Botulinum Toxins, Type A
Clostridium botulinum type A
Clostridium botulinum type E
Clostridium botulinum type B
Clostridium botulinum type D
Clostridium botulinum type F
ADP Ribose Transferases
Clostridium botulinum type C
Lethal Dose 50
Clostridium botulinum type G
rhoB GTP-Binding Protein
Adenosine Diphosphate Ribose
Molecular Sequence Data
Synaptosomal-Associated Protein 25
rhoA GTP-Binding Protein
rho GTP-Binding Proteins
Amino Acid Sequence
Biological Warfare Agents
Rejection of Clostridium putrificum and conservation of Clostridium botulinum and Clostridium sporogenes-Opinion 69. Judicial Commission of the International Committee on Systematic Bacteriology. (1/657)The Judicial Commission rejected the name Clostridium putrificum while conserving Clostridium botulinum for toxigenic strains and conserving Clostridium sporogenes for non-toxigenic strains. (+info)
Biodiversity of Clostridium botulinum type E strains isolated from fish and fishery products. (2/657)The genetic biodiversity of Clostridium botulinum type E strains was studied by pulsed-field gel electrophoresis (PFGE) with two macrorestriction enzymes (SmaI-XmaI and XhoI) and by randomly amplified polymorphic DNA (RAPD) analysis with two primers (OPJ 6 and OPJ 13) to characterize 67 Finnish isolates from fresh fish and fishery products, 15 German isolates from farmed fish, and 10 isolates of North American or North Atlantic origin derived mainly from different types of seafood. The effects of fish species, processing, and geographical origin on the epidemiology of the isolates were evaluated. Cluster analysis based on macrorestriction profiles was performed to study the genetic relationships of the isolates. PFGE and RAPD analyses were combined and resulted in the identification of 62 different subtypes among the 92 type E isolates analyzed. High genetic biodiversity among the isolates was observed regardless of their source. Finnish and North American or North Atlantic isolates did not form distinctly discernible clusters, in contrast with the genetically homogeneous group of German isolates. On the other hand, indistinguishable or closely related genetic profiles among epidemiologically unrelated samples were detected. It was concluded that the high genetic variation was probably a result of a lack of strong selection factors that would influence the evolution of type E. The wide genetic biodiversity observed among type E isolates indicates the value of DNA-based typing methods as a tool in contamination studies in the food industry and in investigations of botulism outbreaks. (+info)
Growth from spores of nonproteolytic Clostridium botulinum in heat-treated vegetable juice. (3/657)Unheated spores of nonproteolytic Clostridium botulinum were able to lead to growth in sterile deoxygenated turnip, spring green, helda bean, broccoli, or potato juice, although the probability of growth was low and the time to growth was longer than the time to growth in culture media. With all five vegetable juices tested, the probability of growth increased when spores were inoculated into the juice and then heated for 2 min in a water bath at 80 degrees C. The probability of growth was greater in bean or broccoli juice than in culture media following 10 min of heat treatment in these media. Growth was prevented by heat treatment of spores in vegetable juices or culture media at 80 degrees C for 100 min. We show for the first time that adding heat-treated vegetable juice to culture media can increase the number of heat-damaged spores of C. botulinum that can lead to colony formation. (+info)
Inhibition of Rho at different stages of thymocyte development gives different perspectives on Rho function. (4/657)Development of thymocytes can be staged according to the levels of expression of the cell-surface markers CD4, CD8, CD44, CD25 and CD2. Thymocyte development is regulated by a complex signalling network , one component of which is the GTPase Rho. The bacterial enzyme C3 transferase from Clostridium botulinum selectively ADP-ribosylates Rho in its effector-binding domain and thereby abolishes its biological function [2,3]. To explore the function of Rho in thymocyte development, we previously used the proximal promoter of the gene encoding the Src-family kinase p56lck to make transgenic mice that selectively express C3 transferase in the thymus [4,6]. In these mice, which lack Rho function from the earliest thymocyte stages, thymocyte numbers are reduced by approximately 50- to 100-fold. Here, we describe transgenic mice that express C3 transferase under the control of the locus control region (LCR) of the CD2 gene; this regulatory element drives expression