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ENTEROBACTERIACEAE basics
ENTEROBACTERIACEAE basics
ENTEROBACTERIACEAE basics
ENTEROBACTERIACEAE basics
ENTEROBACTERIACEAE basics
ENTEROBACTERIACEAE basics
ENTEROBACTERIACEAE basics
ENTEROBACTERIACEAE basics
ENTEROBACTERIACEAE basics
ENTEROBACTERIACEAE basics
ENTEROBACTERIACEAE basics
ENTEROBACTERIACEAE basics
ENTEROBACTERIACEAE basics
ENTEROBACTERIACEAE basics
ENTEROBACTERIACEAE basics
ENTEROBACTERIACEAE basics
ENTEROBACTERIACEAE basics
ENTEROBACTERIACEAE basics
ENTEROBACTERIACEAE basics
ENTEROBACTERIACEAE basics
ENTEROBACTERIACEAE basics
ENTEROBACTERIACEAE basics
ENTEROBACTERIACEAE basics
ENTEROBACTERIACEAE basics
ENTEROBACTERIACEAE basics
ENTEROBACTERIACEAE basics
ENTEROBACTERIACEAE basics
ENTEROBACTERIACEAE basics
ENTEROBACTERIACEAE basics
ENTEROBACTERIACEAE basics
ENTEROBACTERIACEAE basics
ENTEROBACTERIACEAE basics
ENTEROBACTERIACEAE basics
ENTEROBACTERIACEAE basics
ENTEROBACTERIACEAE basics
ENTEROBACTERIACEAE basics
ENTEROBACTERIACEAE basics
ENTEROBACTERIACEAE basics
ENTEROBACTERIACEAE basics
ENTEROBACTERIACEAE basics
ENTEROBACTERIACEAE basics
ENTEROBACTERIACEAE basics
ENTEROBACTERIACEAE basics
ENTEROBACTERIACEAE basics
ENTEROBACTERIACEAE basics
ENTEROBACTERIACEAE basics
ENTEROBACTERIACEAE basics
ENTEROBACTERIACEAE basics
ENTEROBACTERIACEAE basics
ENTEROBACTERIACEAE basics
ENTEROBACTERIACEAE basics
ENTEROBACTERIACEAE basics
ENTEROBACTERIACEAE basics
ENTEROBACTERIACEAE basics
ENTEROBACTERIACEAE basics
ENTEROBACTERIACEAE basics
ENTEROBACTERIACEAE basics
ENTEROBACTERIACEAE basics
ENTEROBACTERIACEAE basics
ENTEROBACTERIACEAE basics
ENTEROBACTERIACEAE basics
ENTEROBACTERIACEAE basics
ENTEROBACTERIACEAE basics
ENTEROBACTERIACEAE basics
ENTEROBACTERIACEAE basics
ENTEROBACTERIACEAE basics
ENTEROBACTERIACEAE basics
ENTEROBACTERIACEAE basics
ENTEROBACTERIACEAE basics
ENTEROBACTERIACEAE basics
ENTEROBACTERIACEAE basics
ENTEROBACTERIACEAE basics
ENTEROBACTERIACEAE basics
ENTEROBACTERIACEAE basics
ENTEROBACTERIACEAE basics
ENTEROBACTERIACEAE basics
ENTEROBACTERIACEAE basics
ENTEROBACTERIACEAE basics
ENTEROBACTERIACEAE basics
ENTEROBACTERIACEAE basics
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ENTEROBACTERIACEAE basics

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ENTEROBACTERIACEAE basics

ENTEROBACTERIACEAE basics

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  • 1. ENTEROBACTERIACEAE basics Chapter I Dr.T.V.Rao MD4/16/2012 Dr.T.V.Rao MD 1
  • 2. Bacteria Gram Gram positive negative Cocci Bacilli Cocci Rods4/16/2012 Dr.T.V.Rao MD 2
  • 3. Enterobacteriaceae• Commonly present in large intestine• Non sporing , Non Acid fast, Gram – bacilli.• A complex family of organisms,• Some are non pathogenic• A few are highly Pathogenic,• Some commensals turn out to be pathogenic. as in UTI after catheterization.4/16/2012 Dr.T.V.Rao MD 3
  • 4. Characters of Enterobacteriaceae• All Enterobacteriaceae – Gram-negative rods – Ferment glucose with acid production – Reduce nitrates into nitrites – Oxidase negative• Facultative anaerobic• Motile except Shigella and Klebsiella• Non-capsulated except Klebsiella• Non-fastidious• Grow on bile containing media (MacConkey agar) 4/16/2012 Dr.T.V.Rao MD 4
  • 5. Basic Tests ……• Basic characters• Catalase +• Oxidase -• Reduce nitrates,• All are Gram negative and non spore forming.• Wide diversity / Antigenic heterogeneity,4/16/2012 Dr.T.V.Rao MD 5
  • 6. Classification of Enterobacteriaceae Enterobacteriaceae Lactose fermenters Non-lactose fermenter E. coli, Citrobacter, Salmonella, Shigella Klebsiella, Enterobacter Proteus, YersiniaThere are several selective and differential media used to isolate distinguishes between LF & LNFThe most important media are: MacConkey agar Eosin Methylene Blue (EMB) agar Salmonella Shigella (SS) agar In addition to Triple Sugar Iron (TSI) agar 4/16/2012 Dr.T.V.Rao MD 6
