Gene Expression Regulation, Bacterial
Infant, Newborn, Diseases
Antigenicity of purified glutaraldehyde-treated cholera toxoid administered orally. (1/590)The antigenicity of orally administered glutaraldehyde-treated cholera toxoid was investigated in healthy volunteers. Fourteen volunteers ingested two or three 2-mg doses of toxoid with saline, with the doses spaced at 28-day intervals. Thirteen other volunteers received comparable toxoid doses with NaHCO3 and milk to neutralize gastric acid. Increments in circulating antitoxin levels were used to assay the antigenicity of oral toxoid. Antitoxin was measured by adrenal cell, rabbit skin permeability factor, and passive hemagglutination assays in sera collected on days 0, 28, 35, 56, 63, and 84 after primary immunization. Adrenal cell and rabbit skin assays exhibited identical sensitivity in detecting antitoxin rises in the 27 vaccinees (19/27) and were significantly more sensitive than passive hemagglutination (11/27) (P less than 0.03). Volunteers who ingested toxoid with NaHCO3 and milk had a higher rate of seroconversion (77%) than those who received toxoid with saline (64%); they also had earlier rises in antitoxin titer and consistently higher geometric mean titers on all days tested. These studies demonstrate that purified cholera toxoid is antigenic in humans after oral administration. The possible role of oral toxoid in enhancing the protective effect of killed whole-cell vaccines can now be investigated. (+info)
Lack of J chain inhibits the transport of gut IgA and abrogates the development of intestinal antitoxic protection. (2/590)Recent publications have provided confusing information on the importance of the J chain for secretion of dimeric IgA at mucosal surfaces. Using J chain-deficient (J chain-/-) mice, we addressed whether a lack of J chain had any functional consequence for the ability to resist challenge with cholera toxin (CT) in intestinal loops. J chain-/- mice had normal levels of IgA plasma cells in the gut mucosa, and the Peyer's patches exhibited normal IgA B cell differentiation and germinal center reactions. The total IgA levels in gut lavage were reduced by roughly 90% as compared with that in wild-type controls, while concomitantly serum IgA levels were significantly increased. Total serum IgM levels were depressed, whereas IgG concentrations were normal. Following oral immunizations with CT, J chain-/- mice developed 10-fold increased serum antitoxin IgA titers, but gut lavage anti-CT IgA levels were substantially reduced. However, anti-CT IgA spot-forming cell frequencies in the gut lamina propria were normal. Anti-CT IgM concentrations were low in serum and gut lavage, whereas anti-CT IgG titers were unaltered. Challenge of small intestinal ligated loops with CT caused dramatic fluid accumulation in immunized J chain-/- mice, and only 20% protection was detected compared with unimmunized controls. In contrast, wild-type mice demonstrated 80% protection against CT challenge. Mice heterozygous for the J chain deletion exhibited intermediate gut lavage anti-CT IgA and intestinal protection levels, arguing for a J chain gene-dosage effect on the transport of secretory IgA. This study unequivocally demonstrates a direct relationship between mucosal transport of secretory SIgA and intestinal immune protection. (+info)
Similarities between the pathogenesis of and immunity to diphtheria and pertussis: the complex nature of serum antitoxin-induced immunity to these two diseases. (3/590)Despite data from animal studies, seroepidemiological surveys, and controlled clinical trials, skepticism persists about immunity to pertussis conferred by serum IgG neutralizing antibodies (antitoxin). This is largely prompted by the absence of a "protective" level of antitoxin. Examination of the similarities between the pathogenesis and immunity to pertussis and diphtheria provides an explanation for this dilemma. As with pertussis, diphtheria toxoid vaccination confers only approximately 70% immunity on an individual basis, individuals with protective levels of antitoxin may contract diphtheria, and about 50% of the entire population, especially adults, have less than protective levels of antitoxin. The virtual disappearance of diphtheria followed vaccination of the entire population with diphtheria toxoid, which blocked transmission of toxigenic Corynebacterium diphtheriae and thus reduced the pathogen to almost undetectable levels. The individual and community-based immunity induced by diphtheria toxoid, we hypothesize, is similar to that of pertussis and pertussis toxoid. (+info)
