"Staph aureus can produce enterotoxins, which can give you significant gastroenteritis in the matter of a half hour to four hours," says Philip Tierno, professor of microbiology and pathology at NYU School of Medicine.
|
|
Reheating it in a microwave won't kill off this bacteria, either, so letting it sit out and then popping it in the microwave puts you at more of a risk of ingesting these enterotoxins.
|
|
Enterotoxins produced by ETEC include heat-labile enterotoxin (LT) and heat- stable enterotoxin (ST).
|
|
In gram-positive bacteria, these are exotoxins or enterotoxins, which may vary depending on the species of bacteria. These are divided into three types. Type I, cell surface-active toxins, disrupt cells without entering, and include superantigens and heat-stable enterotoxins. Type II, membrane-damaging toxins, destroy cell membranes in order to enter and includeF hemolysins and phospholipases.
|
|
GC-C is a key receptor for heat-stable enterotoxins that are responsible for acute secretory diarrhea. Heat-stable enterotoxins are produced by pathogens such as Escherichia coli. Knockout mice deficient in the GC-C gene do not show secretory diarrhea on infection with E. coli, though they do with cholera toxin. This demonstrates the specificity of the GC-C receptor.
|
|
Enterotoxins have a particularly marked effect upon the gastrointestinal tract, causing traveler's diarrhea and food poisoning. The action of enterotoxins leads to increased chloride ion permeability of the apical membrane of intestinal mucosal cells. These membrane pores are activated either by increased cAMP or by increased calcium ion concentration intracellularly. The pore formation has a direct effect on the osmolarity of the luminal contents of the intestines.
|
|
Some strains of E. coli produce heat-stable enterotoxins (ST), which are small peptides that are able to withstand heat treatment at 100 °C. Different STs recognize distinct receptors on the cell surface and thereby affect different intracellular signaling pathways. For example, STa enterotoxins bind and activate membrane- bound guanylate cyclase, which leads to the intracellular accumulation of cyclic GMP and downstream effects on several signaling pathways. These events lead to the loss of electrolytes and water from intestinal cells.
|
|
In molecular biology, the Bacillus haemolytic enterotoxin family of proteins consists of several Bacillus haemolytic enterotoxins (HblC, HblD, HblA, NheA, and NheB), which can cause food poisoning in humans. Haemolysin BL (encoded by HBL) and non-haemolytic enterotoxin (encoded by NHE), represent the major enterotoxins produced by Bacillus cereus. Most of the cytotoxic activity of B. cereus isolates has been attributed to the level of Nhe, which may indicate a highly diarrheic potential. The exact mechanism by which B. cereus causes diarrhoea is unknown.
|
|
Heat-stable enterotoxins (STs) are secretory peptides produced by some bacterial strains, such as enterotoxigenic Escherichia coli which are in general toxic to animals. These peptides keep their 3D structure and remain active at temperatures as high as 100 °C.
|
|
B. cereus is a soil-dwelling bacterium which can colonize the gut of invertebrates as a symbiont and is a frequent cause of food poisoning It produces an emetic toxin, enterotoxins, and other virulence factors. The enterotoxins and virulence factors are encoded on the chromosome, while the emetic toxin is encoded on a 270-kb plasmid, pCER270. B. thuringiensis is an insect pathogen and is characterized by production of parasporal crystals of insecticidal toxins Cry and Cyt. The genes encoding these proteins are commonly located on plasmids which can be lost from the organism, making it indistinguishable from B. cereus.
|
|
Symptoms of Shiga toxin ingestion include abdominal pain as well as watery diarrhea. Severe life-threatening cases are characterized by hemorrhagic colitis (HC). The toxin is associated with hemolytic-uremic syndrome. In contrast, Shigella species may also produce shigella enterotoxins, which are the cause of dysentery.
|
|
Enterotoxins are frequently cytotoxic and kill cells by altering the apical membrane permeability of the mucosal (epithelial) cells of the intestinal wall. They are mostly pore-forming toxins (mostly chloride pores), secreted by bacteria, that assemble to form pores in cell membranes. This causes the cells to die.
