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Review Of Related Literature
A.Bacteria
IINTRODUCTION Help with essay on BacteriaBacteria (Greek bakterion, "little staff"), large group of mostly microscopic, unicellular organisms that lack a distinct nucleus and that usually reproduce by cell division.
Bacteria are tiny, most ranging from 1 to 10 micrometres (1 micrometre equals 1/5,000 in), and are extremely variable in the ways they obtain energy and nourishment. They can be found in nearly all environments from air, soil, water, and ice to hot springs; even the hydrothermal vents on the deep ocean floor are the home of sulphur-metabolizing bacteria. Certain types are found in nearly all food products, and bacteria also occur in various forms of symbiosis with most plants and animals and other kinds of life.
IICLASSIFICATION
In the currently used five-kingdom scheme of classification, bacteria constitute the kingdom Monera, also known as Prokaryotae organisms in whose cells the nucleus is not enclosed by a membrane. About 1,600 species are known. Generally, bacteria are classified into species on the basis of characteristics such as shape cocci (spheres), bacilli (rods), spirochaetes (spirals); cell-wall structure; differential staining (see Grams Stain); ability to grow in the presence or absence of air (aerobes and anaerobes, respectively); metabolic or fermentative capabilities; ability to form dormant spores under adverse conditions; serologic (serum) identification of surface components; and nucleic-acid relatedness.
The most widely used reference for taxonomic classification of bacteria divides them into four major groups based on cell-wall characteristics. The division Gracilicutes encompasses bacteria with thin, gram-negative-type cell walls; the Firmicutes have thick, gram-positive cell walls; the Tenericutes lack cell walls; and the Mendosicutes have unusual cell walls made of material other than typical bacterial peptidoglycan. Among the Mendosicutes are the archaebacteria, a group of unusual organisms that includes methanogens, strict anaerobes that produce methane from carbon dioxide and hydrogen; halobacteria, which grow at high salt concentrations; and thermoacidophiles, which are sulphur-dependent extreme thermophiles. It has been argued that the archaebacteria should be classified into a separate kingdom because recent biochemical studies have shown that they are as different from other bacteria as they are from eukaryotes (the nucleii of which are membrane-bound). The four major bacterial divisions are further subdivided into about 0 numbered sections, some of which are divided into orders, families, and genera. Section 1, for example, is made up of spirochaetes long, corkscrew-shaped bacteria with gram-negative cell walls and internal (between the cell wall and cell membrane) filamentous flagella that provide the organisms with motility (ability to move). Treponema pallidum, causing syphilis, is a spirochaete, a member of the order Spirochaetales, and the family Spirochaetaceae.
Not all bacteria can move, but the mobile ones are generally propelled by screw-like appendages flagella that may project from all over the cell or from one or both ends, singly or in tufts. Depending on the direction in which the flagella rotate, the bacteria either move forward or tumble in place. The duration of runs versus tumbling is linked to receptors in the bacterial membrane; variations enable the bacteria to move towards attractants such as food sources and away from unfavourable environmental conditions. In some aquatic bacteria that contain iron-rich particles, locomotion has been found to be oriented to the Earths magnetic field.
IIIGENETICS
The genetic material of the bacterial cell is in the form of a circular double strand of DNA (see Nucleic Acids). Many bacteria also carry smaller circular DNAs called plasmids, which encode genetic information but are generally not essential for reproduction. Many of these plasmids can be transferred to other bacteria by conjugation, a mechanism of genetic exchange. Other mechanisms whereby bacteria can exchange genetic information include transduction, in which bacterial viruses (see Bacteriophage) transfer DNA, and transformation, in which DNA is taken into the bacterial cell directly from the environment. Bacterial cells multiply by binary fission; the genetic material is duplicated and the bacterium elongates, constricts near the middle, and then undergoes complete division, forming two daughter cells essentially identical to the parent cell. Thus, as with higher organisms, a given species of bacteria reproduces only cells of the same species. Some bacteria divide every 0 to 40 minutes. Under favourable conditions, with one division every 0 minutes, after 15 hours a single cell will have produced roughly 1 billion progeny. This mass, called a colony, may be seen with the naked eye. Under adverse conditions some bacteria may undergo a modified division process to produce spores, dormant forms of the cell that can withstand extremes of temperature and humidity until more favourable conditions return.
IVWORK OF BACTERIA
Two main groups of bacteria exist the saprophytes, which live on dead animal and vegetable matter; and the symbionts, which live on or in living animal or vegetable matter. Saprophytes are important because they decompose dead animals and plants into their constituent elements, making them available as food for plants. Symbiotic bacteria are a normal part of many human tissues, including the alimentary canal and the skin, where they may be indispensable to physiological processes. Such a relationship is called mutualistic. Other symbionts gain nutrients from their living host without causing serious damage; this is commensalism. The third type, parasites, can destroy the plants and animals on which they live.
