How Likely Is a Baby to Develop Botulism From Honey
Infant Botulism
Am Fam Doctor. 2002 April 1;65(seven):1388-1393.
Article Sections
- Abstract
- Pathophysiology
- Epidemiology
- Clinical Presentation
- Differential Diagnosis
- Diagnosis
- Clinical Management
- References
Although the worldwide incidence of infant botulism is rare, the majority of cases are diagnosed in the United States. An infant tin can acquire botulism past ingesting Clostridium botulinum spores, which are found in soil or honey products. The spores germinate into bacteria that colonize the bowel and synthesize toxin. Every bit the toxin is absorbed, information technology irreversibly binds to acetylcholine receptors on motor nerve terminals at neuromuscular junctions. The infant with botulism becomes progressively weak, hypotonic and hyporeflexic, showing bulbar and spinal nerve abnormalities. Presenting symptoms include constipation, lethargy, a weak cry, poor feeding and dehydration. A loftier alphabetize of suspicion is important for the diagnosis and prompt treatment of infant botulism, because this disease can quickly progress to respiratory failure. Diagnosis is confirmed past isolating the organism or toxin in the stool and finding a classic electromyogram pattern. Treatment consists of nutritional and respiratory support until new motor endplates are regenerated, which results in spontaneous recovery. Neurologic sequelae are seldom seen. Some children require outpatient tube feeding and may accept persistent hypotonia.
Infant botulism is caused past a neurotoxin produced by the spore-forming, anaerobic, gram-positive bacilli Clostridium botulinum, which is found globally in soil. Ingestion of spores leads to toxin synthesis and assimilation from the infant'due south abdominal tract. Infant botulism is caused past toxin types A and B.1 The ensuing neuroparalytic disease presents in a subacute mode, initially causing constipation followed by progressive weakness. Doctor awareness of infant botulism is paramount to early recognition and intervention, considering more 70 percent of these infants will eventually crave mechanical ventilation.ii
Pathophysiology
- Abstruse
- Pathophysiology
- Epidemiology
- Clinical Presentation
- Differential Diagnosis
- Diagnosis
- Clinical Management
- References
Baby botulism occurs when ingested spores germinate and colonize the babe's gastrointestinal tract. The cecum is idea to be the initial site of activeness and paralysis of the ileocecal valve might let the colonizing bacteria to extend into the terminal ileum.3 Once the bacteria take colonized, toxin is produced and captivated throughout the intestinal tract. The mechanism by which the toxin is transported to the nerve tissue is unknown.4 The toxin irreversibly binds to presynaptic cholinergic receptors at motor nervus terminals and is afterward internalized. Once inside the cytosol, the toxin behaves as a protease, damaging an integral membrane protein of acetylcholine-containing vesicles, disrupting exocytosis and inhibiting the release of the acetylcholine that is needed to excite muscle.4,5
Epidemiology
- Abstruse
- Pathophysiology
- Epidemiology
- Clinical Presentation
- Differential Diagnosis
- Diagnosis
- Clinical Management
- References
Ninety per centum of the world's cases of babe botulism are diagnosed in the United States, mainly because of medico awareness.5,6 As of 1996, the Centers for Illness Control and Prevention (CDC) has documented more than than ane,400 cases.one The prevalence of infant botulism has surpassed that of food-borne and wound botulism.ane It is estimated that more than 250 cases of infant botulism occur in the United States each year, merely many go unrecognized.7 California, Utah and Pennsylvania have the highest incidence; nearly l percent of all cases are reported in California.2,viii
Soil and honey contamination are the 2 recognized sources of botulinum spores. Extensive research has been conducted to place other sources. In California in the belatedly 1970s, researchers9 analyzed 555 samples of soil, household dust, cereals, baby foods, canned goods, sugar, corn syrup, honey and commercial formulas. Except in the samples of honey and soil, no spores were detected.9 In a study10 performed in New York, no spores were found in any of the 236 products that were tested. According to microbiologic testing, up to 25 pct of honey products accept been found to contain spores.11 A history of honey consumption is seen in 15 percent of the botulism cases reported to the CDC.5,12 As a outcome, dear should not exist given to infants younger than i year.
