User:Khiya04/Clostridium perfringens

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Clostridium perfringens (formerly known as C. welchii, or Bacillus welchii) is a Gram-positive, bacillus (rod-shaped), anaerobic, spore-forming pathogenic bacterium of the genus Clostridium. C. perfringens is ever-present in nature and can be found as a normal component of decaying vegetation, marine sediment, the intestinal tract of humans and other vertebrates, insects, and soil. It has the shortest reported generation time of any organism at 6.3 minutes in thioglycolate medium.

Clostridium perfringens is one of the most common causes of food poisoning in the United States, alongside norovirus, Salmonella, Campylobacter, and Staphylococcus aureus. However, it can sometimes be ingested and cause no harm.

Infections due to C. perfringens show evidence of tissue necrosis, bacteremia, emphysematous cholecystitis, and gas gangrene, also known as clostridial myonecrosis. The specific name, perfringens, is derived from the Latin per (meaning "through") and frango ("burst"), referring to the disruption of tissue that occurs during gas gangrene. The toxin involved in gas gangrene is α-toxin, which inserts into the plasma membrane of cells, producing gaps in the membrane that disrupt normal cellular function. C. perfringens can participate in polymicrobial anaerobic infections. It is commonly encountered in infections as a component of the normal flora. In this case, its role in disease is minor.

C. perfringens toxins are a result of horizontal gene transfer of neighboring cell's plasmids. Shifts in genomic make-up are common for this species of bacterium and contriubute to novel pathogensis. Major toxins are expressed differently in certain populations of C. perfringens; these populations are organized into strains based off there expressed toxins. This especially impacts the food industry, as controlling this microbe is important for preventing foodborne illness. Novel findings in C. perfringens hyper-motility, which was provisionally thought as non-motile, have been discovered as well. Findings in metabolic processes reveal more information concerning C. perfringens pathogenic nature.

Major Toxins[edit]

There are four major toxins produced by Clostridium perfringens. Alpha, beta, and epsilon toxins increase a cells permeability which causes an ion imbalance while iota toxins destroy the cell's actin cytoskeleton. Becoming intoxicated by any of these clostridial proteins eventually leads to the dysfunction of the cell and finally, its death. This can also cause anguish to the host that can then become lethal. These toxins are what allow C. perfringens to strive within a human or animal host.[1] These toxins are made from five different strains of C. perfringens, These strains include A, B, C, D, and G. Each toxin that falls under one of these types is linked to a variety of diseases.[1]

These toxins are made from five different strains of C. perfringens, These strains include A, B, C, D, and E. Each toxin that falls under one of these types is linked to a variety of diseases.[1]

Alpha toxin[edit]

Alpha toxin is a zinc-containing phospholipase C, composed of two structural domains, which destroy a cell's membrane. Alpha toxins are produced by all five types of C. perfringens.This toxin is linked to gas gangrene of humans and animals. Most cases of gas gangrene has been related to a deep wound being contaminated by soil that harbors C. perfringens.[1][2]

Beta toxin[edit]

Beta toxins are a protein that causes hemorrhagic necrotizing enteritis and enterotoxaemia in both animals (type B) and humans (type C) which leads to the infected individual's feces becoming bloody and their intestines necrotizing.[1]

Epsilon toxin[edit]

Epsilon toxin (ETX) is a protein produced by type B and type D strains of C. perfringens. This toxin is currently ranked the third most potent bacterial toxin known.[3] ETX causes enterotoxaemia in mainly goats and sheep, but cattle are sometime susceptible to it as well. A experiment using mice found that ETX had an LD50 of 50-110 ng/kg.[4] The excessive production of ETX increases the permeability of the intestines. This causes severe edema in organs such as the brain and kidneys.[5]

Iota toxin[edit]

Iota toxin is a protein produced by type E strands of C. perfringens. Iota toxins are made up of two, unlinked proteins that form a multimeric complex on cells. Iota toxins prevent the formation of filamentous actin. This causes the destruction of the cells cytoskeleton which in turn leads to the death of the cell as it can no longer maintain homeostasis.[6]

Transmission and pathogenesis[edit]

C. perfringens is most commonly known for foodborne illness, but can translocate from a gastrointestinal source into the bloodstream which causes bacteremia. C. perfringens bacteremia can lead to toxin-mediated intravascular hemolysis and septic shock.[7] This is rare as it makes up less than 1% of bloodstream isolates, but is highly fatal with a reported mortality rate of 27% to 58%.[8]

Clostridium perfringens is the most common bacterial agent for gas gangrene. Some symptoms include blisters, tachycardia, swelling, and jaundice.