at a later stage of thymocyte development than the lck proximal promoter . In these mice, thymocyte numbers were also reduced by 50- to 100-fold, but unlike the lck-C3 mice, in which the reduction predominantly results from defects in cell survival of CD25(+) thymocyte progenitors, the CD2-C3 transgenic mice had a pre-T-cell differentiation block at the CD25(+) stage after rearrangement of the T-cell receptor (TCR) beta chains. Analysis of CD2-C3 mice demonstrated that Rho acts as an intracellular switch for TCR beta selection, the critical thymic-differentiation checkpoint. These results show that Rho-mediated survival signals for CD25(+) pre-T cells are generated by the extracellular signals that act on earlier thymocyte precursors and also that temporal cell-type-specific elimination of Rho can reveal different functions of this GTPase in vivo. (+info)
In situ detection of the Clostridium botulinum type C1 toxin gene in wetland sediments with a nested PCR assay. (5/657)A nested PCR was developed for detection of the Clostridium botulinum type C1 toxin gene in sediments collected from wetlands where avian botulism outbreaks had or had not occurred. The C1 toxin gene was detected in 16 of 18 sites, demonstrating both the ubiquitous distribution of C. botulinum type C in wetland sediments and the sensitivity of the detection assay. (+info)
A predictive model that describes the effect of prolonged heating at 70 to 90 degrees C and subsequent incubation at refrigeration temperatures on growth from spores and toxigenesis by nonproteolytic Clostridium botulinum in the presence of lysozyme. (6/657)Refrigerated processed foods of extended durability such as cook-chill and sous-vide foods rely on a minimal heat treatment at 70 to 95 degrees C and then storage at a refrigeration temperature for safety and preservation. These foods are not sterile and are intended to have an extended shelf life, often up to 42 days. The principal microbiological hazard in foods of this type is growth of and toxin production by nonproteolytic Clostridium botulinum. Lysozyme has been shown to increase the measured heat resistance of nonproteolytic C. botulinum spores. However, the heat treatment guidelines for prevention of risk of botulism in these products have not taken into consideration the effect of lysozyme, which can be present in many foods. In order to assess the botulism hazard, the effect of heat treatments at 70, 75, 80, 85, and 90 degrees C combined with refrigerated storage for up to 90 days on growth from 10(6) spores of nonproteolytic C. botulinum (types B, E, and F) in an anaerobic meat medium containing 2,400 U of lysozyme per ml (50 microg per ml) was studied. Provided that the storage temperature was no higher than 8 degrees C, the following heat treatments each prevented growth and toxin production during 90 days; 70 degrees C for >/=2,545 min, 75 degrees C for >/=463 min, 80 degrees C for >/=230 min, 85 degrees C for >/=84 min, and 90 degrees C for >/=33.5 min. A factorial experimental design allowed development of a predictive model that described the incubation time required before the first sample showed growth, as a function of heating temperature (70 to 90 degrees C), period of heat treatment (up to 2,545 min), and incubation temperature (5 to 25 degrees C). Predictions from the model provided a valid description of the data used to generate the model and agreed with observations made previously. (+info)
Pure botulinum neurotoxin is absorbed from the stomach and small intestine and produces peripheral neuromuscular blockade. (7/657)Clostridium botulinum serotype A produces a neurotoxin composed of a 100-kDa heavy chain and a 50-kDa light chain linked by a disulfide bond. This neurotoxin is part of a ca. 900-kDa complex, formed by noncovalent association with a single nontoxin, nonhemagglutinin subunit and a family of hemagglutinating proteins. Previous work has suggested, although never conclusively demonstrated, that neurotoxin alone cannot survive passage through the stomach and/or cannot be absorbed from the gut without the involvement of auxiliary proteins in the complex. Therefore, this study compared the relative absorption and toxicity of three preparations of neurotoxin in an in vivo mouse model. Equimolar amounts of serotype A complex with hemagglutinins, complex without hemagglutinins, and purified neurotoxin were surgically introduced into the stomach or into the small intestine. In some experiments, movement of neurotoxin from the site of administration was restricted by ligation of the pylorus. Comparison of relative toxicities demonstrated that at adequate doses, complex with