A prospective, example-controlled study12 was performed to decide the run a risk factors of infant botulism. The results showed that decreased frequency of bowel movements (less than one per 24-hour interval) and breast-feeding were take chances factors for the development of disease in infants older than two months. For infants younger than two months, living in a rural farming expanse was the only meaning risk factor, reported past twoscore percent of the families studied. Presumably, these infants would more than likely exist exposed to aerosolized spores from clothing contaminated by soil or from disrupted soil.12
The role of breast-feeding in infant botulism remains controversial. In various studies, breast-feeding occurs in 70 to 90 per centum of infants with botulism.13 Breast-feeding may delay the clinical severity of this condition, assuasive these infants to receive medical attention before the botulism becomes fatal.14 There is no evidence that breast-fed infants have an increased severity of disease when compared with formula-fed infants.12
Historically, infant botulism was thought to contribute to sudden baby death syndrome (SIDS). If the illness went unrecognized, paralysis of the respiratory musculature could lead to rapid hypoxemia and respiratory abort. Two studies identified postmortem C. botulinum colonization in 4 to xv percent of deaths caused by SIDS.xv However, a contempo 10-year prospective report did non find occult botulism to exist a significant cistron for SIDS.xvi
Clinical Presentation
- Abstract
- Pathophysiology
- Epidemiology
- Clinical Presentation
- Differential Diagnosis
- Diagnosis
- Clinical Direction
- References
Infants who acquire botulism range in age from vi weeks to nine months, with the elevation incidence occurring at ii to three months of age. About 90 percent of infants with botulism are younger than six months.4 Infant botulism may be difficult to recognize because of its insidious onset. The classic clinical features include constipation, cranial nerve abnormalities, hypotonia, hyporeflexia and respiratory difficulties. The signs and symptoms commonly present at the fourth dimension of hospital admission are listed in Tabular array 1.ii
Tabular array ane
Signs and Symptoms of Infant Botulism at Hospital Admission
| Signs and symptoms | Incidence (%) |
|---|---|
| Weakness or floppiness | 88 |
| Poor feeding | 79 |
| Constipation | 65 |
| Languor/decreased action | sixty |
| Weak cry | 18 |
| Irritability | 18 |
| Respiratory difficulties | 11 |
| Seizures | 2 |
Constipation may be present in affected infants for a variable length of time and can precede weakness by several weeks.14 Hypotension, neurogenic bladder and other signs of autonomic dysfunction can occur early in the class of the disease. Signs of weakness in the baby with botulism begin with cranial nerve interest and loss of head command. The infant may develop a weak cry, poor sucking ability, impaired gag reflex, pooling of secretions and decreased oral intake. Loss of ocular motility ptosis, mydriasis and facial weakness also may occur.14,15 The weakness progresses in a descending fashion in a matter of days. Affected infants get irritable and lethargic. In severe cases of infant botulism, respiratory difficulties begin as a late sign of disease, quickly leading to respiratory abort.14
Differential Diagnosis
- Abstruse
- Pathophysiology
- Epidemiology
- Clinical Presentation
- Differential Diagnosis
- Diagnosis
- Clinical Management
- References
The differential diagnosis of infant hypotonia is all-encompassing (Tabular array ii).14 An infant with botulism is often diagnosed with sepsis or meningoencephalitis because of symptoms of lethargy and irritability on presentation. Yet, these infants are typically afebrile and the piece of work-up for these entities will be negative.17 Dehydration and other metabolic causes should be properly investigated. Reye's syndrome can be effectively ruled out by determining the serum ammonia level.14 Poisoning besides must be considered. Poliomyelitis is often associated with asymmetric clinical findings and a cerebrospinal fluid pleocytosis, which is non seen in infant botulism.xiv,17 Infantile spinal muscular cloudburst rarely causes pupillary or centre dysfunction.14 Built myasthenia gravis is rare and can be excluded by maternal and neonatal history. Guillain-Barré syndrome presents as an ascending paralysis and is usually not seen in children younger than 1 year.xiv,17 Lastly, acute upper airway obstacle should exist considered in infants with poor feeding, an disability to handle secretions and respiratory distress.
