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Enterobacteriaceae. Enterobacteriaceae. Classification – more than15 different genera Escherichia Shigella Edwardsiella Salmonella Citrobacter Klebsiella Enterobacter Hafnia Serratia. Enterobacteriaceae. Proteus Providencia Morganella Yersinia Erwinia Pectinobacterium.

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  • Classification – more than15 different genera
    • Escherichia
    • Shigella
    • Edwardsiella
    • Salmonella
    • Citrobacter
    • Klebsiella
    • Enterobacter
    • Hafnia
    • Serratia
  • Proteus
  • Providencia
  • Morganella
  • Yersinia
  • Erwinia
  • Pectinobacterium
  • 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)
  • 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
  • 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.
  • 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:
  • 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.
  • 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.
e coli
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.
e coli12
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.
e coli toxins
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.
e coli toxins16
E. coli toxins
  • Both enterotoxins are composed of five beta subunits (for binding) and 1 alpha subunit (has the toxic enzymatic activity).
e coli toxins18
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 that’s part of the 60S subunit
e coli toxins19
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.
e coli22
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.
e coli24
E. coli
  • Clinical significance
    • Is the leading cause of urinary tract infections which can lead to acute cystitis (bladder infection) and pyelonephritis (kidney infection).
urinary tract infections uti
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.
e coli infections
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).
e coli gastroenteritis
E. coli gastroenteritis
  • ETEC – is a common cause of traveler’s 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.





Tir injected

e coli gastroenteritis34
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 mucousbiofilm.
    • 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.
e coli gastroenteritis35
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 O157:H7.
    • 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 O1547:H7 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
e coli37
  • 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
shigella species
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
shigella species39
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 Shigellabefore 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.
shigella species40
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.
  • 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.
  • Antimicrobial therapy
    • Sulfonamides are commonly used as are streptomycin, tetracycline, ampicillin, and chloramphenicol.
    • Resistant strains are becoming increasingly common, so sensitivity testing is required.
  • 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.
  • 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
salmonella virulence factors
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
  • 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.
  • 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.
  • 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.

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)
  • 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.
  • Antimicrobial therapy
    • Enteric fevers – use chloramphenicol usually. Resistant strains have emerged making antimicrobial susceptibility testing essential.
    • Gastroenteritis – usually doesn’t require antimicrobic therapy.
      • Replace lost fluids and electrolytes.
  • 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.
  • 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
  • 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
  • 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
  • Enterobacter
    • NF of GI tract
    • TSI, LIA, and urea give variable results depending upon species
    • Citrate +
    • Clinical significance
      • Nosocomial infections
      • Bacteremia in burn patients
  • 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
  • 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 -
proteus providencia and morganella
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
yersinia species
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)
yersinia species71
Yersinia species
    • TSI K/A no gas
    • LIA K/A
    • Urea –
    • Guinea pig or mouse pathogenicity studies: LD50<10
    • 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
y pestis
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
y pestis73
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.
y pestis75
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
yersinia species77
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
yersinia species78
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.
yersinia species80
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.
yersinia species81
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.
yersinia species82
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.
yersinia species83
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.
yersinia species85
Yersinia species
  • Antimicrobic susceptibility - must do antimicrobial susceptibility testing.