Bacteria are involved in the spoilage of meat, wine, vegetables, and milk and other dairy products. Bacterial action may render such foods unpalatable by changing their composition. Bacterial growth in foods can also lead to food poisoning such as that caused by Staphylococcus aureus or by Clostridium botulinum (see Botulism). On the other hand, bacteria are of great importance in many industries. The fermentative capabilities of various species are manipulated for the production of cheese, yoghurt, pickles, and sauerkraut. Bacteria are also important in the production of tanned leather, tobacco, ensilage, textiles, pharmaceuticals and various enzymes, polysaccharides, and detergents.
Bacteria are found in virtually all environments, where they contribute to various biological processes. For example, they may produce light, such as the phosphorescence of dead fish (see Bioluminescence); and they may produce enough heat to induce spontaneous combustion in haystacks or in hop granaries. By decomposing cellulose (the main constituent of plant cell walls), certain anaerobic forms produce marsh gas in stagnant pools; by oxidizing processes, other bacteria assist in forming deposits of bog iron ore, ochre, and manganese ore.
Bacteria have an immense influence on the nature and composition of the soil. One result of their activities is the complete disintegration of organic remains of plants and animals and of inorganic rock particles. This action produces in the aggregate vast quantities of plant food. In addition, the leguminous plants that enrich soil by increasing its nitrogen content do so with the help of Rhizobium radicicola and other bacteria that infect the roots of the plants and cause nitrogen-fixing nodules to grow (see Nitrogen Fixation).The photosynthetic process on which plant life itself is based was almost certainly first established in bacteria; the recent discovery of an unusual photosynthesizing bacterium called Heliobacterium chlorum may help in understanding this fundamental development in the history of life.
VPATHOGENIC BACTERIA
About 00 species of bacteria are pathogenic, or disease-causing, for humans. Pathogenicity varies widely among various species and is dependent on both the virulence of the particular species and the condition of the host organism. Among the more invasive bacteria responsible for human disease are those that cause cholera, tetanus, gas gangrene, leprosy, plague, bacillary dysentery, tuberculosis, syphilis, typhoid fever, diphtheria, undulant fever, and several forms of pneumonia. Until the discovery of viruses, bacteria were considered the causative agents of all infectious diseases.
The pathogenic effects of bacteria on body tissues may be grouped in four classes as follows (1) effects of the direct local action of the bacteria on the tissues, as in gas gangrene, caused by Clostridium perfringens; () mechanical effects, as when a mass of bacteria blocks a blood vessel, causing an infectious embolus; () effects of the bodys response to certain bacterial infections on body tissues, as in the forming of lung cavities in tuberculosis, or destruction of heart tissue by the bodys own antibodies in rheumatic fever; (4) effects of bacterial-produced toxins, chemical substances that act as poisons to certain tissues. Toxins are generally species specific; for example, the toxin responsible for diphtheria is different from the one responsible for cholera.
However, it is worth noting that an increasing number of scientists are emphasizing the indirectly beneficial effects of mild pathogens. Exposure to germs allows the body to develop immunity (see Immune System, Immunization) to those bugs, and there are some proponents of bacterial inoculation for asthma sufferers, for example. It is believed that a certain level of bacteria is needed to kick-start babies' immune systems in order to prevent allergies, something that may be lacking with the high levels of hygiene in modern homes and hospitals.
VIANTIBIOTICS
Various micro-organisms, including certain fungi and some bacteria, produce chemical substances that are toxic to specific bacteria. Such substances, which include penicillin and streptomycin, are known as antibiotics; they either kill the bacteria or prevent them from growing or reproducing. In recent years antibiotics have played an increasingly important role in medicine in the control of bacterial diseases. See Also Antiseptics; Bacteriology; Disease.
Illustrations
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Anatomy of a Simple Bacterium
A simplified bacterium has three external layers surrounding internal structures the slimy capsule layer protects the rigid cell wall, which in turn covers the semi-permeable cell membrane. The flagellum propels the bacterium, and the pili, hairlike structures that extend beyond the capsule, help the bacterium attach itself to various surfaces. Genetic material is contained in DNA that forms the nucleoid. Ribosomes floating in the cytoplasm help the process of protein synthesis.
Table
Bacteria Types
Microbiologists broadly classify bacteria according to their shape spherical, rod-shaped, and spiral-shaped. Pleomorphic bacteria can assume a variety of shapes. Bacteria may be further classified according to whether they require oxygen (aerobic or anaerobic) and how they react to a test with Gram's stain. Bacteria in which alcohol washes away Gram's stain are called gram-negative, while bacteria in which alcohol causes the bacteria's walls to absorb the stain are called gram-positive.
