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E. coli, risk of infection?

E. coli, risk of infection?


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There has been a warning about E. coli contaminated water in South Florida. Now I'm wondering are there empirical data or historic cases which show a correlation between E.coli levels in tap water and risk of infection in the population drinking this water. Which pathogens, that could be transmitted through tap water, are common in this area?


The maximum temperature for E. coli to survive is dependent on the strain. E. coli from warm areas can easily survive 45 °C and more. The minimum number of E. coli to ingest in order to become ill is also dependent on the strain. Whether you become ill at all is also dependent on the strain. You harbor many billions of E. coli in your digestive tract without becoming ill, so without further information on the released strain, it's really hard to tell.

One of the suggestions from the WHO Guidelines for drinking water quality is to boil the water in order to desinfect it.


One textbook of microbiology suggests that the infectious dose of a specific strain of enterotoxigenic E. coli in adults would be $10^{8}$ cells. Keep in mind that infective dose will vary with species and strain, as well as the health, age and immune-status of the individual ingesting the bacteria. Children, elderly and ill people will generally be affected by a lower infective dose. This does also not consider how well the bacteria can colonize the gastrointestinal system. It is possible for minimal numbers of pathogenic E. coli to colonize in the gut, and only after growing to a infectious level, being to exert pathogenic effects.


Escherichia coli O157:H7

Escherichia coli (or simply E. coli) is one of the many groups of bacteria that live in the intestines of healthy humans and most warm-blooded animals. E. coli bacteria help maintain the balance of normal intestinal flora (bacteria) against harmful bacteria and synthesize or produce some vitamins.

However, there are hundreds of types or strains of E. coli bacteria. Different strains of E. coli have different distinguishing characteristics.

A particular strain of E. coli known as E. coli O157:H7 causes a severe intestinal infection in humans. It is the most common strain to cause illness in people. It can be differentiated from other E. coli by the production of a potent toxin that damages the lining of the intestinal wall causing bloody diarrhea. It is also known as enterohemorrhagic E. coli infection.

The Centers for Disease Control and Prevention (CDC) reports about 70,000 cases of this type of E. coli infection occur in the United States each year.


Potential drug target for dangerous E. coli infections identified

Escherichia coli, known as E. coli, are bacteria which many people associate with causing mild food poisoning, but some types of E. coli can be fatal.

UNSW Science microbiologists studied an E. coli strain that causes a severe intestinal infection in humans: enterohemorrhagic E. coli (EHEC). Their findings were published this week in the Proceedings of the National Academy of Sciences.

EHEC is a food-borne pathogen that releases Shiga toxins during infection, resulting in kidney and neurological damage.

Dr Jai Tree, the study's senior author, said the researchers' discovery of a new molecular pathway that controls Shiga toxin production was important because there was no commercially available treatment for EHEC infections.

"Antibiotic treatment of these infections is generally not recommended because antibiotics stimulate production of the Shiga toxin, leading to an increased risk of kidney failure, neurological damage, and death," Dr Tree said.

"The new pathway that we have found reduces toxin production and is not expected to be stimulated by antibiotic treatment. So, our results identify a potential new target for the development of drugs that can suppress Shiga toxin production during EHEC infection.

"It's still early days, however, and we need to conduct a lot more research to understand if our findings apply to a broad range of clinical EHEC isolates and to both types of Shiga toxins produced by human EHEC isolates."

How EHEC infections start

Dr Tree said there were several ways in which people could become infected with EHEC.

"EHEC is mainly found in the faeces of cows and sheep and people can become infected through contact with farm animals and their faeces, or via person-to-person infection if people come into contact with tiny amounts of faeces from a sick person -- for example, directly or indirectly by touching contaminated surfaces," he said.

"This strain of E. coli can also spread through ingesting the bacteria by eating undercooked minced meat (for example, in hamburgers), eating contaminated fresh produce like salad vegetables, or drinking contaminated water or unpasteurised milk.

