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This topic describes infections caused by Escherichia coli and related members of the family Enterobacteriaceae, excluding genera that principally cause enteric infections. Pathogenesis ETEC produces either a heat-labile toxin (LT), a heat-stable toxin (ST), or both.
Diagnosis After ingestion of food or water that is contaminated with large numbers of ETEC organisms, there is an incubation period of 0 to 2 days before the onset of symptoms. Table 1 Clinical, Epidemiologic, Pathogenetic, and Therapeutic Aspects of Infection with Various Pathotypes of E.
The diagnosis of ETEC infection is often suspected on the basis of epidemiology and the clinical presentation but is rarely confirmed. Treatment As with all diarrheal disease, the initial management of ETEC infection involves ensuring adequate fluid repletion [see 4:III Diarrheal Diseases]. The disease has a low inoculum and can spread from person to person, particularly in day care centers or within the families of young children.
Pathogenesis Animal models have demonstrated that the diarrhea caused by EHEC infection depends on the attaching and effacing effect.27 However, the severe systemic complications of EHEC infection are caused by the expression of Shiga toxins and are independent of the attaching and effacing effect. Diagnosis The classic presentation of EHEC infection begins with watery diarrhea and severe cramps and progresses to bloody diarrhea. HUS is characterized by microangiopathic hemolytic anemia, which results from Shiga toxin-induced damage to endothelial cells, leading to activation of coagulation in the microvascula-ture. The diagnosis of EHEC infection is extremely important, both for the patient (to prevent unnecessary interventions and provide appropriate care) and for public health, because any patient with EHEC could represent the index case of a large outbreak— the detection and interruption of which depend critically upon timely diagnosis and reporting. Treatment The treatment of EHEC infection is supportive and includes oral rehydration, observation, and, if necessary, hospital admission for the management of complications. The risk of EHEC infection can be reduced by routine adherence to good hygienic practice in food preparation.
On a November evening last year, Jennifer Doudna put on a stylish black evening gown and headed to Hangar One, a building at NASAa€™s Ames Research Center that was constructed in 1932 to house dirigibles. Under the looming arches of the hangar, Doudna mingled with celebrities like Benedict Cumberbatch, Cameron Diaz and Jon Hamm before receiving the 2015 Breakthrough Prize in life sciences, an award sponsored by Mark Zuckerberg and other tech billionaires. Doudna, a biochemist at the University of California, Berkeley, and her collaborator, Emmanuelle Charpentier of the Helmholtz Centre for Infection Research in Germany, each received $3 million for their invention of a potentially revolutionary tool for editing DNA known as CRISPR.
Doudna was not a gray-haired emerita being celebrated for work she did back when dirigibles ruled the sky.
It was only in 2012 that Doudna, Charpentier and their colleagues offered the first demonstration of CRISPRa€™s potential.
They crafted molecules that could enter a microbe and precisely snip its DNA at a location of the researchersa€™ choosing. In January 2013, the scientists went one step further: They cut out a particular piece of DNA in human cells and replaced it with another one. In the same month, separate teams of scientists at Harvard University and the Broad Institute reported similar success with the gene-editing tool.
A scientific stampede commenced, and in just the past two years, researchers have performed hundreds of experiments on CRISPR. Some scientists have repaired defective DNA in mice, for example, curing them of genetic disorders. Some researchers are trying to rewrite the genomes of elephants, with the ultimate goal of re-creating a woolly mammoth. The Breakthrough Prize is just one of several prominent awards Doudna has won in recent months for her work on CRISPR; National Public Radio recently reported whispers of a possible Nobel in her future. Even the pharmaceutical industry, which is often slow to embrace new scientific advances, is rushing to get in on the act. In January, the pharmaceutical giant Novartis announced that it would be using Doudnaa€™s CRISPR technology for its research into cancer treatments.
But amid all the black-tie galas and patent filings, ita€™s easy to overlook the most important fact about CRISPR: Nobody actually invented it. Doudna and other researchers did not pluck the molecules they use for gene editing from thin air. Microbes have been using them to edit their own DNA for millions of years, and today they continue to do so all over the planet, from the bottom of the sea to the recesses of our own bodies. Microbes use it as a sophisticated immune system, allowing them to learn to recognize their enemies. The natural history of CRISPR poses many questions to scientists, for which they dona€™t have very good answers yet. Tapping that diversity could lead to more effective gene editing technology, or open the way to applications no one has thought of yet. The scientists who discovered CRISPR had no way of knowing that they had discovered something so revolutionary.