TYPECHARACTERISTICS
Acetic acidRod-shaped, gram-negative, aerobic; highly tolerant of acidic conditions; generate organic acids
ActinomyceteRod-shaped or filamentous, gram-positive, aerobic; common in soils; essential to growth of many plants; source of much of original antibiotic production in pharmaceutical industry
CoccoidSpherical, sometimes in clusters or strings, gram-positive, aerobic and anaerobic; resistant to drying and high-salt conditions; Staphylococcus species common on human skin, certain strains associated with toxic shock syndrome
CoryneformRod-shaped, form club or V shapes, gram-positive, aerobic; found in wide variety of habitats, particularly soils; highly resistant to drying; include Arthrobacter, among most common forms of life on earth
Endospore-
formingUsually rod-shaped, can be gram-positive or gram-negative; have highly adaptable, heat-resistant spores that can go dormant for long periods, possibly thousands of years; include Clostridium (anaerobic) and Bacillus (aerobic)
EntericRod-shaped, gram-negative, aerobic but can live in certain anaerobic conditions; produce nitrite from nitrate, acids from glucose; include Escherichia coli,Salmonella (over 1,000 types), and Shigella
GlidingRod-shaped, gram-negative, mostly aerobic; glide on secreted slimy substances; form colonies, frequently with complex fruiting structures
Lactic acidGram-positive, anaerobic; produce lactic acid through fermentation; include Lactobacillus, essential in dairy product formation, and Streptococcus, common in humans
MycobacteriumPleomorphic, spherical or rod-shaped, frequently branching, no gram stain, aerobic; commonly form yellow pigments; include Mycobacterium tuberculosis, cause of tuberculosis
MycoplasmaSpherical, commonly forming branching chains, no gram stain, aerobic but can live in certain anaerobic conditions; without cell walls yet structurally resistant to lysis; among smallest of bacteria; named for superficial resemblance to fungal hyphae (myco- means fungus)
Nitrogen-fixingRod-shaped, gram-negative, aerobic; convert atmospheric nitrogen gas to ammonium in soil; include Azotobacter, a common genus
Propionic acidRod-shaped, pleomorphic, gram-positive, anaerobic; ferment lactic acid; fermentation produces holes in Swiss cheese from the production of carbon dioxide
PseudomonadRod-shaped (straight or curved) with polar flagella, gram-negative, aerobic; can use up to 100 different compounds for carbon and energy
RickettsiaSpherical or rod-shaped, gram-negative, aerobic; cause Rocky Mountain spotted fever and typhus; closely related to Agrobacterium, a common gall-causing plant bacterium
SheathedFilamentous, gram-negative, aerobic; swarmer (colonizing) cells form and break out of a sheath; sometimes coated with metals from environment
SpirillumSpiral-shaped, gram-negative, aerobic; include Bdellovibrio, predatory on other bacteria
SpirocheteSpiral-shaped, gram-negative, mostly anaerobic; common in moist environments, from mammalian gums to coastal mudflats; complex internal structures convey rapid movement; include Treponemapallidum, cause of syphilis
Sulphate- and Sulphur-reducingCommonly rod-shaped, mostly gram-negative, anaerobic; include Desulfovibrio, ecologically important in marshes
Sulphur- and iron-oxidizingCommonly rod-shaped, frequently with polar flagella, gram-negative, mostly anaerobic; most live in neutral (non-acidic) environment
VibrioRod- or comma-shaped, gram-negative, aerobic; commonly with a single flagellum; include Vibrio cholerae, cause of cholera, and luminescent forms symbiotic with deep-water fishes and squids
Pathogenic E. coli
Left Escherichia coli cells. Right E.coli colonies on EMB Agar
Escherichia coli
The GI tract of most warm-blooded animals is colonized by E. coli within hours or a few days after birth. The bacterium is ingested in foods or water or obtained directly from other individuals handling the infant. The human bowel is usually colonized within 40 hours of birth. E. coli can adhere to the mucus overlying the large intestine. Once established, an E. coli strain may persist for months or years. Resident strains shift over a long period (weeks to months), and more rapidly after enteric infection or antimicrobial chemotherapy that perturbs the normal flora. The basis for these shifts and the ecology of Escherichia coli in the intestine of humans are poorly understood despite the vast amount of information on almost every other aspect of the organisms existence. The entire DNA base sequence of the E. coli genome has been known since 17.
E. coli is the head of the large bacterial family, Enterobacteriaceae, the enteric bacteria, which are faculatively anaerobic Gram-negative rods that live in the intestinal tracts of animals in health and disease. The Enterobacteriaceae are among the most important bacteria medically. A number of genera within the family are human intestinal pathogens (e.g. Salmonella, Shigella, Yersinia). Several others are normal colonists of the human gastrointestinal tract (e.g. Escherichia, Enterobacter, Klebsiella), but these bacteria, as well, may occasionally be associated with diseases of humans.