Shigellosis and Escherichia coli diarrhea: relative importance of invasive and toxigenic mechanisms. (4/590)Shigellae and dysentery-like Escherichia coli must invade the epithelium of the colon to cause disease which can present as dysentery, diarrhea, or both. This paper addresses the possible role of a Shigella dysenteriae-like (Shiga-like) toxin in the pathogenesis of shigellosis and E. coli diarrheal diseases. The possibility for such a role is suggested by the following observations: 1) diarrhea, considered to be a result of secretion of water by the small bowel, is frequently observed in shigellosis, a large bowel disease. 2) Even though shigellae do not invade the jejunum of monkeys fed Shigella flexneri, jejunal secretion is seen in animals with diarrhea. 3) The Shiga toxin of S. dysenteriae has enterotoxic activity and other serotypes of shigellae produce Shiga-like toxins. 4) E. coli 015 RDEC-1 causes a diarrheal disease and frequently death in young rabbits. This organism neither produces E. coli enterotoxins nor is it invasive, but it may produce low levels of a Shiga-like toxin. (+info)
The sigma ligand, igmesine, inhibits cholera toxin and Escherichia coli enterotoxin induced jejunal secretion in the rat. (5/590)BACKGROUND: Cholera toxin, and Escherichia coli heat labile (LT) and heat stable (STa) enterotoxins induce small intestinal secretion in part by activating enteric nerves. Igmesine is a novel sigma receptor ligand that inhibits neurally mediated secretion. AIMS: To assess the antisecretory potential of igmesine in cholera toxin, LT, and STa induced water and electrolyte secretion using an in vivo rat model of jejunal perfusion. METHODS: After pretreatment with igmesine, 0.03-10 mg/kg intravenously, jejunal segments of anaesthetised, adult male Wistar rats were incubated with cholera toxin (25 microg), LT (25 microg), or saline. Jejunal perfusion with a plasma electrolyte solution containing a non-absorbable marker was undertaken. In some cases 200 microg/l STa was added to the perfusate. After equilibration, net water and electrolyte movement was determined. In additional experiments rats received igmesine, intravenously or intrajejunally, after exposure to cholera toxin. RESULTS: Cholera toxin induced net water secretion was inhibited by 1 mg/kg igmesine (median -120 versus -31 microl/min/g, p<0.001). LT and STa induced secretion were also inhibited by 1 mg/kg igmesine (-90 versus -56, p<0.03; and -76 versus -29, p<0.01, respectively). Igmesine reduced established cholera toxin induced secretion. CONCLUSION: The sigma ligand, igmesine, inhibits neurally mediated enterotoxigenic secretion. Its ability to inhibit established secretion makes it an agent with therapeutic potential. (+info)
Vitronectin and its fragments purified as serum inhibitors of Staphylococcus aureus gamma-hemolysin and leukocidin, and their specific binding to the hlg2 and the LukS components of the toxins. (6/590)Staphylococcal gamma-hemolysin and leukocidin are bi-component cytolysins, consisting of LukF (or Hlg1)/Hlg2 and LukF/LukS, respectively. Here, we purified serum inhibitors of gamma-hemolysin and leukocidin from human plasma. Protein sequencing showed that the purified inhibitors of 62, 57, 50 and 38 kDa were the vitronectin fragments with truncation(s) of the C-terminal or both N- and C-terminal regions. The purified vitronectin fragments specifically bound to the Hlg2 component of gamma-hemolysin and the LukS component of leukocidin to form high-molecular-weight complexes with them, leading to inhibition of the toxin-induced lysis of human erythrocytes and human polymorphonuclear leukocytes, respectively. Intact vitronectin also showed inhibitory activity to the toxins. The ability of gamma-hemolysin and leukocidin to bind vitronectin and its fragments is a novel function of the pore-forming cytolysins. (+info)
Monoclonal antibodies against the Androctonus australis hector scorpion neurotoxin I: characterisation and use for venom neutralisation. (7/590)A series of monoclonal antibodies (mAbs) specific for the alpha-neurotoxin I (Aah I) from the venom of the dangerous Androctonus australis hector scorpion were obtained using carrier protein-coupled toxin. Competitive RIA, receptor assays and mouse toxicity tests were performed to characterise mAbs in terms of affinity and neutralisation. Cross-reactivity studies and two-site ELISA results allowed some classification of mAbs into three groups. One mAb, 9C2, was particularly interesting since it recognised the parent toxin I with a K(D) of 0.15 nM and was also reactive with toxins of the same immunological group. Its ability to neutralise the toxic effect of the parent toxin and the venom fraction has been investigated. This anti-Aah I mAb 9C2, associated with anti-Aah II mAb 4C1, provides a valuable tool to neutralise the toxicity of the venom. (+info)
