Antisera from immunized animals that is purified and used as a passive immunizing agent against specific BACTERIAL TOXINS.
An antitoxin used for the treatment of TETANUS.
An antitoxin produced against the toxin of CORYNEBACTERIUM DIPHTHERIAE that is used for the treatment of DIPHTHERIA.
Antiserum given therapeutically in BOTULISM.
A localized infection of mucous membranes or skin caused by toxigenic strains of CORYNEBACTERIUM DIPHTHERIAE. It is characterized by the presence of a pseudomembrane at the site of infection. DIPHTHERIA TOXIN, produced by C. diphtheriae, can cause myocarditis, polyneuritis, and other systemic toxic effects.
Preparations of pathogenic organisms or their derivatives made nontoxic and intended for active immunologic prophylaxis. They include deactivated toxins. Anatoxin toxoids are distinct from anatoxins that are TROPANES found in CYANOBACTERIA.
A disease caused by tetanospasmin, a powerful protein toxin produced by CLOSTRIDIUM TETANI. Tetanus usually occurs after an acute injury, such as a puncture wound or laceration. Generalized tetanus, the most common form, is characterized by tetanic muscular contractions and hyperreflexia. Localized tetanus presents itself as a mild condition with manifestations restricted to muscles near the wound. It may progress to the generalized form.
Toxic substances formed in or elaborated by bacteria; they are usually proteins with high molecular weight and antigenicity; some are used as antibiotics and some to skin test for the presence of or susceptibility to certain diseases.
Specific, characterizable, poisonous chemicals, often PROTEINS, with specific biological properties, including immunogenicity, produced by microbes, higher plants (PLANTS, TOXIC), or ANIMALS.
A disease caused by potent protein NEUROTOXINS produced by CLOSTRIDIUM BOTULINUM which interfere with the presynaptic release of ACETYLCHOLINE at the NEUROMUSCULAR JUNCTION. Clinical features include abdominal pain, vomiting, acute PARALYSIS (including respiratory paralysis), blurred vision, and DIPLOPIA. Botulism may be classified into several subtypes (e.g., food-borne, infant, wound, and others). (From Adams et al., Principles of Neurology, 6th ed, p1208)
The formaldehyde-inactivated toxin of Corynebacterium diphtheriae. It is generally used in mixtures with TETANUS TOXOID and PERTUSSIS VACCINE; (DTP); or with tetanus toxoid alone (DT for pediatric use and Td, which contains 5- to 10-fold less diphtheria toxoid, for other use). Diphtheria toxoid is used for the prevention of diphtheria; DIPHTHERIA ANTITOXIN is for treatment.
Originally an island of the Malay Archipelago, the second largest island in the world. It divided, West New Guinea becoming part of Indonesia and East New Guinea becoming Papua New Guinea.
A species of gram-positive, asporogenous bacteria in which three cultural types are recognized. These types (gravis, intermedius, and mitis) were originally given in accordance with the clinical severity of the cases from which the different strains were most frequently isolated. This species is the causative agent of DIPHTHERIA.
An ENTEROTOXIN from VIBRIO CHOLERAE. It consists of two major protomers, the heavy (H) or A subunit and the B protomer which consists of 5 light (L) or B subunits. The catalytic A subunit is proteolytically cleaved into fragments A1 and A2. The A1 fragment is a MONO(ADP-RIBOSE) TRANSFERASE. The B protomer binds cholera toxin to intestinal epithelial cells, and facilitates the uptake of the A1 fragment. The A1 catalyzed transfer of ADP-RIBOSE to the alpha subunits of heterotrimeric G PROTEINS activates the production of CYCLIC AMP. Increased levels of cyclic AMP are thought to modulate release of fluid and electrolytes from intestinal crypt cells.
Substances that are toxic to the intestinal tract causing vomiting, diarrhea, etc.; most common enterotoxins are produced by bacteria.
A species of anaerobic, gram-positive, rod-shaped bacteria in the family Clostridiaceae that produces proteins with characteristic neurotoxicity. It is the etiologic agent of BOTULISM in humans, wild fowl, HORSES; and CATTLE. Seven subtypes (sometimes called antigenic types, or strains) exist, each producing a different botulinum toxin (BOTULINUM TOXINS). The organism and its spores are widely distributed in nature.
Proteins obtained from ESCHERICHIA COLI.