The Enterobacteriaceae are distinguished from the Pseudomonadaceae in a number of ways known reflexively to competent microbiologists. The pseudomonads are respiratory, never fermentative, oxidase-positive, and motile by means of polar flagella. The enterics ferment glucose producing acid and gas, are typically oxidase-negative, and when motile, produce peritrichous flagella.
Physiologically, E. coli is versatile and well-adapted to its characteristic habitats. It can grow in media with glucose as the sole organic constituent. Wild-type E. coli has no growth factor requirements, and metabolically it can transform glucose into all of the macromolecular components that make up the cell. The bacterium can grow in the presence or absence of O. Under anaerobic conditions it will grow by means of fermentation, producing characteristic mixed acids and gas as end products. However, it can also grow by means of anaerobic respiration, since it is able to utilize NO, NO or fumarate as final electron acceptors for respiratory electron transport processes. In part, this adapts E. coli to its intestinal (anaerobic) and its extraintestinal (aerobic or anaerobic) habitats.
E. coli can respond to environmental signals such as chemicals, pH, temperature, osmolarity, etc., in a number of very remarkable ways considering it is a single-celled organism. For example, it can sense the presence or absence of chemicals and gases in its environment and swim towards or away from them. Or it can stop swimming and grow fimbriae that will specifically attach it to a cell or surface receptor. In response to change in temperature and osmolarity, it can vary the pore diameter of its outer membrane porins to accommodate larger molecules (nutrients) or to exclude inhibitory substances. With its complex mechanisms for regulation of metabolism the bacterium can survey the chemical contents its environment in advance of synthesizing any enzymes necessary to use these compounds. It does not wastefully produce enzymes for degradation of carbon sources unless they are available, and it does not produce enzymes for synthesis of metabolites if they are available as nutrients in the environment.
E. coli is a consistent inhabitant of the human intestinal tract, and it is the predominant facultative organism in the human GI tract; however, it makes up a very small proportion of the total bacterial content. The anaerobic Bacteroides species in the bowel outnumber E. coli by at least 01. however, the regular presence of E. coli in the human intestine and feces has led to tracking the bacterium in nature as an indicator of fecal pollution and water contamination. As such, it is taken to mean that, wherever E. coli is found, there may be fecal contamination by intestinal parasites of humans.
Pathogenesis of E. coli
Over 700 antigenic types (serotypes) are recognized based on O, H, and K antigens. Serotyping is still important in distinguishing the small number of strains that actually cause disease.
E. coli is responsible for three types of infections in humans urinary tract infections (UTI), neonatal meningitis, and intestinal diseases (gastroenteritis). These three diseases depend on a specific array of pathogenic (virulence) determinants. The virulence determinants of various strains of pathogenic E. coli are summarized in Table 1.
Table 1. Summary of the Virulence Determinants of Pathogenic E. coli
Adhesins
CFAI/CFAII
Type 1 fimbriae
P fimbriae
S fimbriae
Intimin (non-fimbrial adhesin)
Invasins
hemolysisn
siderophores and siderophore uptake systems
Shigella-like invasins for intracellular invasion and spread
Motility/chemotaxis
flagella
Toxins
LT toxin
ST toxin
Shiga-like toxin
cytotoxins
endotoxin LPS)
Antiphagocytic surface properties
capsules
K antigens
LPS
Defense against serum bactericidal reactions
LPS
K antigens
Defense against immune responses
capsules
K antigens
LPS
antigenic variation
Genetic attributes
genetic exchange by transduction and conjugation
transmissible plasmids
R factors and drug resistance plasmids
toxin and other virulence plasmids
Urinary tract infections
Uropathogenic E. coli cause 0% of the urinary tract infections (UTI) in anatomically-normal, unobstructed urinary tracts. The bacteria colonize from the feces or perineal region and ascend the urinary tract to the bladder. Bladder infections are 14-times more common in females than males by virtue of the shortened urethra. The typical patient with uncomplicated cystitis is a sexually-active female who was first colonized in the intestine with a uropathogenic E. coli strain. The organisms are propelled into the bladder from the periurethral region during sexual intercourse. With the aid of specific adhesins they are able to colonize the bladder.
The adhesin that has been most closely associated with uropathogenic E. coli is the P fimbria (or pyelonephritis-associated pili [PAP] pili). The letter designation is derived from the ability of P fimbriae to bind specifically to the P blood group antigen which contains a D-galactose-D-galactose residue. The fimbriae bind not only to red cells but to a specific galactose dissaccharide that is found on the surfaces uroepithelial cells in approximately % of the population.
The frequency of the distribution of this host cell receptor plays a role in susceptibility and explains why certain individuals have repeated UTI caused by E. coli. Uncomplicated E. coli UTI virtually never occurs in individuals lacking the receptors.