"Children under five years old and older people are at greatest risk of developing an EHEC infection."

EHEC outbreaks less common but deadly

Dr Tree said while the prevalence of EHEC was low compared to other foodborne pathogens, the disease could be very severe or even fatal. EHEC is a type of STEC (Shiga toxin-producing Escherichia coli).

"EHEC outbreaks occur sporadically in Australia and worldwide. The most significant outbreak occurred in South Australia in 1995 and was caused by contaminated mettwurst, a semi-dry fermented sausage made from raw minced pork preserved by curing and smoking," he said.

"In that outbreak, 143 people were infected -- 23 of them suffered kidney and neurological damage. Many of these severe cases were in infants who suffered permanent kidney damage and later required kidney transplants.

"A four-year-old girl suffered multiple strokes and died three days after admission to hospital. This episode triggered a major food safety investigation and outbreaks since 1995 have been smaller."

Dr Tree said globally, Shiga toxin-producing E. coli was still a major food safety concern after a large outbreak in Germany in 2011.

"The strain in Germany was spread mostly via consumption of contaminated sprouts and in several cases, from close contact with an infected person," he said.

"During this outbreak more than 4000 people were infected and 50 people died."

New pathway 'hiding in plain sight'

Dr Tree said the UNSW research was the first discovery of a new pathway that controls the Shiga toxins in almost 20 years.

"In 2001, researchers at Tufts and Harvard universities first showed how production of the Shiga toxin was controlled by a bacterial virus, known as a bacteriophage, within the genome. This has been the only known pathway that controls Shiga toxin production for almost two decades," he said.

"We have extended that work to show a new mechanism of toxin control that is, surprisingly, buried within the start of the DNA sequence that encodes the Shiga-toxin messenger RNA -- a working copy of the gene.

"We discovered a very short piece of the toxin messenger RNA is made into a regulatory non-coding RNA that silences the toxin and promotes growth of the pathogen."

Dr Tree said their findings were a surprise because Shiga toxin genes have been well studied, with almost 7000 published studies in the past 40 years.

"Only recently have we been able use advances in RNA sequencing technology to detect the presence of the new regulatory non-coding RNA embedded within the Shiga toxin messenger RNA," he said.

"This new regulatory non-coding RNA had been hiding in plain sight for almost 20 years."

Implications for treating EHEC infections

Dr Tree said the researchers' findings opened up new possibilities for the treatment of EHEC infections.

"Patients largely receive supportive care to manage disease symptoms and to reduce the effects of the toxin on the kidneys," he said.

"Our work shows a new mechanism for controlling toxin production that may be amenable to new RNA-based therapeutics to inhibit toxin production during an infection. We anticipate this would expand intervention options and potentially allow use of antibiotics that are currently not recommended because they stimulate Shiga toxin production.

"New treatments could therefore reduce the risk of kidney damage, neurological complications and death. We look forward to testing these new interventions in the next stage of our research."


Identifying the rise of multi drug resistant E. coli

Escherichia coli. Credit: Rocky Mountain Laboratories, NIAID, NIH

Antibiotic resistance in E. coli has been steadily increasing since the early 2000s despite attempts to control it, a new study suggests. In the biggest genomic survey of E. coli to date, that took more than 16 years in Norway, researchers have successfully tracked the spread of antibiotic resistant genes and have shown that these genes are being transferred between E. coli strains.

Researchers from the Wellcome Sanger Institute and University of Oslo have tracked multidrug resistance in Norway and compared this to a previous study from the UK. They found that resistant strains developed around the same time, but increased more rapidly in the UK population.

The results, published today in The Lancet Microbe show that tracking these resistant strains is important in the surveillance and control of drug resistant E. coli, which poses a significant issue in hospitals where it can cause severe infection and mortality. In addition, understanding how these genes are transferred between strains, and what has caused them to acquire drug resistance can help prevent the growth of antibiotic resistance strains.