  • 7. Differentiation between LF & NLF by Growth on MacConkey agar  MacConkey agar is selective & differential medium for Enterobacteriaceae MacConkey Agar ContainsBile salts Crystal violet Lactose Neutral red pH indicatorInhibit growth of G+ve bacteria Cause of differential Acidic: PinkCause of selectivity Lactose feremnters Lactose non feremnters 4/16/2012 Dr.T.V.Rao MD colorless colonies Pink colonies
  • 8. Basic Classification• I Lactose fermenters E.coli, Escherichia Klebsiella,• II Late Lactose fermenters, Shigella sonnei,• III Non Lactose fermenters, Salmonella Shigella,Commonly tested with MacConkey mediumMany are commensals Lactose fermentersAlso called as coli forms , Enteric Bacilli4/16/2012 Dr.T.V.Rao MD 8
  • 9. Enterobacteriaceae Taxonomical• Tribe I Escherichia Genus – 1 Escherichia, 2 Edwardsville 3 Citrobacter 4 Salmonella 5 Shigella4/16/2012 Dr.T.V.Rao MD 9
  • 10. Enterobacteriaceae.• Tribe II; Klebsiella Genus 1. Klebsiella 2.Enterobacter, 3.Hafnia 4 Serratia Tribe III ; Proteeae Genus 1,Proteus 2,Morganella 3 . Providencia4/16/2012 Dr.T.V.Rao MD 10
  • 11. Classification of Enterobacteriaceae ( Contd )• Tribe IV; Erwinieae Genus 1. Erwinia4/16/2012 Dr.T.V.Rao MD 11
  • 12. Identification of EnterobacteriaceaeDifferentiation between LF & NLF by Growth on MacConkey agar • Method: – MacConkey agar is inoculated with tested organism using streak plate technique – Incubate the plate in incubator at 37 C/24 hrs • Results: – LF organism appears as pink colonies (e.g. E. coli) – NLF organism appears as colorless colonies (e.g. Shigella) Flame & Cool 1 2 3 4 Flame & Cool 5 4/16/2012 Dr.T.V.Rao MD 12 Flame & Cool
  • 13. Highly Pathogenic Enterobacteriaceae• Salmonella• Shigella• All are Lactose – non fermenters,• Produce colorless colonies on MacConkey medium• LF also called as Para colons,4/16/2012 Dr.T.V.Rao MD 13
  • 14. Escherichia coli• Named by Escherichia• Wide group of bacteria on basis of Bio typing and Serotyping Produce infections in Humans and Animals Detection of E.coli in water indicates pollution and contamination.4/16/2012 Dr.T.V.Rao MD 14
  • 15. 4/16/2012 Dr.T.V.Rao MD 15
  • 16. E.coli• Morphology Gram - ve Straight rods,• 1-3 X 0.4 -0.7 microns,• Appear in singles or in pairs,• Motile by peritrichate flagella.• Very few strains non motile• Not spore forming, Non acid fast.4/16/2012 Dr.T.V.Rao MD 16
  • 17. E.coli Cultural characters• Aerobic / Facultative Anaerobic• Grows between 10 – 40 c optimal at 37 c• Grown in simple medium• Produce Large grayish ,Thick white , moist smooth opaque colonies• May contain capsule.• On MacConkey medium Produce Bright pink Lactose fermenters.4/16/2012 Dr.T.V.Rao MD 17
  • 18. E.coli on Blood Agar• Many pathogenic strains are haemolytic on blood agar.4/16/2012 Dr.T.V.Rao MD 18
  • 19. E.coli Biochemical Characters,• Glucose,Lactose,Mannitol,Maltose fermented. with A/G Indole + Methyl Red + Voges Proskauer – I,M,Vi,C tests. Citrate – Urease not produced.4/16/2012 Dr.T.V.Rao MD 19
  • 20. E.coli Antigenic Structure• Somatic 0 170• Capsular K 100• Flagella H 75• Virulence factors Surface Antigens Toxins O Endotoxic activity K protects against the phagocytosis Fimbriae promote virulence ( important in UTI )4/16/2012 Dr.T.V.Rao MD 20
  • 21. Virulence Factors• Two types of virulence factors in E.coli• Surface antigens and Toxins• The somatic lipopolysaccharide surface O antigen has endotoxic activity and protects from phagocytosis and bactericidal effects of complement .4/16/2012 Dr.T.V.Rao MD 21