Uropathogenic strains of E. coli possess other determinants of virulence in addition to P fimbriae. E. coli with P fimbriae also possess the gene for Type 1 fimbriae, and there is evidence that P fimbriae are derived from Type 1 fimbriae by insertion of a new fimbrial tip protein to replace the mannose-binding domain of Type 1 fimbria. In any case, Type 1 fimbriae could provide a supplementary mechanism of adherence or play a role in aggregating the bacteria to a specific manosyl-glycoprotein that occurs in urine.
Uropathogenic strains of E. coli usually produce siderophores that probably play an essential role in iron acquisition for the bacteria during or after colonization. They also produce hemolysins which are cytotoxic due to formation of transmembranous pores in host cells. One strategy for obtaining iron and other nutrients for bacterial growth may involve the lysis of host cells to release these substances. The activity of hemolysins is not limited to red cells since the alpha-hemolysins of E. coli also lyse lymphocytes, and the beta-hemolysins inhibit phagocytosis and chemotaxis of neutrophils.
Another factor thought to be involved in the pathogenicity of the uropathogenic strains of E. coli is their resistance to the complement-dependent bactericidal effect of serum. The presence of K antigens is associated with upper urinary tract infections, and antibody to the K antigen has been shown to afford some degree of protection in experimental infections. The K antigens of E. coli are capsular antigens that may be composed of proteinaceous organelles associated with colonization (e.g., CFA antigens), or made of polysaccharides. Regardless of their chemistry, these capsules may be able to promote bacterial virulence by decreasing the ability of antibodies and/or complement to bind to the bacterial surface, and the ability of phagocytes to recognize and engulf the bacterial cells. The best studied K antigen, K-1, is composed of a polymer of N-acetyl neuraminic acid (sialic acid), which besides being antiphagocytic, has the additional property of being an antigenic disguise.
Neonatal Meningitis
Neonatal meningitis affects1/,000-4,000 infants. Eighty percent of E. coli strains involved synthesize K-1 capsular antigens (K-1 is only present 0-40% of the time in intestinal isolates).
E. coli strains invade the blood stream of infants from the nasopharynx or GI tract and are carried to the meninges.
The K-1 antigen is considered the major determinant of virulence among strains of E. coli that cause neonatal meningitis. K-1 is a homopolymer of sialic acid. It inhibits phagocytosis, complement, and responses from the hosts immunological mechanisms. K-1 may not be the only determinant of virulence, however, as siderophore production and endotoxin are also likely to be involved.
Epidemiologic studies have shown that pregnancy is associated with increased rates of colonization by K-1 strains and that these strains become involved in the subsequent cases of meningitis in the newborn. Probably, the infant GI tract is the portal of entry into the bloodstream. Fortunately, although colonization is fairly common, invasion and the catastrophic sequelae are rare.
Neonatal meningitis requires antibiotic therapy that usually includes ampicillin and a third-generation cephalosporin.
Intestinal Diseases Caused by E. coli
As a pathogen, E. coli, of course, is best known for its ability to cause intestinal diseases. Five classes (virotypes) of E. coli that cause diarrheal diseases are now recognized enterotoxigenic E. coli (ETEC), enteroinvasive E. coli (EIEC), enterohemorrhagic E. coli (EHEC), enteropathogenic E. coli (EPEC), and enteroaggregative E. coli (EAggEC). Each class falls within a serological subgroup and manifests distinct features in pathogenesis.
Enterotoxigenic E. coli (ETEC)
ETEC are an important cause of diarrhea in infants and travelers in underdeveloped countries or regions of poor sanitation. The diseases vary from minor discomfort to a severe cholera-like syndrome. ETEC are acquired by ingestion of contaminated food and water, and adults in endemic areas evidently develop immunity. The disease requires colonization and elaboration of one or more enterotoxins. Both traits are plasmid-encoded.
ETEC adhesins are fimbriae which are species-specific. For example, the K-88 fimbrial Ag is found on strains from piglets; K- Ag is found on strains from calves and lambs; CFA I, and CFA II, are found on strains from humans. These fimbrial adhesins adhere to specific receptors on enterocytes of the proximal small intestine.
Enterotoxins produced by ETEC include the LT(heat-labile) toxin and/or the ST (heat-stable) toxin, the genes for which may occur on the same or separate plasmids. The LT enterotoxin is very similar to cholera toxin in both structure and mode of action. It is an 86kDa protein composed of an enzymatically active (A) subunit surrounded by 5 identical binding (B) subunits. It binds to the same identical ganglioside receptors that are recognized by the cholera toxin (i.e., GM1), and its enzymatic activity is identical to that of the cholera toxin.
