Escherichia coli
January 28, 2010 by Staff
Filed under Health Conditions / Ailments
Escherichia coli (commonly abbreviated E. coli; pronounced /ˌɛʃɪˈrɪkiə ˈkoʊlaɪ/, /iː ~/, and named after its discoverer), is a Gram negative rod-shaped bacterium that is commonly found in the lower intestine of warm-blooded organisms (endotherms). Most E. coli strains are harmless, but some, such as serotype O157:H7, can cause serious food poisoning in humans, and are occasionally responsible for product recalls. The harmless strains are part of the normal flora of the gut, and can benefit their hosts by producing vitamin K2, or by preventing the establishment of pathogenic bacteria within the intestine.
E. coli are not always confined to the intestine, and their ability to survive for brief periods outside the body makes them an ideal indicator organism to test environmental samples for fecal contamination. The bacteria can also be grown easily and its genetics are comparatively simple and easily-manipulated or duplicated through a process of metagenics, making it one of the best-studied prokaryotic model organisms, and an important species in biotechnology and microbiology.
E. coli was discovered by German pediatrician and bacteriologist Theodor Escherich in 1885, and is now classified as part of the Enterobacteriaceae family of gamma-proteobacteria.
Strains
Model of successive binary fission in E. coliA strain of E. coli is a sub-group within the species that has unique characteristics that distinguish it from other E. coli strains. These differences are often detectable only at the molecular level; however, they may result in changes to the physiology or lifecycle of the bacterium. For example, a strain may gain pathogenic capacity, the ability to use a unique carbon source, the ability to take upon a particular ecological niche or the ability to resist antimicrobial agents. Different strains of E. coli are often host-specific, making it possible to determine the source of fecal contamination in environmental samples. For example, knowing which E. coli strains are present in a water sample allows to make assumptions about whether the contamination originated from a human, another mammal or a bird.
New strains of E. coli evolve through the natural biological process of mutation, and some strains develop traits that can be harmful to a host animal. These virulent strains typically cause a bout of diarrhea that is unpleasant in healthy adults and is often lethal to children in the developing world. More virulent strains, such as O157:H7 cause serious illness or death in the elderly, the very young or the immunocompromised.
Role as normal flora
E. coli normally colonizes an infant's gastrointestinal tract within 40 hours of birth, arriving with food or water or with the individuals handling the child. In the bowel, it adheres to the mucus of the large intestine. It is the primary facultative organism of the human gastrointestinal tract. As long as these bacteria do not acquire genetic elements encoding for virulence factors, they remain benign commensals.
Therapeutic use of nonpathogenic E. coli
Nonpathogenic Escherichia coli strain Nissle 1917 is used as a probiotic agent in medicine, mainly for the treatment of various gastroenterological diseases, including inflammatory bowel disease.
Role in disease
Virulent strains of E. coli can cause gastroenteritis, urinary tract infections, and neonatal meningitis. In rarer cases, virulent strains are also responsible for hæmolytic-uremic syndrome (HUS), peritonitis, mastitis, septicemia and Gram-negative pneumonia.
Gastrointestinal infection
Certain strains of E. coli, such as O157:H7, O121 and O104:H21, produce potentially-lethal toxins. Food poisoning caused by E. coli is usually caused by eating unwashed vegetables or undercooked meat. O157:H7 is also notorious for causing serious and even life-threatening complications like hemolytic-uremic syndrome (HUS). This particular strain is linked to the 2006 United States E. coli outbreak of fresh spinach. Severity of the illness varies considerably; it can be fatal, particularly to young children, the elderly or the immunocompromised, but is more often mild. Earlier, poor hygienic methods of preparing meat in Scotland killed seven people in 1996 due to E. coli poisoning, and left hundreds more infected. E. coli can harbor both heat-stable and heat-labile enterotoxins. The latter, termed LT, contains one "A" subunit and five "B" subunits arranged into one holotoxin, and is highly similar in structure and function to Cholera toxins. The B subunits assist in adherence and entry of the toxin into host intestinal cells, while the A subunit is cleaved and prevents cells from absorbing water, causing diarrhea. LT is secreted by the Type 2 secretion pathway.
If E. coli bacteria escape the intestinal tract through a perforation (for example from an ulcer, a ruptured appendix, or a surgical error) and enter the abdomen, they usually cause peritonitis that can be fatal without prompt treatment. However, E. coli are extremely sensitive to such antibiotics as streptomycin or gentamicin. This could change since, as noted below, E. coli quickly acquires drug resistance. Recent research suggests that treatment with antibiotics does not improve the outcome of the disease, and may in fact significantly increase the chance of developing haemolytic uraemic syndrome.
Intestinal mucosa-associated E. coli are observed in increased numbers in the inflammatory bowel diseases, Crohn's disease and ulcerative colitis. Invasive strains of E. coli exist in high numbers in the inflamed tissue, and the number of bacteria in the inflamed regions correlates to the severity of the bowel inflammation.
