Clostridium Botulinum Type F with Recent Observations on Other Types

Dolman, C. E.; Murakami, Lily

doi:10.1093/infdis/109.2.107

Cited by 86 publications

(24 citation statements)

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“…The frequency of nucleotide substitutions observed within variants E10 (1 to 7 nucleotides) and E3 (1 or 2 nucleotides) is similar to that reported for variant B4 (1 to 5 nucleotides), a toxin variant generally associated with nonproteolytic C. botulinum (29). Considering such a broad distribution, it is noteworthy that only 2 of the 175 strains included in our study (E1 Dolman, Pacific coast [30] E-RUSS, Sea of Azov [31]) encode BoNT/E1. E1 strains have been previously isolated in Washington State, Alaska, Labrador, Greenland, Denmark, Finland, and Japan (2,12,32).…”

Section: Discussionsupporting

confidence: 82%

Two Novel Toxin Variants Revealed by Whole-Genome Sequencing of 175 Clostridium botulinum Type E Strains

Weedmark

Lambert

Mabon

et al. 2014

Appl Environ Microbiol

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We sequenced 175 Clostridium botulinum type E strains isolated from food, clinical, and environmental sources from northern Canada and analyzed their botulinum neurotoxin (bont) coding sequences (CDSs). In addition to bont/E1 and bont/E3 variant types, neurotoxin sequence analysis identified two novel BoNT type E variants termed E10 and E11. Strains producing type E10 were found along the eastern coastlines of Hudson Bay and the shores of Ungava Bay, while strains producing type E11 were only found in the Koksoak River region of Nunavik. Strains producing BoNT/E3 were widespread throughout northern Canada, with the exception of the coast of eastern Hudson Bay. B otulism, a rare and severe disease characterized by a descending flaccid paralysis, is caused by botulinum neurotoxin (BoNT), the most potent toxin known. BoNT is produced by phylogenetically distinct anaerobic spore-forming bacteria grouped under the taxonomic designation of Clostridium botulinum. Rare botulinogenic strains of related clostridia, such as C. baratii, C. butyricum, and C. argentinense, have also been observed (1, 2). Seven serologically distinct BoNTs (A to G) can be distinguished based on neutralization of toxicity with specific antisera. Recently, a strain of C. botulinum producing botulinum neurotoxin type B (BoNT/B) and another BoNT that is not neutralized by antitoxins to BoNTs A to G has been isolated from a case of infant botulism (3). It has been proposed that this novel neurotoxin is an eighth serotype, BoNT/H (3,4). The botulinum neurotoxins are comprised of three structural domains (translocation [H N ], receptor binding [H C ], and catalytic [LC]). These toxins target different SNARE (soluble N-ethylmaleimide-sensitive factor-attachment protein-receptor) proteins in the neuromuscular junction to block neurotransmitter release (5,6).Heterogeneity within the BoNTs has led to a classification of BoNTs into subtypes. Within a toxin serotype, differences in amino acid sequences can range from 0.9% to 25% (2, 7). Hill and Smith (8) point out that the newer subtypes have been defined based on their DNA sequence and propose the use of the term "subtype/genetic variant" to avoid confusion with the historical use of "subtype," utilized to designate immunological or enzymatic differences among neurotoxins. Two approaches have been used to define new BoNT variants. The first uses a cutoff value of 2.5% difference in amino acid composition (9-11), whereas the second relies on a phylogenetic approach in which variants correspond to clades formed by the clustering of bont sequences (1, 7, 12) Based on these methods, bont/A1 to bont/A5, bont/B1 to bont/ B7, bont/E1 to bont/E9, and bont/F1 to bont/F7 gene variants have been described (1,2,8,10,(12)(13)(14)(15)(16)(17).In Canada, C. botulinum type E is the predominant BoNT serotype associated with food-borne botulism, accounting for 86.2% of all laboratory-confirmed food-borne botulism outbreaks reported between 1985 and 2005 (18). Although variant types E1, E3, and E7 have been identified in t...