To better understand how the gene worked, the scientists also sequenced some of the DNA surrounding it. These repeat sequences were separated from each other by 32-base blocks of DNA, called spacers. This technique a€” called metagenomics a€” revealed those strange genetic sandwiches in a staggering number of species of microbes.
In 2002, Ruud Jansen of Utrecht University in the Netherlands and colleagues dubbed these sandwiches "clustered regularly interspaced short palindromic repeats" a€” CRISPR for short.
Jansena€™s team noticed something else about CRISPR sequences: They were always accompanied by a collection of genes nearby.
Three years later, three teams of scientists independently noticed something odd about CRISPR spacers. At the time, Koonin, an evolutionary biologist at the National Center for Biotechnology Information in Bethesda, Md., had been puzzling over CRISPR and Cas genes for a few years. Scientists didna€™t know enough about the function of CRISPR and Cas enzymes for Koonin to make a detailed hypothesis.
To Barrangou, Koonina€™s idea was not just fascinating, but potentially a huge deal for his employer at the time, the yogurt maker Danisco. ShutterstockDanisco depended on bacteria to convert milk into yogurt, and sometimes entire cultures would be lost to outbreaks of bacteria-killing viruses.
To test Koonina€™s hypothesis, Barrangou and his colleagues infected the milk-fermenting microbe Streptococcus thermophilus with two strains of viruses.
Barrangou and his colleagues found that the bacteria had stuffed DNA fragments from the two viruses into their spacers. Barrangou, now an associate professor at North Carolina State University, said that this discovery led many manufacturers to select for customized CRISPR sequences in their cultures, so that the bacteria could withstand virus outbreaks. In 2007, Blake Wiedenheft joined Doudnaa€™s lab as a postdoctoral researcher, eager to study the structure of Cas enzymes to understand how they worked. Doudna agreed to the plan a€” not because she thought CRISPR had any practical value, but just because she thought the chemistry might be cool. As Wiedenheft, Doudna and their colleagues figured out the structure of Cas enzymes, they began to see how the molecules worked together as a system. As the CRISPR region fills with virus DNA, it becomes a molecular most-wanted gallery, representing the enemies the microbe has encountered. As CRISPRa€™s biology emerged, it began to make other microbial defenses look downright primitive. The microbes shield their own genes, and then attack the naked DNA of viruses and other parasites. In the decades that followed, genetic engineering improved tremendously, but it couldna€™t escape a fundamental shortcoming: Restriction enzymes did not evolve to make precise cuts a€” only to shred foreign DNA. As a result, scientists who used restriction enzymes for biotechnology had little control over where their enzymes cut open DNA. The CRISPR-Cas system, Doudna and her colleagues realized, had already evolved to exert just that sort of control.
To create a DNA-cutting tool, Doudna and her colleagues picked out the CRISPR-Cas system from Streptococcus pyogenes, the bacteria that cause strep throat.
Doudna and her colleagues figured out how to supply Cas9 with an RNA molecule that matched a sequence of DNA they wanted to cut. Using two Cas9 enzymes, the scientists could make a pair of snips, chopping out any segment of DNA they wanted.

Doudna and her colleagues thus invented a biological version of find-and-replace a€” one that could work in virtually any species they chose to work on. As important as these results were, microbiologists were also grappling with even more profound implications of CRISPR.
Before the discovery of CRISPR, all the defenses that microbes were known to use against viruses were simple, one-size-fits-all strategies.
We have innate immunity, too, but on top of that, we also use an entirely different immune system to fight pathogens: one that learns about our enemies.
This so-called adaptive immune system is organized around a special set of immune cells that swallow up pathogens and then present fragments of them, called antigens, to other immune cells. This cycle results in an army of immune cells with receptors that can bind quickly and tightly to a particular type of pathogen, making them into precise assassins.
It takes a few days for the adaptive immune system to learn to recognize the measles virus, for instance, and wipe it out.
And while we need a complex network of different cell types and signals to learn to recognize pathogens, a single-celled microbe has all the equipment necessary to learn the same lesson on its own. CRISPR-Cas systems use a huge number of different enzymes, but all of them have one enzyme in common, called Cas1. Along with their own genes, microbes carry stretches of DNA called mobile elements that act like parasites. Koonin and his colleagues discovered that one group of mobile elements, called casposons, makes enzymes that are pretty much identical to Cas1. In a new paper in Nature Reviews Genetics, Koonin and Mart Krupovic of the Pasteur Institute in Paris argue that the CRISPR-Cas system got its start when mutations transformed casposons from enemies into friends. Their DNA-cutting enzymes became domesticated, taking on a new function: to store captured virus DNA as part of an immune defense. While CRISPR may have had a single origin, it has blossomed into a tremendous diversity of molecules.
