Botulinum Clostridia

Clostridia: rod-shaped, obligate anaerobes, some form endospores, produce potent toxins that cause a variety of diseases in humans. Important in medicine & industry (Botox & oral plaque). Examples of clostridia include C. tetani (cause tetanus), C. perfringens ( causes gangrene), C. botulinum ( causes botulism) and C. difficle (severe diarrhea). Microbes related to Clostridium include: Epulopiscium - a giant bacterium that can be seen without a microscope; Some clostridia are sulfate-reducing microbes – they produce H2S from elemental sulfur during anaerobic respiration; and Selenomonas – a Vibrio-shaped bacteria, live as part of the biofilm (plaque) on teeth of warm-blooded animals. Selenomonas is unusual because even though it has a typical gram-positive RNA sequence, it has a negative Gram reaction – stains pink.

Clostridim difficile was first isolated in1935 by George and his colleagues from a stool found in a healthy infant by the name of Hall and O’Toole (Heinlen and Ballard, 2010). Yet in 1978, C.difficile was known to be associated as disease in human’s antibiotic-associated diarrhea (Heinlen and Ballard, 2010). It is 2 types of C. difficile: one that exists in spore form and the other in vegetative form. Depending on the type of form it exist in, allows it to grow in a certain environment. It is also a gram positive rod bacterium. When Clostridim difficile exist in a spore form, it can live in harsh conditions and in common sterilization techniques (Heinlen and Ballard, 2010). When C. difficile exist in spore form, it will be resistant to temperature

C. diff strains produce multiple toxins. The most well-known are enterotoxin (Clostridium difficile toxin A) and cytotoxin (Clostridium difficile toxin B). These toxins generally agitate the intestines causing C. difficile infections (CDI) including pseudomembranous colitis.

Clostridium difficile is a gram positive, anaerobic, spore forming bacillus. In 1935 it was first described as member of the intestinal flora in healthy neonates [1] , and then in 1978 it was recognised as a cause of diarrhoea [2]. Today it is widely acknowledged as the leading cause of hospital-acquired diarrhoea. This organism can cause a variety of diseases, from mild diarrhoea to severe pseudomembranous colitis, and collectively these are known as C. difficile infections (CDIs) [3]. It is known that the symptoms seen in patients infected with C. difficile are due to the toxins (toxin A and toxin B) that are produced by the organism [4]. Some strains of C. difficile seem to have an increased virulence which can be associated with increased severity, recurrence and increased mortality. This increased virulence is thought to be a result of increased expression of toxins A, B [5]. There is also another toxin produced by C. difficile known as binary toxin, this is also thought to contribute towards increased virulence [6]. A particular strain of C. difficile that does seem to have increased virulence is the strain known as PCR ribotype O27 or North American pulsed (NAP)-field type 01. In Europe PCR ribotype O27 is the sixth most common ribotype [7], and new ribotypes are being detected that appear to have evolved from the O27 lineage [8], making the need for a method to demonstrate strain relatedness highly important. In a hospital setting knowing the

Clostridium perfringens is an anaerobic, spore-forming bacterium that can be found in soil, feces, and water. There are four major toxins (alpha, beta, epsilon and iota) and five strains of C. perfringens (A-E) that cause a variety of symptoms such as food poisoning, gas gangrene, and severe neurological disease in sheep and other ruminants. The latter will be the primary focus of this research paper.

Clostridium botulinum is a kind of bacterium that is responsible for botulism. This is a Gram-positive, rod-shaped bacterium. There are 7 types of toxins caused by C.botulinum, A-G, but only 4 of these toxin are known to cause a disease in humans they are A, B,E, and F. Only type A is universal throughout the world. Toxin G is encoded in the plasmid unlike the rest are encoded in the bacterial chromosome. What is special about type C. Botulinum is that it can only produce its toxin during sporulation. Clostridium botulinum will only become active when the environmental conditions are appropriate but other than that the endospores of Clostridium botulinum will stay “asleep” in contaminated foods. This type

Food-borne botulism is the next type. It is a harmful bacterium that thrives in environments with little to no

Clostridium botulinum produces botulinum toxin which is the strongest human known toxin. This makes it have great potential for use as a bioweapon. The concern for this has risen due to Iraq’s production, under Saddam Hussein’s rule, of 19,000 liters of botulinum toxin in 1995. This amount is enough to kill the entire population of humans on earth, three times over. The use of this neurotoxin could be in the form of aerosol or food contamination. For this reason, it is highly studied. It is also the reason I picked Clostridium botulinum as the bacterium to do my research paper on.

