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Recommended: Botulism case study
An unlikely substance for humans to willingly inject into themselves, botulinum toxin is the endotoxin produced by the gram-negative, acidophilic anaerobe Clostridium botulinum. This neurotoxin, which causes muscular paralysis and can result in death due to respiratory failure, is extremely potent; just 50 grams would be enough to kill every person on the planet (Lindsay, 2013). The earliest recorded case of botulism poisoning occurred in 1735 in Europe. Assumed to be associated with a batch of sausage, it was named for the German word for sausage, “botulus (Sterba, 1982).” Botulism poisoning still occurs today, though with careful food preparation techniques it is incredibly rare. With modern medical attention, the case fatality rate of botulism …show more content…
botulinum was first isolated and identified in 1895. Immediately, intrigue regarding possible therapeutic value of the bacterium’s potent neurotoxin led to extensive research, and ultimately, the pharmacological empire that exists today. The toxin itself was first isolated in the 1920s. By the 1950s, a medical doctor named Vernon Brooks discovered that the toxin blocked the release of acetylcholine from motor nerve endings, which temporarily reduced muscular activity when injected into a hyperactive muscle. Studies conducted by Alan B. Scott, M.D. in the 1960s showed that, in monkeys, intramuscular injection of minute quantities of purified toxin realigned the crossed eyes associated with strabismus. Shortly thereafter, Dr. Scott began testing the toxin on human volunteers (History and Development, …show more content…
As seen by Blasi (1993) found that the light chain acts as a zinc-dependent protease. It targets and cleaves at the carboxy terminus of the SNARE protein SNAP-25. The destruction of this SNARE protein causes the inability for the neurotransmitter vesicles to localize via the synaptobrevin-SNAP 25 interaction. It also disables the SNARE complex from docking or fusing any vesicles. Without neurotransmitter release into the synaptic cleft, there can be no muscular contraction. The neuron still receives the signals from the central nervous system, but is no longer able to pass the signal on though the neuromuscular junction, thus paralyzing the muscles innervated by neurons affected by the
In the beginning phases of muscle contraction, a “cocked” motor neuron in the spinal cord is activated to form a neuromuscular junction with each muscle fiber when it begins branching out to each cell. An action potential is passed down the nerve, releasing calcium, which simultaneously stimulates the release of acetylcholine onto the sarcolemma. As long as calcium and ATP are present, the contraction will continue. Acetylcholine then initiates the resting potential’s change under the motor end plate, stimulates the action potential, and passes along both directions on the surface of the muscle fiber. Sodium ions rush into the cell through the open channels to depolarize the sarcolemma. The depolarization spreads. The potassium channels open while the sodium channels close off, which repolarizes the entire cell. The action potential is dispersed throughout the cell through the transverse tubule, causing the sarcoplasmic reticulum to release
Objective data are observable and measurable. This information is usually obtained through the senses as sight, smell, hearing and touch, during the physical examination of the patient. During Mary was assessed, this is the objective data: symmetrical abdomen, bowel sounds in all quadrants, tender to palpation in the lower quadrants, guarding, skin is warm and moist and her lips and mucous membranes are dry.
Shukla, H.D. and S. K. Sharma. “Clostridium botulinum: A Bug with Beauty and Weapon.” Informa Healthcare 31.1 (2005): n.p. Web. 26 Jan. 2014.
JIU-CONG, Z., LI, S.,& QING-HE, N. (2010). Botulism, where are we now?. Clinical Toxicology (15563650), 48(9), 867-879. doi: 103109/15563650.2010.535003
Simpson LL. Identification of the characteristics that underlie botulinum toxin potency: implications for designing novel drugs. Biochimie 2000:82: 943-953.
