Shiga Toxin 2
Shiga Toxin 1
Shiga-Toxigenic Escherichia coli
Escherichia coli O157
Enterohemorrhagic Escherichia coli
Ribosome Inactivating Proteins
Escherichia coli Vaccines
Botulinum Toxins, Type A
Molecular Sequence Data
Edema Disease of Swine
Polymerase Chain Reaction
RNA, Ribosomal, 28S
Adenylate Cyclase Toxin
P Blood-Group System
Enteropathogenic Escherichia coli
Lethal Dose 50
Amino Acid Sequence
Electrophoresis, Gel, Pulsed-Field
Protein Synthesis Inhibitors
Enzyme-Linked Immunosorbent Assay
Receptors, Cell Surface
Sequence Analysis, DNA
Serum Amyloid P-Component
Antigens, Tumor-Associated, Carbohydrate
Tosylphenylalanyl Chloromethyl Ketone
Vascular ultrastructure and DNA fragmentation in swine infected with Shiga toxin-producing Escherichia coli. (1/321)Shiga toxins (Stx) produced by Escherichia coli cause systemic vascular damage that manifests as edema disease in swine and hemolytic uremic syndrome in humans. In vitro, Stx inhibit protein synthesis and, depending on circumstances, induce necrosis, apoptosis, or both. The mechanism of in vivo Stx-mediated vascular damage is not known. The ability of Stx to cause apoptosis of vasculature in vivo was studied in pigs with edema disease that was produced by oral inoculation with Stx-producing E. coli. Arterioles of ileum and brain were evaluated by terminal dUTP nick-end labeling (TUNEL) assay for DNA fragmentation in myocytes (10 infected pigs, 5 control pigs) and by transmission electron microscopy for ultrastructural changes characteristic of apoptosis (17 infected pigs, 8 control pigs). In comparison with controls, increased numbers of TUNEL-positive arterioles were detected in 6/10 (60%) subclinically affected pigs 14-15 days after inoculation. Ultrastructurally, lesions in myocytes consisted of lysis (necrosis), with cytoplasmic debris and nuclear fragments contained between intact basement membranes. Endothelial cell changes ranged from acute swelling to necrosis and detachment from basement membrane. Subclinically affected pigs (n = 14) tended to have changes predominantly in myocytes, whereas pigs with clinical illness (n = 3) more commonly had changes in endothelial cells. The arteriolar lesions and clinical signs of edema disease are attributed to the effects of Stx on vasculature. Therefore, our findings suggest that the Stx-induced arteriolar lesions seen in this study were primarily necrotic, not apoptotic. We suspect that necrosis was the principal cause of the DNA fragmentation detected. (+info)
Toxin gene expression by shiga toxin-producing Escherichia coli: the role of antibiotics and the bacterial SOS response. (2/321)Toxin synthesis by Shiga toxin-producing Escherichia coli (STEC) appears to be coregulated through induction of the integrated bacteriophage that encodes the toxin gene. Phage production is linked to induction of the bacterial SOS response, a ubiquitous response to DNA damage. SOS-inducing antimicrobial agents, particularly the quinolones, trimethoprim, and furazolidone, were shown to induce toxin gene expression in studies of their effects on a reporter STEC strain carrying a chromosome-based stx2::lacZ transcriptional fusion. At antimicrobial levels above those required to inhibit bacterial replication, these agents are potent inducers (up to 140-fold) of the transcription of type 2 Shiga toxin genes (stx2); therefore, they should be avoided in treating patients with potential or confirmed STEC infections. Other agents (20 studied) and incubation conditions produced significant but less striking effects on stx2 transcription; positive and negative influences were observed. SOS-mediated induction of toxin synthesis also provides a mechanism that could exacerbate STEC infections and increase dissemination of stx genes. These features and the use of SOS-inducing antibiotics in clinical practice and animal husbandry may account for the recent emergence of STEC disease. (+info)
Prevalence of non-O157:H7 shiga toxin-producing Escherichia coli in diarrheal stool samples from Nebraska. (3/321)We determined the prevalence of Shiga toxin-producing Escherichia coli (STEC) in diarrheal stool samples from Nebraska by three methods: cefixime-tellurite sorbitol MacConkey (CT- SMAC) culture, enterohemorrhagic E. coli (EHEC) enzyme immunoassay, and stx1,2 polymerase chain reaction (PCR). Fourteen (4.2%) of 335 specimens were positive by at least one method (CT-SMAC culture [6 of 14], EHEC enzyme immunoassay [13 of 14], stx1,2 PCR [14 of 14]). Six contained serogroup O157, while non-O157 were as prevalent as O157 serogroups. (+info)
Detection and characterization of Shiga toxin-producing Escherichia coli from seagulls. (4/321)Shiga toxin (Stx)-producing Escherichia coli (STEC) strains isolated from a seagull in Japan were examined. A total of 50 faecal samples was collected on a harbour bank in Hokkaido, Japan, in July 1998. Two different STEC strains, whose serotypes were O136:H16 and O153:H-, were isolated from the same individual by PCR screening; both of them were confirmed by ELISA and Vero cell cytotoxicity assay to be producing active Stx2 and Stx1, respectively. They harboured large plasmids, but did not carry the haemolysin or eaeA genes of STEC O157:H7. Based on their plasmid profiles, antibiotic resistance patterns, pulsed-field gel electrophoresis analysis (PFGE), and the stx genes sequences, the isolates were different. Phylogenic analysis of the deduced Stx amino acid sequences demonstrated that the Stx toxins of seagull-origin STEC were closely associated with those of the human-origin, but not those of other animal-origin STEC. In addition, Stx2phi-K7 phage purified from O136 STEC resembled Stx2phi-II from human-origin O157:H7, and was able to convert non-toxigenic E. coli to STEC. These results suggest that birds may be one of the important carriers in terms of the distribution of STEC. (+info)