Over many thousands of years, in other words, evolution behaved like a natural laboratory, coming up with new recipes for altering DNA. To Konstantin Severinov, who holds joint appointments at Rutgers University and the Skolkovo Institute of Science and Technology in Russia, these explanations for CRISPR may turn out to be true, but they barely begin to account for its full mystery. Ita€™s possible that the spacers came from viruses, but viruses that disappeared thousands of years ago. By silencing their genes, the bacteria stop making molecules on their surface that are easily detected by our immune system. If scientists can get a better understanding of how CRISPR works in nature, they may gather more of the raw ingredients for technological innovations. To create a new way to edit DNA, Doudna and her colleagues exploited the CRISPR-Cas system from a single species of bacteria, Streptococcus pyogenes. In January, Editas scientists reported that ita€™s about as efficient at cutting DNA as Cas9 from Streptococcus pyogenes. And as scientists discover more tasks that CRISPR accomplishes in nature, they may be able to mimic those functions, too. But having been surprised by CRISPR before, Doudna expects the biggest benefits from these molecules to surprise us yet again.
Infections caused by Salmonella, Shigella, and Yersinia are described elsewhere [see 7:IX Infections Due to the Enteric Pathogens Campylobacter, Salmonella, Shigella, Yersinia, Vibrio, and Helicobacter]. LT has the same three-dimensional structure, receptor, and mechanism of action as cholera toxin [see 7:IX Infections Due to the Enteric Pathogens Campylobacter, Salmonella, Shigella, Yersinia, Vibrio, and Helicobacter]. Microbiologic diagnosis requires the use of bioassays to identify LT and ST toxins or the use of DNA probing techniques or polymerase chain reaction to detect the genes that encode these toxins; these tests are performed on E. ETEC organisms adhere to intestinal epithelial cells by one of several adhesins known as colonization factor antigens.
The kidney is particularly susceptible, but ischemic necrosis of the bowel, brain, eye, or virtually any organ can occur.
Until proved safe and effective, antibiotics should be regarded as con-traindicated in patients with known or suspected EHEC infection.
Doudna, and actress Cameron Diaz attend the Breakthrough Prize Awards Ceremony at NASA Ames Research Center on November 9, 2014 in Mountain View, California. Their results hint that the technique may fundamentally change both medicine and agriculture. Plant scientists have used CRISPR to edit genes in crops, raising hopes that they can engineer a better food supply. Doudna was one of four winning researchers on the panel at the Breakthrough Prize Breakfast & Symposia on November 10, 2014 in Stanford, California. DNA is made up of building blocks called bases, and the five segments were each composed of the same 29 bases.
By the end of the decade, microbiologists could scoop up seawater or soil and quickly sequence much of the DNA in the sample. They became so common that scientists needed a name to talk about them, even if they still didna€™t know what the sequences were for.
As soon as he learned of the discovery of bits of virus DNA in CRISPR spacers, he realized that microbes were using CRISPR as a weapon against viruses.
Later, when another virus comes along, the bacteria can use the CRISPR sequence as a cheat sheet to recognize the invader. But his thinking was provocative enough for a microbiologist named Rodolphe Barrangou to test it. Now Koonin was suggesting that bacteria could use CRISPR as a weapon against these enemies.
When those resistant bacteria multiplied, their descendants turned out to be resistant too.
She had already made a name for herself as an expert on RNA, a single-stranded cousin to DNA. Cells would make a copy of a gene using RNA, and then use that messenger RNA as a template for building a protein. When a virus invades a microbe, the host cell grabs a little of the virusa€™s genetic material, cuts open its own DNA, and inserts the piece of virus DNA into a spacer. If they encounter genetic material from a virus that matches the CRISPR RNA, the RNA latches on tightly.
Using CRISPR, microbes could, in effect, program their enzymes to seek out any short sequence of DNA and attack it exclusively. Some microbes defend themselves from invasion by using molecules known as restriction enzymes. In the 1970s, molecular biologists figured out how to use restriction enzymes to cut DNA, giving birth to the modern biotechnology industry. It was a system they already understood fairly well, having worked out the function of its main enzyme, called Cas9.