  • 22. Fimbriae• Fimbriae also promote virulence• Present in large numbers causing mannose sensitive Haemagglutination• Colonisation factor antigens is enterotoxigenic E.coli• E.coli produce two kinds of Exotoxins hemolysins and enterotoxins4/16/2012 Dr.T.V.Rao MD 22
  • 23. Toxins and E.coli• E.coli produce Exotoxins• Hemolysins, Enterotoxins causes Diarrheas,• Important toxins produces.• Heat labile HL Heat stable HS Vero toxins VT Like Shigella toxins4/16/2012 Dr.T.V.Rao MD 23
  • 24. 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:4/16/2012 Dr.T.V.Rao MD 24
  • 25. Toxins• 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.4/16/2012 Dr.T.V.Rao MD 25
  • 26. Toxins• Increased cAMP alters the activity of sodium and chloride transporters producing an ion imbalance that results in fluid transport into the bowel.4/16/2012 Dr.T.V.Rao MD 26
  • 27. Toxins in E.coli• Produce Enterotoxin L T and S T• Labile toxin 1956 De experiments in Rabbit ileal loop causes outpouring of fluids• E.coli Labile toxin like Cholera toxin• L T contains component A and B• A = Active B= Binding• B causes Binding with Gm I Ganglioside receptor on Intestinal epithelial cells4/16/2012 Dr.T.V.Rao MD 27
  • 28. E. coli toxins• Both enterotoxins are composed of five beta subunits (for binding) and 1 alpha subunit (has the toxic enzymatic activity).4/16/2012 Dr.T.V.Rao MD 28
  • 29. Toxins E.coli Labile toxin• Component A Activated to A1 and A2• A1 Activates adenyl cyclase in the enterocytes to form cyclic adenosine 5 monophosphate• Causes to increase outflow of water and electrolytes in the gut lumen causes Diarrhea4/16/2012 Dr.T.V.Rao MD 29
  • 30. Toxins of E.coli Stable Toxin• ST A and ST B• ST A Acts by activation of Cyclic guano sine monophosphate.( C GMP )• Causes fluid accumulation in Intestine.• E.coli ( Some ) produce Verocytotoxin causes cytotoxicity to Vero cells.• Acts like Shigella dysentery toxin4/16/2012 Dr.T.V.Rao MD 30
  • 31. 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).4/16/2012 Dr.T.V.Rao MD 31
  • 32. Classification of E.coli1.Enteropathogenic EPEC2.Enterotoxigenic ETEC3.Enteroinvasive EIEC4.Enterohemorrhagic EHEC5.Enteroaggresive EAEC4/16/2012 Dr.T.V.Rao MD 32
  • 33. Enteropathogenic E.coli• Causes diarrheal disease in children,• EPEC O26/O11• Produce Verocytotoxin• Infantile enteritis, Involves upper part of Intestine• Brush border of the intestine is lost• Intimacin – EPEC adhesion factor.• Frequent in summer months• Poor hygiene predisposes.• Out breaks in Institutions4/16/2012 Dr.T.V.Rao MD 33
  • 34. Enteropathogenic E.coli• Causes diarrheal disease in children,• EPEC O26/O11• Produce Verocytotoxin• Infantile enteritis, Involves upper part of Intestine• Brush border of the intestine is lost• Intimacin – EPEC adhesion factor.• Frequent in summer months• Poor hygiene predisposes.• Out breaks in Institutions4/16/2012 Dr.T.V.Rao MD 34
  • 35. EPEC• EPEC are identified by serotyping by their O and B antigens• Diagnosis is difficult during sporadics• Routine culture is done for isolation• The EPEC fails to ferment sorbitol• Causes the disruption of brush border4/16/2012 Dr.T.V.Rao MD 35
  • 36. Laboratory Diagnosis EPEC• Confirm with Polyvalent sera• Test Sero groups with polyvalent and monovalent sera.• HEp2 – adherence.4/16/2012 Dr.T.V.Rao MD 36
  • 37. Enterotoxigenic E.coli• Common and causes endemics in developing countries in all age groups• May be mild watery diarrhoea to fatal conditions• Fimbrial colonization factor antigens4/16/2012 Dr.T.V.Rao MD 37
