Enterobacteriaceae

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Enterobacteriaceae
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Enterobacteriaceae

• Classification more than15 different genera
• Escherichia
• Shigella
• Edwardsiella
• Salmonella
• Citrobacter
• Klebsiella
• Enterobacter
• Hafnia
• Serratia

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Enterobacteriaceae

• Proteus
• Providencia
• Morganella
• Yersinia
• Erwinia
• Pectinobacterium

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Enterobacteriaceae

• Morphology and General Characteristics
• Gram-negative, non-sporing, rod shaped bacteria
• Oxidase
• Ferment glucose and may or may not produce gas in
  the process (aerogenic vs anaerogenic)
• Reduce nitrate to nitrite (there are a few
  exceptions)

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Enterobacteriaceae

• Are facultative anaerobes
• If motile, motility is by peritrichous flagella
• Many are normal inhabitants of the intestinal
  tract of man and other animals
• Some are enteric pathogens and others are urinary
  or respiratory tract pathogens
• Differentiation is based on biochemical reactions
  and differences in antigenic structure

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Enterobacteriaceae

• Most grow well on a variety of lab media
  including a lot of selective and differential
  media originally developed for the the selective
  isolation of enteric pathogens.
• Most of this media is selective by incorporation
  of dyes and bile salts that inhibit G organisms
  and may suppress the growth of nonpathogenic
  species of Enterobacteriaceae.
• Many are differential on the basis of whether or
  not the organisms ferment lactose and/or produce
  H2S.

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Enterobacteriaceae

• On CBA they all produce similar colonies that are
  relatively large and dull gray. They may or may
  not be hemolytic.
• The three most useful media for screening stool
  cultures for potential pathogens are TSI, LIA,
  and urea or phenylalanine agar.
• The antigenic structure is used to differentiate
  organisms within a genus or species.
• Three major classes of antigens are found

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Enterobacteriaceae

• Somatic O antigens these are the heat stable
  polysaccharide part of the LPS.
• Variation from smooth to rough colonial forms is
  accompanied by progressive loss of smooth O
  Antigen.
• Flagellar H antigens are heat labile
• Envelope or capsule K antigens overlay the
  surface O antigen and may block agglutination by
  O specific antisera.
• Boiling for 15 minutes will destroy the K antigen
  and unmask O antigens.
• The K antigen is called the Vi (virulence)
  antigen in Salmonella typhi.

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Antigenic Structure of Enterobacteriaceae
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Enterobacteriaceae

• Escherichia coli
• Normal inhabitant of the G.I. tract.
• Some strains cause various forms of
  gastroenteritis.
• Is a major cause of urinary tract infection and
  neonatal meningitis and septicemia.
• May have a capsule.
• Biochemistry
• Most are motile.

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E. coli

• May be hemolytic on CBA more common in
  pathogenic strains
• KEY tests for the normal strain
• TSI is A/A gas
• LIA K/K
• Urea
• Indole
• Citrate
• Motility
• There is an inactive biotype that is anaerogenic,
  lactose , and nonmotile.

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E. coli

• Antigenic structure - has O, H, and K antigens.
  K1 has a strong association with virulence,
  particularly meningitis in neonates.
• Virulence factors
• Toxins
• Enterotoxins produced by enterotoxigenic
  strains of E. coli (ETEC). Causes a movement of
  water and ions from the tissues to the bowel
  resulting in watery diarrhea. There are two types
  of enterotoxin
• LT is heat labile and binds to specific Gm1
  gangliosides on the epithelial cells of the small
  intestine where it ADP-ribosylates Gs which
  stimulates adenylate cyclase to increase
  production of cAMP.
• Increased cAMP alters the activity of sodium and
  chloride transporters producing an ion imbalance
  that results in fluid transport into the bowel.

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E. coli toxins

• ST is heat stable and binds to specific
  receptors to stimulate the production of cGMP
  with the same results as with LT.

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LT vs ST activity
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E. coli toxins

• Both enterotoxins are composed of five beta
  subunits (for binding) and 1 alpha subunit (has
  the toxic enzymatic activity).

