Commensal Flora
Normally, E. coli is an obligate representative of the intestinal and vaginal microflora. In the colon, the bacterium performs several crucial functions:
- Antagonistic: suppresses the proliferation of Candida fungi, putrefactive flora, and pathogenic enteric bacteria.
- Synthetic: participates in the production of vitamins B, E, and K.
- Metabolic: assists in the breakdown of dietary fiber.
Pathology occurs only in cases of immunodeficiency or when the bacterium enters an unusual niche. This can lead to wound suppuration, secondary pneumonia, or sepsis. In hospital settings, opportunistic strains can acquire R-plasmids, becoming multidrug-resistant agents of nosocomial infections.
Antigenic Structure and Masking Phenomenon
Strain designation uses an antigenic formula (e.g., O12:B6:H2) based on three components:
- O-antigen (over 170 types) determines the serogroup.
- K-antigen (over 97 types, includes types A, B, L) 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 mask the somatic O-antigen. To perform an agglutination reaction and detect the O-antigen, the bacterial culture must be boiled, which destroys the surface layer.
Parenteral (Extraintestinal) Escherichia Infections
Pathogenic strains differ from normal flora by possessing pathogenicity islands, virulence plasmids, or converting phages.
Extraintestinal infections are most frequently caused by uropathogenic strains (urinary tract infections) and agents of generalized disease. The latter are extremely dangerous for newborns: E. coli causes up to 80% of neonatal meningitis cases. Infection occurs during passage through the birth canal. The key virulence factor here is the sialic acid polymer microcapsule, which blocks complement activation and protects the bacterium from phagocytosis (opsonization).
Diarrheagenic Escherichia coli
Agents of acute intestinal infections are divided into several pathogenic groups:
- Enterotoxigenic (ETEC): colonize the small intestine. They secrete heat-labile (similar to cholera toxin) and heat-stable enterotoxins that activate cellular enzyme systems and cause profuse watery diarrhea.
- Enteroinvasive (EIEC): invade the colonic epithelium, multiply intracellularly, and destroy cells. Clinically resembles shigellosis.
- 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 (infection via meat). They produce Shiga-like toxins and a serine protease that cleaves coagulation factor V. They can trigger severe hemolytic uremic syndrome (HUS).
- Enteroaggregative (EAEC): form a thick mucous biofilm resembling a "stacked brick" pattern. Cause prolonged, persistent diarrhea.
Diagnosis and Immunity
Specimens for culture include stool (for 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. Differentiating pathogenic strains from normal flora relies on determining O-serogroups.
Local immunity following 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 sanitation and hygiene.