Toxic proteins produced from the species CLOSTRIDIUM BOTULINUM. The toxins are synthesized as a single peptide chain which is processed into a mature protein consisting of a heavy chain and light chain joined via a disulfide bond. The botulinum toxin light chain is a zinc-dependent protease which is released from the heavy chain upon ENDOCYTOSIS into PRESYNAPTIC NERVE ENDINGS. Once inside the cell the botulinum toxin light chain cleaves specific SNARE proteins which are essential for secretion of ACETYLCHOLINE by SYNAPTIC VESICLES. This inhibition of acetylcholine release results in muscular PARALYSIS.
An ADP-ribosylating polypeptide produced by CORYNEBACTERIUM DIPHTHERIAE that causes the signs and symptoms of DIPHTHERIA. It can be broken into two unequal domains: the smaller, catalytic A domain is the lethal moiety and contains MONO(ADP-RIBOSE) TRANSFERASES which transfers ADP RIBOSE to PEPTIDE ELONGATION FACTOR 2 thereby inhibiting protein synthesis; and the larger B domain that is needed for entry into cells.
The cause of TETANUS in humans and domestic animals. It is a common inhabitant of human and horse intestines as well as soil. Two components make up its potent exotoxin activity, a neurotoxin and a hemolytic toxin.
The etiologic agent of CHOLERA.
Vaccines or candidate vaccines used to prevent infection with VIBRIO CHOLERAE. The original cholera vaccine consisted of killed bacteria, but other kinds of vaccines now exist.
A genus of motile or nonmotile gram-positive bacteria of the family Clostridiaceae. Many species have been identified with some being pathogenic. They occur in water, soil, and in the intestinal tract of humans and lower animals.
An acute diarrheal disease endemic in India and Southeast Asia whose causative agent is VIBRIO CHOLERAE. This condition can lead to severe dehydration in a matter of hours unless quickly treated.
Immunoglobulins produced in a response to BACTERIAL ANTIGENS.
A combined vaccine used to prevent infection with diphtheria and tetanus toxoid. This is used in place of DTP vaccine (DIPHTHERIA-TETANUS-PERTUSSIS VACCINE) when PERTUSSIS VACCINE is contraindicated.
A species of gram-negative, facultatively anaerobic, rod-shaped bacteria (GRAM-NEGATIVE FACULTATIVELY ANAEROBIC RODS) commonly found in the lower part of the intestine of warm-blooded animals. It is usually nonpathogenic, but some strains are known to produce DIARRHEA and pyogenic infections. Pathogenic strains (virotypes) are classified by their specific pathogenic mechanisms such as toxins (ENTEROTOXIGENIC ESCHERICHIA COLI), etc.
The measurement of infection-blocking titer of ANTISERA by testing a series of dilutions for a given virus-antiserum interaction end-point, which is generally the dilution at which tissue cultures inoculated with the serum-virus mixtures demonstrate cytopathology (CPE) or the dilution at which 50% of test animals injected with serum-virus mixtures show infectivity (ID50) or die (LD50).
A reaction that severs one of the sugar-phosphate linkages of the phosphodiester backbone of RNA. It is catalyzed enzymatically, chemically, or by radiation. Cleavage may be exonucleolytic, or endonucleolytic.
A method of measuring the effects of a biologically active substance using an intermediate in vivo or in vitro tissue or cell model under controlled conditions. It includes virulence studies in animal fetuses in utero, mouse convulsion bioassay of insulin, quantitation of tumor-initiator systems in mouse skin, calculation of potentiating effects of a hormonal factor in an isolated strip of contracting stomach muscle, etc.
The most common etiologic agent of GAS GANGRENE. It is differentiable into several distinct types based on the distribution of twelve different toxins.
Any of the processes by which cytoplasmic or intercellular factors influence the differential control of gene action in bacteria.
Deliberate stimulation of the host's immune response. ACTIVE IMMUNIZATION involves administration of ANTIGENS or IMMUNOLOGIC ADJUVANTS. PASSIVE IMMUNIZATION involves administration of IMMUNE SERA or LYMPHOCYTES or their extracts (e.g., transfer factor, immune RNA) or transplantation of immunocompetent cell producing tissue (thymus or bone marrow).
Sensitive tests to measure certain antigens, antibodies, or viruses, using their ability to agglutinate certain erythrocytes. (From Stedman, 26th ed)
Proteins found in any species of bacterium.
