BSCI 424 — PATHOGENIC MICROBIOLOGY — Fall 2000


Enterobacteriaceae Summary


Morphology & Physiology:

  Small Gram-negative non-sporeforming enteric bacilli

  All Enterobacteriaciae:

    1. ferment glucose with acid production

    2. reduce nitrates (NO3 to NO2 or all the way to N2)

    3. are oxidase negative

  All are aerobic but can be facultatively anaerobic

  Motile via peritrichous flagella except Shigella and Klebsiella which are non-motile

  Capsule, slime layer, or neither

  Possess fimbriae (pili)

  Complex cell wall

  Antigenic Structure: plays an important role for some species in epidemiology and classification

 K (capsular) antigens: capsular polysaccharide, particularly heavy in Klebsiella

 H (flagellar) antigens: flagellar proteins of motile genera and species; used for typing; absent in nonmotile genera (Shigella and Klebsiella)
 O (somatic) antigens: O-specific polysaccharide side chain of lipopolysaccharide; used for typing
  Biochemically and metabolically diverse; ferment glucose by the mixed acid pathway; Klebsiella, Enterobacter and Serratia utilize the butanediol pathway

Taxonomy of Enterobacteriaceae:

  Over 30 genera and 120 species

  More than 95% of clinically significant strains fall into 10 genera and less than 25 species

  Family Enterobacteriaceae (clinically important enterics)

 Citrobacter
 Citrobacter freundii  
  Citrobacter diversus
  Enterobacter spp.
 Enterobacter aerogenes  
  Enterobacter agglomerans
  Enterobacter cloacae
  Escherichia coli
 Opportunistic Escherichia coli 
  ETEC = enterotoxigenic E. coli
  EIEC = enteroinvasive E. coli  
  EPEC = enteropathogenic E. coli 
  EHEC = enterohemorrhagic E. coli
  EaggEC = enteroaggregative E. coli
  UPEC = uropathogenic E. coli
   Klebsiella spp.
  Klebsiella pneumoniae  
  Klebsiella oxytoca
  Morganella morganii
  Proteus spp.
  Proteus mirabilis
  Proteus vulgaris
  Providencia spp.
 Providencia alcalifaciens  
  Providencia rettgeri
  Providencia stuartii
 Salmonella spp.
 Salmonella enterica (proper nomenclature; encompasses all Salmonella; taxonomically only one species of Salmonella
  Common nomenclature still in use:
Salmonella typhi
Salmonella paratyphi
Salmonella enteritidis
Salmonella cholerasuis
Salmonella typhimurium
 Serratia spp.
  Serratia marcesans
  Serratia liquifaciens
 Shigella spp.
 Shigella dysenteriae  
  Shigella flexneri
  Shigella boydii
  Shigella sonnei
 Yersinia spp.
  Yersinia enterocolitica
  Yersinia pestis
  Yersinia pseudotuberculosis

Clinical Syndromes:

  Some members of the Enterobacteriaceae are true pathogens

 Salmonella spp.

 Shigella spp.
 Yersinia spp.

  Certain strains of Escherichia coli
 
  ETEC = enterotoxigenic E. coli
  EIEC = enteroinvasive E. coli  
  EPEC = enteropathogenic E. coli 
  EHEC = enterohemorrhagic E. coli
  EaggEC = enteroaggregative E. coli
  UPEC = uropathogenic E. coli

  Most members of the Enterobacteriaceae are opportunistic or cause secondary infections of wounds, the urinary and respiratory tracts, and the circulatory system

 Gram-negative sepsis
 Life-threatening
  Usually nosocomial
  Commonly caused by E. coli
  Clinical Progression:
  Early Phase (REVERSIBLE)
      Decrease in arterial resistance; Increased cardiac output
      Kinins (protein) in plasma due to tissue damage, endotoxin, or antigen-antibody complexes
  Second Phase (REVERSIBLE)
      Increase in arterial resistance; Decreased cardiac output
  Third Phase (IRREVERSIBLE) Vascular collapse with organ failure