hemagglutinins, complex without hemagglutinins, and pure neurotoxin can be absorbed from the stomach. The potency of neurotoxin in complex was greater than that of pure neurotoxin, but the magnitude of this difference diminished as the dosage of neurotoxin increased. Qualitatively similar results were obtained when complex with hemagglutinins, complex without hemagglutinins, and pure neurotoxin were placed directly into the intestine. This work establishes that pure botulinum neurotoxin serotype A is toxic when administered orally. This means that pure neurotoxin does not require hemagglutinins or other auxiliary proteins for absorption from the gastrointestinal system into the general circulation. (+info)
Development of an in vitro bioassay for Clostridium botulinum type B neurotoxin in foods that is more sensitive than the mouse bioassay. (8/657)A novel, in vitro bioassay for detection of the botulinum type B neurotoxin in a range of media was developed. The assay is amplified by the enzymic activity of the neurotoxin's light chain and includes the following three stages: first, a small, monoclonal antibody-based immunoaffinity column captures the toxin; second, a peptide substrate is cleaved by using the endopeptidase activity of the type B neurotoxin; and finally, a modified enzyme-linked immunoassay system detects the peptide cleavage products. The assay is highly specific for type B neurotoxin and is capable of detecting type B toxin at a concentration of 5 pg ml(-1) (0.5 mouse 50% lethal dose ml(-1)) in approximately 5 h. The format of the test was found to be suitable for detecting botulinum type B toxin in a range of foodstuffs with a sensitivity that exceeds the sensitivity of the mouse assay. Using highly specific monoclonal antibodies as the capture phase, we found that the endopeptidase assay was capable of differentiating between the type B neurotoxins produced by proteolytic and nonproteolytic strains of Clostridium botulinum type B. (+info)
1. Foodborne botulism: This type of botulism is caused by eating foods that have been contaminated with the bacteria. Symptoms typically begin within 12 to 72 hours after consuming the contaminated food and can include double vision, droopy eyelids, slurred speech, difficulty swallowing, and muscle weakness.
2. Infant botulism: This type of botulism occurs in infants who are exposed to the bacteria through contact with contaminated soil or object. Symptoms can include constipation, poor feeding, and weak cry.
3. Wound botulism: This type of botulism is caused by the bacteria entering an open wound, usually a deep puncture wound or surgical incision.
Botulism is a rare illness in the United States, but it can be deadly if not treated promptly. Treatment typically involves supportive care, such as mechanical ventilation and fluids, as well as antitoxin injections to neutralize the effects of the toxin. Prevention measures include proper food handling and storage, good hygiene practices, and avoiding consumption of improperly canned or preserved foods.
Some common types of Clostridium infections include:
* Clostridium difficile (C. diff) infection: This is a common type of diarrheal disease that can occur after taking antibiotics, especially in people who are hospitalized or living in long-term care facilities.
* Gas gangrene: This is a severe and potentially life-threatening infection that occurs when Clostridium bacteria infect damaged tissue, causing gas to build up in the affected area.
* Tetanus: This is a serious neurological infection caused by the bacterium Clostridium tetani, which can enter the body through open wounds or puncture wounds.
* Botulism: This is a potentially fatal illness caused by the bacterium Clostridium botulinum, which can be contracted through contaminated food or wounds.
Clostridium infections can cause a range of symptoms, including diarrhea, fever, abdominal pain, and swelling or redness in the affected area. Treatment depends on the type of infection and may include antibiotics, surgery, or supportive care to manage symptoms.
Prevention measures for Clostridium infections include proper hand hygiene, avoiding close contact with people who are sick, and practicing safe food handling practices to prevent the spread of botulism and other clostridial infections. Vaccines are also available for some types of clostridial infections, such as tetanus and botulism.
In summary, Clostridium infections are a diverse group of bacterial infections that can cause a range of illnesses, from mild to severe and life-threatening. Proper prevention and treatment measures are essential to avoid the potential complications of these infections.