The RNA molecule then guided Cas9 along the DNA to the target site, and then the enzyme made its incision. In a few cases, the changes alter the receptor in a way that lets it grab the antigen even more tightly.
Other immune cells produce antibodies that can also grab onto the antigens and help kill the pathogen. Ever since microbiologists began discovering CRISPR-Cas systems in different species, Koonin and his colleagues have been reconstructing the systemsa€™ evolution. The job of this universal enzyme is to grab incoming virus DNA and insert it in CRISPR spacers.
The mobile elements contain genes for enzymes that exist solely to make new copies of their own DNA, cut open their hosta€™s genome, and insert the new copy. The microbes kept holding onto the spacers even when they no longer had to face these enemies. Bacteria that shared the same bar code could recognize each other as relatives and cooperate, while fighting off unrelated populations of bacteria. Recent experiments have shown that some bacteria use CRISPR to silence their own genes, instead of seeking out the genes of enemies. At Editas, a company based in Cambridge, Massachusetts, scientists have been investigating the Cas9 enzyme made by another species of bacteria, Staphylococcus aureus.

But it also has some potential advantages, including its small size, which may make it easier to deliver into cells. Scientists are now working out the structure of distantly related versions of Cas9 that seem to behave very differently from the ones wea€™re now familiar with. Doudna is curious about using CRISPR as a diagnostic tool, searching cells for cancerous mutations, for example.
The family Enter-obacteriaceae comprises facultative anaerobic gram-negative bacilli that ferment sugars. ETEC infections are spread through ingestion of contaminated food and water in regions where sanitation is inadequate.
Like cholera toxin, LT toxin induces a chain of events that leads to an elevation in the intracellular concentration of cyclic adenosine monophosphate (cAMP) and the opening of the cystic fibrosis transmembrane conductance regulator [see Figure 1].
This histopathologic appearance is known as the attaching and effacing effect.12 EPEC strains are distinguished from enterohemorrhagic E. Like EPEC organisms, EHEC organisms induce the attaching and effacing effect on epithelial cells. Shiga toxins catalyze the depurination of ribosomal RNA, leading to a cessation of protein synthesis and to cell death [see Figure 3].29 Microvascular endo-thelial cells, such as those of the kidney, are particularly sensitive to the toxin. However, symptomatic disease may range from heme-negative watery diarrhea to frank hematochesia. Typical EPEC strains produce a plasmid-encoded bundle-forming pilus that is required for reversible aggregation of the bacteria and for full virulence.63 The bacteria are able to inject into host cells a number of proteins, including Tir and EspF, through a specialized chromosome-encoded type III secretion system.
Colonies cultured from the stool of patients with suspected non-O157:H7 Shiga toxin-producing E.
Antimotility agents are also contraindicated in these patients, because their use is associated with a possible risk of HUS31 and with a theoretical risk of increasing the duration of toxin exposure.
Like EPEC, EHEC strains express intimin and Tir and employ the type III secretion system, which cause the attaching and effacing effect on cells.
In 1987, Yoshizumi Ishino and colleagues at Osaka University in Japan published the sequence of a gene called iap belonging to the gut microbe E. The genes encoded enzymes that could cut DNA, but no one could say why they did so, or why they always sat next to the CRISPR sequence. But Doudna and other scientists illuminated many other jobs that RNA can do, such as acting as sensors or controlling the activity of genes.
A few immune cells tailored to measles stay with us for our lifetime, ready to attack again. Several virulence factors are shared by most members of the species; these include the ability to produce a highly reactive lipopolysaccharide in the cell wall, the ability to produce type 1 mannose-binding fimbriae, and, in many strains, the ability to produce an antiphagocytic capsule and to sequester iron.
Thus, it is not surprising that this species has the ability to cause a diverse array of infectious diseases. A relatively large inoculum is required to produce illness; therefore, person-to-person transmission is not significant for this organism.
The efflux of chloride ions into the intestinal lumen is accompanied by sodium ions and water, and diarrhea ensues.
The disease is self-limited, lasting 3 to 5 days in travelers.5 The endemic disease is sometimes more severe, occasionally inducing cholera-like purging in children residing in developing countries. Tir forms a dimer in the host cell membrane, where it serves as a receptor for the bacterial outer membrane protein adhesin intimin, a protein of multiple domains that is also essential for virulence. However, not all microbiology laboratories offer this test, and many of those that perform it do so only on request. However, EHEC also produces Shiga toxins, which are encoded by bacteriophages that stably infect the bacteria. Doudna and her colleagues harnessed one type of CRISPR, but scientists are finding a vast menagerie of different types. Many Enterobacteriaceae species reside principally in the gastrointestinal tract of vertebrates, though some are found primarily in the environment. In fact, the organisms that are commonly referred to as Shigella are actually members of the species E.