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Composition of subunits of enterotoxins
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E. coli toxins

• Shiga-type toxin also called the verotoxin
  -produced by enterohemorrhagic strains of E. coli
  (EHEC) is cytotoxic, enterotoxic, neurotoxic,
  and may cause diarrhea and ulceration of the G.I.
  tract.
• There are two types shiga-like toxin 1 and
  shiga-like toxin 2.
• Inhibit protein synthesis by cleaving a 28S rRNA
  thats part of the 60S subunit

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E. coli toxins

• Enteroaggregative ST-like toxin produced by
  enteroaggregative strains of E. coli (EAEC)
  causes watery diarrhea.
• Hemolysins two different types may be found
  cell bound and secreted.
• They lyse RBCs and leukocytes and may help to
  inhibit phagocytosis when cell bound.
• Endotoxin
• Type III secretion system to deliver effector
  molecules directly into the host cells.
• Involved in inducing uptake of EIEC into
  intestinal cells.
• Involved in development of an attachment and
  effacing lesion in EPEC characterized by
  microvilli destruction and pedestal formation.

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Type III secretion system
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Pedestal formation
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E. coli

• Adhesions are also called colonization factors
  and include both pili or fimbriae and
  non-fimbrial factors involved in attachment (e.g.
  intimin).
• There are at least 21 different types of
  adhesions.
• Antibodies to these may protect one from
  colonization.
• Virulence factors that protect the bacteria from
  host defenses
• Capsule
• Iron capturing ability (enterochelin)
• Outer membrane proteins - are involved in helping
  the organism to invade by helping in attachment
  (acting as adhesion) and in initiating
  endocytosis.

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Types of adhesions
(intimin)
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E. coli

• Clinical significance
• Is the leading cause of urinary tract infections
  which can lead to acute cystitis (bladder
  infection) and pyelonephritis (kidney infection).

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Ascending urinary tract infection
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Urinary tract infections (UTI)

• New evidence in women who suffer from recurrent
  UTIs suggests that this is due to the formation
  of pod-like E. coli biofilms inside bladder
  epithelial cells.
• Bacteria living on the edges of the biofilms nay
  break off leading to a round of infection.

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Pod-like biofilm
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E. coli infections

• Neonatal meningitis is the leading cause of
  neonatal meningitis and septicemia with a high
  mortality rate.
• Usually caused by strains with the K1 capsular
  antigen.
• Gastroenteritis there are several distinct
  types of E. coli that are involved in different
  types of gastroenteritis
• enterotoxigenic E. coli (ETEC),
• enteroinvasive E. coli (EIEC),
• enteropathogenic E. coli (EPEC) ,
• enteroaggregative E. coli (EAEC), and
• enterohemorrhagic E. coli (EHEC).

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Various types of E. coli
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E. coli gastroenteritis

• ETEC is a common cause of travelers diarrhea
  and diarrhea in children in developing countries.
• The organism attaches to the intestinal mucosa
  via colonization factors and then liberates
  enterotoxin.
• The disease is characterized by a watery
  diarrhea, nausea, abdominal cramps and low-grade
  fever for 1-5 days.
• Transmission is via contaminated food or water.
• EPEC Bundle forming pili are involved in
  attachment to the intestinal mucosa.
• The type III secretion system inserts the tir
  (translocated intimin receptor) into target
  cells, and intimate attachment of the
  non-fimbrial adhesion called intimin to tir
  occurs.
• Host cell kinases activated to phosphorylate tir
  which then causes a reorganization of host
  cytoskeletal elements resulting in pedestal
  formation and development of an attaching and
  effacing lesion
• The exact mode of pathogenesis is unclear, but it
  is probably due to the attachment and effacement.
• Diarrhea with large amounts of mucous without
  blood or pus occurs along with vomiting, malaise
  and low grade fever.
• This is a problem mainly in hospitalized infants
  and in day care centers.

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BFP
EPEC
EPEC
EPEC
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Pedestal formation
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EPEC
Tir injected
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E. coli gastroenteritis

• EIEC The organism attaches to the intestinal
  mucosa via pili and outer membrane proteins are
  involved in direct penetration, invasion of the
  intestinal cells, and destruction of the
  intestinal mucosa.
• There is lateral movement of the organism from
  one cell to adjacent cells.
• Symptoms include fever,severe abdominal cramps,
  malaise, and watery diarrhea followed by scanty
  stools containing blood, mucous, and pus.
• EAEC Mucous associated autoagglutinins cause
  aggregation of the bacteria at the cell surface
  and result in the formation of a mucous biofilm.
  
