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[[Image:B2201272-Clostridium_botulinum_bacteria-SPL.jpg|thumb|400 px|right|"Clostridium botulinum". This picture shows the rod-shaped bacteria. Courtesy of[http://www.sciencephotolibrary.com/images/showEnlarged.html/B2201272-Clostridium_botulinum_bacteria-SPL.jpg?id=662201272]]]
[[Image:B2201272-Clostridium_botulinum_bacteria-SPL.jpg|thumb|400 px|right|"Clostridium botulinum". This picture shows the rod-shaped bacteria, C. botulinim, under a scanning electron microscope. Courtesy of Science Photo Library.com [http://www.sciencephotolibrary.com/images/showEnlarged.html/B2201272-Clostridium_botulinum_bacteria-SPL.jpg?id=662201272]]]
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Revision as of 19:13, 7 April 2011

Clostridium botulinum

"Clostridium botulinum". This picture shows the rod-shaped bacteria, C. botulinim, under a scanning electron microscope. Courtesy of Science Photo Library.com [1]





Classification

Taxonomic Classification for Clostridium botulinum

Kingdom: Bacteria

Phylum: Firmicutes

Class: Clostridia

Order: Clostridiales

Family: Clostridiaceae

Genus: Clostridium

Species: botulinum

Description and Significance

Clostridium botulinum is a rod-shaped, gram positive bacteria that produces heat and chemical resistant endospores. The bacterium is a soil dwelling anaerobe that produces a known neurotoxin. The toxin produced by this bacteria is one of the most deadly naturally produced substances known to man. The symptoms of botulism were first described by Justinus Kerner in the early 1820's. Kerner named the disease botulism after the Latin word for sausage, owing to the fact that much of the food poisoning was attributed to the undercooked breakfast meat.

There are seven identified toxins produced by an equal number of strains of the C. botulinum, types A-G. Each strain when cultured has produced toxins of different specificities.
The neurotoxins of Clostridium botulinum cause paralysis and ailments such as infant botulism, wound botulism, and botulism poisoning. Th most common form is food poisoning. Infant botulism most frequently is caused by the ingestion of honey. Wound botulism is much rarer and similar in symptoms to tetanus. The neurotoxin of Clostridium botulinum is also key to the procedure of Botox.

Genome

The complete genome of the A strain of the C. botulinum was sequenced in May 2007 at the Sanger Institute.

The topography found in this organism is a circular model of DNA. The complete chromosome of the bacteria is 3,886,916 nt. In the organism there are 3,776 genes, 81% of which are coding genes.

Similar to other members of the Clostridium genus, there is a low cytosine-guanine, 28% in C. botulinum.

The bacterium contains a 16.3 kilobase plasmid, containing 19 coding genes, with a guanine-cytosine content a little lower than that of the chromosome -- 26.8% [5].

Most of the virulence factors in C. botulinum are encoded within the chromosome and not the plasmid; bioinformatic analysis has shown that the plasmid does not contain the toxin genes or genes for related virulence factors.

The plasmid however does contain several genes needed for replication: dnaE, which encodes for the alpha subunit of DNA polymerase III as well as the genes that encode the ABC-type multidrug transport ATPase.

The C. botulinum genome contains a large number of genes that encode for secreted proteases and enzymes used for the uptake and metabolism of amino acids. [6]

The genome of C. botulinum also shows the bacteria to have the ability to degrade chitin.

The genome shows a significant lack of recently acquired DNA, indicating a stable genomic content.

Cell Structure and Metabolism

Clostridium botulinum is a gram-positive rod-shaped bacteria that forms vegetative endospores. A typical prokaryote, Clostridium botulinum, has no nucleus or other membrane enclosed organelles. The bacteria reproduces through binary fission. Clostridium botulinum has no flagella. The bacteria is a obligate anaerobe and ferments carbohydrates and nitrogenous compounds such as amino acids. C. botulinum uses the Strickland Reaction to ferment amino acids. The amino acids it needs include typtophane, threonine, valine, leucine, isoleucine, methionine, argininie, phenylalanine, and tyrosine.

Ecology

C. botulinum is most commonly found in the soil and freshwater sediment. The bacteria also can live in animal intestines and be found in animal feces. The endospores of C. botulinum can be found in numerous environments, various foods and sewage due to their resistant nature. The spores of the bacteria are not usually found in human feces unless the human has contracted boltulism.

C. botulinum has been isolated all over the world, on every continent but Antarctica, and at both very deep and very high altitude ranges (below 6400ft up to 11,000ft).

The reproduction of endospores requires non-halophilic salinities and anaerobic conditions.

C. botulinum is often found in improperly canned goods; the improper preparation does not heat the cans to a high enough temperature to denature the C. botulinum endospores, allowing the bacteria to survive leading to potential ingestion by human consumers.

Pathology

The C. botulinum neurotoxins are the most potent toxins known, with as little as 30–100 ng constituting a potentially fatal dose. [7]

The most common occurrence of botulism poisoning is caused by ingestion of a toxin that is produced by the Clostridium botulinum bacteria. There are three types of botulism poisoning: the most common is from ingestion of the bacterial spores. Other types include wound botulism, where open wounds can become colonized by the bacteria. The third type of poisoning is infant botulism, where infants ingest the bacterial spores and suffer from the symptoms of the toxin. The toxin is a neuro-active high molecular weight protein, which comes in seven different variations, types A through G.