PSE can be a serious condition, especially in older adults or those with weakened immune systems, as it can lead to life-threatening complications such as inflammation of the bowel wall, perforation of the bowel, and sepsis. PSE is often diagnosed through a combination of clinical symptoms, laboratory tests, and imaging studies such as X-rays or CT scans. Treatment typically involves antibiotics to eradicate the infection, as well as supportive care to manage symptoms such as fluid replacement, pain management, and wound care. In severe cases, surgery may be necessary to remove damaged portions of the intestine.
Prevention measures for PSE include proper hand hygiene, isolation precautions, and environmental cleaning to reduce the transmission of C. diff spores. Probiotics, which are live microorganisms that are similar to the beneficial bacteria found in the gut, have also been shown to be effective in preventing PSE recurrence.
Blepharospasm is a type of movement disorder that affects the eyelids, causing them to twitch or spasm involuntarily. The condition can be caused by a variety of factors, including:
1. Stress and fatigue: High levels of stress and fatigue can lead to muscle tension in the eyelids, resulting in blepharospasm.
2. Caffeine withdrawal: Suddenly stopping or reducing caffeine intake can cause withdrawal symptoms, including blepharospasm.
3. Medications: Certain medications, such as antidepressants and antipsychotics, can cause blepharospasm as a side effect.
4. Neurological disorders: In some cases, blepharospasm may be a symptom of an underlying neurological disorder, such as dystonia or Parkinson's disease.
5. Other causes: Blepharospasm can also be caused by other factors, such as dry eyes, allergies, or exposure to bright lights.
Treatment options for blepharospasm include:
1. Relaxation techniques: Techniques such as deep breathing, progressive muscle relaxation, and visualization can help reduce stress and muscle tension in the eyelids.
2. Botulinum toxin injections: Injecting botulinum toxin into the eyelid muscles can weaken the muscles and reduce the frequency and severity of blepharospasm.
3. Surgery: In severe cases of blepharospasm, surgery may be necessary to remove part of the affected muscle or to alter the position of the eyelid.
4. Medications: Various medications, such as anticholinergic drugs and benzodiazepines, can help reduce the symptoms of blepharospasm.
5. Glasses or contact lenses: In some cases, wearing glasses or contact lenses may help reduce the symptoms of blepharospasm by reducing glare and improving vision.
It is important to note that the best course of treatment will depend on the underlying cause of the blepharospasm, and a healthcare professional should be consulted to determine the appropriate treatment plan.
Examples of Bird Diseases:
1. Avian Influenza (Bird Flu): A viral disease that affects birds and can be transmitted to humans, causing respiratory illness and other symptoms.
2. Psittacosis (Parrot Fever): A bacterial infection caused by Chlamydophila psittaci, which can infect a wide range of bird species and can be transmitted to humans.
3. Aspergillosis: A fungal infection that affects birds, particularly parrots and other Psittacines, causing respiratory problems and other symptoms.
4. Beak and Feather Disease: A viral disease that affects birds, particularly parrots and other Psittacines, causing feather loss and beak deformities.
5. West Nile Virus: A viral disease that can affect birds, as well as humans and other animals, causing a range of symptoms including fever, headache, and muscle weakness.
6. Chlamydophila psittaci: A bacterial infection that can infect birds, particularly parrots and other Psittacines, causing respiratory problems and other symptoms.
7. Mycobacteriosis: A bacterial infection caused by Mycobacterium avium, which can affect a wide range of bird species, including parrots and other Psittacines.
8. Pacheco's Disease: A viral disease that affects birds, particularly parrots and other Psittacines, causing respiratory problems and other symptoms.
9. Polyomavirus: A viral disease that can affect birds, particularly parrots and other Psittacines, causing a range of symptoms including respiratory problems and feather loss.
10. Retinoblastoma: A type of cancer that affects the eyes of birds, particularly parrots and other Psittacines.
It's important to note that many of these diseases can be prevented or treated with proper care and management, including providing a clean and spacious environment, offering a balanced diet, and ensuring access to fresh water and appropriate medical care.
1. The patient experienced a spasm in their leg while running, causing them to stumble and fall.
2. The doctor diagnosed the patient with muscle spasms caused by dehydration and recommended increased fluids and stretching exercises.
3. The athlete suffered from frequent leg spasms during their training, which affected their performance and required regular massage therapy to relieve the discomfort.