A strain of C. perfringens might be implicated in multiple sclerosis (MS) nascent (Pattern III) lesions. Tests in mice found that a two strains of intestinal C. perfringens that produced epsilon toxins (ETX) caused MS-like damage in the brain, and earlier work had identified this strain of C. perfringens in a human with MS. MS patients were found to be 10 times more immune-reactive to the epsilon toxin than healthy people.

Perfringolysin O (pfoA)-positive C. perfringens strains were also associated with the rapid onset of necrotizing enterocolitis in preterm infants.

Prevention[edit]

The growth of C. perfringens spores can be prevented by most cooking food, especially beef and poultry, to recommended temperatures. Leftover food should be refrigerated to a temperature below 40 °F (4 °C) within two hours of preparation. Large pots of food such as soup or stew with meats should be divided into small quantities and covered for refrigeration. Leftovers should be reheated to at least 165 °F (74 °C) before serving. A rule of thumb is that if the food tastes, smells, or looks different from what it is supposed to, then it should be avoided. Even if it looks safe, a food that has been out for a long time can also be dangerous to eat.[9]

The temperature that C. perfringens can multiply within can range anywhere from 59 °F (15 °C) to 122 °F (50 °C).[10]

Treatment[edit]

The most important aspect of treatment is prompt and extensive surgical debridement of the involved area and excision of all devitalized tissue, in which the organisms are prone to grow. Administration of antimicrobial drugs, particularly penicillin, is begun at the same time. Clostridium perfringens is more often susceptible to vancomycin compared to other pathogenic Clostridia.[11] Hyperbaric oxygen may be of help in the medical management of clostridial tissue infections.[12]

Most people who suffer from food poisoning caused by C. perfringens tend to fight off the illness without the need of any antibiotics. Extra fluids should be drank consistently until diarrhea dissipates.[13]

Genome[edit][edit]

Clostridium perfringens has a stable G+C content around 27–28% and average genome size of 3.5 Mb. Genomes of 56 C. perfringens strains have since been made available on NCBI genomes database for the scientific research community. Genomic research has revealed surprisingly high diversity in C. perfringens pangenome, with only 12.6% core genes, identified as the most divergent Gram-positive bacteria reported. Nevertheless, 16S rRNA regions in between C. perfringens strains are found to be highly conserved (sequence identity >99.1%).

The clostridium perfrigens enterotoxin (CPE) producing strain has been identified to be a small portion of the overall population of this Clostridium perfringens (~1-5%) through genomic testing[14]. Advances in gentic information surrounding strain A CPE Clostridium perfringens has allowed techniques such as microbial source tracking (MST) to identify food contamination sources[14]. The CPE gene has been found within chromosomal DNA as well as plasmid DNA[14]. Plasmid DNA has been shown to play and integral role in cell pathogenisis and encodes for major toxins, including CPE[15].

Clostridium perfringens has been shown to carry plasmid containing genes for antibiotic resistance. The pCW3 plasmid is the primary conjugation plasmid responsible for creating antibiotic resistance in Clostridium perfringens. Furthermore, the pCW3 plasmid also encodes for multiple aforementioned toxins found in pathogenic strains of Clostridium perfrigens.[16] Antibiotic resitance genes observed thus far include tetracycline resistance, efflux protein, and aminoglycoside resistance.[17]

Within industrial context, such as food production, sequencing genomes for pathogenic strains of C. perfringens has become an expanding field of research. Poulry production is impacted directly from this trend as antibiotic resistant strains of C. perfringens are becoming more common.[18] By preforming a meta-genome analysis, researches are capable of identifying novel strains of pathogenic strains of bacterium, such as C. perfringens B20.[18]

Metabolic Processes[edit]

C. perfringens is an aerotolerant anaerobe bacterium that live in a variety of environments such as soil and human intestinal tracts.[19] After genomic testing, it is known C. perfringens is incapable of synthesizing multiple amino acids due to the lack of genes require for biosynthesis.[19] Instead, the bacterium produces enzymes and toxins to break down host cells and import nutrients from the degrading cell.[19]

Motility [edit][edit]

Clostridium perfringens is provisionally identified as non-motile. With the exception of Clostridium perfringens, almost all of the genus' members are motile, have peritrichous flagella, and produce spherical or oval endospores that may cause the cell to enlarge.[20]Still, C. perfringens bacteria may glide across surfaces despite lacking flagella because their bodies are completely covered with filaments.