  • 38. Enterotoxigenic E.coli•Produce Heat stable /Heat labile toxins•Adheres to epithelium of small intestine.•Present with Nausea, Vomiting and Lose stool•H L like cholera toxin•Causes accumulation of fluids•Adhesive factors Fimbriae specific receptor in the intestinal epithelium CFAMortality in children < 5 years4/16/2012 Dr.T.V.Rao MD 38
  • 39. ETEC• Causes travelers diarrhea• Water contaminated with Human and Animal feces predisposes.• Laboratory Diagnosis Demonstration of Enterotoxin LT and STTissue culture tests,ELISAPassive agglutination tests.Animal experiments in Rabbit ileal loop test.4/16/2012 Dr.T.V.Rao MD 39
  • 40. Treatment and Prophylaxis in Travelers diarrhea• Doxycycline,• Trimethoprim,• Norfloxacillin• Fluroquinolones• Avoid contaminated food,• Safe protected water ,prefer bottled water,• Hot foods, Hot Drinks,• Boiled milk4/16/2012 Dr.T.V.Rao MD 40
  • 41. Treatment and Prophylaxis in Travelers diarrhea• Doxycycline,• Trimethoprim,• Norfloxacillin• Fluroquinolones• Avoid contaminated food,• Safe protected water ,prefer bottled water,• Hot foods, Hot Drinks,• Boiled milk4/16/2012 Dr.T.V.Rao MD 41
  • 42. Enteroinvasive E.coli• Resembles Shigella in many respects• Non lactose fermenter and non motile• They invade the intestinal epithelium• Penetrate HeLa cells in tissue culture• May produce mild diarrhoea to frank dysentery• Sereny test4/16/2012 Dr.T.V.Rao MD 42
  • 43. Entero invasive E.coli• Some are non motile strains,• Atypical resembles like Shigella.• Clinically mild diarrhea• Sereny test positive animal Rabbit.• ELISA4/16/2012 Dr.T.V.Rao MD 43
  • 44. Enterohemorrhagic E.coli• Produce Verocytotoxin or shiga like toxin• Mild diarrhea - can be fatal hemorrhagic colitis. and uremic syndrome.• Present in Human and Animal feces.• Hemorrhagic complication with O157 in Japan and USA.• Salads vegetables, Radish Proper cooking4/16/2012 Dr.T.V.Rao MD 44
  • 45. 4/16/2012 Dr.T.V.Rao MD 45
  • 46. Enterohemorrhagic E.coli• The primary target for VT appear to be vascular endothelial cells• This may contribute to HUS with characteristic renal lesion is capillary micro angiopathy• The typical EHEC serotype is 0 157 ; H7• The disease may manifest as food poisoning• Occurs due to contamination of feces of 464/16/2012 Dr.T.V.Rao MD humans or animals
  • 47. Enterohemorrhagic E.coli can cause HUS • HUS develops when the toxin from E. coli bacteria, known as Shiga-like toxin (SLT) enters the circulation by binding to special receptors. These Shiga-toxin receptors, known as Gb3 receptors , are probably heterogeneously distributed in the major body organs allowing disparate thrombotic (blood clotting) impacts in different HUS victims, although the greatest receptor concentration appears to be in the kidneys, especially in children.4/16/2012 Dr.T.V.Rao MD 47
  • 48. EHEC ( E.coli )• Culture• DNA detection methods.• Cytotoxic effects on Vero cells.• Detection with monovalent sera O157/H74/16/2012 Dr.T.V.Rao MD 48
  • 49. Enteroaggresive E.coli• They appear aggregated in s stacked brick formation Hep-2 cell• They produce persistent diarrheal• They produce weight heat stable enterotoxin called as low molecular heat stable enterotoxin4/16/2012 Dr.T.V.Rao MD 49
  • 50. Enteroaggresive E.coli EAEC• Stool Culture methods• Detection of Enterotoxin4/16/2012 Dr.T.V.Rao MD 50
  • 51. Treatment – E.coli Gastrointestinal disease• Fluid replacement• Antibiotics – not used usually unless systemic infections prevails –e.g. hemolytic-uremia4/16/2012 syndrome Dr.T.V.Rao MD 51
  • 52. E. coli – Clinical significance • Is the leading cause of urinary tract infections which can lead to acute cystitis (bladder infection) and pyelonephritis4/16/2012 (kidney Dr.T.V.Rao MD 52 infection).