• The organisms attach via pili and liberate a
  cytotoxin distinct from, but similar to the ST
  and LT enterotoxins liberated by ETEC.
• Symptoms include watery diarrhea, vomiting,
  dehydration and occasional abdominal pain.

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E. coli gastroenteritis

• EHEC The organism attaches via pili to the
  intestinal mucosa and liberates the shiga-like
  toxin.
• The symptoms start with a watery diarrhea that
  progresses to bloody diarrhea without pus and
  crampy abdominal pain with no fever or a
  low-grade fever.
• This may progress to hemolytic-uremic syndrome
  that is characterized by low platlet count,
  hemolytic anemia, and kidney failure.
• This is most often caused by serotypes O157H7.
• This strain of E. coli can be differentiated
  from other strains of E. coli by the fact that
  it does not ferment sorbitol in 48 hours (other
  strains do).
• A sorbitol-Mac (SMAC) plate (contains sorbitol
  instead of lactose) is used to selectively
  isolate this organism.
• One must confirm that the isolate is E. coli
  O1547H7 using serological testing and confirm
  production of the shiga-like toxin before
  reporting out results.
• Serotypes of E. coli other than O157H7 have now
  been found to cause this disease

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Summary of E.coli strains that cause
gastroenteritis.
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E.coli

• Antimicrobic therapy- E. coli is usually
  susceptible to a variety of chemotherapeutic
  agents, though drug resistant strains are
  increasingly prevalent.
• It is essential to do susceptibility testing.
• Treatment of patients with EHEC infections is not
  recommended because it can increase the release
  of shiga-like toxins and actually trigger HUS

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Shigella species

• Shigella
• Contains four species that differ antigenically
  and, to a lesser extent, biochemically.
• S. dysenteriae (Group A)
• S. flexneri (Group B)
• S. boydii (Group C)
• S. sonnei (Group D)
• Biochemistry
• TSI K/A with NO gas
• LIA K/A
• Urea
• Motility -
• All ferment mannitol except S. dysenteriae
• S. sonnei may show delayed lactose fermentation

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Shigella species

• Antigenic structure
• Differentiation into groups (A, B, C, and D) is
  based on O antigen serotyping K antigens may
  interfere with serotyping, but are heat labile.
• O antigen is similar to E. coli, so it is
  important to ID as Shigella before doing
  serotyping.
• Virulence factors
• Shiga toxin is produced by S. dysenteriae and
  in smaller amounts by S. flexneri and S. sonnei.
• Acts to inhibit protein synthesis by inactivating
  the 60S ribosomal subunit by cleaving a
  glycosidic bond in the 28S rRNA constituents.
• This plays a role in the ulceration of the
  intestinal mucosa.

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Shigella species

• Outer membrane and secreted proteins
• These proteins are expressed at body temperature
  and upon contact with M cells in the intestinal
  mucosa they induce phagocytosis of the bacteria
  into vacuoles.
• Shigella destroy the vacuoles to escape into the
  cytoplasm.
• From there they spread laterally (Polymerization
  of actin filaments propels them through the
  cytoplasm.) to epithelial cells where they
  multiply but do not usually disseminate beyond
  the epithelium.

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Shigella attachment and penetration
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Shigella attachment
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Shigella penetration
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Shigella invasion continued
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Shigella

• Clinical significance
• Causes shigellosis or bacillary dysentery.
• Transmission is via the fecal-oral route.
• The infective dose required to cause infection is
  very low (10-200 organisms).
• There is an incubation of 1-7 days followed by
  fever, cramping, abdominal pain, and watery
  diarrhea (due to the toxin)for 1-3 days.
• This may be followed by frequent, scant stools
  with blood, mucous, and pus (due to invasion of
  intestinal mucosa).
• It is rare for the organism to disseminate.
• The severity of the disease depends upon the
  species one is infected with.
• S. dysenteria is the most pathogenic followed by
  S. flexneri, S. sonnei and S. boydii.

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Shigella

• Antimicrobial therapy
• Sulfonamides are commonly used as are
  streptomycin, tetracycline, ampicillin, and
  chloramphenicol.
• Resistant strains are becoming increasingly
  common, so sensitivity testing is required.

