Infantile Botulism Research Articles

Infant botulism intoxication and autonomic nervous system dysfunction

Three infants presenting with severe cases of infantile botulism, occurring at 17, 30, and 180 days of life, respectively, are described in this report. All three infants presented with areflexive flaccid coma or apnoeas requiring prolonged ventilation. In serum, type B botulinum neurotoxin (BoNT/B) was detected in two cases and BoNT/A in the third case, confirming the diagnosis of infantile botulism. Despite constant nursing and monitoring, the recovery of motility was progressive, but finally complete. Dysautonomia, measured by recording heart rate variability (HRV), persisted beyond observable physical recovery. Dysautonomia was assessed using a time-domain analysis of the continuous electrocardiogram response (via non-invasive weekly 24 h Holters), which included sympathetic (SDNN) and parasympathetic indices (RMS-SD, pNN50). In all three of our patients, we observed an initial hypotonic period and a major decrease in all HRV indices. Despite observable recovery shortly after extubation, HRV time domain indices remained altered for many weeks. Because of the close monitoring afforded by hospitalization, this change in autonomic function was not accompanied by syncope, complications arising from ventricular arrhythmia, or sudden death. Our observations have important clinical implications since they emphasize the importance of pursuing cardiopulmonary monitoring following apparent functional recovery from the BoNTs.

Index of Suspicion

Index of Suspicion

Infantile Botulism Caused by Clostridium butyricum Type E Toxin

The case of a 9-month-old boy with infantile botulism caused by Clostridium butyricum type E toxin is reported. Because infantile botulism is rare in Japan, it was difficult to diagnose it at an early stage. Electrophysiologic findings were useful for the diagnosis, and were characterized by incremental responses (waxing) to short intervals and rapid repetitive nerve stimulation. A bioassay for botulism in mice indicated that the patient had botulism due to type E or F botulinum toxin. C. butyricum type E was isolated from his feces, confirming the diagnosis. This is the first known case of infantile botulism due to C. butyricum type E toxin in Japan.

Immune Globulin for Infant Botulism

Critical Care| April 01 2006 Immune Globulin for Infant Botulism AAP Grand Rounds (2006) 15 (4): 42–43. https://doi.org/10.1542/gr.15-4-42 Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Twitter LinkedIn Tools Icon Tools Get Permissions Cite Icon Cite Search Site Citation Immune Globulin for Infant Botulism. AAP Grand Rounds April 2006; 15 (4): 42–43. https://doi.org/10.1542/gr.15-4-42 Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search nav search search input Search input auto suggest search filter All PublicationsAll JournalsAAP Grand RoundsPediatricsHospital PediatricsPediatrics In ReviewNeoReviewsAAP NewsAll AAP Sites Search Advanced Search Topics: immunoglobulins, infantile botulism Source: Arnon SS, Schechter R, Maslanka SE, et al. Human botulism immune globulin for the treatment of infant botulism. N Engl J Med. 2006;354:462–471. The authors from the California Department of Health Services report the results of both a randomized, double-blind, placebo-controlled trial of 122 infants with laboratory-confirmed cases of infant botulism, and an open label study of 382 patients with infant botulism treated with botulism immune globulin (BIG) within 18 days after hospital admission. For the randomized study, infants were eligible if they had acute flaccid paralysis consistent with infant botulism according to medical history, physical examination, and laboratory findings at admission. Enrollment was limited to the first 3 days of hospital admission. Stool specimens were sent for Clostridium botulinum toxin and culture; however, patients were generally treated before diagnosis confirmation by these studies. The treatment group received an intravenous infusion of 50... You do not currently have access to this content.

Honey consumption in the state of São Paulo: a risk to human health?

Infantile botulism was recognized in 1976 as a paralyzing disease caused by the ingestion of viable spores that would germinate and colonize the intestinal tract of infants, with local production and absorption of Clostridium botulinum toxin. The possible origins of botulinic spores are dust and honey, which has been identified as a dietary risk factor for infantile botulism. The objectives of the present study were to investigate 100 honey samples obtained in the state of São Paulo (Brazil) in terms of incidence of botulinic spores and of microbiologic quality, in agreement with Decree 367/9. All 100 samples analysed were negative for the presence of Salmonella, Shigella, total coliforms. C. botulinum spores were present in 3 samples (3%) and molds and yeasts, in 64 samples (64%), but only 25 (25%) exceeded established criteria, with counts ranging from zero to 1.5×10 5 CFU/g. The presence of small sporogenic Gram-positive rods was observed in 42 (42%) of the 100 samples tested but these bacteria were not identified.

Biphasic course of infant botulism

The syndrome of infant botulism, characterized by constipation, poor feeding, hypotonia, poor head control, and bulbar involvement, is typically a monophasic disease. We describe a 7-month-old infant with a recurrence of illness 13 days after resolution of the presenting signs. The source of infection was unknown and the only potential risk factors were exclusive breastfeeding and decreased bowel movements, which by themselves cannot explain the recurrence. Although treatment with botulism immunoglobulin is now suggested for the acute phase of infantile botulism, its use for recurrence is controversial.