This is an artist's rendition of a scanning electron microscopy (SEM) image of a cluster of Clostridium perfringens cells.

Hyper-motile Clostridium Perfringens Variations[edit]

Around agar plates, colonies with hypermotile variations like SM101 frequently appear around the borders of the colonies. They appear to create long, thin filaments that enable them to move quickly, much like bacteria with flagella, according to video imaging of their gliding motion. The cause(s) of the hypermotile phenotype and its immediate descendants were found using genome sequencing. The hypermotile offspring of strains SM101 and SM102, SM124 and SM127, respectively, had 10 and 6 nucleotide polymorphisms (SNPs) in comparison to their parent strains. The hypermotile strains have the common trait of gene mutations related to cell division.[21]

Nathan East's contributions[edit]

Added last three paragraphs to the genome section

added 4 refrences within genome section

Metabolic Processes plus the citations

SEM image in the motility section

Added 4th paragraph to the lead section

Mason Taylor's contributions[edit]

Added Toxins section

added/ changed material from existing treatment, prevention, transmission, and pathogenesis sections

deleted/changed gas gangrene section due to plagiarism from previous editor

updated and corrected taxonomy for microbe

Added 16 different references

  1. ^ a b c d e Stiles, Bradley G.; Barth, Gillian; Barth, Holger; Popoff, Michel R. (2013-11-12). "Clostridium perfringens Epsilon Toxin: A Malevolent Molecule for Animals and Man?". Toxins. 5 (11): 2138–2160. doi:10.3390/toxins5112138. ISSN 2072-6651. PMC 3847718. PMID 24284826.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  2. ^ Li, Ming; Li, Ning (2021-06-16). "Clostridium perfringens bloodstream infection secondary to acute pancreatitis: A case report". World Journal of Clinical Cases. 9 (17): 4357–4364. doi:10.12998/wjcc.v9.i17.4357. ISSN 2307-8960.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  3. ^ Alves, Guilherme Guerra; Machado de Ávila, Ricardo Andrez; Chávez-Olórtegui, Carlos Delfin; Lobato, Francisco Carlos Faria (2014-12-01). "Clostridium perfringens epsilon toxin: The third most potent bacterial toxin known". Anaerobe. 30: 102–107. doi:10.1016/j.anaerobe.2014.08.016. ISSN 1075-9964.
  4. ^ Xin, Wenwen; Wang, Jinglin (2019-09-01). "Clostridium perfringens epsilon toxin: Toxic effects and mechanisms of action". Biosafety and Health. 1 (2): 71–75. doi:10.1016/j.bsheal.2019.09.004. ISSN 2590-0536.
  5. ^ Geng, Zhijun; Kang, Lin; Huang, Jing; Gao, Shan; Wang, Jing; Yuan, Yuan; Li, Yanwei; Wang, Jinglin; Xin, Wenwen (2021-07-30). "Epsilon toxin from Clostridium perfringens induces toxic effects on skin tissues and HaCaT and human epidermal keratinocytes". Toxicon. 198: 102–110. doi:10.1016/j.toxicon.2021.05.002. ISSN 0041-0101.
  6. ^ Sakurai, Jun; Nagahama, Masahiro; Oda, Masataka; Tsuge, Hideaki; Kobayashi, Keiko (2009-12-23). "Clostridium perfringens Iota-Toxin: Structure and Function". Toxins. 1 (2): 208–228. doi:10.3390/toxins1020208. ISSN 2072-6651. PMC 3202787. PMID 22069542.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  7. ^ "Cytarabine". Reactions Weekly. 1959 (1): 223–223. 2023-06-03. doi:10.1007/s40278-023-40395-7. ISSN 1179-2051.
  8. ^ Millard, Michael A.; McManus, Kathleen A.; Wispelwey, Brian (2016). "Severe Sepsis due to Clostridium perfringens Bacteremia of Urinary Origin: A Case Report and Systematic Review". Case Reports in Infectious Diseases. 2016: 1–5. doi:10.1155/2016/2981729. ISSN 2090-6625.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  9. ^ "Clostridium perfringens". Center for Disease Control and Prevention. 2015-10-08. Retrieved 2016-09-27.