Entry of ricin and Shiga toxin into cells: molecular mechanisms and medical perspectives. (5/321)A large number of plant and bacterial toxins with enzymatic activity on intracellular targets are now known. These toxins enter cells by first binding to cell surface receptors, then they are endocytosed and finally they become translocated into the cytosol from an intracellular compartment. In the case of the plant toxin ricin and the bacterial toxin Shiga toxin, this happens after retrograde transport through the Golgi apparatus and to the endoplasmic reticulum. The toxins are powerful tools to reveal new pathways in intracellular transport. Furthermore, knowledge about their action on cells can be used to combat infectious diseases where such toxins are involved, and a whole new field of research takes advantage of their ability to enter the cytosol for therapeutic purposes in connection with a variety of diseases. This review deals with the mechanisms of entry of ricin and Shiga toxin, and the attempts to use such toxins in medicine are discussed. (+info)
Shiga toxin activates p38 MAP kinase through cellular Ca(2+) increase in Vero cells. (6/321)We examined whether the mitogen-activated protein kinase (MAPK) pathway is involved in Shiga toxin (Stx)-induced Vero cell injury. Consonant with cell injury, Stx caused a transient extracellular signal-regulated kinase1/2 (ERK1/2) and a sustained p38 MAPK phosphorylation. p38 MAPK inhibitors (SB 203580 and PD 169316), but not an ERK1/2 kinase inhibitor (PD 98059), partially inhibited the Stx-induced cell death. BAPTA-AM, a Ca(2+) chelator, reduced both cell injury and p38 MAPK phosphorylation. Antioxidants reduced Stx1-induced p38 MAPK phosphorylation. These data indicate that Stx activates p38 MAPK through an increase in intracellular Ca(2+) and reactive oxygen species, and this signaling is involved in Stx-induced cell death. (+info)
Rab11 regulates the compartmentalization of early endosomes required for efficient transport from early endosomes to the trans-golgi network. (7/321)Several GTPases of the Rab family, known to be regulators of membrane traffic between organelles, have been described and localized to various intracellular compartments. Rab11 has previously been reported to be associated with the pericentriolar recycling compartment, post-Golgi vesicles, and the trans-Golgi network (TGN). We compared the effect of overexpression of wild-type and mutant forms of Rab11 on the different intracellular transport steps in the endocytic/degradative and the biosynthetic/exocytic pathways in HeLa cells. We also studied transport from endosomes to the Golgi apparatus using the Shiga toxin B subunit (STxB) and TGN38 as reporter molecules. Overexpression of both Rab11 wild-type (Rab11wt) and mutants altered the localization of the transferrrin receptor (TfR), internalized Tf, the STxB, and TGN38. In cells overexpressing Rab11wt and in a GTPase-deficient Rab11 mutant (Rab11Q70L), these proteins were found in vesicles showing characteristics of sorting endosomes lacking cellubrevin (Cb). In contrast, they were redistributed into an extended tubular network, together with Cb, in cells overexpressing a dominant negative mutant of Rab11 (Rab11S25N). This tubularized compartment was not accessible to Tf internalized at temperatures <20 degrees C, suggesting that it is of recycling endosomal origin. Overexpression of Rab11wt, Rab11Q70L, and Rab11S25N also inhibited STxB and TGN38 transport from endosomes to the TGN. These results suggest that Rab11 influences endosome to TGN trafficking primarily by regulating membrane distribution inside the early endosomal pathway. (+info)
Molecular and phenotypic characterization of potentially new Shigella dysenteriae serotype. (8/321)From September 1997 to November 1998, the French National Center for Salmonella and Shigella received 22 Shigella isolates recovered from 22 different patients suffering from dysentery. None of these isolates reacted with any of the antisera used to identify established Shigella serotypes, but all of them agglutinated in the presence of antisera to a previously described potentially new Shigella dysenteriae serotype (represented by strain 96-204) primarily isolated from stool cultures of imported diarrheal cases in Japan. All French isolates, as well as strain 96-204, showed biochemical reactions typical of S. dysenteriae and gave positive results in a PCR assay for detection of the plasmid ipaH gene coding for invasiveness. No Shiga toxin gene was detected by PCR. These isolates were indistinguishable by molecular analysis of ribosomal DNA (ribotyping) and seemed to be related to S. dysenteriae serotypes 3 and 12. However, further characterization by restriction of the amplified O-antigen gene cluster clearly distinguished this new serotype from all other Shigella or Escherichia coli serotypes. (+info)
The symptoms of HUS include:
* Abdominal pain
* Shortness of breath
* Pale or yellowish skin
* Easy bruising or bleeding
If you suspect that someone has HUS, it is important to seek medical attention immediately. A healthcare provider will perform a physical examination and order blood tests to diagnose the condition. Treatment for HUS typically involves addressing the underlying cause of the condition, such as stopping certain medications or treating an infection. In some cases, hospitalization may be necessary to manage complications such as kidney failure.