Immunity appears to be strain specific and may reflect protective responses against particular colonization-factor antigens and toxins. LT is composed of a pentamer of receptor-binding B subunits that are noncovalently attached to a single enzymatically active A subunit. HUS ensues in approximately 5% to 10% of those patients with EHEC O157:H7 infection several days after the onset of diarrhea.
Binding of intimin triggers Tir to activate the cellular machinery for actin polymerization, leading to the formation of the characteristic attaching and effacing pedestals to which the organisms adhere. Therefore, the recognition of sporadic cases and outbreaks of EHEC infection depends largely on the acumen of the astute clinician, who must suspect the diagnosis and request the test. Shiga toxins are similar in quaternary structure to the heat-labile toxin of ETEC; they are composed of a pentamer of receptor-binding B subunits that are noncovalently bound to a single enzymatic A subunit.
They are oxidase negative and catalase positive and are capable of reducing nitrate to nitrite. Like its homologue, ST causes increases in the levels of cyclic guanosine monophosphate (cGMP), which also lead to electrolyte efflux and fluid efflux through the cystic fibrosis transmembrane conductance regulator. For adults traveling to countries where ETEC is endemic, these medications can be provided before they travel, for prompt use if symptoms occur.
The disease often appears in outbreaks associated with the consumption of contaminated food.
After binding its glycolipid receptor and entering the enterocyte, LT is transported retrograde in membrane-bound vesicles to the Golgi apparatus. EspF causes loss of intestinal barrier function through disruption of tight junctions and induces host cell death through apoptosis.
Shiga toxins are able to cross intestinal epithelial monolayers by an unknown mechanism, after which they presumably are spread systemically through the bloodstream.
They cause a variety of diseases, including diarrhea, urinary tract infections (UTIs), and nosocomial infections.
For these toxins to reach their targets in sufficient quantity and for a sufficient duration to induce symptoms, the organisms must adhere to the intestinal mucosa.6 This binding is accomplished through an antigenically and morphologically diverse array of pilus and nonpilus ad-hesins known as colonization factor antigens. Travelers should also be counseled to seek medical care if diarrhea is accompanied by blood or fever or if it persists despite treatment. Undercooked ground beef has been associated with many outbreaks and is the leading risk factor for sporadic cases, but a variety of other foods and beverages, including other beef products, lettuce, sprouts, fruit, fruit juices, and milk, have been implicated. The A subunit reaches its target in the basolateral cell membrane, which is the alpha subunit of the stimulatory heterotrimeric G protein receptor (GA), and catalyzes the adenosine diphosphate (ADP) ribosylation of the target. Various studies have demonstrated that children, the elderly, those who have consumed antimotility agents, and those with high white cell counts have an increased risk of HUS.31,32 Antibiotic therapy may also be a risk factor for HUS.
Travelers can reduce the risk of acquiring ETEC by fastidiously avoiding all food that is not served steaming hot, fruit that they have not peeled, and beverages that are not bottled [see CE:VII Health Advice for International Travelers].
The modified alpha subunit is locked in its guanosine triphosphate (GTP)-bound active form, which forces it to constitutively activate adenylyl cyclase. After binding its glycolipid receptor and entering the host cell, the toxin is transported retrograde in membrane-bound vesicles to the endoplasmic reticulum. Bismuth subsalicylate tablets, taken four times a day, also provide some protection, but difficulty with compliance limits the use of this therapy.7 The prospects for developing an ETEC vaccine are limited by the antigenic heterogeneity of the organisms.
The elevated levels of cyclic adenosine monophosphate (cAMP) that result lead to activation of protein kinase A (PKA) and to phosphorylation and opening of the cystic fibrosis transmembrane conductance regulator (CFTR).
The A subunit induces depuration of a specific adenine residue in ribosomal RNA; this leads to cessation of protein synthesis and death of the cell. The altered surface of the intoxicated endothelial cell serves as a nidus for activation of the coagulation cascade, which leads to the formation of microthrombi and causes distal ischemic necrosis, platelet consumption, and red cell fragmentation—the hallmarks of the hemolytic-uremic syndrome. Like its homologue, ST binds to and activates membrane-bound guanylyl cyclase-C, causing elevations in the levels of cyclic guanosine monophosphate (cGMP).

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