Clinical and Laboratory Comparison of Botulism from Toxin Types A, B, and E in the United States, 1975-1988

Woodruff, Bradley A.; Griffin, Patricia M.; McCroskey, L M; Smart, Joanne F.; Wainwright, Robert B.; Bryant, Raymond G.; Hutwagner, Lori; Hatheway, Charles L.

doi:10.1093/infdis/166.6.1281

Cited by 186 publications

(151 citation statements)

References 11 publications

Supporting

Mentioning

136

Contrasting

Unclassified

Order By: Relevance

“…These babies appear 'floppy,' and may manifest various neurologic signs such as ptosis, ophthalmoplegia, sluggish reaction of the pupils, dysphagia, weak gag reflex and poor anal sphincter tone. 31,32 In seriously ill babies, respiratory arrest may occur.…”

Section: Clinical Manifestationmentioning

confidence: 99%

Infant botulism

Brook

2007

J Perinatol

View full text Add to dashboard Cite

Infant botulism results from the absorption of heat-labile neurotoxin produced in situ by ingested Clostridium botulinum. Honey and environmental exposure are the main sources of acquisition of the organism. Clinical manifestations are owing to progressive neuromuscular blockade, initially of muscles innervated by cranial nerves and later of the trunk, extremities and diaphragm. Presynaptic autonomic nerves are also affected. The diagnosis is made on clinical grounds and is confirmed by recovery of the organism or by detection of toxin in the stool. Management includes meticulous supportive intensive care that may include mechanical ventilation and administration of human botulinum immunoglobulin in severe cases.

show abstract

Section: Clinical Manifestationmentioning

confidence: 99%

Infant botulism

Brook

2007

J Perinatol

View full text Add to dashboard Cite

show abstract

“…Proteolytic Clostridium botulinum (C. botulinum group I) is one of six phylogenetically and physiologically distinct clostridia that forms botulinum neurotoxin. It is responsible for a majority of the cases of infant botulism and wound botulism as well as many cases of classical food-borne botulism (1,2,4,16,17). Nonproteolytic C. botulinum (C. botulinum group II) is responsible for most other cases of food-borne botulism (13).…”

mentioning

confidence: 99%

Diversity of Proteolytic Clostridium botulinum Strains, Determined by a Pulsed-Field Gel Electrophoresis Approach

Nevas

Lindström

Hielm

et al. 2005

Appl Environ Microbiol

View full text Add to dashboard Cite

Pulsed-field gel electrophoresis (PFGE) was applied to the study of the similarity of 55 strains of proteolytic Clostridium botulinum (C. botulinum group I) types A, AB, B, and F. Rare-cutting restriction enzymes ApaI, AscI, MluI, NruI, PmeI, RsrII, SacII, SmaI, and XhoI were tested for their suitability for the cleavage of DNA of five proteolytic C. botulinum strains. Of these enzymes, SacII, followed by SmaI and XhoI, produced the most convenient number of fragments for genetic typing and were selected for analysis of the 55 strains. The proteolytic C. botulinum species was found to be heterogeneous. In the majority of cases, PFGE enabled discrimination between individual strains of proteolytic C. botulinum types A and B. The different toxin types were discriminated at an 86% similarity level with both SacII and SmaI and at an 83% similarity level with XhoI. Despite the high heterogeneity, three clusters at a 95% similarity level consisting of more than three strains of different origin were noted. The strains of types A and B showed higher diversity than the type F organisms which formed a single cluster. According to this survey, PFGE is to be considered a useful tool for molecular epidemiological analysis of proteolytic C. botulinum types A and B. However, epidemiological conclusions based on PFGE data only should be made with discretion, since highly similar PFGE patterns were noticed, especially within the type B strains.The most commonly reported forms of botulism are foodborne botulism, wound botulism, and infant botulism. Foodborne botulism is an intoxication caused by consumption of preformed botulinum neurotoxin, while wound and infant botulism are both infections in which neurotoxin is formed in vivo (13). Proteolytic Clostridium botulinum (C. botulinum group I) is one of six phylogenetically and physiologically distinct clostridia that forms botulinum neurotoxin. It is responsible for a majority of the cases of infant botulism and wound botulism as well as many cases of classical food-borne botulism (1,2,4,16,17). Nonproteolytic C. botulinum (C. botulinum group II) is responsible for most other cases of food-borne botulism (13). The confirmation of food-borne botulism outbreaks has been based on the detection of botulinum toxin or C. botulinum organisms of the same toxin type from both the patient and the suspected food item. In order to be able to confirm the epidemiological relatedness of the strains isolated from patients and from food, a method for genotyping proteolytic C. botulinum isolates is needed. Such a method would also be of utility when investigating cases of wound or infant botulism.Since the first paper on pulsed-field gel electrophoresis (PFGE) typing of C. botulinum type A strains Hall A and 62 A was published (10), no reports on the genetic diversity of strains of proteolytic of C. botulinum as determined by PFGE have been published. With nonproteolytic C. botulinum, a high genetic diversity determined by PFGE and randomly amplified polymorphic DNA (RAPD) analysis has been report...