Preventative measures to reduce the risk of developing HUS include:
* Practicing good hygiene, especially during outbreaks of diarrheal illnesses
* Avoiding certain medications that are known to increase the risk of HUS
* Maintaining a healthy diet and staying hydrated
* Managing any underlying medical conditions such as high blood pressure or diabetes.
Here are some common types of E. coli infections:
1. Urinary tract infections (UTIs): E. coli is a leading cause of UTIs, which occur when bacteria enter the urinary tract and cause inflammation. Symptoms include frequent urination, burning during urination, and cloudy or strong-smelling urine.
2. Diarrheal infections: E. coli can cause diarrhea, abdominal cramps, and fever if consumed through contaminated food or water. In severe cases, this type of infection can lead to dehydration and even death, particularly in young children and the elderly.
3. Septicemia (bloodstream infections): If E. coli bacteria enter the bloodstream, they can cause septicemia, a life-threatening condition that requires immediate medical attention. Symptoms include fever, chills, rapid heart rate, and low blood pressure.
4. Meningitis: In rare cases, E. coli infections can spread to the meninges, the protective membranes covering the brain and spinal cord, causing meningitis. This is a serious condition that requires prompt treatment with antibiotics and supportive care.
5. Hemolytic-uremic syndrome (HUS): E. coli infections can sometimes cause HUS, a condition where the bacteria destroy red blood cells, leading to anemia, kidney failure, and other complications. HUS is most common in young children and can be fatal if not treated promptly.
Preventing E. coli infections primarily involves practicing good hygiene, such as washing hands regularly, especially after using the bathroom or before handling food. It's also essential to cook meat thoroughly, especially ground beef, to avoid cross-contamination with other foods. Avoiding unpasteurized dairy products and drinking contaminated water can also help prevent E. coli infections.
If you suspect an E. coli infection, seek medical attention immediately. Your healthcare provider may perform a urine test or a stool culture to confirm the diagnosis and determine the appropriate treatment. In mild cases, symptoms may resolve on their own within a few days, but antibiotics may be necessary for more severe infections. It's essential to stay hydrated and follow your healthcare provider's recommendations to ensure a full recovery.
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.
The diagnosis of bacillary dysentery is based on a combination of clinical findings and laboratory tests, such as fecal cultures or polymerase chain reaction (PCR) assays. Treatment typically involves antibiotics, which can shorten the duration of diarrhea and reduce the risk of complications. In severe cases, hospitalization may be necessary to manage dehydration and other complications.
Prevention measures include maintaining good hygiene practices, such as washing hands after using the bathroom or before handling food, and avoiding contaminated water or food. Vaccines are also available for some types of Shigella infections.
Edema disease is caused by a picornavirus and is characterized by fever, lethargy, loss of appetite, and difficulty breathing due to severe inflammation of the respiratory tract. The skin becomes edematous (swollen) and hemorrhages occur under the skin and in internal organs such as the lungs and liver. Death can occur within 24 to 48 hours after the onset of symptoms.
The disease is transmitted through direct contact with infected swine or contaminated fomites, and the virus can survive for several days in the environment. The incubation period is typically 3-7 days, and infected animals may not show any clinical signs until they are heavily infected.
There is no specific treatment or vaccine available for edema disease, and control measures are focused on preventing the spread of the virus through proper sanitation, biosecurity measures, and culling of infected animals. The disease is considered highly contagious and can have a significant impact on swine populations if not controlled promptly.
Cattle diseases refer to any health issues that affect cattle, including bacterial, viral, and parasitic infections, as well as genetic disorders and environmental factors. These diseases can have a significant impact on the health and productivity of cattle, as well as the livelihoods of farmers and ranchers who rely on them for their livelihood.