|
|
S. aureus is an enterotoxin producer. Enterotoxins are chromosomally encoded exotoxins that are produced and secreted from several bacterial organisms. It is a heat stable toxin and is resistant to digestive protease. It is the ingestion of the toxin that causes the inflammation and swelling of the intestine.
|
|
Tolevamer was designed to bind the enterotoxins of Clostridium difficile. Since it has no antibiotic properties, it does not harm the gut flora. Early studies used the sodium salt, but it was soon replaced with the potassium sodium salt to prevent hypokalaemia, which is often associated with diarrhea.
|
|
An enterotoxin is a protein exotoxin released by a microorganism that targets the intestines. Enterotoxins are chromosomally encoded or plasmid encodedCarlton Gyles, Magdalene So, Stanley Falkow, Journal of Infectious Diseases (1974) 130 (1): 40-49. exotoxins that are produced and secreted from several bacterial organisms. They are heat labile (>60⁰), and are of low molecular weight and water-soluble.
|
|
A putative catalytic residue in the A1 fragment (Glu112) lies close to a hydrophobic region, which packs two loops together. It is thought that this region might be important for catalysis and membrane translocation. The structural arrangement of E. coli type I and type II heat-labile enterotoxins are very similar, although they are antigenically distinct.
|
|
The pathogenicity of Aeromonas species was believed to be mediated by a number of extracellular proteins such as aerolysin, lipase, chitinase, amylase, gelatinase, hemolysins, and enterotoxins. However, the pathogenic mechanisms are unknown. The recently proposed type-III secretion system (T3SS) has been linked to Aeromonas pathogenesis. T3SS is a specialized protein secretion machinery that exports virulence factors directly to host cells.
|
|
Cooked rice can contain Bacillus cereus spores, which produce an emetic toxin when left at . When storing cooked rice for use the next day, rapid cooling is advised to reduce the risk of toxin production. One of the enterotoxins produced by Bacillus cereus is heat-resistant; reheating contaminated rice kills the bacteria, but does not destroy the toxin already present.
|
|
The purpose of IMF foods is to achieve a water activity that the food can be stored safely without refrigeration. However, the food is not sterile. Staphylococcus aureus is a microorganism of concern as it can grow and produce specific enterotoxins in water activities of 0.83-0.86 under aerobic conditions. Because of this, proper handling, storage, hygiene and good manufacturing practices are necessary to prevent Staphylococcus aureus.
|
|
Increased chloride permeability leads to leakage into the lumen followed by sodium and water movement. This leads to a secretory diarrhea within a few hours of ingesting enterotoxin. Several microbial organisms contain the necessary enterotoxin to create such an effect, such as Staphylococcus aureus and E. coli. The drug linaclotide, used to treat some forms of constipation, is based on the mechanism of enterotoxins.
|
|
Clostridium enterotoxins are toxins produced by Clostridium species. Clostridial species are one of the major causes of food poisoning/gastrointestinal illnesses. They are anaerobic, gram-positive, spore-forming rods that occur naturally in the soil. Among the family are: Clostridium botulinum, which produces one of the most potent toxins in existence; Clostridium tetani, causative agent of tetanus; and Clostridium perfringens, commonly found in wound infections and diarrhea cases.
|
|
While B. cereus vegetative cells are killed during normal cooking, spores are more resistant. Viable spores in food can become vegetative cells in the intestines and produce a range of diarrheal enterotoxins, so elimination of spores is desirable. In wet heat, spores require more than 5 minutes at at the coldest spot to be destroyed. In dry heat, in a sterilizer for 1 hour works for rice, for instance.
|
|
It is the strain behind the deadly June 2011 E. coli outbreak in Europe. Severity of the illness varies considerably; it can be fatal, particularly to young children, the elderly or the immunocompromised, but is more often mild. Earlier, poor hygienic methods of preparing meat in Scotland killed seven people in 1996 due to E. coli poisoning, and left hundreds more infected. E. coli can harbour both heat-stable and heat-labile enterotoxins.
|
|
Arnold G. Wedum, M.D., Ph.D., a civilian scientist who was Director of Industrial Health and Safety at Fort Detrick, was the leader in the development of containment facilities. During the 1960s, the US program underwent a philosophical change, and attention was now directed more towards biological agents that could incapacitate, but not kill. In 1964, research programs involved staphylococcal enterotoxins capable of causing food poisoning. Research initiatives also included new therapy and prophylaxis.