Early diagnosis and treatment of torticollis are crucial to prevent long-term complications and improve quality of life. In children, torticollis can be treated with positioning and exercises, while adults may require more intensive physical therapy and pain management.
Muscle spasticity can cause a range of symptoms, including:
* Increased muscle tone, leading to stiffness and rigidity
* Spasms or sudden contractions of the affected muscles
* Difficulty moving the affected limbs
* Pain or discomfort in the affected area
* Abnormal postures or movements
There are several potential causes of muscle spasticity, including:
* Neurological disorders such as cerebral palsy, multiple sclerosis, and spinal cord injuries
* Stroke or other brain injuries
* Muscle damage or inflammation
* Infections such as meningitis or encephalitis
* Metabolic disorders such as hypokalemia (low potassium levels) or hyperthyroidism
Treatment options for muscle spasticity include:
* Physical therapy to improve range of motion and strength
* Medications such as baclofen, tizanidine, or dantrolene to reduce muscle spasms
* Injectable medications such as botulinum toxin or phenol to destroy excess nerve fibers
* Surgery to release or sever affected nerve fibers
* Electrical stimulation therapy to improve muscle function and reduce spasticity.
It is important to note that muscle spasticity can have a significant impact on an individual's quality of life, affecting their ability to perform daily activities, maintain independence, and engage in social and recreational activities. As such, it is important to seek medical attention if symptoms of muscle spasticity are present to determine the underlying cause and develop an appropriate treatment plan.
Foodborne diseases, also known as food-borne illnesses or gastrointestinal infections, are conditions caused by eating contaminated or spoiled food. These diseases can be caused by a variety of pathogens, including bacteria, viruses, and parasites, which can be present in food products at any stage of the food supply chain.
Examples of common foodborne diseases include:
1. Salmonella: Caused by the bacterium Salmonella enterica, this disease can cause symptoms such as diarrhea, fever, and abdominal cramps.
2. E. coli: Caused by the bacterium Escherichia coli, this disease can cause a range of symptoms, including diarrhea, urinary tract infections, and pneumonia.
3. Listeria: Caused by the bacterium Listeria monocytogenes, this disease can cause symptoms such as fever, headache, and stiffness in the neck.
4. Campylobacter: Caused by the bacterium Campylobacter jejuni, this disease can cause symptoms such as diarrhea, fever, and abdominal cramps.
5. Norovirus: This highly contagious virus can cause symptoms such as diarrhea, vomiting, and stomach cramps.
6. Botulism: Caused by the bacterium Clostridium botulinum, this disease can cause symptoms such as muscle paralysis, respiratory failure, and difficulty swallowing.
Foodborne diseases can be diagnosed through a variety of tests, including stool samples, blood tests, and biopsies. Treatment typically involves antibiotics or other supportive care to manage symptoms. Prevention is key to avoiding foodborne diseases, and this includes proper food handling and preparation practices, as well as ensuring that food products are stored and cooked at safe temperatures.