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Salmonella

• Salmonella
• Classification has been changing in the last few
  years.
• There is now 1 species S. enteritica, and 7
  subspecies 1, 2 ,3a ,3b ,4 ,5, and 6.
• Subgroup 1 causes most human infections
• Clinically Salmonella isolates are often still
  reported out as serogroups or serotypes based on
  the Kauffman-White scheme of classification.
• Based on O and H (flagella) antigens
• The H antigens occur in two phases 1 and 2 and
  only 1 phase is expressed at a given time.
• Polyvalent antisera is used followed by group
  specific antisera (A, B, C1, C2, D, and E)
• Salmonella typhi also has a Vi antigen which is a
  capsular antigen.

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Phase variation of Salmonella
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Salmonella

• Biochemistry
• TSI K/A gas and H2S S. typhi produces only a
  small amount of H2S and no gas , and S. paratyphi
  A produces no H2S
• LIA K/K with H2S with S. paratyphi A giving K/A
  results
• Urea
• Motility
• Citrate /-
• Indole -
• Virulence factors
• Endotoxin may play a role in intracellular
  survival
• Capsule (for S. typhi and some strains of S.
  paratyphi)
• Adhesions both fimbrial and non-fimbrial

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Salmonella virulence factors

• Type III secretion systems and effector molecules
  2 different systems may be found
• One type is involved in promoting entry into
  intestinal epithelial cells
• The other type is involved in the ability of
  Salmonella to survive inside macrophages
• Outer membrane proteins - involved in the ability
  of Salmonella to survive inside macrophages
• Flagella help bacteria to move through
  intestinal mucous
• Enterotoxin - may be involved in gastroenteritis
• Iron capturing ability

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Salmonella

• Clinical Significance causes two different
  kinds of disease enteric fevers and
  gastroenteritis.
• Both types of disease begin in the same way, but
  with the gastroenteritis the bacteria remains
  restricted to the intestine and with the enteric
  fevers, the organism spreads
• Transmission is via a fecal-oral route, i.e., via
  ingestion of contaminated food or water.

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Salmonella

• The organism moves through the intestinal mucosa
  and adheres to intestinal epithelium.
• Effector proteins of the type III secretion
  system mediate invasion of enterocytes and M
  cells via an induced endocytic mechanism.
• Salmonella multiplies within the endosome.

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Salmonella invasion of epithelial cells
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Salmonella

• The endosome moves to the basal side of the cell
  and Salmonella are released and may be
  phagocytosed by macrophages.
• For gastroenteritis the Salmonella multiply and
  their presence induces a strong inflammatory
  response which causes most of the symptoms seen
  in gastroenteritis (mild to moderate fever with
  diarrhea and abdominal cramps).
• The inflammatory response prevents the spread
  beyond the GI tract and eventually kills the
  bacteria.
• In enteric fevers (typhoid and paratyphoid) the
  Salmonella disseminate before they multiply to
  high enough levels to stimulate a strong
  inflammatory response so the initial symptoms are
  only a low-grade fever and constipation.

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Salmonella

• The bacteria move via the lymphatics and
  bloodstream to the liver and spleen where
  phagocytosis and multiplication occurs.
• The bacteria re-enter the bloodstream to
  disseminate throughout the body to all organs
  causing fever, headaches, myalgia, and GI
  problems.
• Rose spots (erythematous, muculopapular lesions)
  are seen on the abdomen. Osteomyelitis,
  cystitis, and gall bladder infections may occur.
• Symptoms of paratyphoid fevers (due to S.
  paratyphi A, B, or C) are similar to but less
  severe than those that occur with typhoid fever
  (due to S. typhi)

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Salmonella

• Diagnosis of typhoid fever
• Blood cultures are positive during the first week
  and after the second week
• Stool cultures and sometimes urine cultures are
  positive after the second week
• The Widal test is a serological test for
  antibodies against Salmonella typhi. One looks
  for a 4-fold rise in titer between acute and
  convalescent stages.
• 10 of those infected become short term carriers
  and a smaller become long-term carriers due to
  persistence of the bacteria in the gallbladder or
  urinary bladder.

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Salmonella

• Antimicrobial therapy
• Enteric fevers use chloramphenicol usually.
  Resistant strains have emerged making
  antimicrobial susceptibility testing essential.
• Gastroenteritis usually doesnt require
  antimicrobic therapy.
• Replace lost fluids and electrolytes.

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Comparison of Shigella versus Salmonella invasion
Shigella
Salmonella
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Enterobacteriaceae

• Citrobacter
• TSI K/A or A/A both gas and H2S
• LIA K/A H2S
• Urea usually
• Motility
• Are opportunistic pathogens causing urinary tract
  or respiratory tract infections and occasionally
  wound infections, osteomyelitis, endocarditis,
  and meningitis.

