General Characteristics and Morphology
The family is characterized by immense diversity and is the largest group among pathogenic and opportunistic bacteria. The DNA GC-content is highly heterogeneous: microorganisms range from low GC-content (38–42% in Proteus and Providencia) to high GC-content (52–60% in Klebsiella and Enterobacter). The type genus Escherichia, along with Shigella and Salmonella, occupy a central position with 50–53% GC-content.
Enterobacteriaceae are small to medium-sized Gram-negative rods (1–5 × 0.4–0.8 µm). They never form spores, although some genera can synthesize a protective polysaccharide capsule. Many species are motile via peritrichous flagella, but non-motile species also exist.
Physiology and Biochemical Properties
Most enterobacteria are non-fastidious and grow readily on standard nutrient media. In liquid media, they cause diffuse turbidity, while on solid media they form convex, shiny colonies (mucoid if a capsule is present). The optimal growth temperature is typically 37 °C, with the exception of the genus Yersinia, whose members exhibit peak metabolic activity at lower temperatures.
In terms of respiration, they are facultative anaerobes combining fermentative and respiratory metabolism. Key differential features of the family include a negative oxidase test, a positive catalase test, and the ability to reduce nitrates (nitrate reductase).
Glucose is fermented with acid production via one of two pathways:
- Mixed acid fermentation: Produces numerous organic acids and sometimes gas. Detected by the methyl red test.
- Butanediol fermentation: End products include 2,3-butanediol and ethanol. Detected by the Voges-Proskauer test.
Virulence Factors
The synthesis of aggression factors in enterobacteria is encoded by genes located on specialized pathogenicity islands, plasmids, or within converting bacteriophage genomes. Major factors include:
- Endotoxin (somatic O-antigen) — present in all species and released only upon bacterial cell wall lysis.
- Exotoxins — heat-stable and heat-labile enterotoxins, as well as various cytotoxins.
- Adhesion factors — type IV pili and type III secretion system (T3SS) filamentous structures necessary for epithelial attachment.
- Aggression enzymes — DNase, phosphatase, neuraminidase.
- Capsule — reliably protects the microbe from phagocytosis and complement-mediated lysis.
Types of Interaction with Intestinal Epithelium
The mechanism of infection depends on the depth of tissue penetration and degree of cellular damage:
- Superficial without damage: Bacteria (e.g., enterotoxigenic E. coli) multiply directly on the cell surface without disrupting the intestinal architecture.
- Superficial with damage: Microbes destroy microvilli, causing a cytopathic effect on the apical surface (enteropathogenic and enterohemorrhagic E. coli).
- Invasive with cytotoxicity: Bacteria invade large bowel enterocytes, multiply inside them, and cause cell death (Shigella species, enteroinvasive E. coli).
- Transcithosis and systemic spread: Pathogens penetrate through M cells into Peyer's patches, subsequently multiplying within macrophages (Salmonella and Yersinia species).