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- Foodborne botulism is a severe neuroparalytic disease caused by consumption of botulinum neurotoxin formed by strains of proteolytic Clostridium botulinum and non-proteolytic C. botulinum during their growth in food. (nih.gov)
- The spontaneous production of botulinum toxin in the infant gut by ingested Clostridium botulinum organisms is the underlying cause of infant botulism, recognised as an infectious disease only in late 1976. (nih.gov)
- Faecal specimens from 160 age-matched healthy infants who served as controls in studies of inpatient infant botulism cases were negative for both C. botulinum organisms and toxin, except for one specimen that contained only C. botulinum type A organisms. (nih.gov)
- These findings suggest that intestinal production of botulinum toxin by C. botulinum is one cause of S.I.D.S. The strikingly similar age-distribution of 62 inpatient infant botulism cases and the 211 S.I.D.S. cases is also consistent with this concept. (nih.gov)
- The recall was initiated after routine sampling conducted by the Washington State Department of Agriculture revealed that one batch of Zesty Sweet Peppers had a pH level high enough to support the formation of the Clostridium botulinum toxin, which causes botulism poisoning. (sprayandscrap.com)
- A case of botulism in the Czech Republic and current possibilities for detecting the neurotoxin produced by Clostridium botulinum]. (bvsalud.org)
- Botulism is a rare but serious illness caused by Clostridium botulinum bacteria. (medlineplus.gov)
- Infant botulism occurs when a baby eats Clostridium botulinum spores and the bacteria grow in the baby's intestines. (medlineplus.gov)
- Norton LE, Schleiss MR. Botulism ( Clostridium botulinum ). (medlineplus.gov)
- Infant botulism is when Clostridium botulinum spores grow in a baby's intestinal tract. (livescience.com)
- Botulism, which is a potentially fatal form of food poisoning caused by Clostridium botulinum bacteria, has been linked to the Bio Gaudiano branded olives since two people were infected after eating them. (foodnavigator.com)
- Take Clostridium botulinum - as in botulism - which can't grow in a pH below 4.6 . (nutsvolts.com)
- Agam Rao] Botulism is treated with management in an intensive care unit, mechanical ventilation when needed, and botulinum antitoxin. (cdc.gov)
- People who get botulism from food get it from eating foods that contain the actual botulinum toxin. (cdc.gov)
- A second way people can develop botulism is when botulinum toxin is produced in a wound that has C. botulinum in it. (cdc.gov)
- In the US these days, wound botulism most often occurs in injection drug users who introduce the C. botulinum into wounds when they skin-pop black tar heroin. (cdc.gov)
- But people can also get wound botulism when C. botulinum from soil contaminates other kinds of wounds, like open fractures and wounds from motor vehicle accidents. (cdc.gov)
- A third way to get botulism is when C. botulinum gets into infant's intestines. (cdc.gov)
- Usually the source of infant botulism isn't known, but we do know that C. botulinum can be found in honey, and since it's also often in environmental sources like dust, it's easy to see how C. botulinum could be ingested. (cdc.gov)
- And finally, the last way of getting botulism can happen when people get too high a dose of botulinum toxin from medical treatment. (cdc.gov)
- But because botulinum toxin is injected, people can get botulism if the dose is too high. (cdc.gov)
- Botulism is an acute neurologic disorder that causes potentially life-threatening paralysis due to a neurotoxin produced by Clostridium botulinum or related species ( C baratii and C. butyricum) . (medscape.com)
- Wound cultures that grow C botulinum suggest the presence of wound botulism. (medscape.com)
- Botulism is caused by toxins produced by Clostridium botulinum bacteria. (thepoultrysite.com)
- Among the 23 deaths, 22 were attributed to bacterial etiologies (nine to Listeria monocytogenes, five Salmonella , four STEC O157, three Clostridium perfringens, and one Shigella ), and one to norovirus. (cdc.gov)
- The usual suspects include Escherichia coli O157:H7, Salmonella , Listeria monocytogenes, Clostridium perfringens, and Campylobacter , which we must also manage with commercially produced meat. (ufl.edu)
Made from a toxin produced1
- Botox is actually made from a toxin produced by Clostridium botulinum . (livescience.com)
- Patient samples were analyzed using affinity carriers and MALDI mass spectrometry , a modern highly sensitive technique for detecting the presence of botulinum neurotoxins . (bvsalud.org)
- In this manuscript we describe an outbreak of Clostridium (C.) botulinum neurotoxin (BoNT) intoxication in a Saxony-Anhalt dairy cow stock of 286 Holstein-Friesian cows and offspring in spring/summer 2009 and its diagnostic approach. (vetline.de)