A prokaryotic ATP-dependent protease that plays a role in the degradation of many abnormal proteins. It is a tetramer of 87-kDa subunits, each of which contains a proteolytic site and a ATP-binding site.
Protein synthesized by CLOSTRIDIUM TETANI as a single chain of ~150 kDa with 35% sequence identity to BOTULINUM TOXIN that is cleaved to a light and a heavy chain that are linked by a single disulfide bond. Tetanolysin is the hemolytic and tetanospasmin is the neurotoxic principle. The toxin causes disruption of the inhibitory mechanisms of the CNS, thus permitting uncontrolled nervous activity, leading to fatal CONVULSIONS.
A species of temperate bacteriophage in the genus P1-like viruses, family MYOVIRIDAE, which infects E. coli. It is the largest of the COLIPHAGES and consists of double-stranded DNA, terminally redundant, and circularly permuted.
Fluids originating from the epithelial lining of the intestines, adjoining exocrine glands and from organs such as the liver, which empty into the cavity of the intestines.
Drugs which have received FDA approval for human testing but have yet to be approved for commercial marketing. This includes drugs used for treatment while they still are undergoing clinical trials (Treatment IND). The main heading includes drugs under investigation in foreign countries.
A TETRACYCLINE analog isolated from the actinomycete STREPTOMYCES rimosus and used in a wide variety of clinical conditions.
Toxins produced, especially by bacterial or fungal cells, and released into the culture medium or environment.
A severe condition resulting from bacteria invading healthy muscle from adjacent traumatized muscle or soft tissue. The infection originates in a wound contaminated with bacteria of the genus CLOSTRIDIUM. C. perfringens accounts for the majority of cases (over eighty percent), while C. noyvi, C. septicum, and C. histolyticum cause most of the other cases.
An increased liquidity or decreased consistency of FECES, such as running stool. Fecal consistency is related to the ratio of water-holding capacity of insoluble solids to total water, rather than the amount of water present. Diarrhea is not hyperdefecation or increased fecal weight.
An acute infection caused by the spore-forming bacteria BACILLUS ANTHRACIS. It commonly affects hoofed animals such as sheep and goats. Infection in humans often involves the skin (cutaneous anthrax), the lungs (inhalation anthrax), or the gastrointestinal tract. Anthrax is not contagious and can be treated with antibiotics.
A family of enzymes that catalyze the endonucleolytic cleavage of RNA. It includes EC 3.1.26.-, EC 3.1.27.-, EC 3.1.30.-, and EC 3.1.31.-.
A vaccine consisting of DIPHTHERIA TOXOID; TETANUS TOXOID; and whole-cell PERTUSSIS VACCINE. The vaccine protects against diphtheria, tetanus, and whooping cough.
Diseases of newborn infants present at birth (congenital) or developing within the first month of birth. It does not include hereditary diseases not manifesting at birth or within the first 30 days of life nor does it include inborn errors of metabolism. Both HEREDITARY DISEASES and METABOLISM, INBORN ERRORS are available as general concepts.
A suspension of killed Bordetella pertussis organisms, used for immunization against pertussis (WHOOPING COUGH). It is generally used in a mixture with diphtheria and tetanus toxoids (DTP). There is an acellular pertussis vaccine prepared from the purified antigenic components of Bordetella pertussis, which causes fewer adverse reactions than whole-cell vaccine and, like the whole-cell vaccine, is generally used in a mixture with diphtheria and tetanus toxoids. (From Dorland, 28th ed)
The major immunoglobulin isotype class in normal human serum. There are several isotype subclasses of IgG, for example, IgG1, IgG2A, and IgG2B.

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
* Headache
* 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.

An antitoxin is an antibody with the ability to neutralize a specific toxin. Antitoxins are produced by certain animals, plants ... To prevent serum sickness, it is often best to use an antitoxin obtained from the same species (e.g. use human antitoxin to ... 4 December 2018). "Medical definition of antitoxin". 2289. Antitoxins at the US National Library of Medicine ... When the antitoxin is obtained from the blood, it is purified and injected into a human or other animal, inducing temporary ...
... was developed and came into medical use in the late 1800s. It is on the World Health Organization's List ... Diphtheria antitoxin (DAT) is a medication made up of antibodies used in the treatment of diphtheria. It is no longer ... Diphtheria antitoxin is made from the blood plasma of horses that have been immunized against diphtheria toxin. It works by ... Diphtheria Antitoxin at the US National Library of Medicine Medical Subject Headings (MeSH) Portal: Medicine (Articles with ...