The bacterium, Escherichia coli is a common cause of bloodstream infections world-wide*, which seem to be increasing over the last decade. E. coli is commonly found in the gut, where it does not cause harm, but if it gets into the bloodstream due to a weakened immune system it can cause severe and life threatening infections. As an added challenge for health care providers, multi-drug resistance (MDR) has become a frequent feature of such infections, and in a worrying number of cases the available treatment options are becoming limited.

In the largest study of its kind, and only the second systematic longitudinal genomic study of bacteremia E. coli, researchers from the Wellcome Sanger Institute and the University of Oslo processed a nation-wide catalogue of samples from more than 3,200 patients to track antibiotic resistance over 16 years. By harnessing the power of large-scale DNA sequencing, they tracked the emergence of drug resistance and compared this to a similar study conducted in the UK**.

The team found that MDR started to increase and show in more strains in the early 2000s due to antibiotic pressure, and now multiple MDR E. coli strains are present in Norway. However, MDR E. coli seems to be more widely present in the UK, despite similar policies in place around antibiotic use. The UK population however is considerably larger than Norway which could explain some of the differences. Further research is needed to allow for closer comparison and to identify the exact factors that cause rapid spread in some locations compared to others.

MDR is relatively rare in bacteria. However, this new study has identified that lineages that previously were not thought to have MDR have acquired drug-resistance genes, showing the increased ability of E. coli to share MDR genes that move horizontally between strains.

Professor Jukka Corander, co-author and Associate Faculty member at the Wellcome Sanger Institute, said: "The high number of samples from the Norwegian population and the level of genomic detail on the strains of bacteria enabled us to make much more far-reaching conclusions than were ever possible before. This study demonstrates the power arising from a systematic national surveillance of resistant organisms, which both collects and makes the data available for in-depth analyses. Without these in place, it would have been impossible to approach the central research questions formulated in the study and find answers to them."

The researchers hope to conduct similar research in the UK to build on previous studies and gain a full data set of 16 years in the UK in order to more closely track MDR resistant E. coli.

Dr. Rebecca Gladstone, lead author of the study and Bioinformatician at the University of Oslo, Norway, said: "Being able to estimate the expansion timelines of the MDR clones of E. coli and to identify multiple occasions of novel acquisition of resistance genes is particularly exciting as this is the first time that this has been possible. Understanding and tracking the movement of these drug resistance genes and the strains that carry them are necessary for controlling the spread of drug-resistant bacteria, which is a huge issue in healthcare."

Professor Julian Parkhill, co-author and Professor in the Department of Veterinary Medicine at University of Cambridge, said: "Long-term studies such as this one provide in-depth understanding about the complex epidemiology underlying bloodstream infections. The next step would be further research to detail the factors determining the success of emerging pathogenic clones of these bacteria, to help find a way to control and possibly minimise the spread of multidrug resistance."

*Kern WV, Rieg S. (2020) Burden of bacterial bloodstream infection - A brief update on epidemiology and significance of multidrug-resistant pathogens. Clin Microbiol Infect 26: 151-7.

**Teemu Kallonen et al. Systematic longitudinal survey of invasiveEscherichia coliin England demonstrates a stable population structure only transiently disturbed by the emergence of ST131, Genome Research (2017). DOI: 10.1101/gr.216606.116


Potential drug target for dangerous E. coli infections identified

Escherichia coli. Credit: Rocky Mountain Laboratories, NIAID, NIH

Escherichia coli, known as E. coli, are bacteria which many people associate with causing mild food poisoning, but some types of E. coli can be fatal.

UNSW Science microbiologists studied an E. coli strain that causes a severe intestinal infection in humans: enterohemorrhagic E. coli (EHEC). Their findings were published this week in the Proceedings of the National Academy of Sciences.

