Online citations, reference lists, and bibliographies.
← Back to Search

Clostridium Botulinum , Clostridium Perfringens , Clostridium Difficile

A. Bhunia
Published 2018 · Medicine

Save to my Library
Download PDF
Analyze on Scholarcy Visualize in Litmaps
Reduce the time it takes to create your bibliography by a factor of 10 by using the world’s favourite reference manager
Time to take this seriously.
Get Citationsy
Members of the genus Clostridium cause a variety of diseases in humans and animals, sometimes with fatal consequences. These organisms are anaerobic spore-forming rod-shaped bacteria and mostly associated with soil and sediments. Three species, Clostridium botulinum, C. perfringens and C. difficile, have a significant importance because these pathogens are responsible for neuroparalytic botulism (intoxication), food poisoning (toxicoinfection), and antibiotic-associated diarrhea and pseudomembranous colitis (infection) diseases, respectively. Clostridium botulinum strains are grouped into proteolytic and non-proteolytic due to their ability to produce proteases. C. botulinum produces eight antigenically distinct botulinum toxins (A, B, C, D, E, F, G, and H). In foodborne botulism, the botulinum toxin is produced in the food during anaerobic growth. Botulinum toxin is an A–B-type toxin with a zinc-dependent endopeptidase activity. It cleaves SNARE protein complex, which is responsible for the release of neurotransmitter, acetylcholine, from the synaptic vesicles into the neuromuscular junction for transmission of nerve impulse. Lack of acetylcholine release impedes nerve impulse propagation resulting in the onset of flaccid paralysis. The symptoms appear as early as 2 h after ingestion of toxin, and the severity and progression of the disease depend on the amount of toxins being ingested. Early medical intervention involves administration of antibotulinal antisera. C. perfringens causes food poisoning, necrotic enteritis, gas gangrene, myonecrosis, and toxemia. It produces at least 20 different toxins and causes toxicoinfection. There are five types of C. perfringens (A, B, C, D, and E), classified based on the production of four types of extracellular toxins: alpha (α), beta (β), epsilon (e), and iota (ι). C. perfringens type A strain is generally associated with the foodborne disease. After consumption of vegetative cells, the bacterium begins to sporulate as it encounters acidic pH of the stomach. The enterotoxin (CPE) is produced during sporulation. The enterotoxin binds to the claudin receptor in the tight junction (TJ) and forms a large protein complex with other membrane proteins to form a pore in the membrane that alters the membrane permeability to cause Ca2+ influx and fluid and ion (Na+, Cl−) losses. CPE alters the paracellular membrane permeability and promotes diarrhea. Food poisoning is generally self-limiting requiring bed rest and fluid therapy, but in rare cases, myonecrosis and necrotic enteritis diseases could be life-threatening thus patients require hospitalization and antibiotic therapy. Clostridium difficile is a nosocomial (hospital-acquired) human pathogen and causes Clostridium difficile antibiotic-associated diarrhea (CDAD) and pseudomembranous colitis. It produces toxin A (TcdA), toxin B (TcdB), and CDT which cause diarrhea and mucus membrane damage, inflammation leading to diarrhea, and sometimes life-threatening pseudomembranous colitis and megacolon and intestinal perforation. C. difficile association with meat animals and routine isolation from meats support its possible involvement as a foodborne pathogen. Prevention of C. difficile infection is possible by revising the antibiotic prescription practices such as the type of antibiotics, frequency, and duration of use. Probiotics supplement and fecal bacteriotherapy to repopulate the patient’s gut with healthy microbiota, and the surgical removal of infected section of the intestine are used to control recurrent infection.
This paper references
Antibiotic-associated pseudomembranous colitis due to toxin-producing clostridia.
J. Bartlett (1978)
Botulinum toxin as a biological weapon: medical and public health management.
S. S. Arnon (2001)
Clostridium botulinum and its neurotoxins: a metabolic and cellular perspective.
E. Johnson (2001)
Clostridium perfringens and foodborne infections.
S. Brynestad (2002)
New insights into the cytotoxic mechanisms of Clostridium perfringens enterotoxin.
B. McClane (2004)
William H. Welch, MD, and the discovery of Bacillus welchii.
B. Lucey (2004)
Botulinum Toxins – Cause of Botulism and Systemic Diseases?
H. Böhnel (2005)
The story of Clostridium botulinum: from food poisoning to Botox.
P. Ting (2004)
Genomics of clostridial pathogens: implication of extrachromosomal elements in pathogenicity.
H. Brüggemann (2005)
Quantitative Detection of Clostridium perfringens in the Broiler Fowl Gastrointestinal Tract by Real-Time PCR
M. Wise (2005)
Clostridium botulinum and Clostridium perfringens.
J. S. Novak (2005)
Laboratory Diagnostics of Botulism
M. Lindström (2006)
Clostridium perfringens Iota-Toxin: Structure and Function
J. Sakurai (2009)
Clostridia as agents of zoonotic disease.
J. Songer (2010)
Clostridium difficile: its potential as a source of foodborne disease.
M. Rupnik (2010)
Specificity of Interaction between Clostridium perfringens Enterotoxin and Claudin-Family Tight Junction Proteins
L. Mitchell (2010)
Molecular basis of toxicity of Clostridium perfringens epsilon toxin
M. Bokori-Brown (2011)
Clostridium difficile Infection and Inflammatory Bowel Disease: A Review
P. Sinh (2011)
Clostridium botulinum in the post-genomic era.
M. Peck (2011)
Clostridium perfringens: A Dynamic Foodborne Pathogen
S. García (2011)
New insights into the mode of action of the actin ADP-ribosylating virulence factors Salmonella enterica SpvB and Clostridium botulinum C2 toxin.
H. Barth (2011)
Novel insights into the epidemiology of Clostridium perfringens type A food poisoning.
M. Lindström (2011)
Treatment of recurrent Clostridium difficile infection: a systematic review
J. C. O’Horo (2014)
Clostridium difficile binary toxin CDT
D. Gerding (2013)
John G. Bartlett: Contributions to the discovery of Clostridium difficile antibiotic-associated diarrhea.
S. Gorbach (2014)
A novel strain of Clostridium botulinum that produces type B and type H botulinum toxins.
J. R. Barash (2014)
Towards an understanding of the role of Clostridium perfringens toxins in human and animal disease.
F. Uzal (2014)
Botulinum neurotoxins: genetic, structural and mechanistic insights
O. Rossetto (2014)
Clostridial C3 Toxins Target Monocytes/Macrophages and Modulate Their Functions
H. Barth (2015)
Clostridium perfringens Enterotoxin: Action, Genetics, and Translational Applications
J. C. Freedman (2016)
Clostridium difficile colitis: pathogenesis and host defence
M. Abt (2016)
Clostridium perfringens Sialidases: Potential Contributors to Intestinal Pathogenesis and Therapeutic Targets
Jihong Li (2016)

This paper is referenced by
Semantic Scholar Logo Some data provided by SemanticScholar