E. Coli (Escherichia Coli)- An Overview

Habitat of E. coli

  1. Theodor Escherich isolated E. coli from the excrement of infants and found it in 1885.
  2. The typical flora of the human body includes E. coli.
  3. The presence of nutrients in the host species’ intestines determines E. coli’s niche.
  4. coli’s primary habitat is the gastrointestinal (GI) tract of humans and numerous other warm-blooded animals.
  5. It can be discovered in the epithelium or mucus on the intestine’s wall.
  6. most frequently inside the colon of the large intestine.
  7. Most of them are opportunistic and harmless.
  8. Between E. coli and its host, a symbiotic connection develops.
  9. coli aids in the colon’s ability to absorb vitamin K and other vitamins.
  10. The majority of the bacteria in the gut belong to this category.
  11. Between 0.1 and 1 percent of the bacteria in the GI tract are E. coli.
  12. A facultative aerobe, that is.
  13. Human faeces also contain E. coli.
  14. coli can only live for a short period of time after leaving the digestive tract.
  15. Outside of the body, E. coli can be found in feces-contaminated surroundings including water, mud, or sediments.
  16. Vegetable leaves may get infected if E. coli comes into touch with them while they are still fresh.
  17. Additionally, E. coli may be found in hotter areas, such as the border of hot springs.
  18. Due to processing at the slaughterhouse, E. coli is also discovered on ground beef.
  19. The E. coli O157:H7 found in cattle is more likely to infect people.

Morphology of E. coli

  • coli is a rod-shaped, gram-negative (-ve) bacterium.
  • It has dimensions of 1-3 x 0.4–0.7 m and a volume of 0.6–0.7 m.
  • It may be installed singly or in doubles.
  • It is mobile due to the peritrichous flagella.
  • Unmotile strains persist.
  • Fimbriated strains can exist. Both motile and non-motile strains have the type 1 (hemagglutinating & mannose-sensitive) fimbriae.
  • There are several E. coli strains with polysaccharide capsules that have been identified from extraintestinal infections.
  • They don’t spore.
  • They only have one or two peptidoglycan layers in their thin cell wall.
  • They can tolerate anaerobes.
  • From 15 to 45 °C, growth can take place in a wide temperature range.

Antigenic Structure

The most important cell wall antigen of E is heat stable lipopolysaccharide (LPS). coli.

  1. H, O, K, and F are the four antigens found in coli.

H or Flagellar Antigen

  • Alcohol and heat labile protein
  • available on the flagella
  • specific to genera
  • monophasic and present
  • There are 75 known “H” antigens.

O or Somatic Antigen

  • Heat stable; up to two hours of boiling resistance. one hour
  • occur on the outer membrane’s surface.
  • a crucial component of the cell wall
  • There are 173 known “O” antigens.

Capsular Antigen or K

  • Heat unstable
  • There is an antigen for acidic polysaccharides in the envelope.
  • The K antigen is removed by boiling.
  • suppress phagocytosis
  • There are 103 known “K” antigens.

F or Fimbrial Antigen

  • Heat-sensitive proteins
  • available in the fimbriae
  • K99 and K88 antigens

Cultural Characteristics of E. coli

  1. A facultative anaerobe is E. coli.
  2. Its optimal development temperature, which varies from 10 to 40 degrees Celsius, is 37 degrees.
  3. E. coli on Nutrient Agar (NA)
  1. They have a big, round, low convex, moist, smooth, opaque, greyish, white appearance.
  2. They come in two varieties: smooth (S) and rough (R).
  3. In saline, smooth forms can be emulsified.
  4. There is smooth to rough variance as a result of repeated culturing (S-R variation).

E. coli on Blood Agar (BA)

  1. Colonies are large, round, greyish, and humid.
  2. The formation of non-hemolytic colonies (gamma-hemolysis) (Above Figure) OR beta () hemolytic colonies.

E.coli on MacConkey Agar (MAC)


  1. Colonies have a complete edge, are round, and are wet.
  2. Colonies have a flat, pink appearance.
  3. These colonies digest lactose.

E.coli on Mueller Hinton Agar (MHA)

  1. Colonies are pale straw-colored.

E. coli on Eosin Methylene Blue (EMB) Agar

  1. Green Metallic sheen colonies are formed.

E. coli on m-ENDO Agar

  1. Colonies have a metallic shine of green.
  2. Lactose is metabolised, resulting in the generation of acid and aldehyde.

E. coli on Violet Red Bile Agar (VRBA)

  1. Pink to scarlet red colonies develop.
  2. Under UV, bluish glow may be noticed near colonies.

Cystine Lactose Electrolyte-Deficient (CLED) Agar with E. coli

They produce yellow colonies that are lactose-positive.

E.coli on Liquid Media

  1. Within 12 to 18 hours, they exhibit uniform turbid development.
  2. R form spontaneously agglutinates, depositing sediment at the test tube bottom.
  3. On the surface of liquid medium, pellicles develop after a lengthy incubation (>72 hours).
  4. Large deposits are created, which scatter when shaken.