Tabular array ii
Differential Diagnosis of Hypotonia in Infants
| Infectious |
| Sepsis |
| Meningitis |
| Encephalitis |
| Metabolic |
| Electrolyte abnormalities (hyponatremia) |
| Reye'due south syndrome |
| Hepatic encephalopathy |
| Hypothyroidism |
| Organic acidurias |
| Subacute necrotizing encephalomyelitis |
| Toxins |
| Heavy metals |
| Alcohols |
| Organophosphates |
| Anticholinergics |
| Narcotics |
| Neuromuscular |
| Poliomyelitis |
| Infantile spinal muscular cloudburst |
| Acute polyneuropathy (Guillain-Barré syndrome) |
| Congenital myasthenia gravis |
| Muscular dystrophy and congenital myopathy |
| Tick paralysis |
Diagnosis
- Abstruse
- Pathophysiology
- Epidemiology
- Clinical Presentation
- Differential Diagnosis
- Diagnosis
- Clinical Management
- References
A definitive diagnosis can be fabricated with the detection of botulinum toxin and the isolation of C. botulinum from stool samples. Additionally, electromyogram (EMG) studies tin support an early diagnosis.
A passed stool is the preferred specimen for culture and toxin investigation. In a constipated infant, information technology may be necessary to perform colonic irrigation with limited amounts of sterile saline. A 25-g stool or a 25-mL effluent sample should exist nerveless in a sterile container and refrigerated.5 A serum sample should be obtained for a toxin assay. Other potential source samples, such every bit dust, soil from wearable, honey, corn syrup or foods, should besides be collected for investigation.
Testing is commonly performed by land health departments or the CDC. Organism identification is established using conventional microbiologic techniques. Identification of botulinum toxin is completed using a mouse neutralization bioassay. Polymerase chain reaction and enzyme-linked immunosorbent assays accept been adult to test for baby botulism. Nevertheless, the unavailability of reagents and lack of standardization among laboratories take kept these tests from replacing the mouse bioassay as the preferred testing method.5,8,18
Researchers have proposed that standardized electrodiagnostic testing be performed in infants with suspected botulism, looking for the EMG triad to aid in early confirmation of the diagnosis (Table 3)19 Hypermagnesemia is the only other consideration in infants who brandish all three diagnostic features.19 Because EMG results can exist normal early in the disease, series testing may exist required, beginning 1 week to 10 days from the onset of symptoms.2,15 Also, resolution of EMG findings do not correlate with the recovery of spontaneous ventilation.20
Tabular array iii
EMG Evaluation of Suspected Cases of Baby Botulism
| EMG standard battery |
| Motor and sensory nerve conduction velocity in ane arm and ane leg |
| Two-Hz nerve stimulation to two distal muscles |
| Supramaximal single nerve stimulation, followed by 50-Hz tetanization for 10 seconds and immediately thereafter by single nerve stimuli at xxx-second intervals until amplitude of compound muscle potentials return to baseline |
| Diagnostic triad for baby botulism |
| Chemical compound musculus action potentials of decreased amplitude in at least two muscle groups |
| Tetanic and post-tetanic facilitation defined by an amplitude of more 120 percent of baseline |
| Prolonged mail-tetanic facilitation of more than 120 seconds and absence of post-tetanic exhaustion |
Clinical Management
- Abstract
- Pathophysiology
- Epidemiology
- Clinical Presentation
- Differential Diagnosis
- Diagnosis
- Clinical Direction
- References
Supportive care is the mainstay of therapy. Infants with botulism should stay in an intensive care unit considering they frequently require airway management, nasogastric tube feedings, and physical and occupational therapy. Parents are usually permitted 24-60 minutes visitation and should exist encouraged to participate in the care of their baby.
A diverseness of complications can occur in these infants during hospitalization (Table 4).two Aminoglycosides should exist avoided considering their utilize can lyse bacteria, releasing additional intracellular toxin into the babe gut.5,17 Cathartics have not been found to shorten the grade of the illness.1,17
TABLE 4
General Complications in Patients Hospitalized with Infant Botulism
| Complexity | Incidence (%) |
|---|---|
| Syndrome of inappropriate secretion of antidiuretic hormone | sixteen |
| Autonomic instability | 12 |
| Apnea | 12 |
| Urinary tract infection | xi |
| Pneumonia | 7 |
| Sepsis | 5 |
| Seizure | 5 |
| Deterioration with gentamicin | iv |
| Respiratory arrest | 4 |
Historically, administration of antitoxin involved an equine-derived production. Side effects, including anaphylaxis, occurred in 20 percent of patients, and the antitoxin is no longer considered beneficial given the cocky-limiting course of baby botulism.11 Recently, the California Department of Wellness Services conducted a five-year clinical investigation of botulinum allowed globulin, a human-derived antitoxin for the handling of infant botulism. The use of botulinum immune globulin in infants has successfully reduced the time spent in the infirmary and the need for mechanical ventilation and tube feeding.21
The prognosis is excellent, with a instance-fatality charge per unit of less than two pct.17 Recovery results from the regeneration of nerve terminals and motor endplates. Diaphragmatic function returns before peripheral muscle recovery.