  • 53. Ascending urinary tract infection4/16/2012 Dr.T.V.Rao MD 53
  • 54. Urinary Tract Infections• E.coli produce urinary tract infection.• Majority of UTI s are produce by E.coli.• Instrumentation, Prostatic enlargement, Urinary caliculi,Pregnancy,• Asymptomatic Bacteriuria in pregnant women,• Pyelonephritis, 4/16/2012 Dr.T.V.Rao MD 54
  • 55. Facts on UTI• Women suffer more than males Short urethra Pregnancy, Sexual intercourse /Honey moon cystitis.• Other factors Urethral obstruction, Urinary stones Congenital malformations Neurological disorders, Catheterization , CystoscopyUsually cystitis is produced from fecal strains entering urethra4/16/2012 Dr.T.V.Rao MD 55
  • 56. Culturing for E.coli• Mid stream sample/semi quantitative culturing (Kass et al ) >_ 1.00,000/ml of urine. ( significant Bacteriuria )• Urine should not be kept in wards for > 2 hours and to be preserved at 4 c• Culture by standard loop method.• Fixed volume cultured on MacConkey agar Lactose fermenters I M Vi C• Antibiotic sensitivity tested.4/16/2012 Dr.T.V.Rao MD 56
  • 57. Other Bacteria and UTI• Majority of UTI are caused by E.coli• Other agents which cause UTI,1 Staphylococcus2.Proteus.3.Pseudomonas,4.Klebsilella spp,Citrobacter,5.Enteococcus.4/16/2012 Dr.T.V.Rao MD 57
  • 58. Other infection with E.coli• Pyogenic infections.• Intraabdominal infections• Peritonitis. Abscess.• Septicemias• Produce Drug resistant infections.4/16/2012 Dr.T.V.Rao MD 58
  • 59. 4/16/2012 Dr.T.V.Rao MD 59
  • 60. Klebsiella, Enterobacter, Serratia & Hafnia sp.• Usually found in intestinal tract• Wide variety of infections, primarily pneumonia, wound, and UTI• General characteristics: – Some species are non-motile – Simmons citrate positive – H2S negative – Phenylalanine deaminase negative – Some weakly urease positive – MR negative; VP positive4/16/2012 Dr.T.V.Rao MD 60
  • 61. Klebsiella species• Usually found in GI tract• Four major species• K. pneumoniae is mostly commonly isolated species – Possesses a polysaccharide capsule, which protects against phagocytosis and antibiotics AND makes the colonies moist and mucoid – Has a distinctive “yeasty” odor – Frequent cause of nosocomial pneumonia4/16/2012 Dr.T.V.Rao MD 61
  • 62. Klebsiella• Klebsiella is a genus of non-motile, Gram- negative, oxidase-negative, rod-shaped bacteria with a prominent polysaccharide- based capsule. It is named after the German microbiologist Edwin Klebs (1834–1913). Frequent human pathogens, Klebsiella organisms can lead to a wide range of disease states, notably pneumonia, urinary tract infections, septicaemia, and Dr.T.V.Raotissue infections. 624/16/2012 soft MD
  • 63. Klebsiella• The genus was originally divided into 3 main species based on biochemical reactions. Today, 7 species with demonstrated similarities in DNA homology are known. These are (1) Klebsiella pneumoniae, (2) Klebsiella ozaenae, (3) Klebsiella rhinoscleromatis, (4) Klebsiella oxytoca, (5) Klebsiella planticola, (6) Klebsiella terrigena, and (7) Klebsiella ornithinolytica4/16/2012 Dr.T.V.Rao MD 63
  • 64. Klebsiella• K pneumoniae is the most medically important species of the group. K oxytoca and K rhinoscleromatis have also been demonstrated in human clinical specimens. In recent years, klebsiellae have become important pathogens in nosocomial infections.4/16/2012 Dr.T.V.Rao MD 64
  • 65. Klebsiella• 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 antigens4/16/2012 Dr.T.V.Rao MD 65