Combining phage display and molecular modeling to map the epitope of a neutralizing antitoxin antibody. (8/590)Crotoxin is a potent presynaptic neurotoxin from the venom of the rattlesnake Crotalus durissus terrificus. It is composed of the noncovalent and synergistic association of a weakly toxic phospholipase A2, CB, and a nontoxic three-chain subunit, CA, which increases the lethal potency of CB. The A-56.36 mAb is able to dissociate the crotoxin complex by binding to the CA subunit, thereby neutralizing its toxicity. Because A-56.36 and CB show sequence homology and both compete for binding to CA, we postulated that A-56.36 and CB had overlapping binding sites on CA. By screening random phage-displayed libraries with the mAb, phagotopes bearing the (D/S)GY(A/G) or AAXI consensus motifs were selected. They all bound A-56.36 in ELISA and competed with CA for mAb binding, although with different reactivities. When mice were immunized with the selected clones, polyclonal sera reacting with CA were induced. Interestingly, the raised antibodies retained the crotoxin-dissociating effect of A-56.36, suggesting that the selected peptides may be used to produce neutralizing antibodies. By combining these data with the molecular modeling of CA, it appeared that the functional epitope of A-56.36 on CA was conformational, one subregion being discontinuous and corresponding to the first family of peptides, the other subregion being continuous and composed of amino acids of the second family. Phage-displayed peptides corresponding to fragments of the two identified regions on CA reacted with A-56.36 and with CB. Our data support the hypothesis that A-56.36 and CB interact with common regions of CA, and highlight residues which are likely to be critical for CA-CB complex formation. (+info)
The symptoms of diphtheria typically develop within 2-5 days after exposure and may include:
* Sore throat and difficulty swallowing
* Fever and chills
* Swollen and tender lymph nodes in the neck
* Difficulty breathing or shortness of breath
* Skin lesions or rashes
* Nerve damage, leading to weakness, paralysis, and other neurological symptoms.
If left untreated, diphtheria can lead to serious complications such as respiratory failure, heart failure, and death. Treatment typically involves antibiotics, which can help clear the infection and prevent further damage. In severe cases, hospitalization may be required to provide supportive care, such as mechanical ventilation or cardiac support.
Diphtheria is a vaccine-preventable disease, and immunization programs have been instrumental in reducing the incidence of this disease worldwide. However, outbreaks still occur in some areas, particularly among unvaccinated individuals or those living in areas with low vaccination coverage.
In addition to its clinical features, diphtheria has several key characteristics that are important to note:
* It is highly contagious and can be transmitted through respiratory droplets, close contact with an infected person, or by touching contaminated surfaces and objects.
* The bacteria can survive for weeks outside the body, making it a significant risk for transmission through fomites.
* Immunity to diphtheria is not lifelong, and booster doses of the vaccine are recommended every 10 years to maintain protection.
The symptoms of tetanus can develop anywhere from 3 days to 3 weeks after exposure to the bacteria, and they can include:
* Muscle stiffness and spasms, especially in the neck, jaw, and limbs
* Difficulty swallowing or speaking
* Fever and sweating
* Headache and fatigue
* Rigidity and spasticity of muscles
* Abdominal cramps and diarrhea
* In severe cases, tetanus can cause serious complications such as pneumonia, heart problems, and death.
Tetanus is diagnosed through a physical examination, medical history, and laboratory tests. Treatment typically involves administering antitoxin medication to neutralize the effects of the bacterial toxins, as well as providing supportive care such as pain management and wound care.
Prevention is key in avoiding tetanus, and this can be achieved through:
* Vaccination: Tetanus vaccines are available and recommended for individuals of all ages, especially for those who have open wounds or injuries.