Types of Cattle Diseases
There are many different types of cattle diseases, including:
1. Bacterial diseases, such as brucellosis, anthrax, and botulism.
2. Viral diseases, such as bovine viral diarrhea (BVD) and bluetongue.
3. Parasitic diseases, such as heartwater and gapeworm.
4. Genetic disorders, such as polledness and cleft palate.
5. Environmental factors, such as heat stress and nutritional deficiencies.
Symptoms of Cattle Diseases
The symptoms of cattle diseases can vary depending on the specific disease, but may include:
1. Fever and respiratory problems
2. Diarrhea and vomiting
3. Weight loss and depression
4. Swelling and pain in joints or limbs
5. Discharge from the eyes or nose
6. Coughing or difficulty breathing
7. Lameness or reluctance to move
8. Changes in behavior, such as aggression or lethargy
Diagnosis and Treatment of Cattle Diseases
Diagnosing cattle diseases can be challenging, as the symptoms may be similar for different conditions. However, veterinarians use a combination of physical examination, laboratory tests, and medical history to make a diagnosis. Treatment options vary depending on the specific disease and may include antibiotics, vaccines, anti-inflammatory drugs, and supportive care such as fluids and nutritional supplements.
Prevention of Cattle Diseases
Preventing cattle diseases is essential for maintaining the health and productivity of your herd. Some preventative measures include:
1. Proper nutrition and hydration
2. Regular vaccinations and parasite control
3. Sanitary living conditions and frequent cleaning
4. Monitoring for signs of illness and seeking prompt veterinary care if symptoms arise
5. Implementing biosecurity measures such as isolating sick animals and quarantining new animals before introduction to the herd.
It is important to work closely with a veterinarian to develop a comprehensive health plan for your cattle herd, as they can provide guidance on vaccination schedules, parasite control methods, and disease prevention strategies tailored to your specific needs.
Cattle diseases can have a significant impact on the productivity and profitability of your herd, as well as the overall health of your animals. It is essential to be aware of the common cattle diseases, their symptoms, diagnosis, treatment, and prevention methods to ensure the health and well-being of your herd.
By working closely with a veterinarian and implementing preventative measures such as proper nutrition and sanitary living conditions, you can help protect your cattle from disease and maintain a productive and profitable herd. Remember, prevention is key when it comes to managing cattle diseases.
Foodborne diseases, also known as food-borne illnesses or gastrointestinal infections, are conditions caused by eating contaminated or spoiled food. These diseases can be caused by a variety of pathogens, including bacteria, viruses, and parasites, which can be present in food products at any stage of the food supply chain.
Examples of common foodborne diseases include:
1. Salmonella: Caused by the bacterium Salmonella enterica, this disease can cause symptoms such as diarrhea, fever, and abdominal cramps.
2. E. coli: Caused by the bacterium Escherichia coli, this disease can cause a range of symptoms, including diarrhea, urinary tract infections, and pneumonia.
3. Listeria: Caused by the bacterium Listeria monocytogenes, this disease can cause symptoms such as fever, headache, and stiffness in the neck.
4. Campylobacter: Caused by the bacterium Campylobacter jejuni, this disease can cause symptoms such as diarrhea, fever, and abdominal cramps.
5. Norovirus: This highly contagious virus can cause symptoms such as diarrhea, vomiting, and stomach cramps.
6. Botulism: Caused by the bacterium Clostridium botulinum, this disease can cause symptoms such as muscle paralysis, respiratory failure, and difficulty swallowing.
Foodborne diseases can be diagnosed through a variety of tests, including stool samples, blood tests, and biopsies. Treatment typically involves antibiotics or other supportive care to manage symptoms. Prevention is key to avoiding foodborne diseases, and this includes proper food handling and preparation practices, as well as ensuring that food products are stored and cooked at safe temperatures.
Enteroaggregative Escherichia coli
2011 Germany E. coli O104:H4 outbreak
Peter K. Olitsky
Escherichia coli O104:H4
Shigatoxigenic and verotoxigenic Escherichia coli
Horizontal gene transfer
Escherichia coli O157:H7
Escherichia coli O121
P1PK blood group system
AP-1 transcription factor
Function-spacer-lipid Kode construct
List of foodborne illness outbreaks in the United States
American Meat Institute
Vibrio regulatory RNA of OmpA
Causes of seizures
DNA damage-inducible transcript 3
Pathogenic Escherichia coli
List of International Organization for Standardization standards, 12000-13999
Binding immunoglobulin protein
Free statistical software
Lambda holin family
Shiga Toxin-producing E. coli and Leafy Greens | DFWED | CDC
Case Count Maps | Multistate Outbreak of Shiga toxin-producing Escherichia coli O157:H7 Linked to I.M. Healthy Brand SoyNut...
112 - Moved: Shiga toxin-producing E. coli (STEC) Studies | Case Control, Cohort, and Other Studies | FoodNet | CDC
Attributing illness caused by Shiga toxin-producing Escherichia coli (STEC) to specific foods: report
WHO EMRO | Shiga toxin-producing bacteria as emerging enteric pathogens associated with outbreaks of foodborne illness in the...