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Enterobacteriaceae

• Edwardsiella tarda
• TSI K/A gas and H2S
• LIA K/K H2S
• Urea
• Citrate
• Indole
• Clinical significance causes GI disease in
  tropical and subtropical countries

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Enterobacteriaceae

• Klebsiella
• NF of GI tract, but potential pathogen in other
  areas
• TSI A/A gas
• LIA K/K
• Urea
• Citrate
• MR-, VP
• Motility -
• Has both O and K antigens

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Klebsiella

• Virulence factors
• Capsule
• Adhesions
• Iron capturing ability
• Clinical significance
• Causes pneumonia, mostly in immunocompromised
  hosts.
• Permanent lung damage is a frequent occurrence
  (rare in other types of bacterial pneumonia)
• A major cause of nosocomial infections such as
  septicemia and meningitis

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Enterobacteriaceae

• Enterobacter
• NF of GI tract
• TSI, LIA, and urea give variable results
  depending upon species
• Citrate
• Clinical significance
• Nosocomial infections
• Bacteremia in burn patients

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Enterobacteriaceae

• Serratia
• A free-living saprophyte
• TSI A/A or K/A /- gas (does not ferment
  lactose)
• LIA usually K/K
• Citrate
• Motility
• Urea /-
• Has been found in RT and UT infections
• Is resistant to many antimicrobics

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Enterobacteriaceae

• Proteus, Providencia, and Morganella
• Are all part of the NF of the GI tract (except
  Providencia).
• All motile, with Proteus swarming
• PA
• Lysine deamination (LIA R/A)
• Urea for most, strongly for Proteus
• TSI variable (know the reactions for each in the
  lab!)
• Indole only P. mirabilis is -

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Proteus, Providencia, and Morganella

• Virulence factors
• Urease the ammonia produced may damage the
  epithelial cells of the UT
• Clinical Significance
• UT infections, as well as pneumonia, septicemia,
  and wound infections
• Yersinia
• Three species are important pathogens in man
• Yersinia pestis causes plague
• Yersinis enterocolitica enteropathogenic
• Yersinia pseudotuberculosis enteropathogenic

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Yersinia species

• Identification
• Y. pestis can be separated from Y. enterocolitica
  and Y. pseudotuberculosis by the fact that it is
  non-motile. Y. enterocolitica and Y.
  pseudotuberculosis are both non-motile at 370 C,
  and motile at 220 C.
• Y. pestis is identified based on the following
• Non-motile
• Bipolar staining
• Slow growth of small colonies on ordinary culture
  media it grows better at lower temperature
  (25-300 C)

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Yersinia pestis bipolar staining
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Yersinia species

• TSI K/A no gas
• LIA K/A
• Urea
• Guinea pig or mouse pathogenicity studies
  LD50lt10
• Direct fluorescent antibody test
• New DNA probe test
• Yersinia pestis virulence characteristics
• Endotoxin is responsible for many of the
  symptoms
• Murine toxin causes edema and necrosis in mice
  and rats, but has not been shown to play a role
  in human disease

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Y. pestis

• Fraction 1 a protein component of the
  antiphagocytic protein capsule. Also blocks flea
  digestion.
• V antigen a secreted protein that controls
  expression of many of the virulence genes plus it
  appears to have another unknown function that is
  essential for virulence
• Pla a protease that activates plasminogen
  activator (acts as a fibrinolysin) and degrades
  C3b (prevents formation of complement membrane
  attack complex) and C5a (prevents attraction of
  phagocytes)
• Psa a pilus adhesion for attachment
• Iron acquisition and sequestering system
• Type III secretion system
• YopB and YopD disrupt actin cytoskeleton in
  phagocytic cells to evade phagocytosis

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Y. pestis

• Y. pestis clinical significance
• In man plague occurs in two forms bubonic and
  pneumonic
• Bubonic plague transmitted by fleas from an
  infected rodent (is endemic in our local
  mountains).
• The bacteria travel in the blood to the nearest
  lymph node where they are engulfed by fixed
  macrophages.
• A high fever develops and the lymph nodes in the
  groin and armpit become enlarged (buboes) as the
  bacteria proliferate and stimulate an
  inflammatory response.
• The bacteria growing in the lymph node leak into
  the bloodstream.
• Lysis of the bacteria releases LPS, causing
  septic shock.
• Subcutaneous hemorrhages, probably due to LPS
  causing DIC gave the disease the name, the black
  death, in the middle ages.
• The untreated mortality rate is quite high.