* Proper wound care: Keeping wounds clean and covered can help prevent the entry of bacteria into the body.
* Avoiding risky behaviors: Avoiding activities that can cause injury, such as playing contact sports or engaging in dangerous hobbies, can reduce the risk of developing tetanus.
Overall, tetanus is a serious medical condition that requires prompt treatment and prevention measures to avoid complications and ensure a full recovery.
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.
The symptoms of cholera include:
1. Diarrhea: Cholera causes profuse, watery diarrhea that can last for several days.
2. Dehydration: The loss of fluids and electrolytes due to diarrhea can lead to severe dehydration, which can be life-threatening if not treated promptly.
3. Nausea and vomiting: Cholera patients may experience nausea and vomiting, especially in the early stages of the disease.
4. Abdominal cramps: The abdomen may become tender and painful due to the inflammation caused by the bacteria.
5. Low-grade fever: Some patients with cholera may experience a mild fever, typically less than 102°F (39°C).
Cholera is spread through the fecal-oral route, which means that it is transmitted when someone ingests food or water contaminated with the bacteria. The disease can also be spread by direct contact with infected fecal matter, such as through poor hygiene practices or inadequate waste disposal.
There are several ways to diagnose cholera, including:
1. Stool test: A stool sample can be tested for the presence of Vibrio cholerae using a microscope or a rapid diagnostic test (RDT).
2. Blood test: A blood test can detect the presence of antibodies against Vibrio cholerae, which can indicate that the patient has been infected with the bacteria.
3. Physical examination: A healthcare provider may perform a physical examination to look for signs of dehydration and other symptoms of cholera.
Treatment of cholera typically involves replacing lost fluids and electrolytes through oral rehydration therapy (ORT) or intravenous fluids. Antibiotics may also be given to shorten the duration of diarrhea and reduce the risk of complications. In severe cases, hospitalization may be necessary to provide more intensive treatment.
Prevention of cholera involves maintaining good hygiene practices, such as washing hands with soap and water, and avoiding consumption of contaminated food and water. Vaccines are also available to protect against cholera, particularly for people living in areas where the disease is common.
In conclusion, cholera is a highly infectious disease that can cause severe dehydration and even death if left untreated. Early diagnosis and treatment are critical to preventing complications and reducing the risk of transmission. Prevention measures such as vaccination and good hygiene practices can also help control the spread of the disease.
The symptoms of gas gangrene can include sudden onset of severe pain, swelling, redness, and warmth in the affected area. The skin may also be tender to the touch and feel firm or hard. In severe cases, the infection can spread quickly and lead to sepsis, shock, and even death.
Gas gangrene can occur as a result of trauma, such as a wound or injury, or it can be caused by a surgical incision that becomes infected. The infection can also spread to other parts of the body through the bloodstream.
Treatment of gas gangrene typically involves antibiotics and surgical debridement (removal of dead tissue) to remove the infected tissue and promote healing. In severe cases, amputation of the affected limb may be necessary. Early diagnosis and treatment are essential to prevent serious complications and improve outcomes.
In summary, gas gangrene is a life-threatening bacterial infection that can occur in muscle tissue, causing sudden pain, swelling, and warmth in the affected area. Prompt diagnosis and treatment are crucial to prevent serious complications and improve outcomes.
There are several types of diarrhea, including:
1. Acute diarrhea: This type of diarrhea is short-term and usually resolves on its own within a few days. It can be caused by a viral or bacterial infection, food poisoning, or medication side effects.
2. Chronic diarrhea: This type of diarrhea persists for more than 4 weeks and can be caused by a variety of conditions, such as irritable bowel syndrome (IBS), inflammatory bowel disease (IBD), or celiac disease.
3. Diarrhea-predominant IBS: This type of diarrhea is characterized by frequent, loose stools and abdominal pain or discomfort. It can be caused by a variety of factors, including stress, hormonal changes, and certain foods.
4. Infectious diarrhea: This type of diarrhea is caused by a bacterial, viral, or parasitic infection and can be spread through contaminated food and water, close contact with an infected person, or by consuming contaminated food.