Genes encoding Shiga toxin and the intimin receptor detected in faecal samples collected from wild canids
An outbreak of Shiga toxin-producing Escherichia coli O157:H7 linked to a mud-based obstacle course, England, August 2018. |...
Escherichia coli O157: H7 strains harbor at least three distinct sequence types of Shiga toxin 2a-converting phages<...
Details for: Escherichia coli O157:H7 and other shiga toxin-producing E. coli strains / › WHO HQ Library catalog
FoodNet Fast | CDC
IMSEAR at SEARO: Detection & characterization of Shiga toxin producing Escherichia coli (STEC) & enteropathogenic Escherichia...
Research - The epidemiology of Shiga toxin-producing Escherichia coli serogroup O157 in England, 2009-2019 | FoodWorld
DHS Search Results | Wisconsin Department of Health Services
Hemolytic Uremic Syndrome: Background, Pathophysiology, Epidemiology
Evaluation of Process Control to Prevent Contamination of Beef with Non O157 Shiga Toxin producing Escherichia coli (STEC) in U...
The role of periplasmic antioxidant enzymes (superoxide dismutase and thiol peroxidase) of the Shiga toxin-producing...
Multidrug resistance in Shiga toxin-producing Escherichia coli (STEC) isolated from broiler chickens at slaughter | Portal de...
Hemolytic anemia in a 26-year-old woman with vomiting and fatigue | CMAJ
DeCS 2008 - Changed terms
- Leafy greens, such as romaine lettuce and spinach, are commonly associated with outbreaks of Shiga toxin-producing E. coli (STEC) and other enteric infections. (cdc.gov)
- To evaluate the potential public health risk caused by sec- healthy adults examined, 398 (0.08%) were positive for ondary Shiga toxin-producing Escherichia coli (STEC) STEC. (cdc.gov)
- 60 isolates were O higa toxin-producing Escherichia coli (STEC), which serogroup untypeable (online Technical Appendix Table). (cdc.gov)
- Multiple teams of scientists are looking into how E. coli causes disease, including enterohemmaorrhagic Shiga toxin-producing E. coli (known to scientists as EHEC/STEC). (nih.gov)
- Large-scale outbreaks of Shiga toxin-producing Escherichia coli (STEC) infection have revealed the great disease-causing potential of this organism, especially among children and elderly persons. (nih.gov)
- In 2016, a multijurisdictional team investigated an outbreak of Shiga toxin-producing Escherichia coli (STEC) serogroup O121 and O26 infections linked to contaminated flour from a large domestic producer. (nih.gov)
- Although Escherichia coli O157 has been is the most prevalent Shiga toxin producing serotype of Escherichia coli (STEC) in the United States, more than 900 isolates of non-O157 STEC, including serogroups O26, O111, O121, O45 and O145, were cultured from people with sporadic illnesses from 43 different states between 1983 and 2002. (beefresearch.org)
- In all countries outside North America, non-O157 serogroups of Shiga toxin-producing E. coli (STEC) have emerged as the cause about four times as many cases of human disease as E. coli O157. (beefresearch.org)
- This hypothesis is supported by laboratory experiments that have demonstrated the potential for bacteriophages from E. coli O157 that encode Shiga toxins to lysogenize new host bacteria, making them STEC. (beefresearch.org)
- Background: Enteropathogenic Escherichia coli (EPEC) and Shiga toxin-producing E. coli (STEC) are diarrheagenic E. coli that can cause disease in humans. (ufrgs.br)
- Discussion: The carrier's animals of STEC and EPEC strains do not have receptors for the Shiga toxin, serving as asymptomatic vehicle. (ufrgs.br)
- In conclusion, the identification of genes encoding Shiga toxin and the intimin receptor in wild canids feces highlight that STEC and EPEC pathogens could be spread by these wild animals. (ufrgs.br)
- Shiga toxin-producing Escherichia coli (STEC) are estimated to cause more than 265,000 illnesses each year in the United States. (cdc.gov)
- In recent years, the number of clinical laboratories that use tests that detect Shiga toxin or Shiga toxin genes has increased, resulting in increased detection of both O157 and non-O157 STEC infections. (cdc.gov)
- Hybrid Shiga toxin-producing Escherichia coli (STEC) and uropathogenic E. coli (UPEC) strains can cause both diarrhoea and urinary tract infections and are phylogenetically located between STEC and UPEC (UTIs). (tsijournals.com)
- IMSEAR at SEARO: Detection & characterization of Shiga toxin producing Escherichia coli (STEC) & enteropathogenic Escherichia coli (EPEC) in poultry birds with diarrhoea. (who.int)
- Dutta T K, Roychoudhury P, Bandyopadhyay S, Wani S A, Hussain I. Detection & characterization of Shiga toxin producing Escherichia coli (STEC) & enteropathogenic Escherichia coli (EPEC) in poultry birds with diarrhoea. (who.int)