EHEC is a food-borne pathogen that releases Shiga toxins during infection, resulting in kidney and neurological damage.

Dr. Jai Tree, the study's senior author, said the researchers' discovery of a new molecular pathway that controls Shiga toxin production was important because there was no commercially available treatment for EHEC infections.

"Antibiotic treatment of these infections is generally not recommended because antibiotics stimulate production of the Shiga toxin, leading to an increased risk of kidney failure, neurological damage, and death," Dr. Tree said.

"The new pathway that we have found reduces toxin production and is not expected to be stimulated by antibiotic treatment. So, our results identify a potential new target for the development of drugs that can suppress Shiga toxin production during EHEC infection. It's still early days, however, and we need to conduct a lot more research to understand if our findings apply to a broad range of clinical EHEC isolates and to both types of Shiga toxins produced by human EHEC isolates."

How EHEC infections start

Dr. Tree said there were several ways in which people could become infected with EHEC.

"EHEC is mainly found in the feces of cows and sheep and people can become infected through contact with farm animals and their feces, or via person-to-person infection if people come into contact with tiny amounts of feces from a sick person—for example, directly or indirectly by touching contaminated surfaces," he said.

"This strain of E. coli can also spread through ingesting the bacteria by eating undercooked minced meat (for example, in hamburgers), eating contaminated fresh produce like salad vegetables, or drinking contaminated water or unpasteurised milk. Children under five years old and older people are at greatest risk of developing an EHEC infection."

EHEC outbreaks less common but deadly

Dr. Tree said while the prevalence of EHEC was low compared to other foodborne pathogens, the disease could be very severe or even fatal. EHEC is a type of STEC (Shiga toxin-producing Escherichia coli).

"EHEC outbreaks occur sporadically in Australia and worldwide. The most significant outbreak occurred in South Australia in 1995 and was caused by contaminated mettwurst, a semi-dry fermented sausage made from raw minced pork preserved by curing and smoking," he said.

"In that outbreak, 143 people were infected—23 of them suffered kidney and neurological damage. Many of these severe cases were in infants who suffered permanent kidney damage and later required kidney transplants. A four-year-old girl suffered multiple strokes and died three days after admission to hospital. This episode triggered a major food safety investigation and outbreaks since 1995 have been smaller."

Dr. Tree said globally, Shiga toxin-producing E. coli was still a major food safety concern after a large outbreak in Germany in 2011.

"The strain in Germany was spread mostly via consumption of contaminated sprouts and in several cases, from close contact with an infected person," he said.

"During this outbreak more than 4000 people were infected and 50 people died."

New pathway hiding in plain sight

Dr. Tree said the UNSW research was the first discovery of a new pathway that controls the Shiga toxins in almost 20 years.

"In 2001, researchers at Tufts and Harvard universities first showed how production of the Shiga toxin was controlled by a bacterial virus, known as a bacteriophage, within the genome. This has been the only known pathway that controls Shiga toxin production for almost two decades," he said.

"We have extended that work to show a new mechanism of toxin control that is, surprisingly, buried within the start of the DNA sequence that encodes the Shiga-toxin messenger RNA—a working copy of the gene. We discovered a very short piece of the toxin messenger RNA is made into a regulatory non-coding RNA that silences the toxin and promotes growth of the pathogen."

Dr. Tree said their findings were a surprise because Shiga toxin genes have been well studied, with almost 7,000 published studies in the past 40 years.

"Only recently have we been able use advances in RNA sequencing technology to detect the presence of the new regulatory non-coding RNA embedded within the Shiga toxin messenger RNA," he said.

"This new regulatory non-coding RNA had been hiding in plain sight for almost 20 years."

Implications for treating EHEC infections

Dr. Tree said the researchers' findings opened up new possibilities for the treatment of EHEC infections.

"Patients largely receive supportive care to manage disease symptoms and to reduce the effects of the toxin on the kidneys," he said.