 Urinary tract infections

 Greatest incidence in young individuals and middle-aged females
  Incidence increases with age in males
  Most commonly caused by E. coli
  Diagnosis by microscopic and cultural examination of urine
   Obtain urine by catheter through urethra into bladder, suprapubic tap

 Pneumonia

 Nosocomial; Spread by personnel and equipment
  Frequently caused by K. pneumoniae
  Often in middle-aged males who abuse alcohol
  Difficult to diagnose because of commensals in sputum

 Abdominal sepsis

 Caused by flora of the gastrointestinal tract
  Infections usually polymicrobi

 Meningitis

 Usually nosocomial
  Frequently caused by E. coli
  Diagnosis by microscopic and cultural examination of cerebrospinal fluid

 Spontaneous bacterial peritonitis

 Usually in patients with liver ailments
  Commonly caused by E. coli, but also anaerobes and Gram-positive cocci (S. pneumoniae)

 Endocarditis

 Vascular endocardial surface inflammation
  Mostly caused by Gram-positive cocci, but 1-3% caused by aerobic Gram-negative rods
  Diagnosis by blood culture
  Difficult to treat; treatment is of long duration

Epidemiology:

  Found in soil, water and decaying matter

  Some of the normal inhabitants of the small and large intestine included in the family: therefore, are sometimes referred to as enteric bacilli or simply enterics

  Enterics are responsible for a majority of nosocomial infections

 About two million patients per year in the United States are estimated to acquire nosocomial infections

 Approximately 5% to 10% of the total hospital population acquire such infections

Pathogenesis & Immunity:

  Endotoxin: important virulence factor with wide-ranging effects on host

  Capsule: antiphagocytic

  Antigenic phase variation: capability to alternately express or not express either capsule or flagella and thus avoid host immunity

  Sequestration of nutritional factors, in particular, iron by production of siderophores which are extracellular iron-chelating compounds (e.g., enterobactin, aerobactin)

 Iron is important compound for both host and pathogen and is limited in supply and thus must be competed for

 Much of iron in host body is sequestered in heme proteins (e.g., hemoglobin, myoglobin) and in iron-chelating proteins (e.g., transferrin, lactoferrin)

  Resistance to serum killing: many bacteria are inherently sensitive to nonspecific bloodborne components and to circulating complement and the resultant complement-mediated clearance, but Enterobacteriaceae and other bloodborne pathogens can resist such killing

  Antimicrobial resistance

  True pathogenic members of the Enterobacteriaceae may possess specific virulence features, which are unique to individual genera or species

 Adhesins

 Exotoxins, (e.g., enterotoxins which act in the small intestine)

  Antigens which stimulate antibody production by the host include:

Laboratory Identification:

  Specimens whether pus, tissue, sputum, fluids, rectal swabs, or feces should be cultured immediately or placed on special media to prevent overgrowth

  Special isolation media: contain various substances including indicators, inhibitors, etc.

  Media and tests to differentiate the genera of the family

  Tests that divide species of the genera, e.g., patterns of acid production from various carbohydrates

  Various species differ in the carbohydrates from which acid may be produced and end products that may be formed from various substrates

  Culture:

 Colony morphology: moist, gray (except Serratia marcescans which appears red) smooth colonies on non-selective media

 Special differential and selective media used for separation of genera and species

 Some strains are beta hemolytic on blood agar

Treatment, Prevention & Control:

  Major problem

  Various options; must consider resistance

 


Miscellaneous Opportunists of the Enterobacteriaceae

Citrobacter: environmental sources and in feces of man and animals

Enterobacter: inhabit soil and water and to a lesser extent, the human intestine

Serratia: inhabitants of water and soil

Morganella / Providencia: airborne organisms that frequently colonize burn wounds and are often antibiotic resistant in vivo

Edwardsiella: rarely causes wound infections; also rarely seen in sepsis, meningitis, and gastroenteritis in humans

   Go to Pathogen List

 

 

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Revised: August 2000
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