- The mouse bioassay turned out positive (wasp-waist) in three preselected organ samples and the neutralization test of one sample with type-specific antitoxin confirmed the presence of BoNT type D. We succeeded in isolating a C. botulinum strain from a liver sample which was typed as a D/C mosaic strain by sequence analysis of the toxin gene. (vetline.de)
- Bei 122 Tieren fielen klinische Anzeichen einer Intoxikation mit Clostridium (C.) botulinu m Neurotoxin (BoNT) auf. (vetline.de)
- Der Neutralisationstest einer ausgewählten Probe mit typspezifischen Antitoxinen bestätigte die Anwesenheit von BoNT Typ D. Aus einer Leberprobe gelang die Isolierung eines C. botulinum -Stammes. (vetline.de)
- We found C. botulinum organisms in 10 infants, all of whom died suddenly and unexpectedly. (nih.gov)
- In 2 of these 10 sudden deaths both C. botulinum organisms and botulinum toxin were identified, and from the spleen of 1, C. botulinum organisms were isolated. (nih.gov)
- Spore formation and spore germination of anaerobic food spoilage organisms, especially Clostridium botulinum. (nih.gov)
- Biology and genomic analysis of Clostridium botulinum. (nih.gov)
- Because of the recognition of the pathophysiology of this disease and because the known potency and action of botulinum toxin can lead to rapid respiratory arrest, it appeared possible that the in-vivo production of botulinum toxin could cause the sudden death of some infants. (nih.gov)
- In this nomination document, we discuss a number of potential refinement and replacement methods to the mouse LD50 assay for botulinum toxin potency, and we recommend that these methods be assessed and prioritized for prevalidation and validation studies. (nih.gov)
- The unintended variability in potency of botulinum toxin-based products stemming from the use of the mouse bioassay would be reduced with the use of a more analytical type of assay. (nih.gov)
- You may not know that Botox® and Dysport® are trade names for botulinum toxin. (cdc.gov)
- 8. Role of guanine nucleotide-binding proteins in Clostridium botulinum pathology: purification of substrates for Clostridium botulinum C3 ADP-ribosyltransferase with different requirements for GTP and phospholipids. (nih.gov)
- Botulinum toxin (BTX) is a type of nerve blocker. (nih.gov)
- Botulinum toxin has beneficial effects only on wrinkles caused by muscular contractions. (medscape.com)
- Botulinum toxin is not an appropriate treatment for wrinkles caused by solar exposure or other degenerative processes of the dermal tissues. (medscape.com)
- Botulinum toxin is used in dermatology for the treatment of facial wrinkles caused by muscular contractions. (medscape.com)
- Botulinum toxin is appropriate only for the treatment of wrinkles caused by muscular action. (medscape.com)
- 4. Differentiation-induced increase in Clostridium botulinum C3 exoenzyme-catalyzed ADP-ribosylation of the small GTP-binding protein Rho. (nih.gov)
- 7. ADP-ribosylation and de-ADP-ribosylation of the rho protein by Clostridium botulinum exoenzyme C3. (nih.gov)
- 16. [ras oncogene-related small molecular weight GTP-binding protein, rho gene product and botulinum C3 ADP-ribosyltransferase]. (nih.gov)
- The common mechanism in these disorders is the paralysis of various muscles caused by the botulinum toxin. (medscape.com)
- Botulinum antitoxin is most helpful if administered early during the patient's illness, so it's really important that physicians get that antitoxin as soon as possible when they find out about a patient's illness. (cdc.gov)
- The botulinum neurotoxin is the most potent substance known, with as little as 30-100 ng potentially fatal, and consumption of just a few milligrams of neurotoxin-containing food is likely to be sufficient to cause illness and potentially death. (nih.gov)
- A rare but serious form of food poisoning caused by the nerve toxin botulinum. (medic8.com)
- Clostridium botulinum are found in soil and untreated water throughout the world. (medlineplus.gov)
- To better control the botulinum neurotoxin-forming clostridia, it is important to understand spore resistance mechanisms, and the physiological processes involved in germination and lag phase during recovery from this dormant state. (nih.gov)
- The different types of botulinum toxin have different molecular sizes, degrees of activation, and mechanisms of action. (medscape.com)
- The 9 S.I.D.S. cases with evidence of C. botulinum infection comprised 4.3% of the 211 S.I.D.S. cases examined over 12 months. (nih.gov)
- Clostridium botulinum : ecology and control in foods / edited by Andreas H. W. Hauschild, Karen L. Dodds. (who.int)
- However, one's poison is another's medicine, because botulinum toxin is useful in the treatment of certain diseases. (medscape.com)
- To test this hypothesis, serum, selected tissues, and bowel contents from 280 dead infants were examined for the presence of C. botulinum toxin and/or organsisms. (nih.gov)
- Note that the specimens for toxin analysis should be refrigerated, but culture samples of C botulinum should not be refrigerated. (medscape.com)