The illness of topic that is rare but potentially fatal that is caused by a toxin is Botulism. In the United States, health care providers report an average of 110 cases per year. The botulinum toxin is a neurotoxin protein. The causative organism that makes up this toxin is Clostridium botulism and sometimes Clostridium butyricum or Clostridium baratii. They are the gram-positive, rod-shaped, spore-forming, obligate anaerobic bacteria. The bacteria that make this toxin are naturally found in many places and it is rare for them to make people sick. This bacterium makes spores that act like a protective coating. The spores help these bacteria survive in the environment, even in very extreme conditions. The spores even when eaten usually do not make people sick but under certain conditions they can grow and become

Botulism2What is the significance of clostridium botulinum being anaerobic?Botulinum bacteria can live in the absence of oxygen. This means that they can live and grow in number, and produce the botulin toxin in a sealed jar or can. Clostridium botulinum spores are quite widespread throughout the world, inhabiting soil as well as both freshwater and saltwater in mud. Clostridium botulinum organism

Vultures are a sign of death, yet they have a curious immunity to species of bacteria that would kill a normal human. One of the most dangerous of these bacteria is Clostridium botulinum, which causes paralysis in most animals. Through such differences from people, animals provide examples of natural survival techniques that scientists research to help society. I intend to enter the research field in order to solve mysteries such as the vulture’s bacteria immunity and help my community by applying such discoveries to human ailments.

The strategy used to determine the unknown organism was to first perform a gram stain to determine if the organism was either a gram negative or gram positive bacteria based on the color of cells. A TSA plate was inoculated to streak for isolation and purity. After colonies were incubated characteristics of colony morphology were recorded and a TSB broth and TSA slant were inoculated to determine characteristics of growth in broth and slant. Another TSA plate was inoculated to determine growth under anaerobic conditions. The next step was to look over the class results for biochemical test and create a dichotomous key to determine which test were useful and which were unnecessary to perform. The gram stain helped determine that the organism

Botulinum neurotoxins (BoNTs) are the most toxic bacterial toxins known and are produced by the anaerobic spore forming bacteria Clostridium botulinum, C. butyricum, or C. baratii [1]. When contaminated food is ingested the toxin induces botulism, a disease characterized by descending flaccid paralysis that can lead to death by respiratory failure when untreated [2]. Due to BoNTs high toxicity (intraperitoneal LD50: 1 ng/kg [3]) it is regarded as a potential bioweapon [4], but it has also broad medical and cosmetic applications due to its highly specific inhibition of neurotransmitter release in the neuromuscular junction [5-7]. Both its potency and specificity can be attributed to an elaborate and elegant mode of action, mediated by the different domains of the 150 kDa molecule [8]. First, the 50 kDa C-terminal domain of the 100 kDa heavy chain (HC) mediates high affinity binding to specific receptors on the presynaptic membrane. Next, BoNT is taken up into recycling synaptic vesicles whereupon acidification the 50 kDa N-terminal domain (HN) forms a pore through which the 50 kDa light chain (LC) is released in the cytoplasm. Finally, LC-mediated substrate cleavage of different members of the SNARE-protein complex inhibits fusion of neurotransmitter-filled vesicles at cholinergic synapses hereby inhibiting cargo release and transmission of the stimulus to the attached muscle [9].

The symptoms are caused by tetanospasmin, a neurotoxin produced by the bacterium Clostridium tetani. The average incubation period is seven to ten days, and

In addition, Mtx2 shares homology with epsilon toxin from Clostridium, suggests its mode of action as pore forming toxin [2]. The mtx2 gene encodes a 31.8 kDa protein which is moderately toxic to Culex and Aedes larvae [3], and specificity determinant of the protein depends on amino acid at position 224 where lysine and threonine renders toxicity towards Culex and Aedes larvae, respectively [4]. Study of truncated Mtx2 proteins showed that amino acid position 23-26 in the N terminus are required for full toxicity and the C terminus is important for folding and toxicity of the Mtx2