Opportunistic flora
Normally, E. coli is an obligate member of the intestinal and vaginal microflora. In the large intestine, the bacterium performs several crucial functions:
- Antagonistic: inhibits the proliferation of fungi of the genus Candida, putrefactive flora, and pathogenic intestinal bacteria.
- Synthetic: participates in the production of vitamins B, E, and K.
- Metabolic: assists in breaking down fiber.
Diseases occur only during immunodeficiencies or when the bacterium enters an uncharacteristic habitat. This can lead to wound suppuration, secondary pneumonia, or sepsis. In hospitals, opportunistic strains can acquire R-plasmids, becoming multiresistant causative agents of nosocomial infections.
Antigenic structure and masking phenomenon
An antigenic formula (e.g., O12:B6:H2) is used to designate strains. It is based on three components:
- O-antigen (over 170 types) determines the serogroup.
- K-antigen (over 97 types, comes in A, B, L types) is a surface antigen.
- H-antigen (over 57 types) determines the serovar.
An interesting feature is the O-inagglutinability phenomenon. The capsular K-antigen can physically block the somatic O-antigen. To perform the agglutination reaction and identify the O-antigen, the bacterial culture must be boiled, which destroys the surface layer.
Parenteral (extraintestinal) escherichiosis
Pathogenic strains differ from normal flora by the presence of pathogenicity islands, virulence plasmids, or converting phages.
Extraintestinal infections are most frequently caused by uropathogenic strains (urinary tract infections) and agents of generalized forms. The latter are extremely dangerous for newborns: E. coli causes up to 80% of neonatal meningitis. Infection occurs during passage through the birth canal. A key virulence factor here is a microcapsule made of sialic acid polymer, which blocks complement activation and protects the bacterium from phagocytosis (opsonization).
Diarrheagenic Escherichia coli
Causative agents of acute intestinal infections are divided into several pathogroups:
- Enterotoxigenic (ETEC): colonize the small intestine. Release a heat-labile (resembling cholera toxin) and heat-stable enterotoxigenic factors that activate cell enzyme systems and cause profuse watery diarrhea.
- Enteroinvasive (EIEC): invade the epithelium of the large intestine, multiply inside cells, and destroy them. Clinically, this resembles dysentery.
- Enteropathogenic (EPEC): a frequent cause of diarrhea in infants. They attach to the small intestine and flatten its epithelium, destroying microvilli.
- Enterohemorrhagic (EHEC): cause bloody diarrhea and affect the large intestine. Cattle serve as the reservoir of infection (transmission via meat). They produce Shiga-like toxins and serine protease, which destroys coagulation factor V. They can trigger severe hemolytic uremic syndrome.
- Enteroaggregative (EAEC): form a thick mucous biofilm resembling a "brick wall." Cause prolonged persistent diarrhea.
Diagnostics and immunity
Specimens for culture include feces (in intestinal forms), urine, blood, or wound discharge. Inoculation is performed on lactose-containing differential media (e.g., Endo agar) and incubated for 18 hours at 37 °C. Determining O-serogroups helps differentiate pathogenic strains from normal flora.
Local immunity after intestinal infections is mediated by secretory IgA. In infants, protection is provided by maternal IgG, breastfeeding, and early colonization of the intestine with bifidobacteria (by the 5th day of life). Specific vaccines have not been developed; prevention relies on compliance with sanitary standards.
Briefly: answers to topical questions
What specific virulence factors (adhesins, toxins) do uropathogenic E. coli strains possess?
Uropathogenic strains of Escherichia coli possess specific virulence factors that provide adhesion, protection against the immune system, and toxic effects.
- Fimbriae (pili) provide adhesiveness, allowing bacteria to attach to uroepithelial cells and migrate retrogradely against the urine flow.
- Capsular K-antigens determine anti-phagocytic activity by blocking the processes of opsonization, phagocytosis, and complement-dependent bactericidal action of blood.
- Hemolysin is a toxin whose production stimulates bacterial colony growth and increases the resistance of microorganisms to antibiotic therapy.
What differential-diagnostic nutrient media are used for bacteriological culture of Escherichia coli?
Differential lactose-containing nutrient media are used for the bacteriological culture of Escherichia coli.
- Endo agar is used for culturing the test material, except for blood.
- Eosin Methylene Blue (EMB) agar (Levine's formulation) is used for the isolation of enterobacteria.
During microbiological diagnostics of escherichioses, specimens other than blood are inoculated onto differential lactose-containing media, such as Endo and Levine agars. On solid media, Escherichia form S-form or R-form colonies.
Which antibiotic groups are the drugs of choice for etiotropic treatment of extraintestinal escherichiosis?
In the cited sources, the drugs of choice for extraintestinal escherichiosis are specified using urinary tract infections during pregnancy as an example.
- Oral 3rd-generation cephalosporins: the susceptibility of Escherichia coli to cefixime is >90%, making them the drugs of choice in empirical UTI therapy.
- Fosfomycin: activity against E. coli is 95.6%.
- Nitrofurantoin: activity against E. coli is 100%.
In other cases, sources indicate that antibiotics are prescribed after determining the antibiogram of the isolated pathogen.
It is easy to remember the causative agents of infant nosocomial diarrhea: EPEC = EnteroPathogenic = Pediatric (children in their first year of life).
Class and exam questions
Why can infection with ETEC lead to the development of immunity against cholera?
The heat-labile enterotoxin (LT) of Escherichia shares structural homology with cholera toxin (especially their B-subunits), leading to the development of cross-immunity.
How to differentiate the dangerous EHEC O157 strain in the laboratory?
Unlike most other strains, the O157 serovar is unable to ferment sorbitol. This property is used as a reliable metabolic marker in bacteriological culture.
What is the mechanism of penetration in enteroinvasive strains?
They use specific surface proteins (IPA antigens) to invade large intestine cells, and the VirG protein ensures the assembly of cellular actin for their movement inside the epitheliocyte.
What else to study on this topic
- Genetic control of virulence factors: the role of converting phages, pathogenicity islands, and plasmids
- Molecular mechanism of action of heat-stable and heat-labile enterotoxins of ETEC
- Pathogenesis of hemolytic uremic syndrome (HUS) in enterohemorrhagic strain infection
- Structural features of the K1 microcapsule and the mechanism of evasion from the complement system
- The "attaching and effacing" phenomenon at the cellular level
Study the full topic in the «Microbiology» course
This is a summary. The course covers everything tested in classes and exams.
- Complete study guide on "Escherichia coli" and 4,383 other subject pages
- Assignments and quizzes after every topic — just like in a colloquium
- AI tutor answers questions on the topic anytime
- 141 video lectures on the subject
Other topics in the section "Gram-negative facultatively anaerobic rods (Enterobacteriaceae, Vibrio, Haemophilus, Pasteurella)"
Free video lessons: microbiologyShort lessons with study notes — no registration required.
Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.