The ST enterotoxin is actually a family of toxins which are peptides of molecular weight about ,000 daltons. Their small size explains why they are not inactivated by heat. ST causes an increase in cyclic GMP in host cell cytoplasm leading to the same effects as an increase in cAMP. STa is known to act by binding to a guanylate cyclase that is located on the apical membranes of host cells, thereby activating the enzyme. This leads to secretion of fluid and electrolytes resulting in diarrhea.
Symptoms ETEC infections include diarrhea without fever. The bacteria colonize the GI tract by means of a fimbrial adhesin, e.g. CFA I and CFA II, and are noninvasive, but produce either the LT or ST toxin.
Enteroinvasive E. coli (EIEC)
EIEC closely resemble Shigella in their pathogenic mechanisms and the kind of clinical illness they produce. EIEC penetrate and multiply within epithelial cells of the colon causing widespread cell destruction. The clinical syndrome is identical to Shigella dysentery and includes a dysentery-like diarrhea with fever. EIEC apparently lack fimbrial adhesins but do possess a specific adhesin that, as in Shigella, is thought to be an outer membrane protein. Also, likeShigella, EIEC are invasive organisms. They do not produce LT or ST toxin and, unlike Shigella, they do not produce the shiga toxin.
Enteropathogenic E. coli (EPEC)
EPEC induce a watery diarrhea similar to ETEC, but they do not possess the same colonization factors and do not produce ST or LT toxins. They produce a non fimbrial adhesin designated intimin, an outer membrane protein, that mediates the final stages of adherence. Although they do not produce LT or ST toxins, there are reports that they produce an enterotoxin similar to that of Shigella. Other virulence factors may be related to those in Shigella.
Adherence of EPEC strains to the intestinal mucosa is a very complicated process and produces dramatic effects in the ultrastructure of the cells resulting in rearrangements of actin in the vicinity of adherent bacteria. The phenomenon is sometimes called attaching and effacing of cells. EPEC strains are said to be moderately-invasive meaning they are not as invasive as Shigella, and unlike ETEC or EAggEC, they cause an inflammatory response. The diarrhea and other symptoms of EPEC infections probably are caused by bacterial invasion of host cells and interference with normal cellular signal transduction, rather than by production of toxins.
Some types of EPEC are referred to as Enteroadherent E. coli (EAEC), based on specific patterns of adherence. They are an important cause of travelers diarrhea in Mexico and in North Africa.
Enteroaggregative E. coli (EAggEC)
The distinguishing feature of EAggEC strains is their ability to attach to tissue culture cells in an aggregative manner. These strains are associated with persistent diarrhea in young children. They resemble ETEC strains in that the bacteria adhere to the intestinal mucosa and cause non-bloody diarrhea without invading or causing inflammation. This suggests that the organisms produce a toxin of some sort. Recently, a distinctive heat-labile plasmid-encoded toxin has been isolated from these strains, called the EAST (EnteroAggregative ST) toxin. They also produce a hemolysin related to the hemolysin produced by E. coli strains involved in urinary tract infections. The role of the toxin and the hemolysin in virulence has not been proven. The significance of EAggEC strains in human disease is controversial.
Enterohemorrhagic E. coli (EHEC)
EHEC are represented by a single strain (serotype O157H7), which causes a diarrheal syndrome distinct from EIEC (and Shigella) in that there is copious bloody discharge and no fever. A frequent life-threatening situation is its toxic effects on the kidneys (hemolytic uremia).
EHEC has recently been recognized as a cause of serious disease often associated with ingestion of inadequately cooked hamburger meat. Pediatric diarrhea caused by this strain can be fatal due to acute kidney failure (hemolytic uremic syndrome [HUS]). EHEC are also considered to be moderately invasive. Nothing is known about the colonization antigens of EHEC but fimbriae are presumed to be involved. The bacteria do not invade mucosal cells as readily as Shigella, but EHEC strains produce a toxin that is virtually identical to the Shiga toxin. The toxin plays a role in the intense inflammatory response produced by EHEC strains and may explain the ability of EHEC strains to cause HUS. The toxin is phage encoded and its production is enhanced by iron deficiency.