|
|
Different STs recognize distinct receptors on the surface of animal cells and thereby affect different intracellular signaling pathways. For example, STa enterotoxins bind and activate membrane-bound guanylate cyclase, which leads to the intracellular accumulation of cyclic GMP and downstream effects on several signaling pathways. These events lead to the loss of electrolytes and water from intestinal cells. Heat-stable toxin 1 of entero-aggregative Escherichia coli (EAST1) is a small toxin.
|
|
Guanylin is a 15 amino acid polypeptide that is secreted by goblet cells in the colon. Guanylin acts as an agonist of the guanylyl cyclase receptor GC-C and regulates electrolyte and water transport in intestinal and renal epithelia. Upon receptor binding, guanylin increases the intracellular concentration of cGMP, induces chloride secretion and decreases intestinal fluid absorption, ultimately causing diarrhoea. The peptide stimulates the enzyme through the same receptor binding region as the heat-stable enterotoxins.
|
|
The protein contains a putative 30- amino-acid signal peptide; removal of the signal sequence gives a predicted molecular weight of 25.787 kDa for the secreted protein. Both a promoter and a ribosome binding site (Shine-Dalgarno sequence) are present upstream of the gene. A transcriptional terminator is located 69 bases downstream from the translational termination codon. The carboxy terminal portion of the protein exhibits extensive homology with the carboxy terminus of Staphylococcus aureus enterotoxins B and C1.
|
|
Examples of virulence factors for Staphylococcus aureus are hyaluronidase, protease, coagulase, lipases, deoxyribonucleases and enterotoxins. Examples for Streptococcus pyogenes are M protein, lipoteichoic acid, hyaluronic acid capsule, destructive enzymes (including streptokinase, streptodornase, and hyaluronidase), and exotoxins (including streptolysin). Examples for Listeria monocytogenes include internalin A, internalin B, lysteriolysin O, and actA, all of which are used to help colonize the host. Examples for Yersinia pestis are an altered form of lipopolysaccharide, type three secretion system, and YopE and YopJ pathogenicity.
|
|
When the United States renounced its offensive biological warfare program in 1969 and 1970, the vast majority of its biological arsenal was composed of these plant diseases. Enterotoxins and Mycotoxins were not affected by Nixon's order. Though herbicides are chemicals, they are often grouped with biological warfare and chemical warfare because they may work in a similar manner as biotoxins or bioregulators. The Army Biological Laboratory tested each agent and the Army's Technical Escort Unit was responsible for the transport of all chemical, biological, radiological (nuclear) materials.
|
|
The pathogenesis of EAEC involves the aggregation of and adherence of the bacteria to the intestinal mucosa, where they elaborate enterotoxins and cytotoxins that damage host cells and induce inflammation that results in diarrhea. EAEC is now recognized as an emerging enteric pathogen. In particular, EAEC are reported as the second most common cause of traveler's diarrhea, second only to Enterotoxigenic E. coli, and a common cause of diarrhea amongst pediatric populations. It has also been associated with chronic infections in the latter, as well as in immunocompromised hosts, such as HIV-infected individuals.
|
|
Enterotoxigenic E. coli (ETEC) is the most common cause of traveler's diarrhea, with as many as 840 million cases worldwide in developing countries each year. The bacteria, typically transmitted through contaminated food or drinking water, adheres to the intestinal lining, where it secretes either of two types of enterotoxins, leading to watery diarrhea. The rate and severity of infections are higher among children under the age of five, including as many as 380,000 deaths annually. In May 2011, one E. coli strain, O104:H4, was the subject of a bacterial outbreak that began in Germany.
|
|
In healthy individuals, pyrin-mediated inflammasome assembly (which leads to the caspase 1) dependent processing and secretion of the pro-inflammatory cytokines (such as interleukin-18 (IL-18) and IL-1β) is a response to enterotoxins from certain bacteria. The gain-of-function mutations in the MEFV gene render Pyrin hyperactive, and subsequently, the formation of the inflammasomes becomes more frequent. The pathophysiology of familial Mediterranean fever has recently undergone significant advances: at basal state, pyrin is kept inactive by a chaperone protein (belonging to the family of 14.3.3 proteins) linked to pyrin through phosphorylated serine residues.