Biochemical Characteristics of Escherichia coli (E. coli)

Pathogenicity of E. coli

  • The most prevalent and significant member of the Escherichia genus is E. coli.
  • It is a rod-shaped, Gram-negative bacteria that often lives in the lower intestine of warm-blooded species. It is also facultatively anaerobic (endotherms).
  • Human Escherichia coli strains are classified depending on their genetic traits and clinical outcomes as commensal microbiota E. coli, enterovirulent E. coli, as well as extraintestinal pathogenic E. coli.
  • Except for neonatal meningitis and gastroenteritis, the majority of illnesses are endogenous,which means that when a patient’s defences are weakened, E. coli from their regular microbial flora can spread illness (e.g., through trauma or immune suppression).
  • Numerous illnesses,this bacteria has been related to gastroenteritis and extraintestinal infections such as UTIs, meningitis, as well as sepsis.
  • There are several strains that can spread illness, and certain serotypes are known to be more virulent than others.

Virulence Factors of E. coli

  • There is a wide variety of virulence factors present in E. coli.
  • Escherichia strains have unique virulence factors that fall into two categories: adhesins and exotoxins, addingto the generic traits shared by all members of the Enterobacteriaceae family.

ETEC (Enterotoxigenic E. coli)

  • Antigens for colonisation factors (CFA/I, CFA/II, and CFA/III)
  • Heat-stable toxin; heat-labile toxin (LT-1) (STa)

EPEC (Enteropathogenic E. coli) (Enteropathogenic E. coli)

  • Intimin; Bundle Forming Pili (BFP)

EAEC (Enteroaggregative E. coli)

  • Adherence fimbriae (AAF/I, AAF/II, and AAF/III) in aggregate
  • Toxin that enteroaggregates and is heat-stable; plasmid-encoded toxin

STEC (Shiga toxin-producing E. coli)

  • BFP and immin
  • the shiga toxins (Stx1, Stx2)

EIEC (Enteroinvasive E. coli)

  • plasmid antigen that is invasive
  • Hemolysin (HlyA)


  • P pili
  • Fimbriae, Dr.


Clinical Feature of E. coli


  • Infants with ETEC develop baby diarrhoea or traveler’s diarrhoea. Plasmid-mediated, heat-stable (ST) and heat-labile (LT) enterotoxins that promote fluid and electrolyte oversecretion are involved in pathogenesis.
  • Infant diarrhoea is brought on by EPEC in underdeveloped nations. Diarrhea and malabsorption are caused by the disruption of normal microvillus structure, which is caused by plasmid-mediated A/E histopathology.
  • Along with traveler’s diarrhoea, EAEC also causes newborn diarrhoea in developing and maybe developed nations. Plasmid-mediated aggregative rod adhesion (“stacked bricks”), bleeding, mononuclear infiltration, and shortening of microvilli are all part of the pathogenesis. Fluid absorption is also diminished.
  • Hemorrhagic colitis is brought on by STEC. STEC developed from EPEC; A/E lesions with intestinal microvilli destroyed, reducing absorption; disease caused by cytotoxic Shiga toxins (Stx1, Stx2), which interfere with protein synthesis
  • EIEC produces a sickness that is uncommon in both developed and developing nations. Plasmid-mediated invasion and apoptosis of colon epithelial cells are hallmarks of the pathogenesis process.

Urinary Tract Infection

  • The majority of gram-negative rods that cause UTIs start off in the colon, get into the urethra, climb up into the bladder, and then occasionally go on to the kidney or prostate.
  • Although UTIs can be caused by the majority of E. coli strains, certain particular serogroups are more prone to the condition.
  • Due to their ability to generate hemolysin HlyA which lyses erythrocytes and other cell types as well as adhesins (mainly P pili, AAF/I, AAF/III, and Dr) which adhere to cells lining the bladder as well as upper urinary tract and inhibit the bacteria from being removed in urine, these bacteria are particularly virulent (resulting in the release of cytokines and the induction of an inflammatory reaction).


  • Sepsis may develop when E coli enters the circulation due to insufficient human defences.
  • Due to the absence of IgM antibodies, newborns may be more vulnerable to E coli sepsis.
  • Urinary tract infection may contribute to sepsis.


  • The most common germs that cause meningitis in young children are E coli and group B streptococci.
  • The K1 antigen is present in around 75% of E coli from meningitis patients.
  • The group B capsular polysaccharide of N meningitidis interacts with this antigen.
  • Unknown is the mechanism of pathogenicity linked to the K1 antigen.

Clinical Manifestations of E. coli


  • red or watery diarrhoea
  • vomiting
  • cramping
  • nausea
  • minimal fever
  • dehydration
  • stomach pains

Urinary tract infection

Escherichia coli is the bacterium most frequently discovered to cause UTIs (E. coli).Although there are other bacteria that can cause UTIs, E. coli is the main offender roughly 90% of the time. The following are some of the infection’s main symptoms:

  • an intense, constant need to urinate
  • an uncomfortable burning when urinating
  • tummy pressure
  • Lower abdominal pain
  • uncomfortable and frequent urination
  • urethral blood

Acute bacterial meningitis

  • Fevers and failure to grow are common symptoms of E. coli meningitis in newborns, as are aberrant neurologic signals.
  • Other neonatal symptoms include jaundice, decreased eating, apneic episodes, and listlessness.
  • Patients under a month old frequently exhibit lethargy, irritability, vomiting, anorexia, and convulsions.