Virulence properties
Enteric E. coli (EC) are classified on the basis of serological characteristics and virulence properties. Virotypes include:
| Name | Hosts | Description |
|---|---|---|
| Enterotoxigenic E. coli (ETEC) | causative agent of diarrhea (without fever) in humans, pigs, sheep, goats, cattle, dogs, and horses | ETEC uses fimbrial adhesins (projections from the bacterial cell surface) to bind enterocyte cells in the small intestine. ETEC can produce two proteinaceous enterotoxins:
ETEC strains are non-invasive, and they do not leave the intestinal lumen. ETEC is the leading bacterial cause of diarrhea in children in the developing world, as well as the most common cause of traveler's diarrhea. Each year, ETEC causes more than 200 million cases of diarrhea and 380,000 deaths, mostly in children in developing countries.[25] |
| Enteropathogenic E. coli (EPEC) | causative agent of diarrhea in humans, rabbits, dogs, cats and horses | Like ETEC, EPEC also causes diarrhea, but the molecular mechanisms of colonization and etiology are different. EPEC lack fimbriae, ST and LT toxins, but they utilize an adhesin known as intimin to bind host intestinal cells. This virotype has an array of virulence factors that are similar to those found in Shigella, and may possess a shiga toxin. Adherence to the intestinal mucosa causes a rearrangement of actin in the host cell, causing significant deformation. EPEC cells are moderately-invasive (i.e. they enter host cells) and elicit an inflammatory response. Changes in intestinal cell ultrastructure due to "attachment and effacement" is likely the prime cause of diarrhea in those afflicted with EPEC. |
| Enteroinvasive E. coli (EIEC) | found only in humans | EIEC infection causes a syndrome that is identical to Shigellosis, with profuse diarrhea and high fever. |
| Enterohemorrhagic E. coli (EHEC) | found in humans, cattle, and goats | The most famous member of this virotype is strain O157:H7, which causes bloody diarrhea and no fever. EHEC can cause hemolytic-uremic syndrome and sudden kidney failure. It uses bacterial fimbriae for attachment (E. coli common pilus, ECP),[26] is moderately-invasive and possesses a phage-encoded Shiga toxin that can elicit an intense inflammatory response. |
| Enteroaggregative E. coli (EAEC) | found only in humans | So named because they have fimbriae which aggregate tissue culture cells, EAEC bind to the intestinal mucosa to cause watery diarrhea without fever. EAEC are non-invasive. They produce a hemolysin and an ST enterotoxin similar to that of ETEC. |
Epidemiology of gastrointestinal infection
Transmission of pathogenic E. coli often occurs via fecal-oral transmission. Common routes of transmission include: unhygienic food preparation, farm contamination due to manure fertilization, irrigation of crops with contaminated greywater or raw sewage, feral pigs on cropland, or direct consumption of sewage-contaminated water. Dairy and beef cattle are primary reservoirs of E. coli O157:H7, and they can carry it asymptomatically and shed it in their feces. Food products associated with E. coli outbreaks include raw ground beef, raw seed sprouts or spinach, raw milk, unpasteurized juice, and foods contaminated by infected food workers via fecal-oral route.
According to the U.S. Food and Drug Administration, the fecal-oral cycle of transmission can be disrupted by cooking food properly, preventing cross-contamination, instituting barriers such as gloves for food workers, instituting health care policies so food industry employees seek treatment when they are ill, pasteurization of juice or dairy products and proper hand washing requirements.
Shiga toxin-producing E. coli (STEC), specifically serotype O157:H7, have also been transmitted by flies, as well as direct contact with farm animals, petting zoo animals, and airborne particles found in animal-rearing environments.
Urinary tract infection
Uropathogenic E. coli (UPEC) is responsible for approximately 90% of urinary tract infections (UTI) seen in individuals with ordinary anatomy. In ascending infections, fecal bacteria colonize the urethra and spread up the urinary tract to the bladder as well as to the kidneys (causing pyelonephritis), or the prostate in males. Because women have a shorter urethra than men, they are 14-times more likely to suffer from an ascending UTI.
Uropathogenic E. coli utilize P fimbriae (pyelonephritis-associated pili) to bind urinary tract endothelial cells and colonize the bladder. These adhesins specifically bind D-galactose-D-galactose moieties on the P blood group antigen of erythrocytes and uroepithelial cells. Approximately 1% of the human population lacks this receptor, and its presence or absence dictates an individual's susceptibility to E. coli urinary tract infections. Uropathogenic E. coli produce alpha- and beta-hemolysins, which cause lysis of urinary tract cells.
UPEC can evade the body's innate immune defenses (e.g. the complement system) by invading superficial umbrella cells to form intracellular bacterial communities (IBCs). They also have the ability to form K antigen, capsular polysaccharides that contribute to biofilm formation. Biofilm-producing E. coli are recalcitrant to immune factors and antibiotic therapy and are often responsible for chronic urinary tract infections. K antigen-producing E. coli infections are commonly found in the upper urinary tract.
Descending infections, though relatively rare, occur when E. coli cells enter the upper urinary tract organs (kidneys, bladder or ureters) from the blood stream.
Neonatal meningitis
It is produced by a serotype of Escherichia coli that contains a capsular antigen called K1. The colonisation of the new born's intestines with these stems, that are present in the mother's vagina, lead to bacteriemia, which leads to meningitis. And because of the absence of the igM antibodies from the mother (these do not cross the placenta because they are too big), plus the fact that the body recognises as self the K1 antigen, as it resembles the cerebral glicopeptides, this leads to a severe meningitis in the neonates.