show abstract

“…Il test solitamente richiede dalle 24 alle 48 ore. Nel frattempo, la terapia specifica deve essere instaurata anche solo sulla base del fondato sospetto clinico, indipendentemente dalla gravità di presentazione. La sensibilità del test varia dal 33 al 44% 10,11 , essendo inversamente proporzionale al tempo trascorso dalla contaminazione. In genere, trascorsa una settimana dalla contaminazione, la tossina non è più presente nel siero mentre resta più a lungo nelle feci e nei cibi contaminati.…”

Section: Discussioneunclassified

Green beans are the ones to blame

2010

View full text Add to dashboard Cite

Una famiglia composta da padre (67 anni), madre (57 anni) e figlia (36 anni), sono inviati al Pronto Soccorso dal medico curante per sospetta meningite. Da circa 4 giorni presentano una sintomatologia ingravescente comune caratterizzata da annebbiamento visivo ed astenia marcata con associata, solo nella madre, una sintomatologia gastrointestinale. L'anamnesi patologica è negativa per patologie di rilievo ed i parametri vitali sono nella norma. L'esame obiettivo rileva in tutti e tre i casi una midriasi bilaterale non reagente alla luce. La madre presenta inoltre ptosi palpebrale con ipostenia dei muscoli orbicolari bilaterale, ipomobilità del velo pendulo, disfagia e disartria. Lamenta anche dispnea soggettiva, ma obiettivamente è eupnoica e l'emogasanalisi evidenzia una normale pressione parziale dei gas arteriosi in assenza di alterazioni dell'equilibrio acido-base. Nella stessa, gli esami di laboratorio rilevano una discreta elevazione dell'amilasemia (431 U/l) ed una lieve ipokaliemia (3,1 mmol/l). La diagnostica d'immagine (radiografia standard del torace e tomografia computerizzata dell'encefalo) non fornisce elementi diagnostici. L'elettrocardiogramma e l'elettroencefalogramma sono nella norma. Diagnostica differenzialeQuesto quadro clinico è comune, nelle sue linee essenziali, a diverse patologie neurologiche con caratteristiche cliniche simili ma con aspetti fisiopatologici ed epidemiologici molto diversi: la patologia infettiva meningo-encefalica, la miastenia gravis, la patologia demielinizzante acuta (sindrome di Guillain-Barrè), patologie vascolari e proliferative cerebrali, la sindrome di Eaton-Lambert e le intossicazioni acute esogene. La presentazione "epidemica" del caso tuttavia indirizza il sospetto clinico verso una patologia infettiva o ambientale che possa spiegare il coinvolgimento contemporaneo di più persone accomunate dallo stesso ambiente ed abitudini di vita. La meningite infettiva può essere ritenuta poco probabile in considerazione del fatto che nessuno dei familiari ne presentava gli aspetti clinici caratteristici: febbre, cefalea o rigor nucae to sono quelle da tossici inalatori, da contatto o alimentari. Rimane la difficoltà di individuare quale tra le molteplici sostanze tossiche note possa esserne la causa. L'anamnesi escludeva un'intossicazione da Shellfish, da tetrodotossina, da atropinici, metanolo e paralisi da zecche [2][3] . I valori di carbossiemoglobina erano nella norma. L'elemento chiave per la diagnosi definitiva è emerso proprio da un'accurata anamnesi alimentare, e cioè il consumo da parte di tutti i familiari di verdure (fagiolini) confezionate in casa e conservate sott'olio, 24 ore prima della comparsa dei sintomi. Questo dato anamnestico comune unitamente alla caratteristica modalità di presentazione clinica ha orientato i sospetti verso la diagnosi di intossicazione botulinica. Accertamenti specifici e trattamentoPrima di iniziare il trattamento specifico sono stati prelevati campioni di feci e sangue e conservati a 4 °C (dopo sieraggio del campione ematico) p...

show abstract

Clinical and Laboratory Comparison of Botulism from Toxin Types A, B, and E in the United States, 1975-1988

Cited by 186 publications

References 11 publications

Infant botulism

Infant botulism

Diversity of Proteolytic Clostridium botulinum Strains, Determined by a Pulsed-Field Gel Electrophoresis Approach

Green beans are the ones to blame

Contact Info

Product

Resources

About