|
|
The intestinal epithelium helps protect the intestinal mucosa from the external environment and luminal contents. Tight junctions are intercellular complexes that facilitate the low level of permeability present in the intestinal epithelial layer by monitoring the movement of materials between the intestinal lumen and the intestinal mucosa. Enterotoxins released by pathogens, in particular TNF-ct, result in an increase in the level of epithelial permeability. Lactobacillus mucosae strain ME-340 expressing the gene Lam29, which encodes for a protein that is believed to be related to the cysteine-binding transporter, shows a significant adhesion for human blood group A and B antigens.
|
|
Enterotoxigenic Escherichia coli (ETEC) is a type of Escherichia coli and one of the leading bacterial causes of diarrhea in the developing world, as well as the most common cause of travelers' diarrhea. Insufficient data exist, but conservative estimates suggest that each year, about 157,000 deaths occur, mostly in children, from ETEC. A number of pathogenic isolates are termed ETEC, but the main hallmarks of this type of bacteria are expression of one or more enterotoxins and presence of fimbriae used for attachment to host intestinal cells. The bacteria was identified by the Bradley Sack lab in Kolkata in 1968.
|
|
SAgs are produced intracellularly by bacteria and are released upon infection as extracellular mature toxins. The sequences of these toxins are relatively conserved among the different subgroups. More important than sequence homology, the 3D structure is very similar among different SAgs resulting in similar functional effects among different groups. Crystal structures of the enterotoxins reveals that they are compact, ellipsoidal proteins sharing a characteristic two-domain folding pattern comprising an NH2-terminal β barrel globular domain known as the oligosaccharide / oligonucleotide fold, a long α-helix that diagonally spans the center of the molecule, and a COOH terminal globular domain.
|
|
Domain A1 (approximately 22kDa in cholera toxin or heat labile enterotoxins) is the part of the toxin responsible for its toxic effects. Domain A2 (approximately 5kDa in cholera toxin or heat labile enterotoxin) provides a non-covalent linkage to the B subunit through the B subunit's central pore. The A1 chain for cholera toxin catalyzes the transfer of ADP-ribose from Nicotinamide adenine dinucleotide(NAD) to arginine or other guanidine compounds by utilizing ADP- ribosylation factors (ARFs). In the absence of arginine or simple guanidino compounds, the toxin mediated NAD+ nucleosidase (NADase) activity proceeds using water as a nucleophile.
|
|
Fasano began his career as a pediatric gastroenterologist interested in treating debilitating diarrhea, as well as a researcher determined to find a vaccine for cholera. He was responsible for the discovery of several new enterotoxins involved in the diarrheal pathogenesis of several pathogens, including Shigella, E. coli, and V. cholerae. These discoveries led to the engineering of attenuated enteric vaccines, some of them currently used in clinical practice. The course of this research path eventually led him and his team to the “serendipitous” discovery of zonulin in 2000, a protein responsible for regulating intestinal tight- junctions (and the over secretion of which causes “leaky-gut”).
|
|
His early career was devoted to characterize the receptor-mediated responses to atrial natriuretic peptide (ANP) in vascular smooth muscle and other cell types, especially its stimulation of guanylyl cyclase to cause the intracellular accumulation of cGMP in the context of vasodilatory phenomena. His subsequent studies on the ANP-like stimulation of guanylyl cyclase by enterotoxins eventually led to new research venues into the study of guanylyl cyclase C and its role in the pathogenesis of colorectal cancer. Recently, Waldman has extensively explored concepts surrounding the role of membrane- bound GUCY2C receptors lining the gastrointestinal tract in relation to the homeostatic regulation of the crypt-surface axis by paracrine hormones uroguanylin and guanylin. His recent research includes the experimental targeting of such receptors in various ways for the treatment of inflammatory bowel disease and colorectal neoplasias, including (under his leadership) a phase-I clinical trial to test a recombinant vaccine against colorectal cancer aimed to immunize against GUCY2C receptors.
|
|