"Our work shows a new mechanism for controlling toxin production that may be amenable to new RNA-based therapeutics to inhibit toxin production during an infection. We anticipate this would expand intervention options and potentially allow use of antibiotics that are currently not recommended because they stimulate Shiga toxin production. New treatments could therefore reduce the risk of kidney damage, neurological complications and death. We look forward to testing these new interventions in the next stage of our research."


Prevention

How can I prevent or avoid an E. coli infection?

The most important thing you can do to protect against E. coli infection is to wash your hands – frequently. Always wash your hands thoroughly before and after cooking and after handling raw meat or poultry.

Wash your hands after using the restroom, changing diapers or after contact with animals.

If you’ve been infected with E. coli, scrub your hands vigorously with soap and clean under your fingernails where bacteria can get caught. Dry your hands with paper towels instead of cloth towels to avoid transferring bacteria.

You can also reduce your risk of an E. coli infection by following these food preparation and cooking tips.

When thawing meats:

  • Don’t defrost frozen meat unwrapped on the counter.
  • Keep frozen meat in a separate plastic bag (for example, a plastic grocery bag) when thawing.

When prepping foods:

  • Don’t rinse meat before cooking. It’s not necessary. Washing the meat could spread bacterial to nearby surfaces, utensils and other food.
  • Use a plastic or ceramic cutting board to cut raw meat. These materials can be cleaned more easily and thoroughly than wooden cutting boards.
  • Don’t “cross-contaminate” a prepping surface. If you had raw meat or chicken on a prepping surface, such as a cutting board, wash it thoroughly with soap and hot water before putting another type of food (such as a raw vegetable) on it. Better yet, use different cutting boards for the foods you are preparing.
  • Rinse all raw fruits and vegetables under cold running water before eating them. It’s ok to scrub firm produce but don’t use detergent or soap.

When cooking and serving meats:

  • Cook all meat well (undercooked meat is another source of E. coli contamination). Cooking foods well kills bacteria.
  • Use a food thermometer when cooking meat, and cook all meat and other foods to the safe temperatures recommended by the United States Department of Agriculture (see references for link).
  • Don’t put a cooked hamburger on a plate that had raw ground beef or any other raw meat on it.
  • Refrigerate leftovers right away.

Colonization of Cattle

E. coli O157:H7 naturally colonizes the gastrointestinal tracts of cattle, and the lymphoid follicle-dense mucosa at the terminal rectum, called the rectoanal junction (RAJ) mucosa, is known as a principal site of colonization in cattle [39, 48].

Three distinct patterns of E. coli O157:H7 carriage in cattle have been described previously [14, 39, 58]. First, animals can be transiently culture positive for short durations of a few days and are considered passive shedders and are likely not colonized at the RAJ mucosa. Second, cattle can be colonized and shed the bacteria for an average of 1 month and typically not longer than 2 months. Third, a few rare animals are colonized for a long duration and shed the bacteria from 3 to 12 months or longer. This unique situation, in which a few animals develop long-duration colonization (Ϣ months) with E. coli O157:H7, is likely due to bacterial association at the RAJ mucosa however, it may be due to unique colonization by the bacteria at a site(s) in addition to the RAJ mucosa.

Age, diet, and immunity of individual cattle could also potentially affect bacterial colonization. Cray and Moon [14] reported that calves shed E. coli O157:H7 longer than adult cattle given the same level of E. coli O157:H7 inoculums.

Reducing the level of carriage of E. coli O157:H7 in cattle, as a major source of E. coli O157:H7 infection, would play a key role in decreasing the risk of human infection. The understanding of colonization factors of E. coli O157:H7 will be necessary to develop effective strategies for reducing or preventing bovine carriage of E. coli O157:H7.