In molecular biology, the epsilon antitoxin, produced by various prokaryotes, forms part of a post-segregational killing system ...
CDC/MMWR (March 19, 2010): "Investigational Heptavalent Botulinum Antitoxin (HBAT) to Replace Licensed Botulinum Antitoxin AB ... The Botulism Antitoxin Heptavalent (A, B, C, D, E, F, G) - (Equine) - BAT, made by Emergent BioSolutions Canada Inc. (formerly ... A related product - Botulism AntiToxin, Heptavalent, Equine, Types A, B, C, D, E, F and G (HE-BAT) - is also available to the U ... This action left BAT as the only botulinum antitoxin available in the US for naturally occurring non-infant botulism. On March ...
... and the antitoxin, DarG, removes the toxic modification. ghoST is a type V toxin-antitoxin system, in which the antitoxin (GhoS ... Type I toxin-antitoxin systems rely on the base-pairing of complementary antitoxin RNA with the toxin mRNA. Translation of the ... Type III toxin-antitoxin systems rely on direct interaction between a toxic protein and an RNA antitoxin. The toxic effects of ... Type II toxin-antitoxin systems are generally better-understood than type I. In this system a labile proteic antitoxin tightly ...
TADB is a database of Type 2 toxin-antitoxin loci in bacterial and archaeal genomes. Toxin-antitoxin system Shao, Yucheng; ... a web-based resource for Type 2 toxin-antitoxin loci in bacteria and archaea". Nucleic Acids Res. England. 39 (Database issue ...
The SrnB-SrnC toxin-antitoxin system of the F plasmid is homologous to the hok/sok system of R1. Like the hok/sok system, it ... v t e (Orphaned articles from June 2020, All orphaned articles, RNA antitoxins, All stub articles, Bacteria stubs). ... an antitoxin with complementarity to srnB. The suspected method of regulation has not been directly tested for this system, ...
The TisB-IstR toxin-antitoxin system is the first known toxin-antitoxin system which is induced by the SOS response in response ... Toxin-antitoxin system Sib RNA hok/sok system Vogel J, Argaman L, Wagner EG, Altuvia S (December 2004). "The small RNA IstR ... There are two small RNAs encoded by the IstR locus: IstR-1 and IstR-2, of which IstR-1 works as antitoxins against the toxic ... Fozo EM, Makarova KS, Shabalina SA, Yutin N, Koonin EV, Storz G (June 2010). "Abundance of type I toxin-antitoxin systems in ...
SymE-SymR is a type I toxin-antitoxin system, and is under regulation by the antitoxin, SymR. The SymE-SymR complex is believed ... In contrast to other common toxin-antitoxin systems, the SymR antitoxin is more stable than the SymE toxin. Following DNA ... Page for SymR antitoxin at Rfam (CS1: long volume value, Antisense RNA, RNA antitoxins). ... Toxin-antitoxin system Hok/sok system Kawano M, Aravind L, Storz G (May 2007). "An antisense RNA controls synthesis of an SOS- ...
Toxin-antitoxin system IstR RNA RdlD RNA Sib RNA SymR RNA ptaRNA1 Loh SM, Cram DS, Skurray RA (June 1988). "Nucleotide sequence ... The FlmA-FlmB toxin-antitoxin system consists of FlmB RNA (F leading-region maintenance B), a family of non-coding RNAs and the ... Fozo EM, Makarova KS, Shabalina SA, Yutin N, Koonin EV, Storz G (June 2010). "Abundance of type I toxin-antitoxin systems in ... Gerdes K, Wagner EG (April 2007). "RNA antitoxins". Curr. Opin. Microbiol. 10 (2): 117-124. doi:10.1016/j.mib.2007.03.003. PMID ...
Page for rdlD antitoxin at Rfam (Protein pages needing a picture, Antisense RNA, RNA antitoxins, Toxins). ... as is common with Type 1 toxin-antitoxin systems. Toxin-antitoxin system Hok/sok system RatA Kawano M, Oshima T, Kasai H, Mori ... This is in keeping with other type I toxin-antitoxin systems. Northern blots showed that ldrD and rdlD are both transcribed and ... Fozo EM, Makarova KS, Shabalina SA, Yutin N, Koonin EV, Storz G (June 2010). "Abundance of type I toxin-antitoxin systems in ...