Guillain-Barré syndrome: Perspectives with infants and children

An acute flaccid paraparesis or ascending quadriparesis in an infant or child constitutes a very important pediatric neurology emergency. The Guillain-Barré syndrome (GBS) is the most frequent cause. This is primarily an autoimmune, post-infectious, demyelinating, peripheral nervous system process. A small percentage of children develop a primary axonal process not unlike that identified more commonly in China. Because of the potential for acute respiratory compromise, any child suspected of having GBS needs immediate hospitalization. The major considerations in differential diagnosis include transverse myelitis, toxic neuropathies, tick paralysis, infantile botulism, myasthenia gravis, and dermatomyositis. On occasion, some younger children present with an acute severe pain syndrome that may mask as a pseudo-encephalopathy. Another clinical variant is the Miller-Fisher syndrome characterized by ataxia, ophthalmoparesis, and areflexia. This is associated with a high frequency of the anti-GQ-1-b antibodies. Although most children with GBS have a relatively benign clinical course, some become very ill and require intubation with intensive care monitoring. Immunomodulating treatment should be used for any child who loses the ability to walk. To date, no well-controlled study has been completed analyzing the relative merits of the two most commonly used therapies, namely plasmapheresis or intravenously administered immunoglobulin.

Infantile botulism: Clinical and laboratory observations of a rare neuroparalytic disease

A 3-month-old male infant was admitted to the University Hospital of Los Andes with a history of constipation, weak crying, poor feeding, flaccidity and later bilateral ptosis and hyporeflexia. The admission diagnosis was septicaemia until an electrophysiological study reported postetanic facilitation with 50 Hz/seg stimulations four days later. The Clostridium botulinum toxin type B was isolated from the infant's stool samples and the organism grew in anaerobic cultures. The patient recovered completely and was discharged 2 months later. Although infant botulism is an uncommon disease in our environment, this diagnosis must be suspected in all afebrile infants with constipation, affected cranial nerves and generalized hypotonia. The principal differential diagnoses are Landry-Guillain-Barré syndrome, poliomyelitis, myasthenia gravis and infant muscular atrophy.

Permanent Sixth Nerve Paralysis in Infantile Botulism

Permanent Sixth Nerve Paralysis in Infantile Botulism

Electrodiagnosis of infantile botulism.

Analysis of the literature on the electrophysiologic features of infantile botulism was undertaken. Small compound muscle action potential amplitude is a very sensitive feature but lacks specificity. The decremental response to 2- to 3-Hz repetitive nerve stimulation is inconsistent and not a reliable sign. Tetanic and posttetanic facilitation are highly sensitive and highly specific. Absence of posttetanic exhaustion is also highly specific for infant botulism and shared only by hypermagnesemia. We conclude that the findings of low compound muscle action potential amplitude in combination with tetanic facilitation or posttetanic facilitation and absence of posttetanic exhaustion constitute the triad on which the electrodiagnosis of infantile botulism can be supported.

Early severe infantile botulism

Two neonates with a history of diarrhea, abrupt apnea, and suspected sepsis were proved to have infantile botulism. Initial symptoms in both infants suggested other diagnoses. Electrophysiologic studies were important in confirming the diagnosis. Early severe infantile botulism may be rare but should be considered in neonates who have hypotonia and respiratory arrest or a sepsis-like clinical picture.

Disorders of neuromuscular transmission in infants and children.

Disorders of neuromuscular transmission in infants and children can be divided into two groups. The first group includes conditions similar to those seen in adults: autoimmune myasthenia gravis, Lambert-Eaton myasthenic syndrome, and botulism. The second includes several disorders that are unique to this age group, such as the congenital myasthenias and infantile botulism. This review discusses the diseases of neuromuscular transmission found in the pediatric population, with emphasis on electrodiagnosis. The distinctive clinical and electrophysiologic features allow the clinician to identify these illnesses correctly, so that appropriate treatment can be instituted or further specialized investigation can be undertaken.

Value of bacteriologic studies within the scope of forensic autopsies

The various questions regarding bacteriological investigations within the scope of forensic autopsies are discussed in the light of our own cases and with regard to the relevant literature: estimate of the age of the corpse on the basis of decomposition changes caused by bacteria; determination of so-called bacteriograms from the point of view of criminalistics; supplementary investigations of the cause of death. Iatrogenic infections (e.g., gangrene) are gone into in more detail, as is so-called infantile botulism within the scope of the "sudden infant death syndrome". Finally, it is pointed out that when doing forensic autopsies, thought should also be given to illnesses that have only been known for a few years, examples being legionnaires' disease and the toxic shock syndrome ("tampon sickness").

Hypotonia in Infants and Children

Many diseases in the pediatric population present with hypotonia and/or weakness. In order to ensure proper diagnosis and facilitate appropriate treatment, the nurse must be familial with those diseases which produce motor unit dysfunction in infants and children; among these conditions are infantile botulism and Guillain-Barré Syndrome. An understanding of the particular features which distinguish central from peripheral hypotonia is essential for the nurse. It is also important to obtain detailed histories and to ensure thorough physical examination. The nurse should also be aware of those laboratory studies that evaluate hypotonia and weakness, including the EMG, PNCT, muscle biopsy, and lumbar puncture.

Letters to the Editor

Dr Shaw expresses concern over withholding honey from large numbers of infants in an effort to prevent infantile botulism. He suggests that the finding of spores in a few samples of honey does not justify withholding honey from a large number of children and also suggests that there is no proof that the spores grow in the honey and produce toxin. In our study of infants in Utah with infantile botulism we did fmd two honey specimens in which organism could be isolated.

Infantile botulism

Botulism has not traditionally been considered as occurring in infants under one year of age because they generally do not ingest foods potentially containing preformed Clostridium botulinum toxin. We report a case of infantile botulism in a 3 1/2 month old infant who presented as a "floppy baby," and discuss the probable pathobiology involved.