Prion Diseases Biology & Genetics

Scientists at NIAID’s Rocky Mountain Laboratories (RML) in Hamilton, Montana, have studied prion diseases since the 1960s when Dr. William Hadlow spearheaded work on the sheep brain disease known as scrapie, which was later shown to be a prion disease. RML is one of the world's premier laboratories for studying prion diseases. Primary to their mission is understanding how abnormal prion protein cause disease at the molecular, biochemical, cellular, and animal-model levels.

NIAID scientists at RML are studying how cells in the nervous system interact with prion protein and whether those interactions affect disease progression. These studies have shown how prions move through the brain and how cells in the brain called microglia help slow down disease.

Other studies at RML have looked at different types of CJD in human tissue and how different types of CJD may occur. These studies have shown how human prions interact with cells. They have also shown that prions derived from slightly different forms of the prion protein gene can influence how prions accumulate in the brain.

NIAID scientists at RML also have shown that, in response to damage to the brain, normal prion protein acquires properties similar to those of infectious prion protein. These studies show that prion protein, like the tau protein in chronic traumatic encephalopathy (CTE), acts abnormally following brain injury. They also suggest that damage to the brain might be a way in which CJD infection starts in some people.

RML chronic wasting disease studies have focused on whether infectious prions can cross species from cervids, like deer and elk, into people. During research that took 13 years of observation, NIAID scientists published a series of studies, the latest in 2018, showing that CWD from deer or elk does not cause disease in prion models that are susceptible to infection by human prions. These studies reinforce the belief that a strong barrier to CWD infection exists between cervids and people.

Studies of prion disease infection of cerebral organoid (“minibrain”) cultures in incubators began at RML in 2017. These studies could provide a new model for scientists to study how prion diseases affect the human brain. Cerebral organoids are small balls of human brain cells – developed from skin stem cells – that range in size from a poppy seed to a small pea. Their organization, structure, and electrical signaling mimic some aspects of brain tissue.


What causes an EHEC infection?

EHEC is a strain of E. coli that produces a toxin called Shiga toxin. The toxin causes damage to the lining of the intestinal wall. In 1982, EHEC was found as the cause of bloody diarrhea that developed after eating undercooked or raw hamburger meat contaminated with the bacteria. Since that time, outbreaks of EHEC have been linked with other types of foods, such as spinach, lettuce, sprouts, unpasteurized milk, unpasteurized apple juice or apple cider, salami, and well water or surface water areas frequently visited by animals. Outbreaks have also been traced to animals at petting zoos and day care centers.

EHEC is found in the intestines of healthy cattle, goats, deer, and sheep. According to the CDC, the spread of these bacteria to humans may occur in the following manner:

  • Meat, such as beef from cows, may become contaminated when organisms are accidently mixed in with beef, especially when it is ground. Meat contaminated with EHEC does not smell or taste bad and looks normal. For this reason, it is important to thoroughly cook beef.
  • Infection may occur after swimming in or drinking water that has been contaminated with EHEC.
  • The bacteria can also be spread from person-to-person in families and in child care and other institutional care centers.

A Structure-Function Toolbox for Membrane Transporter and Channels

Jacopo Marino , . Eric R. Geertsma , in Methods in Enzymology , 2017

Abstract

Escherichia coli is one of the most widely used expression hosts for membrane proteins. However, establishing conditions for its recombinant production of membrane proteins remains difficult. Attempts to produce membrane proteins frequently result in either no expression or expression as misfolded aggregates. We developed an efficient pipeline for improving membrane protein overexpression in E. coli that is based on two approaches. The first involves transcriptional fusions, small additional RNA sequences upstream of the target open reading frame, to overcome no or poor overall expression levels. The other is based on a tunable promoter in combination with a fusion to green fluorescent protein serving as a reporter for the folding state of the target membrane protein. The latter combination allows adjusting the membrane protein expression rate to the downstream folding capacity, in order to decrease the formation of protein aggregates. This pipeline has proven successful for the efficient and parallel optimization of a diverse set of membrane proteins.