Enterobacteriaceae Characteristics and Pathogenesis
Physiology and Structure of Enterobacteriaceae
Enterobacteria are Gram-negative bacilli ranging from 1 to 6 μm in size. They are non-spore-forming, generally motile, and function as facultative anaerobes. Some species possess capsules, fimbriae, and pili.
These bacteria utilize a wide variety of enzymes, which are used for biochemical diagnosis. They are nutritionally undemanding, ferment glucose, reduce nitrate, and are catalase-positive and oxidase-negative.
Clinical Significance and Pathogenic Species
The Enterobacteriaceae family includes several clinically relevant species:
- Citrobacter freundii and C. koseri
- Enterobacter aerogenes and E. cloacae
- Escherichia coli
- Klebsiella pneumoniae and K. oxytoca
- Morganella morganii
- Proteus mirabilis and P. vulgaris
- Salmonella enterica
- Serratia marcescens
- Shigella sonnei and S. flexneri
- Yersinia pestis, Y. enterocolitica, and Y. pseudotuberculosis
Habitat and Ecological Niche
Their common habitats include soil, water, vegetation, and the intestines of animals. Some species have a limited ecological niche, such as Salmonella typhi, which is found only in humans.
Associated Infections
While common in the intestine, they can colonize the perianal and perigenital regions. They may cause extraintestinal infections involving Enterobacter cloacae, E. coli, Klebsiella spp., Proteus spp., Citrobacter spp., Serratia spp., and Morganella spp.
Key associated infections include:
- Respiratory infections
- Wound and soft tissue infections
- Bacteremia and Central Nervous System (CNS) infections
- Septicemia: 30%–35% of cases
- Urinary Tract Infections (UTI): 70% of cases
- Intestinal infections
Antigenic Structure and Classification
The serological classification of Enterobacteria is based on cell wall antigens:
- Antigen O (Somatic): Located in the bacterial cell wall; consists of polysaccharides.
- Antigen H (Flagellar): Located in the flagella; proteinaceous and thermolabile.
- Antigen K (Capsular): Formed by polysaccharides; thermolabile.
The thermoset lipopolysaccharide consists of the somatic O polysaccharide, common polysaccharide antigens, and Lipid A (endotoxin).
Pathogenesis and Immunity
Virulence is driven by several factors, including endotoxins, capsules, antigenic variation, sequestration of growth factors, and resistance to serum bactericidal effects.
Key Virulence Mechanisms
- Endotoxin: Triggers complement activation, cytokine release, leukocytosis, thrombocytopenia, disseminated intravascular coagulation (DIC), fever, endotoxic shock, and death.
- Capsule: Protects against phagocytosis by repelling phagocytes via hydrophilic surfaces. It interferes with antibody binding and is poorly immunogenic.
- Antigenic Phase Variation: Regulates the expression of K and H antigens, protecting the bacteria from antibody-mediated cell death.
- Type III Secretion System: A critical virulence factor; its absence renders the bacteria non-pathogenic.
- Sequestration of Growth Factors: Bacteria use siderophores (such as enterobactin and aerobactin) and hemolysins to compete for iron (Fe) from hemoglobin, myoglobin, lactoferrin, and transferrin.
- Resistance to Serum Bactericidal Effect: Evasion of the complement system to avoid bacterial elimination.
- Antimicrobial Resistance: Often encoded on transferable plasmids that are interchangeable between species, genera, and families of bacteria.