Laboratory Diagnosis of E. coli

Urinary Tract Infection

  • By using the clean-catch midstream approach, the majority of urine samples are collected from adult patients.
  • Gram staining of centrifuged urine specimens, Gram staining of uncentrifuged urine specimens, or direct viewing of bacteria in urine specimens can all be used to diagnose bacteriuria microscopically.
  • E coli appears stained as a Gram-negative, rod-shaped bacteria that does not produce spores.
  • For the semi-quantitative approach, routine urine cultures should be plated using calibrated loops.
  • Note:The presence of 105 CFU per millilitre of urine is the standard for determining serious bacteriuria.
  • The only media types that should be used for standard cultures are blood agar and MacConkey’s agar.
  • Before reading, urine cultures should be cultured for a whole night at 35°C–37°C in room air.

Reactions to tests

Indole, lysine decarboxylase, lactose, and mannitol fermentation tests for E. coli often provide positive findings, and it also generates gas from glucose. When an isolate from urine exhibits hemolysis on blood agar, characteristic colonial morphology with an iridescent “sheen” on differential medium like EMB agar, and a positive spot indole test result, the isolate can be immediately recognised as E. coli. For the substrate 4-methylumbelliferyl-glucuronide, more than 90% of E. coli isolates are -glucuronidase positive (MUG).


  • ETEC: PCR tests are utilised with clinical specimens, and commercial immunoassays are available for identifying ST in clinical specimens and cultures.
  • EPEC: a plasmid-encoded bundle-forming pili and gene targets on the “locus of enterocyte effacement” pathogenicity island, as well as characteristic adhesion to HEp-2 or HeLa cells.
  • EAEC: DNA probe and amplification assays created for conserved plasmid; distinctive adhesion to HEp-2 cells.
  • STEC: Use sorbitol MacConkey agar to test for O157:H7; confirm with serology; use immunoassays (ELISA, latex agglutination) to identify the Stx toxins in stool samples and grown bacteria; create DNA amplification tests for the Stx genes.
  • EIEC includes the Sereny test for keratoconjunctivitis in guinea pigs, the HeLa cell plaque assay, and probes and amplification tests for genes influencing invasion (cannot discriminate between EIEC and Shigella).

Treatment of E. coli infections

  • The enterics are significantly affected by the antibacterial activities of the sulfonamides, ampicillin, cephalosporins, fluoroquinolones, and aminoglycosides, although there is wide variation in sensitivity, necessitating laboratory testing for antibiotic susceptibility.
  • Antibiotics, like cephalosporins of the third generation, are required to cure E. coli meningitis (eg, ceftriaxone).
  • Respiratory assistance, sufficient oxygenation, and medications like third-generation cephalosporins or fluoroquinolones are all necessary for treating E. coli pneumonia.
  • Rarely are antibiotics prescribed for diarrheal sickness. The most effective treatment for an E. coli infection  is to get as much rest as you can and drink lots of fluids to prevent dehydration. However, patients should stay away from dairy products since they might temporarily create lactose intolerance, which aggravates diarrhoea.

Prevention and Control of E. coli infections

  • In places with poor environmental cleanliness, it is generally advised to exercise caution while consuming food and drink and to replace early and short treatment (e.g., with ciprofloxacin or trimethoprim-sulfamethoxazole) for prevention.
  • Handwashing, thorough asepsis, equipment sterilisation, disinfection, constraint in intravenous treatment, and stringent care to maintain the urinary tract’s sterility are all necessary for their management (ie, closed drainage).

References and Sources

  • Ananthanarayan and Paniker. Textbook of Microbiology.
  • Bailey and Scott’s Diagnostic Microbiology. Part 3. Section 7. Chapter 22. Enterobacteriaceae, 323.
  • Mackie and McCartney Practical Medical Microbiology. Section B. Bacteria and Related Organisms. Chapter 20. Escherichia, 361.
  • Murray, P. R., Rosenthal, K. S., & Pfaller, M. A. (2013). Medical microbiology. Philadelphia: Elsevier/Saunders
  • Sastry A.S. & Bhat S.K. (2016). Essentials of Medical Microbiology. New Delhi: Jaypee Brothers Medical Publishers.
  • Scaletsky, I. C., Fabbricotti, S. H., Carvalho, R. L., Nunes, C. R., Maranhão, H. S., Morais, M. B., & Fagundes-Neto, U. (2002). Diffusely adherent Escherichia coli as a cause of acute diarrhea in young children in Northeast Brazil: a case-control study. Journal of clinical microbiology, 40(2), 645-8.
  • Subhash Chandra Parija. Textbook of Microbiology & Immunology.
  • Topley and Wilson’s Microbiology and Microbial Infection. Bacteriology Volume 2. Part VI. Organisms and their biology. Chapter 36. Escherichia, 1360.
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