The dinQ-agrB type I toxin-antitoxin (TA) system was initially identified in Escherichia coli. This type I TA system is induced ...
Toxin-antitoxin system Hok/sok system RdlD RNA Bacillus subtilis BSR sRNAs Bacillus subtilis type I antitoxin SR6 Silvaggi JM, ... Page for RNA anti-toxin A at Rfam (Antisense RNA, RNA antitoxins). ... The toxin-antitoxin system contained within skin forces the inheritance of this element, which is acting as a selfish gene. The ... It consists of a non-coding 222nt sRNA called RatA (RNA anti-toxin A) and a protein toxin named TxpA (Toxic protein A). RatA ...
In type I toxin-antitoxin (TA) systems the antitoxin is a small RNA that neutralizes a toxin protein. Several type I TA systems ... txpA/RatA bsrG/SR4, bsrE/SR5 Durand S, Jahn N, Condon C, Brantl S (December 2012). "Type I toxin-antitoxin systems in Bacillus ... SR6 is a 100 nucleotide long antisense RNA antitoxin that overlaps 2 toxins: 3' end of yonT and yoyJ at its 5'end. ... Reif C, Löser C, Brantl S (February 2018). "Bacillus subtilis Type I antitoxin SR6 Promotes Degradation of Toxin yonT mRNA and ...
The parDE type II toxin-antitoxin system is one example of the bacterial toxin-antitoxin (TA) systems that encode two proteins ... The antitoxin protein of each system interacts with its cognate toxin to neutralise the activity of the toxin and in the ... Toxin-antitoxin database Jensen RB, Gerdes K (1995). "Programmed cell death in bacteria: proteic plasmid stabilization systems ... Oberer M, Zangger K, Prytulla S, Keller W (January 2002). "The anti-toxin ParD of plasmid RK2 consists of two structurally ...
These observations are in accordance with those made of Type I toxin-antitoxin systems. In type I toxin-antitoxin systems, the ... Type I toxin-antitoxin loci are frequently found in both prokaryotic chromosomes and plasmids. The secondary structure of ... Hok/sok system Toxin-antitoxin system Findeiss S, Schmidtke C, Stadler PF, Bonas U (March 2010). "A novel family of plasmid- ... Gerdes K, Wagner EG (April 2007). "RNA antitoxins". Curr. Opin. Microbiol. 10 (2): 117-124. doi:10.1016/j.mib.2007.03.003. PMID ...
Louis children died from contaminated diphtheria antitoxin. The horse from which the antitoxin was derived died of tetanus. ... Behring used this antitoxin (now known to consist of antibodies that neutralize the toxin produced by C. diphtheriae) for human ... They also immunized goats and horses in the same way and showed that an "antitoxin" made from serum of immunized animals could ... Protection can be verified by measuring the antitoxin level in the blood. Diphtheria can be prevented in those exposed as well ...
27 (Associated Press).-Nome has a diphtheria epidemic and no antitoxin. The nearest known supply of antitoxin is at Anchorage, ... "DOGS RUSH ANTI-TOXIN FOR NOME EPIDEMIC; Two Fliers Volunteer Services". The New York Times. Associated Press. January 29, 1925 ... The antitoxin units are to leave Seattle Saturday on the steamship Alameda. . . . WASHINGTON, Jan. 29.-Possibility that an ... This is reminiscent of the 1925 serum run to Nome, a sled dog relay carrying antitoxin that was responsible for halting a ...
The products included diagnostic reagents and procedures, drugs, vaccines, toxoids, and antitoxins. Emphasis is placed on ... Antitoxins for diseases such as botulism; Human immune globulin preparations (passive antibody protection) against various ...
Olitsky, Peter K.; Kligler, I. J. (1920). "Toxins and Antitoxins of Bacillus Dysenteriæ Shiga". Journal of Experimental ...
Antitoxins are used to prevent further harm. Antibiotics are also used to fight the infection. Typical antibiotics that are ...
Discovered the diphtheria antitoxin. It was the world's first cure for a disease (1891). He was awarded history's first Nobel ... Emil von Behring: Discovery of diphtheria antitoxin Fabian Gottlieb von Bellingshausen: Navigator and explorer. Discovered the ...