- Background & objectives Limited information is available on shiga toxin producing Escherichia coli (STEC) in animals and birds from India. (who.int)
- The PST2 cluster, identified in two clade 8 strains, was related to stx2a-converting phages previously identified in non-O157 Shiga-toxin producing E. coli (STEC) strains associated with a high incidence of HUS. (elsevier.com)
- The European Commission (EC) integrated approach to food safety  defines a case of Shiga-like toxin-producing E. coli (STEC) diarrhea caused by O104:H4 by an acute onset of diarrhea or bloody diarrhea together with the detection of the Shiga toxin 2 (Stx2) or the Shiga gene stx2 . (wikipedia.org)
- To diagnose infection with STEC, a patient's stool (feces) can be tested in a laboratory for the presence of Shiga toxin. (wikipedia.org)
- Shiga toxin-producing Escherichia coli (STEC) serogroup O157 is a zoonotic, foodborne gastrointestinal pathogen of major public health concern. (kswfoodmicro.com)
- This study examined the role of the periplasmic oridative defense proteins, copper, zinc superoxide dismutase (SodC), and thiol peroxidase (Tpx), from the Shiga toxin-producing Escherichia coli O157:H7 (STEC) in the formation of biofilms. (korea.ac.kr)
- Broiler chickens and derived products are a key source of Shiga toxin-producing Escherichia coli (STEC) in humans. (bvsalud.org)
- Scientists at USDA's Agricultural Research Service Western Regional Research Center in Albany, CA, have come up with a less-expensive way to detect biologically active Shiga toxin, a product of pathogenic Escherichia coli serotype O157:H7. (foodsafetynews.com)
- While Shigella dysenteriae serotype 1 most commonly produces this toxin, other members of the Enterobacteriaceae family, such as Shiga toxin-producing Escherichia coli and enterohaemorrhagic E. coli, as well as Citrobacter spp. (who.int)
- Secondly, it is considered possible that new strains of Shiga toxin-producing E. coli may emerge by acquiring the ability to produce Shiga toxin from E. coli O157 following the exchange of genetic material. (beefresearch.org)
- The Shiga toxin gene was replaced with an antibiotic marker (chloramphenicol acetyl transferase, CAT) gene among isolates of E. coli O157 and isolates of E. coli O26. (beefresearch.org)
- Eight, 12-week-old wean calves were inoculated with an E. coli O157 strain in which the Shiga toxin gene had been replaced with a kanamycin resistance gene ( E. coli O157 stxÄkan). (beefresearch.org)
- A toxin produced by certain pathogenic strains of ESCHERICHIA COLI such as ESCHERICHIA COLI O157. (ucdenver.edu)
- Isolation of E. coli from a clinical specimen with detection of Shiga toxin or Shiga toxin genes. (cdc.gov)
- Whole-Genome Sequencing of Shiga Toxin-Producing Escherichia coli OX18 from a Fatal Hemolytic Uremic Syndrome Case. (bvsalud.org)
- We report a fatal case of hemolytic uremic syndrome with urinary tract infection in Japan caused by Shiga toxin-producing Escherichia coli . (bvsalud.org)
- Escherichia coli O157:H7 and other shiga toxin-producing E. coli strains / editors: James B. Kaper, Alison D. O'Brien. (who.int)
- Background: Shiga toxin-producing Escherichia coli O157:H7 is a foodborne pathogen that causes severe human diseases including hemolytic uremic syndrome (HUS). (elsevier.com)
- Analysis of genomic sequences obtained by BGI Shenzhen shows that the O104:H4 outbreak strain is an enteroaggregative E. coli (EAEC or EAggEC) type that has acquired Shiga toxin genes, presumably by horizontal gene transfer . (wikipedia.org)
- Persistent infizierte Rinder sind das wichtigste Reservoir für humanpathogene Shigatoxin-bildende E. coli. (uni-giessen.de)
- Persistently infected ruminants are the main reservoir of Shiga toxin-producing E. coli which can be pathogenic for humans. (uni-giessen.de)
- Effect of rifampicin and gentamicin on Shiga toxin 2 expression level and the SOS response in Escherichia Coli O104:H4. (metaorganism-research.com)
- could also carry different Shiga toxin (stx) genes and their variants (stx1 and/or stx2) (1,2). (who.int)
- All colony forming units (CFU) were collected by plate washing with ultrapure water (2 mL) and posterior freezing at -20°C. The total bacterial DNA from the CFU collected was extracted, followed by PCR assay to search for three genes: stx1, stx2 (responsible for the synthesis of the Shiga toxin) and tir, which encodes the translocated intimin receptor, related to the A/E lesion formation. (ufrgs.br)
- Within 2 months, two water sources in a karst area in Switzerland were sampled 9 times each, and analyzed by real-time PCR for 6 EHEC O-types, Shiga-like-toxin (stx1 and stx2) and intimin (eae) genes. (usda.gov)
- Detection of Shiga toxin or Shiga toxin genes in a clinical specimen using a culture-independent diagnostic test (CIDT) and no known isolation of Shigella from a clinical specimen. (cdc.gov)