Symptoms of diarrhea may include:
* Frequent, loose, and watery stools
* Abdominal cramps and pain
* Bloating and gas
* Nausea and vomiting
* Fever and chills
* Fatigue and weakness
Diagnosis of diarrhea is typically made through a physical examination, medical history, and laboratory tests to rule out other potential causes of the symptoms. Treatment for diarrhea depends on the underlying cause and may include antibiotics, anti-diarrheal medications, fluid replacement, and dietary changes. In severe cases, hospitalization may be necessary to monitor and treat any complications.
Prevention of diarrhea includes:
* Practicing good hygiene, such as washing hands frequently and thoroughly, especially after using the bathroom or before preparing food
* Avoiding close contact with people who are sick
* Properly storing and cooking food to prevent contamination
* Drinking safe water and avoiding contaminated water sources
* Avoiding raw or undercooked meat, poultry, and seafood
* Getting vaccinated against infections that can cause diarrhea
Complications of diarrhea can include:
* Dehydration: Diarrhea can lead to a loss of fluids and electrolytes, which can cause dehydration. Severe dehydration can be life-threatening and requires immediate medical attention.
* Electrolyte imbalance: Diarrhea can also cause an imbalance of electrolytes in the body, which can lead to serious complications.
* Inflammation of the intestines: Prolonged diarrhea can cause inflammation of the intestines, which can lead to abdominal pain and other complications.
* Infections: Diarrhea can be a symptom of an infection, such as a bacterial or viral infection. If left untreated, these infections can lead to serious complications.
* Malnutrition: Prolonged diarrhea can lead to malnutrition and weight loss, which can have long-term effects on health and development.
Treatment of diarrhea will depend on the underlying cause, but may include:
* Fluid replacement: Drinking plenty of fluids to prevent dehydration and replace lost electrolytes.
* Anti-diarrheal medications: Over-the-counter or prescription medications to slow down bowel movements and reduce diarrhea.
* Antibiotics: If the diarrhea is caused by a bacterial infection, antibiotics may be prescribed to treat the infection.
* Rest: Getting plenty of rest to allow the body to recover from the illness.
* Dietary changes: Avoiding certain foods or making dietary changes to help manage symptoms and prevent future episodes of diarrhea.
It is important to seek medical attention if you experience any of the following:
* Severe diarrhea that lasts for more than 3 days
* Diarrhea that is accompanied by fever, blood in the stool, or abdominal pain
* Diarrhea that is severe enough to cause dehydration or electrolyte imbalances
* Diarrhea that is not responding to treatment
Prevention of diarrhea includes:
* Good hand hygiene: Washing your hands frequently, especially after using the bathroom or before preparing food.
* Safe food handling: Cooking and storing food properly to prevent contamination.
* Avoiding close contact with people who are sick.
* Getting vaccinated against infections that can cause diarrhea, such as rotavirus.
Overall, while diarrhea can be uncomfortable and disruptive, it is usually a minor illness that can be treated at home with over-the-counter medications and plenty of fluids. However, if you experience severe or persistent diarrhea, it is important to seek medical attention to rule out any underlying conditions that may require more formal treatment.
There are three main forms of anthrax:
1. Cutaneous (skin) anthrax: This is the most common form of the disease and causes skin lesions that can progress to severe inflammation and scarring.
2. Inhalational (lung) anthrax: This is the most deadly form of the disease and causes serious respiratory problems, including fever, chills, and difficulty breathing.
3. Gastrointestinal (GI) anthrax: This form of the disease causes symptoms such as diarrhea, abdominal pain, and vomiting.
Anthrax can be diagnosed through a variety of tests, including blood tests and imaging studies. Treatment typically involves antibiotics, but the effectiveness of treatment depends on the severity of the infection and the timing of treatment.
Prevention of anthrax primarily involves vaccination of animals and control of animal products to prevent the spread of the bacteria. In addition, public health measures such as surveillance and quarantine can help prevent the spread of the disease to humans.
The medical management of anthrax involves a combination of antibiotics, supportive care, and wound management. Early diagnosis and treatment are critical to preventing serious complications and death.
1. Respiratory distress syndrome (RDS): This is a breathing disorder that occurs when the baby's lungs are not fully developed, causing difficulty in breathing. RDS can be treated with oxygen therapy and other medical interventions.
