death? Bacteriological
results obtained in Central Germany. Eur J Pediatr. 2001;160:
623-628.
44. Byard RW, Moore L, Bourne AJ, Lawrence AJ, Goldwater PN. Clos-
tridium botulinum and sudden infant death syndrome: a 10 year
prospective study. J Paediatr Child Health. 1992;28:156-157.

Any fool can criticize, condemn and complaindand most fools do.

Benjamin Franklin