- Polymorphisms between phage genomes may help explain differences in Stx2a production between strains, however our data indicates that genes encoded external to the phage affect toxin production as well. (elsevier.com)
- Testing methods used include direct detection of the toxin by immunoassay , or detection of the stx2 gene or other virulence-factor genes by PCR . (wikipedia.org)
- In order to compete with commensal microbes, strains passing into the small and large intestines must be able to colonise the intestinal epithelium - and then may express various toxins after coming in close association with the intestinal mucosa [ 1 ]. (tsijournals.com)
Detect Shiga toxin1
- Rasooly says that while the cost of technology used to detect Shiga toxin and other pathogens is not a concern for wealthy countries, the equipment is typically too expensive for developing ones, where the risk of foodborne illness and outbreaks is greatest. (foodsafetynews.com)
- Insbesondere wurden die Zellen durchflusszytometrisch auf die Expression von Stx1-Rezeptoren (Gb3/CD77) sowie die Fähigkeit zur Bindung der B-Untereinheit des Toxins untersucht und die Zusammensetzung der IEL-Subpopulationen mit der aus Zäkum und Kolon verglichen. (uni-giessen.de)
- Genome assembly and copy-number analysis both confirmed that two copies of the Shiga toxin stx2 prophage gene cluster are a distinctive characteristic of the genome of the O104:H4 outbreak strain. (wikipedia.org)
- Affordable, sensitive devices like this are needed to reduce the sources and incidence of foodborne illness, says Reuven Rasooly, who works in the center's Foodborne Toxin Detection and Prevention Research Unit. (foodsafetynews.com)
- The camera method, which can easily be adapted for detecting other foodborne toxins,was compared to a commercial fluorometer for detecting active Shiga toxin, Rasooly adds. (foodsafetynews.com)
- This study investigated the prevalence of Shiga toxin-producing bacteria in stool samples of patients with diarrhoea associated with outbreaks of foodborne illness in the Islamic Republic of Iran. (who.int)
- Cooperation of Shiga toxins with other virulence factors, such as aggregative adhesin and intimin (eae), could induce more severe disease in infected patients (3). (who.int)
- By studying the human genome, researchers have identified special, small molecules that stop bacteria from producing toxins and other molecules that can cause a severe bacterial infection and illness or death. (nih.gov)
- A total of 532 stool and rectal swab samples from 70 sporadic outbreaks during May 2014 to August 2015 were examined for infection with Shiga toxin-producing bacteria. (who.int)
- Shiga toxin-producing bacteria are the main cause of bloody or non-bloody diarrhoea. (who.int)
- The virulence factor that mediates HUS, Shiga toxin (Stx), is encoded within the genome of a lambdoid prophage. (elsevier.com)
- Antimicrobials may have a potentially harmful role, possibly by inducing intestinal production of Shiga toxin during the diarrheal phase of illness. (nih.gov)
- The toxins cause illness and the associated symptoms by sticking to the intestinal cells and aggravating the cells along the intestinal wall. (wikipedia.org)
- Both instruments had the same level of toxin detection. (foodsafetynews.com)
- The toxin in the sample inhibited the synthesis of GFP - reducing GFP production in relation to the amount of toxin present. (foodsafetynews.com)
- The expression of the toxin receptor Gb3/CD77, the binding of rStxB1 to IEL, and differences between the lymphocyte subpopulations of ileum, cecum and colon were all investigated. (uni-giessen.de)
- Receptor-mediated internalization to the endoplasmic reticulum (ER) and subsequent retro-translocation to the cytosol are essential sequential processes required for the productive intoxication of susceptible mammalian cells by Shiga-like toxin-1 (SLTx). (ox.ac.uk)
- A recent clinical trial evaluating an intraluminal Shiga toxin-binding agent to ameliorate HUS showed no improvement in outcome. (nih.gov)
- Determining the activity of the toxin is very important, because the active form poses a threat to humans. (foodsafetynews.com)
- Shiga Toxin 2" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus, MeSH (Medical Subject Headings) . (ucdenver.edu)
- A portion of a Shiga toxin-containing food sample was incubated with cells designed to produce GFP. (foodsafetynews.com)
- This graph shows the total number of publications written about "Shiga Toxin 2" by people in this website by year, and whether "Shiga Toxin 2" was a major or minor topic of these publications. (ucdenver.edu)
- Current immunological tests, such as the ELISA, cannot distinguish between the active and inactive form of Shiga toxin. (foodsafetynews.com)
