Enterobacteriaceae Intro and coli

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     Chapter 31
 “Enteric Bacteria”
 Gram-negative rods
 Ubiquitous
 Cause 30%-35% of all septicemias, more
  than 70% of UTIs, and many intestinal
 Pathogens:
     Normal flora – opportunistic infections
     Animal reservoirs
     Human carriers
 Box 31-1
BOX 31-1. Common Medically
Important Enterobacteriaceae
   Citrobacter freundii, Citrobacter koseri
   Enterobacter aerogenes, Enterobacter cloacae
   Escherichia coli
   Klebsiella pneumoniae, Klebsiella oxytoca
   Morganella morganii
   Proteus mirabilis, Proteus vulgaris
   Salmonella enterica
   Serratia marcescens
   Shigella sonnei, Shigella flexneri
   Yersinia pestis, Yersinia enterocolitica, Yersinia
Physiology and Structure
 Facultative anaerobes
 Ferment glucose, are catalase
  positive, and oxidase negative
 Lactose fermenting strains (e.g.
  Escherichia, Klebsiella, Enterobacter)
 Non-lactose fermenting (e.g.
  Salmonella, Shigella, and Yersinia)
Differentiating Similar Strains
Antigen detection
 O polysaccharides
   Part of LPS
 Capsular K
 Flagellar H proteins
 E. coli O157:H7
Pathogenesis and Immunity
Common virulence factors
 Endotoxin
   Lipid A portion of LPS causes many of the systemic
     manifestations of infection
 Capsule
   Interferes with antibody binding
   Capsular antigens are hydrophilic (phagocytic cell
     surface is hydrophobic)
   Poor antigenicity
 Antigenic phase variation
   Capsular K and flagellar H antigens are under genetic
   Can be expressed or not expressed
Pathogenesis and Immunity
 Sequestration of growth factors
   Iron: Bacteria produce competitive
    siderophores or iron-chelating
    compounds, hemolysins
Escherichia coli
Pathogenesis (Box 31-3)
 Adhesins: Essential for colonization
   Prevents the organism from being
    flushed out of the urinary or
    gastrointestinal tract
 Exotoxins
   Specific target tissue
   Result in altered cell function or cell
Epidemiology and Clinical Diseases
 Many infections are endogenous (septicemia and
 Septicemia-originate from UT or GI infections leading
  to intraabdominal infection
 Neonatal meningitis, Intraabdominal infections
 UTIs-originate in the colon -> contaminate urethra ->
  ascend into the bladder
   Production of adhesins
   ~80% of all community-acquired UTIs
 Gastroenteritis-caused by five major groups
   May include: watery diarrhea, abdominal cramps,
      fever, and vomiting
   (Table 31-1)
Gastroenteritis (ETEC)
   Estimated 80,000 cases in US travelers annually (650
    million worldwide)
   In small intestine; watery diarrhea, cramps, vomiting, fever
   Occurs in developing countries usually in children or
    travelers (traveler’s diarrhea)
   1-2 day incubation, 3-4 duration
   Infectious dose is high so person to person spread does not
   Two classes of enterotoxins: heat-labile (LT-I, LT-II) and
    heat-stable (STa, STb)
       LT-I increases secretion of chloride and inhibits absorption of
        sodium and chloride (the same as cholera toxin)
       STa causes a hypersecretion of fluids
           Both contributing to watery diarrhea
   Disease similar to cholera, but milder
Gastroenteritis (ETEC)

Imodium mode of action:
Gastroenteritis (EHEC)
 73,000 cases with 60 deaths annually
 In large intestine; vomiting, abdominal cramps, fever
 Severity ranges from diarrhea to hemorrhagic
  colitis (bacterial dysentery)
 3-4 day incubation, 4-10 day duration
 Infectious dose is less than 100 bacteria, O157:H7
  serotype is the most common
 Read text page 329
 Shiga toxins (Stx-1, Stx-2)
   Bind to 28S rRNA and disrupt protein synthesis
   Tissue destruction leads to the symptoms (bloody
Gastroenteritis (EHEC)
 Spinach Outbreak Information
Salmonella Characteristics
 Similar to E. coli except no lactose
 Historically there have been many
  different species (~2000)
   All are really one species:
   Salmonella enterica
Salmonella Virulence factors