"Eleven Killed by Antitoxin". Chicago Daily Tribune. November 2, 1901. p. 1. Hamowy, Ronald (2008). Government and Public Health ... Louis was the first of 13 from a contaminated antitoxin distributed by that city's health department, would lead to the United ... Behring had discovered the antitoxin to cure the disease of diphtheria, and then applied the same principles of blood serum ...
"Diphtheria and its antitoxin". The Laryngoscope. 1 (2): 105-106. August 1896. doi:10.1288/00005537-189608000-00011. Lee, Elmer ...
Hall, F. D. (1894). "Antitoxin Treatment of Diphtheria". British Medical Journal. 2 (1757): 513. doi:10.1136/bmj.2.1757.513. ...
"Tetanus Antitoxin Successfully Administered". Reading Times. 1898-10-20. p. 2. Retrieved 2017-10-27. "General Hospital May ...
"Antitoxin and Serum Therapy". The History of Vaccines. Philadelphia: The College of Physicians of Philadelphia. 2020. Retrieved ... serum antitoxin) by Emil von Behring 1896 - First vaccine for typhoid fever by Almroth Edward Wright, Richard Pfeiffer, and ...
Rees, Anthony R. (2015). The Antibody Molecule: From Antitoxins to Therapeutic Antibodies. Oxford University Press. pp. 104-120 ...
... -antitoxin system Harper, Douglas. "toxin". Online Etymology Dictionary. "toxin - Definition from the Merriam-Webster ...
The second antitoxin, heptavalent (A,B,C,D,E,F,G) botulinum antitoxin, is derived from "despeciated" equine IgG antibodies ... This human-derived antitoxin has been shown to be both safe and effective for the treatment of infant botulism. However, the ... To avoid this, a human-derived antitoxin has been developed and approved by the U.S. FDA in 2003 for the treatment of infant ... 2018). "Efficacy of Antitoxin Therapy in Treating Patients With Foodborne Botulism: A Systematic Review and Meta-analysis of ...
... Botulism antitoxin for patients with signs and symptoms of human foodborne or wound botulism is ... The results of these tests are helpful in evaluating the need for botulism antitoxin. Reported by Enteric Diseases Br, Div of ... A list of daytime and 24-hour telephone numbers (if available) is published to assist those seeking botulism antitoxin (Table 2 ... Any health-care provider requesting botulism antitoxin should first contact his/her state health department. ...
Diphtheria antitoxin was one of these medicines. Doctors used diphteria antitoxin to treat and prevent diphtheria, an often ... How did they make diphtheria antitoxin?. Scientists learned to harness the immune systems of some animals to produce antitoxin ... As an immune response, the animals blood produces diphtheria antitoxin.. 3. Scientists collect blood from the horses and ... 4. Then, researchers purify the antitoxin serum for use as a medicine for people. ...
Diphtheria antitoxin (DAT). Dose given depends on site of infection and length of time patient is symptomatic. In US, DAT ... Antitoxins. Class Summary. These agents are administered to neutralize toxin responsible for diphtheria. ... For C diphtheriae infection, the therapy is antitoxin and antibiotic treatment. Many antibiotics previously were effective, ...
In particular, antitoxins have been shown to be beneficial in several forms of severe acute infections such as diphtheria, ... Anthrax Antitoxins No authors listed In: LiverTox: Clinical and Research Information on Drug-Induced Liver Injury [Internet]. ... In particular, antitoxins have been shown to be beneficial in several forms of severe acute infections such as diphtheria, ... Systematic review of the literature on animal studies of the efficacy of antitoxin therapy for anthrax).] - PMC - PubMed ...
PRODUCTION OF BOTULINUM ANTI-TOXIN IMMUNOGLOBULIN Release Date: June 13, 2002 NOTICE: NOT-AI-02-030 National Institute of ... in supporting the development and licensure of botulinum anti-toxin immunoglobulin as a part of our Biodefense program. NIAID ...
In particular, antitoxins have been shown to be beneficial in several forms of severe acute infections such as diphtheria, ... Systematic review of the literature on animal studies of the efficacy of antitoxin therapy for anthrax). ... Antitoxin treatment of inhalation anthrax: a systematic review. Health Secur. 2015;13:365-77. [PMC free article: PMC4710135] [ ... In particular, antitoxins have been shown to be beneficial in several forms of severe acute infections such as diphtheria, ...