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Section: Discussionsupporting

confidence: 82%

Two Novel Toxin Variants Revealed by Whole-Genome Sequencing of 175 Clostridium botulinum Type E Strains

Weedmark

Lambert

Mabon

et al. 2014

Appl Environ Microbiol

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“…In the worst-case scenario, should a BoNT/E laden fish be improperly cooked or eaten raw, the public health risk is still minimal. The estimated lethal dose of BoNT/E for humans is between 1,500 and 2,500 MLD kg Ϫ1 (6). Thus, for a 65-kg person, this would be between 97,500 to 162,000 MLD.…”

Section: Public Health Implications the High Proportion Ofmentioning

confidence: 99%

Persistence of Clostridium botulinum Neurotoxin Type E in Tissues from Selected Freshwater Fish Species: Implications to Public Health

Yule

Austin

Barker

et al. 2006

Journal of Food Protection

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Rainbow trout (Oncorhynchus mykiss), round gobies (Neogobius melanostomas), yellow walleye (Stizostedion vitreum), and yellow perch (Perca flavescens) were given Clostridium botulinum neurotoxin type E (BoNT/E) at four doses (0, 800, 1,500, and 4,000 mouse lethal doses). BoNT/E was sought in the fish tissues at death or at the conclusion of the experiment (10 days after treatment). Fish were divided into a ''fillet'' (axial musculature) and a ''nonfillet'' sample before testing for BoNT/E toxicity with a mouse bioassay. BoNT/E was detected in all species. The percentage of positive BoNT samples ranged across the species and doses from 0 (trout, perch, and walleye) to 17% (round goby) in fillet tissues and from 0 (perch) to 92% (round goby) in nonfillet tissues. The lack of positive fillet samples in three key commercial fish species suggests that the public health implications of eating these fish are minimal. However, the presence of toxin in the nonfillet compartment of a high proportion of fish supports the hypothesis that live intoxicated fish are a vehicle for the transfer of BoNT/E to fisheating birds, which are then in turn, intoxicated.

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“…Two cases of foodborne botulism linked to BoNT C and one case of infant botulism attributed to C. botulinum serotype C1 have been reported [8,9], and BoNT D organisms were found in tainted ham that caused mild botulism in several persons [9]. However, BoNT C1 and D are predominantly known for causing avian or mammalian botulism [10][11][12].…”

Section: Introductionmentioning

confidence: 99%

Protection with recombinant Clostridium botulinum C1 and D binding domain subunit (Hc) vaccines against C and D neurotoxins

Webb¹,

Smith²,

Wright³

et al. 2007

Vaccine

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Recombinant botulinum Hc (rBoNT Hc) vaccines for serotypes C1 and D were produced in the yeast Pichia pastoris and used to determine protection against four distinct BoNT C and D toxin subtypes. Mice were vaccinated with rBoNT/C1 Hc, rBoNT/D Hc, or with a combination of both vaccines and challenged with BoNT C1, D, C/D, or D/C toxin. Mice receiving monovalent vaccinations were partially or completely protected against homologous toxin and not protected against heterologous toxin. Bivalent vaccine candidates completely survived challenges from all toxins except D/C toxin. These results indicate the recombinant C1 and D Hc vaccines are not only effective in a monovalent formula but offer complete protection against both parental and C/D mosaic toxin and partial protection against D/C mosaic toxin when delivered as a bivalent vaccine.

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Clostridium Botulinum Type F with Recent Observations on Other Types

Cited by 86 publications

References 0 publications

Two Novel Toxin Variants Revealed by Whole-Genome Sequencing of 175 Clostridium botulinum Type E Strains

Two Novel Toxin Variants Revealed by Whole-Genome Sequencing of 175 Clostridium botulinum Type E Strains

Persistence of Clostridium botulinum Neurotoxin Type E in Tissues from Selected Freshwater Fish Species: Implications to Public Health

Protection with recombinant Clostridium botulinum C1 and D binding domain subunit (Hc) vaccines against C and D neurotoxins

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