E. coli- Pathogenicity and Clinical Manifestations

E. coli- Pathogenicity and Clinical Manifestations

  • E. coli is the most common and important member of the genus Escherichia.
  • It is a Gram-negative, facultative anaerobic, rod-shaped bacterium that is commonly found in the lower intestine of warm-blooded organisms (endotherms).
  • Human Escherichia coli strains are classified as commensal microbiota E. coli, enterovirulent E. coli, and extraintestinal pathogenic E. coli on the basis of their genetic features and clinical outcomes.
  • Most infections (with the exception of neonatal meningitis and gastroenteritis) are endogenous; that is, the E. coli that are part of the patient’s normal microbial flora are able to establish infection when the patient’s defenses are compromised (e.g., through trauma or immune suppression).
  • This organism is associated with a variety of diseases, including gastroenteritis and extra-intestinal infections such as UTIs, meningitis, and sepsis.
  • A multitude of strains are capable of causing disease, with some serotypes associated with greater virulence.

E. coli- Pathogenicity and Clinical Manifestations

Image Source: https://doi.org/10.1038/nrmicro818 and https://doi.org/10.1371/journal.ppat.1006238

Pathogenicity

Virulence Factors

  • E. coli possesses a broad range of virulence factors.
  • In addition to the general factors possessed by all members of the family Enterobacteriaceae, Escherichia strains possess specialized virulence factors that can be placed into two general categories: adhesins and exotoxins.

ETEC (Enterotoxigenic E. coli):

  • Colonization factor antigens (CFA/I, CFA/II, CFA/III)
  • Heat-labile toxin (LT-1); heat-stable toxin (STa)

EPEC (Enteropathogenic E. coli):

  • Bundle Forming Pili (BFP); intimin

EAEC (Enteroaggregative E. coli):  

  • Aggregative adherence fimbriae (AAF/I, AAF/II, AAF/III)
  • Enteroaggregative heat-stable toxin; plasmid-encoded toxin

STEC (Shiga toxin-producing E. coli):

  • BFP; intimin
  • Shiga toxins (Stx1, Stx2)

EIEC (Enteroinvasive E. coli):

  • Invasive plasmid antigen
  • Hemolysin (HlyA)

Uropathogens

  • P pili
  • Dr fimbriae

Pathogenesis

Gastroenteritis

  • ETEC causes traveler’s diarrhea or infant diarrhea in infants. Pathogenesis involves plasmid-mediated, heat-stable (ST) and heat-labile (LT) enterotoxins that stimulate hypersecretion of fluids and electrolytes.
  • EPEC causes infant diarrhea in developing countries. Pathogenesis involves plasmid-mediated A/E histopathology, with disruption of normal microvillus structure resulting in malabsorption and diarrhea.
  • EAEC causes infant diarrhea in developing and probably developed countries along with traveler’s diarrhea. Pathogenesis involves plasmid-mediated aggregative adherence of rods (“stacked bricks”) with shortening of microvilli, mononuclear infiltration, and hemorrhage; decreased fluid absorption.
  • STEC causes hemorrhagic colitis. STEC evolved from EPEC; A/E lesions with the destruction of intestinal microvilli, resulting in decreased absorption; pathology mediated by cytotoxic Shiga toxins (Stx1, Stx2), which disrupt protein synthesis
  • EIEC causes disease which is rare in developing and developed countries. Pathogenesis involves plasmid-mediated invasion and destruction of epithelial cells lining the colon.

Urinary Tract Infection

  • Most gram-negative rods that produce UTIs originate in the colon, contaminate the urethra, ascend into the bladder, and may migrate to the kidney or prostate.
  • Although most strains of E. coli can produce UTIs, the disease is more common with certain specific serogroups.
  • These bacteria are particularly virulent because of their ability to produce adhesins (primarily P pili, AAF/I, AAF/III, and Dr) that bind to cells lining the bladder and upper urinary tract (preventing elimination of the bacteria in voided urine) and hemolysin HlyA that lyses erythrocytes and other cell types (leading to cytokine release and stimulation of an inflammatory response).

Sepsis

  • When normal host defenses are inadequate, E coli may reach the bloodstream and cause sepsis.
  • Newborns may be highly susceptible to E coli sepsis because they lack IgM antibodies.
  • Sepsis may occur secondary to urinary tract infection.

Meningitis

  • E coli and group B streptococci are the leading causes of meningitis in infants.
  • Approximately 75% of E coli from meningitis cases have the K1 antigen.
  • This antigen cross-reacts with the group B capsular polysaccharide of N meningitidis.
  • The mechanism of virulence-associated with the K1 antigen is not understood.

Clinical Manifestations

Gastroenteritis

  • watery or bloody diarrhea
  • vomiting
  • cramps
  • nausea
  • low-grade fever
  • dehydration
  • abdominal cramps

Urinary tract infection

The most common bacteria found to cause UTIs is Escherichia coli (E. coli). Other bacteria can cause UTI, but E. coli is the culprit about 90 percent of the time. The major manifestations of the infection include:

  • A strong, persistent urge to urinate
  • A burning sensation when urinating
  • Pelvic pressure
  • Lower abdomen discomfort
  • Frequent, painful urination
  • Blood in urine

Acute bacterial meningitis

  • Newborns with E. coli meningitis present with fever and failure to thrive or abnormal neurologic signs.
  • Other findings in neonates include jaundice, decreased feeding, periods of apnea, and listlessness.
  • Patients younger than 1 month present with irritability, lethargy, vomiting, lack of appetite, and seizures.

References

  1. Murray, P. R., Rosenthal, K. S., & Pfaller, M. A. (2013). Medical microbiology. Philadelphia: Elsevier/Saunders
  2. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5156508/
  3. Sastry A.S. & Bhat S.K. (2016). Essentials of Medical Microbiology. New Delhi: Jaypee Brothers Medical Publishers.
  4. 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.
  5. https://cmr.asm.org/content/27/4/823
  6. https://bmcmicrobiol.biomedcentral.com/articles/10.1186/1471-2180-13-22
  7. https://cmr.asm.org/content/11/1/142
  8. https://nios.ac.in/media/documents/dmlt/Microbiology/Lesson-21.pdf
  9. https://www.mayoclinic.org/diseases-conditions/e-coli/symptoms-causes/syc-20372058
  10. https://emedicine.medscape.com/article/217485-clinical

E. coli- Pathogenicity and Clinical Manifestations

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2 thoughts on “E. coli- Pathogenicity and Clinical Manifestations”

  1. Is total Coliform
    and faecal Coliform interrelated to each other???
    In membrane filter technique,Total coliform and faecal coloform both can be seen ,but total coliform is absent and faecal coliform is present….can this be happen?

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