  • 66. Klebsiella species• Usually found in GI tract• Four major species• K. pneumoniae is mostly commonly isolated species – Possesses a polysaccharide capsule, which protects against phagocytosis and antibiotics AND makes the colonies moist and mucoid – Has a distinctive “yeasty” odor – Frequent cause of nosocomial pneumonia4/16/2012 Dr.T.V.Rao MD 66
  • 67. Klebsiella species (cont’d) – Significant biochemical reactions • Lactose positive • Most are urease positive • Non-motile4/16/2012 Dr.T.V.Rao MD 67
  • 68. 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 meningitis4/16/2012 Dr.T.V.Rao MD 68
  • 69. Enterobacter species• Comprised of 12 species; E. cloacae and E. aerogenes are most common• Isolated from wounds, urine, blood and CSF• Major characteristics – Colonies resemble Klebsiella – Motile – MR negative; VP positive4/16/2012 Dr.T.V.Rao MD 69
  • 70. Serratia species• Seven species, but S. marcescens is the only one clinically important• Frequently found in nosocomial infections of urinary or respiratory tracts• Implicated in bacteremic outbreaks in nurseries, cardiac surgery, and burn units• Fairly resistant to antibiotics4/16/2012 Dr.T.V.Rao MD 70
  • 71. Serratia species (cont’d)• Major characteristics – Ferments lactose slowly – Produce characteristic pink pigment, especially when cultures are left at room temperature S. marscens on nutrient agar →4/16/2012 Dr.T.V.Rao MD 71
  • 72. Hafnia species• Hafnia alvei is only species• Has been isolated from many anatomical sites in humans and the environment• Occasionally isolated from stools• Delayed citrate reaction is major characteristic4/16/2012 Dr.T.V.Rao MD 72
  • 73. Other 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 -4/16/2012 Dr.T.V.Rao MD 73
  • 74. Proteus, Morganella & Providencia species• All are normal intestinal flora• Opportunistic pathogens• Deaminate phenylalanine• All are lactose negative4/16/2012 Dr.T.V.Rao MD 74
  • 75. Proteus species• P. mirabilis and P. vulgaris are widely recognized human pathogens• Isolated from urine, wounds, and ear and bacteremic infections• Both produce swarming colonies on non-selective media and have a distinctive “burned chocolate” odor• Both are strongly urease positive• Both are phenylalanine deaminase positive4/16/2012 Dr.T.V.Rao MD 75
  • 76. Proteus species (cont’d)• A exhibits characteristic “swarming”• B shows urease positive on right4/16/2012 Dr.T.V.Rao MD 76
  • 77. Morganella species• Morganella morganii is only species• Documented cause of UTI• Isolated from other anatomical sites• Urease positive• Phenylalanine deaminase positive4/16/2012 Dr.T.V.Rao MD 77
  • 78. Providencia species• Providencia rettgeri is pathogen of urinary tract and has caused nosocomial outbreaks• Providenicia stuartii can cause nosocomial outbreaks in burn units and has been isolated from urine• Both are phenylalanine deaminase positive4/16/2012 Dr.T.V.Rao MD 78
  • 79. Citrobacter species• Citrobacter freundii associated with nosocomial infections (UTI, pneumonias, and intraabdominal abscesses)• Ferments lactose and hydrolyzes urea slowly• Resembles Salmonella sp.4/16/2012 Dr.T.V.Rao MD 79
  • 80. • Programme Created by Dr.T.V.Rao MD for benefit of Medical and Paramedical Students as e-learning Resource • Email • doctortvrao@gmail4/16/2012 Dr.T.V.Rao MD 80

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