- The association of Shiga-like toxin with detergent-resistant membranes is modulated by glucosylceramide and is an essential requirement in the endoplasmic reticulum for a cytotoxic effect. (ox.ac.uk)
- Reduction in glucosylceramide (GlcCer) levels led to complete protection against SLTx and a reduced cell surface association of bound toxin with DRM. (ox.ac.uk)
- However, toxin sequestration within DRM of the ER was abolished under reduced GlcCer conditions, suggesting that an association of toxin with lipid microdomains or rafts in the ER (where these are defined by detergent insolubility) is essential for a later step leading to or involving retro-translocation of SLTx across the ER membrane. (ox.ac.uk)
Hemolytic uremic s5
- The antibodies are intended to neutralize circulating Shiga toxins (Stx1 and Stx2), thereby treating the disease and preventing serious complications such as gastrointestinal disease, bloody diarrhea, destruction of red blood cells and platelets, and hemolytic uremic syndrome (HUS). (medscape.com)
- Correction to: C3 levels and acute outcomes in Shiga toxin-related hemolytic uremic syndrome. (bvsalud.org)
- Shiga toxin associated hemolytic uremic syndrome. (medscape.com)
- Joseph A, Cointe A, Mariani Kurkdjian P, Rafat C, Hertig A. Shiga Toxin-Associated Hemolytic Uremic Syndrome: A Narrative Review. (medscape.com)
- Hemolytic uremic syndrome revisited: Shiga toxin, factor H, and fibrin generation. (medscape.com)
- and the European Medicines Evaluation Agency has approved orphan drug status for 2 therapeutic monoclonal antibodies in the treatment of Shiga-toxin producing Escherichia coli infections. (medscape.com)
- While Shigella dysenteriae serotype 1 most commonly produces this toxin, other members of the Enterobacteriaceae family, such as Shiga toxin-producing Escherichia coli and enterohaemorrhagic E. coli, as well as Citrobacter spp. (who.int)
- Unlike the atypical form, the typical form is caused by infection with certain strains of Escherichia coli bacteria that produce toxic substances called Shiga-like toxins. (medlineplus.gov)
- Shiga-toxin-producing Escherichia coli and haemolytic uraemic syndrome. (medscape.com)
- Epidemic profile of Shiga-toxin-producing Escherichia coli O104:H4 outbreak in Germany. (medscape.com)
- Clinical laboratories should report and send E. coli O157 isolates and Shiga toxin-positive samples to state or local public health laboratories as soon as possible for additional characterization. (cdc.gov)
- Strains may carry one Shiga toxin or both at the same time. (cdc.gov)
- Strains that produce Shiga toxin 2 tend to be more virulent. (cdc.gov)
- Infections by bacterial strains that carry Shiga toxin, however, can lead to dangerous complications, including severe bloody diarrhea, kidney failure and even death. (nih.gov)
- could also carry different Shiga toxin (stx) genes and their variants (stx1 and/or stx2) (1,2). (who.int)
- Shiga toxins (Stx) comprise a family of potent cytotoxins that are involved in severe human disease. (nih.gov)
- Shiga toxin, however, escapes this route by leaving the endosome and traveling through the Golgi apparatus to the cell's protein production machinery. (nih.gov)
- Once there, the toxin halts protein production and kills the cell. (nih.gov)
- In earlier research, scientists directed by Dr. Adam Linstedt of Carnegie Mellon University found that Shiga toxin uses a specific cellular protein, called GPP130, to bypass the cell's defenses and avoid destruction. (nih.gov)
- Curious about the connection between GPP130 and Shiga toxin, the researchers broke the GPP130 protein into pieces. (nih.gov)
- They found that Shiga toxin binds directly to one section of the GPP130 protein. (nih.gov)
- When cells of the digestive tract take up Shiga toxin, it interferes with cellular functions and the cells die. (nih.gov)
- 13. Trafficking of Shiga toxin/Shiga-like toxin-1 in human glomerular microvascular endothelial cells and human mesangial cells. (nih.gov)
- 19. Gastric Adenocarcinomas Express the Glycosphingolipid Gb3/CD77: Targeting of Gastric Cancer Cells with Shiga Toxin B-Subunit. (nih.gov)
- 3. Endoplasmic Reticulum-Targeted Subunit Toxins Provide a New Approach to Rescue Misfolded Mutant Proteins and Revert Cell Models of Genetic Diseases. (nih.gov)
- However, with further research, the scientists hope to find a manganese treatment that can be used as a preventative measure or at disease onset to prevent Shiga toxin-related death. (nih.gov)
- 8. Alteration of the glycolipid binding specificity of the pig edema toxin from globotetraosyl to globotriaosyl ceramide alters in vivo tissue targetting and results in a verotoxin 1-like disease in pigs. (nih.gov)
- All patients with Shiga toxin-positive diarrheal illness or HUS should be reported to health departments. (cdc.gov)