... the 1st International Standard for Diphtheria Antitoxin Human should be used as the reference antitoxin (National Institute for ... Diphtheria antitoxin for therapeutic use is in limited supply. A potential source might be affinity-purified antibodies ... Access to diphtheria antitoxin for therapy and diagnostics. Euro Surveill. 2014;19:20830. ... Postbooster Antibodies from Humans as Source of Diphtheria Antitoxin. Emerging Infectious Diseases. 2016;22(7):1265-1267. doi: ...
Get up-to-date information on Tetanus Antitoxin side effects, uses, dosage, overdose, pregnancy, alcohol and more. Learn more ... How was your experience with Tetanus Antitoxin?. First, a little about yourself. Male Female ... Tetanus Antitoxin falls into category C:. In animal studies, pregnant animals were given this medication and had some babies ... Tetanus Antitoxin should be used during pregnancy only if the possible benefit outweighs the possible risk to the unborn baby. ...
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Spaun, J. & Lyng, J. (‎1970)‎. Replacement of the International Standard for Tetanus Antitoxin and the Use of the Standard in ... Replacement of the International Standard for Tetanus Antitoxin and the Use of the Standard in the Flocculation Test. ...
The HigA antitoxin binds to and inactivates the HigB toxin when cells are not in a stressed state. Structural investigation ... 6.7 Mechanism of antitoxin inhibition of toxin function. 224. 6.8 Molecular mechanisms of cleavage of mRNA by ribosome- ... Structural and functional studies of a toxin-anti toxin system involved in translational inhibition Open Access. Schureck, Marc ... Structural and functional studies of a toxin-anti toxin system involved in translational inhibition () 2018-08-28 14:27:06 - ...
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Lukas joined ANTITOXIN in 2019 following a career in pharmaceutical and IVD industry. He holds a Master of Science degree in ... ANTITOXIN was owner-managed by professional specialists in IVD since its beginning. Lukas Quidenus succeeded Dr. Ortwin Walla, ...
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Start Over You searched for: Subjects Diphtheria Antitoxin -- administration & dosage ✖Remove constraint Subjects: Diphtheria ...
Diphtheria Antitoxin I.P. (Liquid). *DESCRIPTION:. Diphtheria Antitoxin is a preparation containing the specific globulin ... Diphtheria antitoxin should be administered as soon as the clinical evidence of the disease appears. Administration of the ... In case of positive skin test, Diphtheria antitoxin may be administered after desensitization and/or under the cover of anti- ... Each ml of Diphtheria Antitoxin serum contains:. - Enzyme refined Equine globulin , or =1000 IU. - Preservative, Phenol , or = ...
Keywords: Toxin-antitoxin. Selfish gene leaves bacteria behind. A. York, Nature Reviews Microbiology, 2021. Mitochondrial ...
Medicine: Anti-toxin Pill is one of the Ninja Skills in Nioh2. Medicine: Anti-toxin pill is a jutsu skill that allows you to ... Medicine: Anti-toxin Pill , Nioh 2 Wiki Edit. 1. 2. …. * Create new page ... Medicine: Anti-toxin Pill Description. Allows you to ready Anti-toxic pill. When taken, these pills neutralise poison and ... Anti-toxin Pill I ♦ Kodama Transformation I ♦ Kunai I ♦ Levitation ♦ Makibishi ♦ Makibishi Ball ♦ Medicine: Power Pill I ♦ ...
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Although best effort has been made to ensure the information provided is correct and updated, users are advised to visit HSA Official website whenever in doubt. Please see Disclaimers ...
Antitoxin definition, A medicine or substance produced by your body which stops the effects of a poison.. See more. ... In 1891, Emil von Behring produced an antitoxin from the blood of animals for curing diphtheria. ...
Topic: Diphtheria and Diphtheria antitoxins. (Please note that the documents listed below are sorted by date.). Toxigenic ...
Further, MazEF6 acts independently of other Maz family toxin:antitoxin pairs. Notably, soj Mtb and mazEF6 transcripts where ... functions as an mRNA interferase leading to bacteriostasis that can be prevented by interaction with its cognate antitoxin, ... MazE6-HIS antitoxin and MazF6-HSV toxin functionally and physically interact in vivo. A) Growth of E. coli BL21 (DE3) pLysE ... Table 3 Growth kinetics in cultures co-expressing the mazF6 toxin with cognate and non-cognate antitoxins Full size table. ...