Table . Pathogenic E. coli Summary of Virulence Characteristics of Intestinal Pathogens
ETEC
fimbrial adhesins e.g. CFA I, CFAII, K88. K
non invasive
produce LT and/or ST toxin
watery diarrhea in infants and travelers; no inflammation, no fever
EIEC
nonfimbrial adhesins, possibly outer membrane protein
invasive (penetrate and multiply within epithelial cells)
does not produce shiga toxin
dysentery-like diarrhea (mucous, blood), severe inflammation, fever
EPEC
non fimbrial adhesin (intimin)
moderately invasive (not as invasive as Shigella or EIEC)
does not produce LT or ST; some reports of shiga-like toxin
usually infantile diarrhea; watery diarrhea similar to ETEC, some inflammation, no fever; symptoms probably result mainly from invasion rather than toxigenesis
EAggEC
adhesins not characterized
non invasive
produce ST-like toxin (EAST) and a hemolysin
persistent diarrhea in young children without inflammation, no fever
EHEC
adhesins not characterized, probably fimbriae
moderately invasive
does not produce LT or ST but does produce shiga toxin
pediatric diarrhea, copious bloody discharge (hemorrhagic colitis), intense inflammatory response, may be complicated by hemolytic uremia
E. coli info #
the labels on frozen steak products
Frequently Asked Questions
•What is Escherichia coli O157H7?
•How is E. coli O157H7 spread?
•What illness does E.coli O157H7 cause?
•How is E. coli O157H7 infection diagnosed?
•How is the illness treated?
•What are the long term consequences of infection?
•What can be done to prevent the infection?
•What can you do to prevent E. coli O157H7 infection?
Escherichia coli O157H7 is an emerging cause of foodborne illness. An estimated 7,000 cases of infection and 61 deaths occur in the United States each year. Infection often leads to bloody diarrhea, and occasionally to kidney failure. Most illness has been associated with eating undercooked, contaminated ground beef. Person-to-person contact in families and child care centers is also an important mode of transmission. Infection can also occur after drinking raw milk and after swimming in or drinking sewage-contaminated water.
Consumers can prevent E. coli O157H7 infection by thoroughly cooking ground beef, avoiding unpasteurized milk, and washing hands carefully.
Because the organism lives in the intestines of healthy cattle, preventive measures on cattle farms and during meat processing are beinginvestigated.
What is Escherichia coli O157H7?
E. coli O157H7 is one of hundreds of strains of the bacterium Escherichia coli. Although most strains are harmless and live in the intestines of healthy humans and animals, this strain produces a powerful toxin and can cause severe illness.
E. coli O157H7 was first recognized as a cause of illness in 18 during an outbreak of severe bloody diarrhea; the outbreak was traced to contaminated hamburgers. Since then, most infections have come from eating undercooked ground beef.
The combination of letters and numbers in the name of the bacterium refers to the specific markers found on its surface and distinguishes it from other types of E. coli.
How is E. coli O157H7 spread?
The organism can be found on a small number of cattle farms and can live in the intestines of healthy cattle. Meat can become contaminated during slaughter, and organisms can be thoroughly mixed into beef when it is ground. Bacteria present on the cows udders or on equipment may get into raw milk.
Eating meat, especially ground beef, that has not been cooked sufficiently to kill E. coli O157H7 can cause infection. Contaminated meat looks and smells normal. Although the number of organisms required to cause disease is not known, it is suspected to be very small.
Among other known sources of infection are consumption of sprouts, lettuce, salami, unpasteurized milk and juice, and swimming in or drinking sewage-contaminated water.
Bacteria in diarrheal stools of infected persons can be passed from one person to another if hygiene or handwashing habits are inadequate.
This is particularly likely among toddlers who are not toilet trained. Family members and playmates of these children are at high risk of becoming infected.
Young children typically shed the organism in their feces for a week or two after their illness resolves. Older children rarely carry the organism without symptoms.
What illness does E. coli O157H7 cause?
E. coli O157H7 infection often causes severe bloody diarrhea and abdominal cramps; sometimes the infection causes nonbloody diarrhea or no symptoms. Usually little or no fever is present, and the illness resolves in 5 to 10 days.
In some persons, particularly children under 5 years of age and the elderly, the infection can also cause a complication called hemolytic uremic syndrome, in which the red blood cells are destroyed and the kidneys fail. About %-7% of infections lead to this complication. In the United States, hemolytic uremic syndrome is the principal cause of acute kidney failure in children, and most cases of hemolytic uremic syndrome are caused by E. coli O157H7.
How is E. coli O157H7 infection diagnosed?
Infection with E. coli O157H7 is diagnosed by detecting the bacterium in the stool. Most laboratories that culture stool do not test for E. coli O157H7, so it is important to request that the stool specimen be tested on sorbitol-MacConkey (SMAC) agar for this organism. All persons who suddenly have diarrhea with blood should get their stool tested for E. coli O157H7.
How is the illness treated?
Most persons recover without antibiotics or other specific treatment in 5-10 days. There is no evidence that antibiotics improve the course of disease, and it is thought that treatment with some antibiotics may precipitate kidney complications. Antidiarrheal agents, such as loperamide (Imodium), should also be avoided.
Hemolytic uremic syndrome is a life-threatening condition usually treated in an intensive care unit. Blood transfusions and kidney dialysis are often required. With intensive care, the death rate for hemolytic uremic syndrome is %-5%.
What are the long-term consequences of infection?