2. Jaundice: Jaundice is a yellowish tint to the skin and eyes caused by high levels of bilirubin in the blood. It is a common condition in newborns, but if left untreated, it can lead to brain damage. Treatment may involve phototherapy or blood exchange transfusions.
3. Neonatal jaundice: This is a milder form of jaundice that occurs in the first few days of life. It usually resolves on its own within a week, but if it persists, treatment may be necessary.
4. Premature birth: Premature babies are at risk for various health issues, including respiratory distress syndrome, intraventricular hemorrhage (bleeding in the brain), and retinopathy (eye problems).
5. Congenital heart disease: This is a heart defect that occurs during fetal development. It can range from mild to severe and may require surgical intervention.
6. Infections: Newborns are susceptible to bacterial and viral infections, such as group B strep, pneumonia, and urinary tract infections. These can be treated with antibiotics if caught early.
7. Hypoglycemia (low blood sugar): This is a condition that occurs when the baby's blood sugar levels drop too low. It can cause seizures, lethargy, and other symptoms. Treatment involves feeding or providing glucose supplements.
8. Hyperbilirubinemia (high bilirubin levels): Bilirubin is a yellow pigment produced during the breakdown of red blood cells. High levels can cause jaundice, which can lead to kernicterus, a condition that can cause brain damage and hearing loss.
9. Intracranial hemorrhage (bleeding in the brain): This is a serious condition that occurs when there is bleeding in the baby's brain. It can be caused by various conditions, including premature birth, abruption, and vasculitis.
10. Meconium aspiration: This occurs when the baby inhales a mixture of meconium (a substance produced by the intestines) and amniotic fluid during delivery. It can cause respiratory problems and other complications.
It's important to note that while these conditions can be serious, many babies born at 37 weeks gestation do not experience any complications. Proper prenatal care and a healthy pregnancy can help reduce the risk of these conditions.
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- Diphtheria antitoxin was one of these medicines. (nih.gov)
- As an immune response, the animal's blood produces diphtheria antitoxin. (nih.gov)
- Plasma from vaccinated persons is used to produce horse (challenged with sublethal dose of Corynebacterium Anthrasil (Cangene Corporation, Winnipeg, Manitoba, diphtheriae ) to develop equine diphtheria antitoxin (DAT), Canada), a fully human polyclonal antianthrax intrave- which seemed to confer passive immunity to patients with nous immunoglobulin (IVIG) licensed in the United States. (cdc.gov)
- Diphtheria antitoxin should be administered as soon as the clinical evidence of the disease appears. (crikasauli.nic.in)
- CAES Seminar Series: 'Toxin-Antitoxin Systems: Implications for Plant Disease? (ctgardenclubs.org)
- Dr. Teja Shiodre , Dept of Plant Pathology and Ecology, CAES will present 'Toxin-Antitoxin Systems: Implication for Plant Disease? (ctgardenclubs.org)
- The possibility of rendering toxic a non-toxic toxin-antitoxin mixture by the addition of toxoid is confirmed. (gla.ac.uk)
- When the excess of antitoxin is too great it is technically impossible to bring together the necessary amount of toxoid with the toxin and antitoxin in a volume that would allow of subcutaneous injection of a guinea pig. (gla.ac.uk)
- Under otherwise similar conditions the difficulty of rendering toxic a non-toxic toxin-antitoxin mixture by means of the addition of toxoid becomes greater, the longer the toxin-antitoxin mixture has stood. (gla.ac.uk)
- If when at a temperature of 40 C. one exposes a neutral toxin-antitoxin mixture to the dissociative action of toxoid, then the following is seen. (gla.ac.uk)
- The toxin-antitoxin compound which is bound to the floccules can again pass into the surrounding fluid where it can be demonstrated by means of toxoid. (gla.ac.uk)
- If in a neutral toxin-antitoxin mixture or in mixtures of varying degrees of over-neutralisation, one knows the amount of toxin used in the production of the given mixture, then through dissociation of the compound by means of toxoid one is able to find how much antitoxin per cc. is present in the mixture. (gla.ac.uk)