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Buboes and pneumonia
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Y. pestis

• Eventually bacteria reach the lungs where they
  are ingested by lung macrophages to cause
  pneumonic plague.
• Pneumonic plague this can be transmitted
  directly to others via aerosol. Direct
  inhalation of aerosols containing the organism
  produces a form of the disease that progresses
  much more rapidly and the mortality rate is close
  to 100.
• Treatment for plague
• Streptomycin or tetracycline are effective

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Yersinia species

• Yersinia enterocolitica and Yersinia
  pseudotuberculosis identification
• Both are motile at 22-250 C, but non-motile at
  370 C
• Both exhibit bipolar staining
• Both grow better at lower temperatures and
  produce small colonies at 370 C
• TSI A/A (sucrose, not lactose fermentation) for
  Y. enterocolitica K/A for Y. pseudotuberculosis
• LIA K/A for both
• Urea for both
• ODC for Y. enterocolitica only

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Yersinia species

• Cefsulodin-irgasan-novobiocin (CIN) agar is a
  selective media developed specifically for the
  isolation of Y. enterocolitica from
  gastrointestinal specimens.
• The media also contains mannitol and phenol red
  to differentiate mannitol from non-mannitol
  fermenting organisms.
• The media is incubated at room temperature and
  Yersinia are the only Enterobacteriaceae that
  will grow on the media.
• Aeromonas and Pleisiomonas, both members of the
  Vibrionaceae will also grow.
• After 48 hours at RT, Y. enterocolitica and Y.
  pseudotuberculosis both produce typical pink
  (from mannitol fermentation) colonies with a
  bulls-eye appearance.

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Y. enterocolitica growth on CIN
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Yersinia species

• Y. enterocolotica virulence factors
• Enterotoxin similar to E. coli ST (increases cGMP
  leading to watery diarrhea)
• Adhesions include both fimbrial and
  non-fimbrial adhesions.
• At least four different adhesions have been
  identified thus far.
• Antiphagocytic proteins include both outer
  membrane and secreted proteins.
• Some are actually injected directly into the host
  via a type III secretion mechanism.
• Some interfere with signal transduction in host
  cells, thus interfering with the ability of PMNs
  to respond to signals leading them to the
  invading bacteria.
• Others disrupt the actin cytoskeleton and lead to
  death of the PMNs.

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Yersinia species

• V antigen - a secreted protein that controls
  expression of many of the virulence genes plus it
  appears to have another unknown function that is
  essential for virulence
• Iron capturing ability
• Yad A an outer membrane protein that interferes
  with C3b binding to bacteria thus preventing the
  formation of a membrane attack complex.
• Endotoxin
• Y. pseudotuberculosis virulence factors
• Has all of the same virulence factors as Y.
  enterocolitica except the enterotoxin.

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Yersinia species

• Yersinia enterocolitica and Y. pseudotuberculosis
  clinical significance
• Both are acquired by ingestion of contaminated
  food or water.
• Y. enterocolitica is a common cause of human
  disease, whereas, Y. pseudotuberculosis is mainly
  a disease of other animals.
• Both cause a disease involving fever and
  abdominal pain. Y. enterocolitica also causes a
  watery diarrhea.
• After ingestion, the bacteria invade the
  intestinal epithelium by invasion of M cells.
• They are transcytosed through the M cells and
  released at the basal surface.
• Once through the intestional epithelium, the
  bacteria penetrate into the underlying lymphoid
  tissue, where they multiply both inside and
  outside host cells.

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Yersinia species

• Multiplication of the bacteria produces an
  inflammatory response that is responsible for the
  extreme pain associated with the infections
  (resembles acute appendicitis)
• Fever is due to the activity of the LPS
  endotoxin.
• Sometimes they drain into adjacent mesenteric
  lymph nodes, causing mesenteric lymphadenitis.
• Reactive arthritis may occur in some people
  following Y. enterocolitica infection.
• It is thought to be due to cross reacting T cells
  or antibodies that attack the joints.

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Summary of Yersinia infections
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Yersinia species

• Antimicrobic susceptibility - must do
  antimicrobial susceptibility testing.