Effects of Toxin-Antitoxin System HicAB on Biofilm Formation by Extraintestinal Pathogenic E. coli.. Hou, Bo; Wang, Chen-Yan; ... The type II toxin-antitoxin (T-A) HicAB system is abundant in several bacteria and archaea, such as Escherichia coli, ...
Diphtheria antitoxin Diphtheria antitoxin must be given early without waiting for culture confirmation because the antitoxin ... IV administration of antitoxin is contraindicated in patients who are allergic to the antitoxin. ... CAUTION: Diphtheria antitoxin is derived from horses; therefore, a skin (or conjunctival) test to rule out sensitivity Specific ... In the US, antitoxin must be obtained from the Centers for Disease Control and Prevention (CDC) through the CDCs Emergency ...
  • Diphtheria antitoxin was one of these medicines. (
  • As an immune response, the animal's blood produces diphtheria antitoxin. (
  • 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. (
  • Diphtheria antitoxin should be administered as soon as the clinical evidence of the disease appears. (
  • CAES Seminar Series: 'Toxin-Antitoxin Systems: Implications for Plant Disease? (
  • Dr. Teja Shiodre , Dept of Plant Pathology and Ecology, CAES will present 'Toxin-Antitoxin Systems: Implication for Plant Disease? (
  • The possibility of rendering toxic a non-toxic toxin-antitoxin mixture by the addition of toxoid is confirmed. (
  • 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. (
  • 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. (
  • 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. (
  • 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. (
  • 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. (
  • The HigA antitoxin binds to and inactivates the HigB toxin when cells are not in a stressed state. (
  • 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. (
  • Introduction: Toxin-antitoxin systems. (
  • 1.10 Transcriptional regulation of toxin-antitoxin systems. (
  • 1.12 Toxin-antitoxin systems and persister cell formation. (
  • 1.13 Other roles of toxin-antitoxin systems. (
  • 1.16 The HigB-HigA toxin-antitoxin system. (
  • Structure of the P. vulgaris HigB-(HigA)2-HigB toxin-antitoxin complex. (
  • Effects of Toxin-Antitoxin System HicAB on Biofilm Formation by Extraintestinal Pathogenic E. coli. (
  • 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 . (
  • Further, MazEF6 acts independently of other Maz family toxin:antitoxin pairs. (
  • 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. (
  • TA loci encode an unstable antitoxin immediately upstream of a toxin and these proteins form a complex with one another under optimal growth conditions. (
  • We previously reported on an SOS-induced toxin, TisB, in Escherichia coli and its regulation by the RNA antitoxin IstR-1. (
  • 3. Scientists collect blood from the horses and separate out the antitoxin rich serum. (
  • 4. Then, researchers purify the antitoxin serum for use as a medicine for people. (
  • Anti-tetanic Serum (1898) and Tetanus Antitoxin (ca 1953) are different names for the same product. (
  • 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. (
  • Any health-care provider requesting botulism antitoxin should first contact his/her state health department. (
  • A list of daytime and 24-hour telephone numbers (if available) is published to assist those seeking botulism antitoxin (Table 2). (
  • The results of these tests are helpful in evaluating the need for botulism antitoxin. (
  • The medicine is called botulism antitoxin. (
  • Antitoxins: therapy for stressed bacteria. (
  • Edmond Nocard demonstrated the protection and immunization of tetanus by using passively transferred antitoxin as well as deactivating the bacteria and spores. (
  • Scientists learned to harness the immune systems of some animals to produce antitoxin serums to use as medicines. (
  • 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. (
  • For C diphtheriae infection, the therapy is antitoxin and antibiotic treatment. (
  • The more antitoxin the mixture contains, the greater must be the amount of toxoid added in order to render the mixture toxic. (
  • 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. (
  • 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. (
  • Doctors used diphteria antitoxin to treat and prevent diphtheria, an often deadly childhood disease. (
  • In 1891, Emil von Behring produced an antitoxin from the blood of animals for curing diphtheria. (
  • of alternative antitoxins of human origin. (
  • Heptavalent antitoxin (toxins A through G) is available at the Centers for Disease Control and Prevention (CDC). (
  • 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. (
  • Doctors used diphteria antitoxin to treat and prevent diphtheria, an often deadly childhood disease. (
  • 4. Then, researchers purify the antitoxin serum for use as a medicine for people. (