- The HigA antitoxin binds to and inactivates the HigB toxin when cells are not in a stressed state. (emory.edu)
- This structure reveals that HigA does not inactivate HigB through direct interactions with the HigB active site, as observed in many other toxin-antitoxin complexes. (emory.edu)
- Introduction: Toxin-antitoxin systems. (emory.edu)
- 1.10 Transcriptional regulation of toxin-antitoxin systems. (emory.edu)
- 1.12 Toxin-antitoxin systems and persister cell formation. (emory.edu)
- 1.13 Other roles of toxin-antitoxin systems. (emory.edu)
- 1.16 The HigB-HigA toxin-antitoxin system. (emory.edu)
- Structure of the P. vulgaris HigB-(HigA)2-HigB toxin-antitoxin complex. (emory.edu)
- Effects of Toxin-Antitoxin System HicAB on Biofilm Formation by Extraintestinal Pathogenic E. coli. (bvsalud.org)
- The type II toxin- antitoxin (T-A) HicAB system is abundant in several bacteria and archaea , such as Escherichia coli , Burkholderia Pseudomallei , Yersinia pestis , Pseudomonas aeruginosa , and Streptococcus pneumoniae . (bvsalud.org)
- Further, MazEF6 acts independently of other Maz family toxin:antitoxin pairs. (biomedcentral.com)
- There is growing evidence that genome encoded toxin:antitoxin (TA) loci have important roles in Mtb biology and they are increasingly being associated with stress responses. (biomedcentral.com)
- TA loci encode an unstable antitoxin immediately upstream of a toxin and these proteins form a complex with one another under optimal growth conditions. (biomedcentral.com)
- We previously reported on an SOS-induced toxin, TisB, in Escherichia coli and its regulation by the RNA antitoxin IstR-1. (nih.gov)
- Botulism antitoxin for patients with signs and symptoms of human foodborne or wound botulism is released to physicians by CDC from its quarantine stations located throughout the United States. (cdc.gov)
- Any health-care provider requesting botulism antitoxin should first contact his/her state health department. (cdc.gov)
- A list of daytime and 24-hour telephone numbers (if available) is published to assist those seeking botulism antitoxin (Table 2). (cdc.gov)
- The results of these tests are helpful in evaluating the need for botulism antitoxin. (cdc.gov)
- The medicine is called botulism antitoxin. (medlineplus.gov)
- Scientists learned to harness the immune systems of some animals to produce antitoxin serums to use as medicines. (nih.gov)
- The laboratory, I think, was Kinyoun's lab something like that that…I can't remember the names of all the … But there was a succession of entities which dealt with what we now call biologics and dealt with vaccines and serums and antitoxins. (nih.gov)
- For C diphtheriae infection, the therapy is antitoxin and antibiotic treatment. (medscape.com)
- The more antitoxin the mixture contains, the greater must be the amount of toxoid added in order to render the mixture toxic. (gla.ac.uk)
- In the measurement of a toxoid the Lf value alone does not give a complete picture of its antigenic action, for this method refers only to the binding power of the toxoid, while the other methods the Lb, Lba and Lbp which have been discussed in this work, allow of the determination not only of the binding power but also of the affinity of a toxoid to an antitoxin. (gla.ac.uk)
- The affinity can be expressed thus R = Lbp/Lba The lower the value of R is, then the stronger is the affinity of the toxoid to the antitoxin. (gla.ac.uk)
- Doctors used diphteria antitoxin to treat and prevent diphtheria, an often deadly childhood disease. (nih.gov)
- In 1891, Emil von Behring produced an antitoxin from the blood of animals for curing diphtheria. (learnthat.org)
- of alternative antitoxins of human origin. (cdc.gov)
- Heptavalent antitoxin (toxins A through G) is available at the Centers for Disease Control and Prevention (CDC). (medscape.com)
- The European Centre for Disease Prevention and Control and the US Centers for Disease Control and Prevention encourage searching for new providers of equine DAT and promote the development of alternative antitoxins of human origin. (cdc.gov)
- Doctors used diphteria antitoxin to treat and prevent diphtheria, an often deadly childhood disease. (nih.gov)
- 4. Then, researchers purify the antitoxin serum for use as a medicine for people. (nih.gov)