  10. ^ Taormina, Peter J.; Dorsa, Warren J. (July 2004). "Growth Potential of Clostridium perfringens during Cooling of Cooked Meats". Journal of Food Protection. 67 (7): 1537–1547. doi:10.4315/0362-028X-67.7.1537.
  11. ^ Di Bella, Stefano; Antonello, Roberta Maria; Sanson, Gianfranco; Maraolo, Alberto Enrico; Giacobbe, Daniele Roberto; Sepulcri, Chiara; Ambretti, Simone; Aschbacher, Richard; Bartolini, Laura; Bernardo, Mariano; Bielli, Alessandra (June 2022). "Anaerobic bloodstream infections in Italy (ITANAEROBY): A 5-year retrospective nationwide survey". Anaerobe. 75: 102583. doi:10.1016/j.anaerobe.2022.102583. hdl:11368/3020691. PMID 35568274. S2CID 248736289.
  12. ^ Jawetz Melnick & Adelbergs Medical Microbiology - 27E.
  13. ^ CDC (2023-03-24). "Prevent Illness From C. perfringens". Centers for Disease Control and Prevention. Retrieved 2023-10-01.
  14. ^ a b c Miyamoto, Kazuaki; Li, Jihong; McClane, Bruce A. (2012). "Enterotoxigenic Clostridium perfringens: Detection and Identification". Microbes and environments. 27 (4): 343–349. doi:10.1264/jsme2.ME12002. ISSN 1342-6311.
  15. ^ Gulliver, Emily L.; Adams, Vicki; Marcelino, Vanessa Rossetto; Gould, Jodee; Rutten, Emily L.; Powell, David R.; Young, Remy B.; D’Adamo, Gemma L.; Hemphill, Jamia; Solari, Sean M.; Revitt-Mills, Sarah A.; Munn, Samantha; Jirapanjawat, Thanavit; Greening, Chris; Boer, Jennifer C. (2023-04-20). "Extensive genome analysis identifies novel plasmid families in Clostridium perfringens". Microbial Genomics. 9 (4). doi:10.1099/mgen.0.000995. ISSN 2057-5858.
  16. ^ Adams, Vicki; Han, Xiaoyan; Lyras, Dena; Rood, Julian I. (2018-09). "Antibiotic resistance plasmids and mobile genetic elements of Clostridium perfringens". Plasmid. 99: 32–39. doi:10.1016/j.plasmid.2018.07.002. {{cite journal}}: Check date values in: |date= (help)
  17. ^ Kiu, Raymond; Caim, Shabhonam; Alexander, Sarah; Pachori, Purnima; Hall, Lindsay J. (2017-12-12). "Probing Genomic Aspects of the Multi-Host Pathogen Clostridium perfringens Reveals Significant Pangenome Diversity, and a Diverse Array of Virulence Factors". Frontiers in Microbiology. 8. doi:10.3389/fmicb.2017.02485. ISSN 1664-302X.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  18. ^ a b Elnar, Arxel G.; Kim, Geun-Bae (2021-11-30). "Complete genome sequence of Clostridium perfringens B20, a bacteriocin-producing pathogen". Journal of Animal Science and Technology. 63 (6): 1468–1472. doi:10.5187/jast.2021.e113. ISSN 2672-0191.
  19. ^ a b c Ohtani, Kaori; Shimizu, Tohru (2016-07-05). "Regulation of Toxin Production in Clostridium perfringens". Toxins. 8 (7): 207. doi:10.3390/toxins8070207. ISSN 2072-6651.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  20. ^ Wambui, Joseph; Cernela, Nicole; Stevens, Marc J. A.; Stephan, Roger (2021-09-13). "Whole Genome Sequence-Based Identification of Clostridium estertheticum Complex Strains Supports the Need for Taxonomic Reclassification Within the Species Clostridium estertheticum". Frontiers in Microbiology. 12. doi:10.3389/fmicb.2021.727022. ISSN 1664-302X.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  21. ^ Liu, Hualan; McCord, Kristin D.; Howarth, Jonathon; Popham, David L.; Jensen, Roderick V.; Melville, Stephen B. (2014-7). "Hypermotility in Clostridium perfringens Strain SM101 Is Due to Spontaneous Mutations in Genes Linked to Cell Division". Journal of Bacteriology. 196 (13): 2405–2412. doi:10.1128/JB.01614-14. ISSN 0021-9193. PMC 4054169. PMID 24748614. {{cite journal}}: Check date values in: |date= (help)