 Box 31-2 and 31-5
 Some bacteria can survive stomach
 Able to enter M cells (peyer’s
 Cause cell death and spread to
  surrounding cells.
 Figure
  Colonize virtually all animal species
Salmonella Diseases
 Most common form of disease
   40,000 cases in the US in 2004
 Mostly spread by eating contaminated food
   (Poultry, eggs, dairy products)
 Can be fecal-oral in children
 Infectious dose 106 to 108
 Symptoms 6-48hrs after consumption
     nausea, vomiting, non-bloody
     diarrhea, fever, abdominal cramps
 Usually ends without intervention in a week
  or less
Salmonella Diseases
(Typhoid Fever)
 Typhoid Fever
 Human reservoir (person-to-person spread)
 Pass through intestinal lining and engulfed
  by phagocytes
   Replicate in liver, spleen, bone marrow
 Cause fever, myalgia, gastroenteritis
 Asymptomatic colonization (1-5% patients)
   Story Time - “Typhoid Mary”
Salmonella Treatment
 Preventative - safe food preparation
   Antibiotics not recommended for enteritis
 Typhoid Fever - antibiotics
 Characteristics
 Gram - facultative anaerobe, rod
 DNA hybridization reveals they’re actually
  biogroups of E. coli.
 Don’t ferment lactose
 Intracellular pathogen
Shigella Virulence Factors
 Adhere to, invade, and replicate in M cells
  (Peyer’s Patches).
 Spread to macrophages and cause lysis of
  phagocytic vacuole
   They then replicate in the cytoplasm
 Cause apoptosis, and release of IL-1β
  which attract polymorphonulear leukocytes
  which destroy intestinal tissue.
 Shiga toxin—disrupts protein synthesis
   Remember E. coli O157:H7
Shigella Epidemiology
 Estimated 450,000 cases in U.S.
   150 million world wide
 Spread by fecal oral route (yummy).
 Primarily a pediatric disease
   70% occur in children 15 and under.
 Highest risk in daycares, nurseries,
  custodial institutions
 Low infectious dosage (~200 cells)
 Symptoms appear 1-3 days after ingestion
 Begin with watery diarrhea.
 Progress to abdominal cramps and pus in
  bloody stool.
 Usually clears up on its own
   Antibiotics are given to reduce the chance of
 Small percentage of asymptomatic
Yersinia Species
 Y. pestis – causes the plague
   Highly virulent pathogen causing a systemic
 Y. enterocolitica - causes enterocolitis
Yersinia Virulence Factors
 Found on plasmids
 Capsule
 Antiphagocytic proteins
 Proteins which cause apoptosis in
 Proteases which inactivate compliment
 Fibrinases which break down blood clots
Yersinia Epidemiology
 Humans are accidental hosts
   Most infections in other animals are fatal (not
    normal flora)
 Y. enterocolitica
   Reservoir rabbits, rodents, pigs, livestock
   Primarily in colder climates
   90% infections associated with ingestion of
    contaminated meat, milk, water
     Mostly in children
Yersinia entercolitica
 Symptoms include: diarrhea, abdominal
  pain, fever
   Can mimic acute appendicitis
 Usually lasts 1 to 2 weeks
 Because of growth at low temperature
  (4°C) can spread in blood products
Yersinia pestis Epidemiology
Sylvatic Plague
 Reservoir is small
   livestock etc.
 Too widespread for
   animal control
 Can spread by
   contaminated food
Yersinia Pestis Epidemiology
Urban plague
 Reservoir is rats,
  transmitted by
 Rare due to good
  hygiene, and rat
 Three great
Plague History
 Egypt 541 AD. lasted 200yrs
   Spread to most of the “old world”
   Killed a majority of the population
 1320s, over 5 year period 25 million
  died in Europe (30-40% of
 China 1860s spread world wide
 About 10 cases in the U.S. per year
   Sylvatic plague
Yersinia Diseases
Bubonic Plague
  incubation of no more than 7 days
  cause bubos (swelling of lymph
  nodes) in groin and armpit
  75% mortality in untreated cases
Yersinia Diseases
Pneumonic Plague
  short (2-3 day) incubation
  fever, malaise, pulmonary signs
  highly infectious
  90% mortality for untreated patients
Yersinia Treatment
 Y. pestis–streptomycin, tetracyclines,
 Enteric infections usually clear on
  there own
 Urban plague is controlled by
  reducing the rodent population

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