General characteristics of the Enterobacteriaceae family
Enterobacteria are a large family of Gram-negative rod-shaped bacteria that inhabit primarily the large intestine of humans and animals. Many species are part of the normal microflora, while others are obligate or opportunistic pathogens causing intestinal and extraintestinal infections. Clinically significant genera belonging to this family include Escherichia, Salmonella, Shigella, Klebsiella, Proteus, Yersinia, Enterobacter, and Serratia.
All enterobacteria share four key characteristics:
- Facultative anaerobes — grow both in the presence and absence of oxygen.
- Ferment glucose with the production of acid (and sometimes gas); the ability to ferment other sugars (lactose, sucrose, mannitol) varies and is used for differentiation.
- Oxidase-negative — lack cytochrome c oxidase.
- Reduce nitrates to nitrites at one of the metabolic stages.
These features distinguish enterobacteria from clinically significant non-fermenting Gram-negative bacteria, such as Pseudomonas aeruginosa, a strict aerobe that is oxidase-positive, does not ferment glucose, and does not reduce nitrates.
Pathogenicity factors
The cell wall of all enterobacteria contains endotoxin — lipid A, which is a component of the lipopolysaccharide (LPS) characteristic of Gram-negative bacteria. The release of endotoxin upon microbial death is accompanied by fever, hypotension, activation of the complement and coagulation systems, and, in severe cases, septic shock.
Many species produce exotoxins. For example, E. coli and Vibrio cholerae (a family closely related to enterobacteria) secrete enterotoxins that activate adenylate cyclase in small intestinal enterocytes, leading to secretory diarrhea. Shigellae produce Shiga toxin with cytotoxic action.
Antigenic structure
Serological differentiation of enterobacteria is based on a set of antigens:
- O-antigen — somatic, represented by the variable polysaccharide part of the cell wall LPS; determines the serogroup.
- H-antigen — flagellar protein (flagellin); present only in motile species (Salmonella, Escherichia, Proteus).
- K-antigen — capsular polysaccharide antigen found in species that form a capsule (e.g., Klebsiella).
- Vi-antigen — a specific variant of the capsular antigen in Salmonella Typhi, the causative agent of typhoid fever; associated with virulence.
Laboratory diagnostics
The basis of diagnosis is the bacteriological method. Material is inoculated simultaneously onto blood agar and selective-differential media containing lactose: Endo agar, MacConkey agar, and eosin methylene blue (EMB) agar. Lactose-positive colonies (E. coli, Klebsiella) become colored, while lactose-negative colonies (Salmonella, Shigella) remain colorless.
For in-depth biochemical identification, triple sugar iron (TSI) agar is used, which contains ferrous sulfate and three sugars: glucose, lactose, and sucrose. The medium is poured as a butt with a slanted surface; the bottom is the anaerobic zone, and the slant is the aerobic zone. Possible results include:
- Fermentation of lactose and/or sucrose — yellowing of the entire medium (both slant and butt) due to a large amount of acid.
- Fermentation of glucose only — only the butt turns yellow, while the slant remains red (acid is oxidized in the aerobic zone).
- Absence of fermentation — the color of the medium does not change.
- Gas production — bubbles and fissures in the agar.
- H₂S production — blackening of the medium due to the formation of iron sulfide (FeS).
Urea agar is used to detect the enzyme urease. Under the action of urease, urea is split into ammonia and CO₂, the medium becomes alkaline, and the phenol red indicator changes color from orange to purple. Urease is a pathogenicity factor in Proteus and Helicobacter pylori.
Additionally, motility (presence of flagella) is evaluated, which is important for identification and understanding pathogenesis — for example, the ascending spread of E. coli through the urinary tract. Serological methods are represented by agglutination reactions with specific sera.
Principles of treatment
Treatment of infections caused by enterobacteria is based on antibiotic therapy. Before the results of culture and antibiogram are available, broad-spectrum drugs are prescribed empirically, after which therapy is adjusted according to the pathogen's susceptibility.
Applicable antibiotic groups include:
- Penicillins and cephalosporins — inhibit cell wall synthesis.
- Aminoglycosides, tetracyclines, chloramphenicol — disrupt protein synthesis on ribosomes.
- Fluoroquinolones — block DNA gyrase.
- Sulfonamides — competitive inhibitors of folic acid synthesis.
A serious problem is antibiotic resistance. Many strains produce β-lactamases, including extended-spectrum β-lactamases (ESBLs), which destroy the β-lactam ring of penicillins and cephalosporins. Modifications of drug targets and the action of efflux pumps are also possible. In such cases, inhibitor-protected β-lactams, carbapenems, or combination therapy are used.
Key points
- Enterobacteria are Gram-negative facultatively anaerobic bacilli of the intestinal microflora.
- Four general characteristics: glucose fermentation, oxidase negativity, reduction of nitrates to nitrites, facultative anaerobiosis.
- Endotoxin is lipid A of the cell wall LPS; a number of species also produce exotoxins.
- Key antigens: O, H, K, and Vi-antigen in S. Typhi.
- Differentiation on lactose-containing media (Endo, MacConkey, EMB) and TSI medium.
- The urease test detects Proteus, H. pylori; H₂S production causes blackening of TSI.
- Basic therapy involves β-lactams, aminoglycosides, and fluoroquinolones after an antibiogram.
- The main mechanism of resistance is the production of β-lactamases, including ESBLs.