If food containing spores of this organism is ingested, the bacteria can grow and produce the toxins which are then taken up by the body. The symptoms of the toxin do not manifest until about one to two months after the ingestion of the contaminated food. It starts by affecting several groups of nerves in the head. These symptoms can appear as drooping eyes, loss of facial expression and difficulty chewing and swallowing. The paralysis is descending and spreads to the rest of the body. The toxin effects not only voluntary muscles, but also the involuntary muscles. This can manifest in respiratory problems. The toxin also affects various parts of the autonomic nervous system. This can lead to symptoms such as dry mouth, and hypotension, and constipation. Overall the most clinically recognized symptoms are descending paralysis, lack of fever, and clear mental abilities.

Current Research

Cool Factor

BOTOX Botox works by cutting off communication between nerve cells and destroying a protein that controls neurotransmitters – SNAP-25. The result is a temporary paralysis of muscles that form furrows, wrinkles, and various other facial lines. This effect generally stays for 4 to 6 months, and then the paralysis wears off.

The bacteria produces one of the most potent and deadly neurotoxins: a single gram of toxin from C. botulinum is a lethal dose for 200,000 mice, and a cup of the toxin in its pure form would be enough to depopulate the entire earth!

Sources

  1. http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&id=1491&lvl=3&keep=1&srchmode=1&unlock&lin=s

  2. http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6TCS-43VJ7K0-9&_user=2403224&_coverDate=11%2F30%2F2001&_rdoc=1&_fmt=high&_orig=search&_origin=search&_sort=d&_docanchor&view=c&_searchStrId=1637460128&_rerunOrigin=scholar.google&_acct=C000057194&_version=1&_urlVersion=0&_userid=2403224&md5=31a01ba61aa9d2025fa99a77dad6b624&searchtype=a

  3. http://www.sciencedirect.com/science?_ob=GatewayURL&_origin=inwardhub&_urlversion=4&_method=citationSearch&_piikey=S004101010100157X&_version=1&_referrer=http%3A%2F%2Fwww.google.com%2Fsearch%3Fclient%3Dsafari%26rls%3Den%26q%3DThe%2Bmost%2Bcommon%2Bhabitats%2Bof%2Bclostridia%2Bare%2Bthe%2Bsoil%2B%28Dodds%3B%2BPopoff%2Band%2BSmith%29%2Band%2Bthe%2Bfeces%2Bof%2Bhumans%2Band%2Banimals%2B%28%2BGeorge%2Band%2BHatheway%29%2C%2Bbut%2Bthe%2Bspores%2Bare%2Bresistant%2Bto%2Benvironmental%2Bstresses%2Band%2Bare%2Balso%2Bfound%2Bin%2Bvarious%2Bfoods%2C%2Bsewage%2C%2Band%2Bother%2Benvironments.%2BUnlike%2Bmany%2Bother%2Bclostridial%2Bspecies%2C%2BC.%2Bbotulinum%2Bspores%2Bare%2Brarely%2Bfound%2Bin%2Bhuman%2Bfeces%2Bunless%2Bthe%2Bindividuals%2Bhave%2Bcontracted%2Bbotulism%2C%2Band%2Bcoproexamination%2Bhas%2Bbeen%2Bsuggested%2Bas%2Ba%2Bpartial%2Bdiagnosis%2Bof%2Bbotulism%2B%28%2BDowell%2C%2BV.R.J.%2C%2BMcCroskey%2C%2BL.M.%2C%2BHatheway%2C%2BC.L.%2C%2BLombard%2C%2BG.L.%2C%2BHughes%2C%2BJ.M.%2Band%2BMerson%2C%2BM.H.%2C%2B1977.%2BCoproexamination%2Bfor%2Bbotulinal%2Btoxin%2Band%2BClostridium%2Bbotulinum.%2BA%2Bnew%2Bprocedure%2Bfor%2Blaboratory%2Bdiagnosis.%2BJ.%2BAmer.%2BMed.%2BAssoc.%2B238%2C%2Bpp.%2B1829%25E2%2580%25931832.%2BView%2BRecord%2Bin%2BScopus%2B%257C%2BCited%2BBy%2Bin%2BScopus%2B%2822%29%2BDowell%2Bet%2Bal.%2C%2B1977%29.%2Bhe%2Btaxonomy%2Bof%2Bthe%2Bclostridia%2Bhas%2Btraditionally%2Bbeen%2Bdetermined%2Bby%2Bcultural%2Bproperties%2C%2Bmorphological%2Bcharacters%2Bincluding%2Bthe%2Bvegetative%2Brod-shape%2Band%2Bproduction%2Bof%2Bendospores%2C%2Bphenotypic%2Bproperties%2Bincluding%2Bfermentation%2Bpatterns%2Bof%2Bcarbohydrates%2Band%2Bnitrogenous%2Bsubstrates%2C%2Bvolatile%2Bacid%2Bformation%2C%2Bcell%2Bwall%2Bstructure%2C%2Band%2Bgenetic%2Bmethods%2Bsuch%2Bas%2Bdetermination%2Bof%2BDNA%25E2%2580%2593DNA%2Bhybridization%2C%2B16S%2BrRNA%2Bsequence%2Bhomology%2C%2Band%2Bmol%25&md5=88162bb70bcb0b55687fd9f22a7ef241

  4. http://www.jwildlifedis.org/cgi/reprint/6/4/205

  5. Dressler D, Adib Saberi F. Botulinum Toxin: Mechanisms of Action. European Neurology [serial online]. March 2005;53(1):3-9. Available from: Academic Search Premier, Ipswich, MA. Accessed March 31, 2011.