For infants who require mechanical ventilation, the boilerplate duration is 23 days. On average, infants were able to feed orally 51 days from admission.ii Parents should be aware that the course of this affliction consists of minor improvements and setbacks. The average hospital stay is 44 days.2 Typically, neurologic sequelae is seldom seen. Persistent hypotonia may be nowadays at the time of infirmary discharge, merely full recovery tin be expected with time.14,15
Relapse of babe botulism has been reported in infants demonstrating complete resolution of symptoms.22 All relapses occurred inside 13 days of hospital discharge. No predictors of relapse were identified.22 Therefore, close follow-up is important during the first month after discharge.
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REFERENCES
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1. Shapiro RL, Hatheway C, Swerdlow DL. Botulism in the The states: a clinical and epidemiologic review. Ann Intern Med. 1998;129:221–viii. ...
2. Schreiner MS, Field E, Cerise R. Babe botulism: a review of 12 years' experience at the Children's Hospital of Philadelphia. Pediatrics. 1991;87:159–65.
iii. Mills DC, Arnon SS. The large intestine as the site of Clostridium botulinum colonization in homo infant botulism. J Infect Dis. 1987;156:997–viii.
four. Ferrari ND, Weisse ME. Botulism. Adv Pediatr Infect Dis. 1995;ten:81–91.
5. Midura TF. Update: infant botulism. Clin Microbiol Rev. 1996;9:119–25.
six. Faucheux RC, Shetty AK, Cowan GS. Infant botulism. Clin Pediatr. 1997;36:591–iv.
7. Mygrant BI, Renaud MT. Infant botulism. Heart Lung. 1994;23:164–8.
8. Hatheway CL. Botulism: the present status of the illness. Curr Top Microbiol Immunol. 1995;195:55–75.
9. Chin J, Arnon SS, Midura TF. Food and environ mental aspects of infant botulism in California. Rev Infect Dis. 1979;1:693–7.
10. Guilfoyle DE, Yager JF. Survey of baby foods for Clostridium botulinum spores. J Assoc Off Anal Chem. 1983;66:1302–4.
11. Cherington Chiliad. Clinical spectrum of botulism. Musculus Nerve. 1998;21:701–x.
12. Spika JS, Shaffer N, Hargrett-Edible bean Northward, Collin S, MacDonald KL, Blake PA. Risk factors for infant botulism in the United States. Am J Dis Child. 1989;143:828–32.
13. Golding J, Emmett PM, Rogers IS. Does breast feeding protect against non-gastric infections? Early Hum Dev. 1997;49(suppl)S10520.
14. Schmidt RD, Schmidt TW. Baby botulism: a case series and review of the literature. J Emerg Med. 1992;10:713–8.
15. Wigginton JM, Thill P. Infant botulism: a review of the literature. Clin Pediatr. 1993;32:669–74.
sixteen. Byard RW, Moore L, Bourne AJ, Lawrence AJ, Goldwater PN. Clostridium botulinum and sudden infant death syndrome: a 10 twelvemonth prospective written report. J Paediatr Kid Health. 1992;28:156–seven.
17. Cochran DP, Appleton RE. Infant botulism—is it that rare? Dev Med Child Neurol. 1995;37:274–8.
xviii. Szabo EA, Pemberton JM, Gibson AM, Eyles MJ, Desmarchelier PM. Polymerase concatenation reaction for detection of Clostridium botulinum types A, B and E in food, soil and infant faeces. J Appl Bacteriol. 1994;76:539–45.
nineteen. Gutierrez AR, Bodensteiner J, Gutmann L. Electrodiagnosis of infantile botulism. J Child Neurol. 1994;ix:362–5.
twenty. Wohl DL, Tucker JA. Infant botulism: considerations for airway direction. Laryngoscope. 1992;102:1251–iv.
21. American Academy of Pediatrics. Clostridial infections. In: Pickering LK, ed. 2000 Blood-red book: study of the Committee on Infectious Diseases. 25th ed. Elk Grove Hamlet, III.: American Academy of Pediatrics, 2000:212–4.
22. Glauser TA, Maguire HC, Sladky JT. Relapse of babe botulism. Ann Neurol. 1990;28:187–nine.
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