Taxonomy and morphology
Escherichia coli belongs to the genus Escherichia of the family Enterobacteriaceae and is a classic representative of gram-negative bacteria of the large intestine. For exam purposes, it is sufficient to know the genus — Escherichia, and the species — coli.
Morphologically, they are straight rods, motile due to peritrichously arranged flagella. A number of strains have a microcapsule made of a sialic acid homopolymer; such strains are designated as K+. Cell dimensions are important in comparative characterization with other enterobacteria (Vibrio cholerae, Campylobacter, etc.).
Tinctorial, biochemical, and cultural properties
By Gram stain, the bacteria stain red — gram-negative. Biochemical characterization is the key to identification within the Enterobacteriaceae family:
- ferment glucose and lactose with gas production;
- do not utilize urea;
- produce indole from tryptophan;
- do not produce hydrogen sulfide;
- decarboxylate lysine, use acetate as the sole carbon source.
E. coli is a facultative anaerobe. It is cultivated on blood agar, Endo agar, MacConkey agar, and Russell's medium. On Russell's medium, fermentation of lactose and glucose results in yellowing of both the slant and the butt with agar cracks (gas production). On solid media, it forms S-form colonies (smooth, shiny) or R-form colonies (rough); the colony type depends on the structure of the cell wall lipopolysaccharide. In liquid media, it causes uniform turbidity with a bottom sediment.
Antigenic structure and pathogenicity factors
Three types of antigens are distinguished, which determine serogroups and serovars:
- O-antigen — somatic, determines the serogroup;
- K-antigen — capsular;
- H-antigen — flagellar.
Pathogenicity factors include pili (adhesins), microcapsule (protection against phagocytosis), endotoxin (LPS, common to all gram-negative bacteria), as well as exotoxins — heat-labile and heat-stable enterotoxins, and Shiga-like toxins.
Ecology and strain categories
E. coli is an obligate representative of the microflora of the large intestine. It performs a protective function (antagonism against pathogens), participates in the synthesis of vitamins B, E, and K, and partially digests fiber. When immunity decreases, opportunistic strains cause endogenous infections; the ability to develop drug resistance is well known.
Pathogenic E. coli are divided into causative agents of parenteral escherichiosis (uropathogenic — UPEC, as well as strains causing neonatal sepsis and meningitis) and diarrheagenic ones. Among the latter, five categories are distinguished:
- ETEC (enterotoxigenic) — cholera-like watery diarrhea; heat-labile and heat-stable enterotoxins encoded by a plasmid; small intestine colonization factors;
- EIEC (enteroinvasive) — dysentery-like disease; invasion of the large intestinal epithelium via IpA antigens and VirG proteins (actin assembly);
- EPEC (enteropathogenic) — diarrhea in infants in the first year of life; type IV pili, intimin protein, type III secretion system; contact transmission route;
- EHEC (enterohemorrhagic) — hemorrhagic colitis; Shiga-like toxins encoded by bacteriophages, serine protease (disrupts clotting, acts on factor V), hemolysin; source — cattle;
- EAEC (enteroaggregative) — persistent diarrhea; adhesins, dispersin protein, biofilm formation, heat-stable toxin.
Clinical presentation and immunity
Clinical forms of escherichiosis are diverse: intestinal infections, urinary tract infections (pyelonephritis, cystitis), neonatal meningitis and sepsis, peritonitis, and "traveler's diarrhea". EHEC causes bloody diarrhea with crampy abdominal pain and fever as a manifestation of intoxication syndrome.
Parenteral escherichioses occur predominantly against the background of immunodeficiency; persistent immunity is not formed. In intestinal forms, local immunity mediated by secretory IgA develops. In infants in their first year of life, protection is provided by passive transplacental immunity (IgG) and breast milk; intestinal colonization by bifidobacteria is completed by the fifth day of life.
Laboratory diagnostics, treatment, and prevention
Material for research depends on the form of infection: stool in intestinal escherichioses; urine, wound discharge, blood, and CSF in parenteral ones. Stages:
- microscopy of a Gram-stained smear;
- inoculation onto differential diagnostic lactose-containing media (Endo, MacConkey);
- biochemical identification (indole+, lysine decarboxylase+, acetate utilization, motility);
- serological identification in the agglutination reaction with O- and H-sera to determine the serogroup.
Treatment depends on the focus of infection and the antibiotic resistance of the strain. In diarrheagenic escherichiosis, antibiotic therapy is generally not indicated; the mainstay of treatment is rehydration and restoration of water and electrolyte balance. Specific prevention (vaccine) has not been developed. Non-specific measures: compliance with sanitary and hygienic rules, avoidance of raw water and thermally unprocessed foods, timely replacement of urinary and intravenous catheters, and maintenance of immunity (vitamin C, including cranberry juice).
Key points
- E. coli is a gram-negative motile rod, peritrichous, facultative anaerobe of the large intestine.
- Biochemical profile: lactose+, glucose+, indole+, H₂S−, urea−.
- Antigenic structure: O (serogroup), K (capsule), H (flagella).
- Five categories of diarrheagenic Escherichia: ETEC, EIEC, EPEC, EHEC, EAEC.
- EHEC produces Shiga-like toxins and causes hemorrhagic colitis.
- Extraintestinal forms: UTIs, neonatal meningitis and sepsis, peritonitis.
- Protection in the intestinal form is provided by secretory IgA; in infants, by maternal IgG and breast milk.
- The basis of diarrhea treatment is rehydration; vaccine prophylaxis is absent.