Persons who only have diarrhea usually recover completely.
About one-third of persons with hemolytic uremic syndrome have abnormal kidney function many years later, and a few require long-term dialysis. Another 8% of persons with hemolytic uremic syndrome have other lifelong complications, such as high blood pressure, seizures, blindness, paralysis, and the effects of having part of their bowel removed.
What can be done to prevent the infection?
E. coli O157H7 will continue to be an important public health concern as long as it contaminates meat. Preventive measures may reduce the number of cattle that carry it and the contamination of meat during slaughter and grinding. Research into such prevention measures is just beginning.
What can you do to prevent E. coli O157H7 infection?
Cook all ground beef and hamburger thoroughly. Because ground beef can turn brown before disease-causing bacteria are killed, use a digital instant-read meat thermometer to ensure thorough cooking. Ground beef should be cooked until a thermometer inserted into several parts of the patty, including the thickest part, reads at least 160º F. Persons who cook ground beef without using a thermometer can decrease their risk of illness by not eating ground beef patties that are still pink in the middle.
If you are served an undercooked hamburger or other ground beef product in a restaurant, send it back for further cooking. You may want to ask for a new bun and a clean plate, too.
Avoid spreading harmful bacteria in your kitchen. Keep raw meat separate from ready-to-eat foods. Wash hands, counters, and utensils with hot soapy water after they touch raw meat. Never place cooked hamburgers or ground beef on the unwashed plate that held raw patties. Wash meat thermometers in between tests of patties that require further cooking.
Drink only pasteurized milk, juice, or cider. Commercial juice with an extended shelf-life that is sold at room temperature (e.g. juice in cardboard boxes, vacuum sealed juice in glass containers) has been pasteurized, although this is generally not indicated on the label. Juice concentrates are also heated sufficiently to kill pathogens.
Wash fruits and vegetables thoroughly, especially those that will not be cooked. Children under 5 years of age, immunocompromised persons, and the elderly should avoid eating alfalfa sprouts until their safety can be assured. Methods to decontaminate alfalfa seeds and sprouts are being investigated.
Drink municipal water that has been treated with chlorine or other effective disinfectants.
Avoid swallowing lake or pool water while swimming. See more information about this.
Make sure that persons with diarrhea, especially children, wash their hands carefully with soap after bowel movements to reduce the risk of spreading infection, and that persons wash hands after changing soiled diapers. Anyone with a diarrheal illness should avoid swimming in public pools or lakes, sharing baths with others, and preparing food for others.
For more information about reducing your risk of foodborne illness, visit the US Department of Agriculture's Food Safety and Inspection Service website at http//www.fsis.usda.gov or the Partnership for Food Safety Education at For more advice on cooking ground beef, visit the U.S. Department of Agriculture web site at http//www.fsis.usda.gov/OA/topics/gb.htm
The term E. coli is an abbreviation for the bacteria Escherichia coli.
E. coli bacteria were discovered in the human colon in 1885 by German bacteriologist Theodor Escherich. Dr. Escherich also showed that certain strains of the bacteria were responsible for infant diarrhea and gastroenteritis - an important public health discovery. Although the bacteria were initially called Bacterium coli, the name was later changed to Escherichia coli to honor its discoverer.
Soon after its discovery, E. coli became a very popular lab organism because scientists could grow it quickly on both simple and complex mediums. E. coli can grow in air, using oxygen as a terminal electron acceptor (aerobically) or without air, by what is called fermentative metabolisman (aerobically). The ability to grow both aerobically and anaerobically classifies the E. coli bacteria as a facultative anaerobe.
Although E. coli has been often in the news as a foodborne pathogen, the vast majority of E. coli strains are harmless, including those commonly used by scientists in genetics laboratories. E. coli is found in the family of bacteria named Enterobacteriaceae, which is informally referred to as the enteric bacteria. Other enteric bacteria are the Salmonella bacteria (also a very large family, with many different members), Klebsiella pneumoniae, and Shigella, which many people consider to be part of the E. coli family.
E. coli O157 H7
Because there are so many different strains of E. coli, microbiologists classify it into more than 170 serogroups. Within each serogroup, there are one or more serotypes. For example, O16H and O16H7 represent two serotypes of E. coli, with the O16 signifying the particular serogroup to which these serotypes belong. E. coli O157H7 was identified for the first time at the U. S. Centers for Disease Control (CDC) in 175. However, it was not until seven years later, in 18, that E. coli O157H7 was conclusively determined to be a cause of enteric disease. Specifically, in 18, following outbreaks of foodborne illness that involved several cases of bloody diarrhea, E. coli O157 H7 was firmly associated with hemorrhagic colitis.1 As a result of this association, E. coli O157 H7 was designated as an enterohemorrhagic E. coli, or EHEC.
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