Muscle contraction is a long process. It goes through many different steps. First, an electrical signal, action potential, travels down a nerve cell, causing it to release a chemical message, known as neurotransmitter,into a small gap between the nerve cell and muscle cell. This gap is called the synapse.The chemical message, neurotransmitter, crosses the gap, and attaches to a protein called a receptor on the muscle-cell membrane and causes an electrical signal, action potential, in the muscle cell.The chemical signal, action potential, spreads quickly along the muscle cel...
perfringens is the most common cause of foodborne illness in the United States, with a million cases each year (CDC, 2014). C. perfringens is able to produce up to 15 different toxins, making it versatile. These toxins are used to isolate the five different types of C. perfringes: type A, B, C, D, and E. The four toxins that are primarily used to isolate the different types include alpha, beta, epsilon, and iota-toxins. Type A is the most common and most variable, and subdivided into entertoxigenic and non-enterotoxigenic strains (Herholz et al., 1999). Enterotoxigenic type A and C are associated with equine enterocolitis, gas gangrene, infections, avian and canine necrotic enteritis, colitis in horses, and diarrhea in pigs (Divers and Ball, 1996). Types B, C, D, and E can cause severe enteritis, dysentery, toxemia, and high mortality rates in young lambs, calves, pigs, and foals. Types B, C, D, and E have been intermittently associated with foal enterocolitis, and equine antibiotic associated diarrhea (Divers and Ball, 1996). Even though the alpha toxin is noted to be relatively nonpathogenic, the beta2 toxin plays a significant role in digestive disease, specifically, enterocolitis in equine (Herholz et al., 1999). This is mainly due to the C. perfringens entertoxin (CPE), the main virulence factor that initiates many critical gastrointestinal diseases across species (Herholz et al. 1999). CPE works in a four-step mechanism against membrane action (CDC, 2014). First,
Shier, W. 2008, “Introduction to the Special Issue on Lethal Toxin Neutralizing Factor", Toxin Reviews, vol. 27, pp. 79-80.
These microglial cells then induced inflammation in the cerebellum, which resulted in the learning and coordination problems (Rettner para.5). Considering it is nearly impossible to test for the drug it poses a control problem.
An illness, a disease, a neurotoxin that is fatal. Beginning in crowded areas with massive populations and an abundance of homes, businesses and infrastructure. Targeting everyone despite age, gender and race. A toxin so powerful that an epidemic was declared in the state of New York within hours.
Most natural toxins happen naturally in just few foods and other natural toxins are produced when the food is damaged or when mould or fungi growth on the food,
The botulinum bacteria if left to grow will produce spores and create a deadly toxin that can result in food borne botulism. The bacterium, C. botulinum is present in soil and in marine sediment. The spores can be found on fruits and vegetables, but the spores are harmless at this stage, because to grow and to create toxins, it needs a low oxygen, low acid environment.
The patient has experienced fever, chills on body, headaches and anorexia as well as sweating especially during the night. The patient has also been feeling fatigued, muscle aches and nausea as well as vomiting especially after eating (WHO, 2010, p. 117). These symptoms started forty eight hours ago, and the patient has not taken any medication except for some aspirin.
The detailed mechanism of BoNT pathogenicity and the structure-function relationship of BoNT provide invaluable targets for development of the antidotes and inhibitors against botulism. The BoNT molecule is divided in clear functional domains that can operate independently. This feature provides multiple targets for designing therapeutics to treat botulism. High throughput screening and the combinatorial chemistry provide another useful tool for screening the inhibitors against botulism (Cai and Singh, 2007). Early work with zinc metalloprotease inhibitors focused on the well-characterized agents captopril ((2S)-1-[(2S)-2-methyl-3-sulfanyl-propanoyl] pyrrolidine-2-carboxylic acid) and phosphoramidon (N-alpha-L-rhamno pyranosyl oxy [hydroxyl phosphinyl]-L-leucyl-L-tryptophan). These compounds, however, were found to have little inhibitory activity against BoNT (Adler et al., 1994, 1999a). Phosphoramidon analogs in which Leu–Trp was replaced by Phe–Glu to resemble the cleavage site of synaptobrevin exhibited little increase in inhibitory activity (Adler et al., 1999a).
“Botox is a neurotoxin derived from Clostridium botulinum, an organism found in the natural environment where it is largely inactive and non-toxic” (Nichols). It temporarily paralyzes the muscles. Clostridium botulinum can be found in the forest and cultivated soils, and in the sediments of lakes, streams and untreated waters. The bacteria can be found also in the intestines of mammals and fish. It can also be found in the organs of crabs and other shellfish. This