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ENTEROBACTERIACEAE

ENTEROBACTERIACEAE. Dr Gehan Panagoda Division of Microbiology Faculty of Dental Sciences University of Peradeniya. Gram -ve bacilli/rods Natural habitat - Intestinal tract of humans/animals Facultative anaerobes/aerobes. Ferment CHO, Often produce gas

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ENTEROBACTERIACEAE

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  1. ENTEROBACTERIACEAE Dr Gehan Panagoda Division of Microbiology Faculty of Dental Sciences University of Peradeniya

  2. Gram -ve bacilli/rods • Natural habitat - Intestinal tract of humans/animals • Facultative anaerobes/aerobes

  3. Ferment CHO, Often produce gas • Enterics found in water is used as a proof of contamination with sewerage.

  4. There are more than 25 genera,110 species. • Clinically significant 25 species.

  5. Grow on peptone or meat extract. • Grow well on McConkey agar. • Catalase +ve • Oxydase -ve.

  6. Antigenic structure. • Complex • Lipopolisaccharides/Somatic or O antigen • Heat stable.more than 150 types • Most external in the cell wall • detected by bacterial agglutination • Antibody produced is predominantly IgM

  7. Capsular/K antigen • Sometimes external to O antigen but not always • Can be polysaccharides or protein • Flagella /H antigen • Heat and alcohol labile.

  8. Colicines/Bacteriocines • Produced by many Gram -ves • Virus like bactericidal substance • Active against some other bacteria of similar • or closely related species

  9. Production is controlled by plasmids • E coli - colicines • Serratia - marcescines • Pseudomonas - Pyocines THIS MAY BE ONE OF THE REASONS FOR THEIR SUCCESS AS COMMENSALS

  10. Toxins/Enzymes • Endotoxins- Complex LPS in the cell wall • Exotoxins

  11. Relevance in clinical medicine • Normally nonpathogenic. • In some instances, they even contribute to normal. • function and nutrition. • Other species cause hospital/community acquired • disease • Become pathogenic when they change their habitat. • When the host defense is reduced, act as opportunistic • pathogens.

  12. Common infections • UTI • RTI • Diarrhoea • Enterocolitis • Wound infection

  13. E. Coli Klebsiella Serratia Enterobacter Shigella Salmonella Proteus Yersinia Lactose fermenters Non lactose fermenters

  14. Relevance in clinical medicine • Primary pathogens - Shigella sp Salmonella typhi • Common infections - UTI ( E. coli, Proteus) • Less common but important - • Respiratory - Klebsiella • Enterocolitis - Yersinia

  15. Hospital infections - due to colonization - Contamination - Compromised patients

  16. E SCHERICHIA COLI UTI Most common cause for UTI,90% UTI in young women is due to E coli. Diarrhoea E coli is classified on the basis of virulence and the mechanism of causing diarrhoea

  17. A.Enteropathogenic E coli (EPEC) • Important cause of diarrhoea ininfantsof developing countries. • Adhere to mucosal cells in small bowel,loss of microvilli, NONINVASIVE • enter to cell body. result in watery diarrhoea. • Self limiting ,can be chronic. • Normally do not produce toxins • Few EPEC produce 0114, 0128 calledVETEC ( Vero cytotoxin producing ) (Viteka ?)

  18. B.Enterotoxigenic E coli ( ETEC) • Common cause for travelers diarrhoea, and watery diarrhoea in children. • Colonisation factor facilitates the attachment to the • intestinal epithelium. • Some ETEC produces heat labile exotoxin LT and heat stable or either of the toxins • LT has two sub units A B • Action -Activate Adenylate cyclase Increase local CAMP Intense, prolonged hypersecretion of water , Lumen of gut fill with water Hypermobility and diarrhoea results.

  19. LT is antigenic and cross reacts with the enterotoxin of Vibrio cholerae.

  20. Some ETEC produces heat stable enterotoxin STa/b • STa activates guanylyl cyclase. • STb activates cyclic nucleotides. • Releases water

  21. C. Enterohemorrhagic E coli ( EHEC) • Produce verotoxin which has similarities to Shiga toxin • Associated with hemorrhagic colitis, severe form of diarrhoea. • Hemolytic uremic syndrome Disease can be prevented by thorough cooking.

  22. D.Enteroinvasive E coli (EIEC) • Produces disease similar to shigellosis. • In adults this has been isolated with Shigella • Commonly affect children in developing countries, • and travelers. • Disease is due to invasion into mucosal cells of the intestine • multiply inside the cells and destruction /inflammation/ulceration • diarrhoea with blood • EIEC are nonlactose fermenter,or late lactose fermenter • and non motile.

  23. E. Enteroaggregative E coli (EAEC) • Produce acute/chronic diarrhoea in persons in developing countries. • Sepsis When normal host defense is poor ,sepsis can happen.Common in new born babies whose IgM level is low.

  24. Treatment of E.coli related diarrhoea 1st Line • Nitrofurantoin • Nalidixic acid • Norfloxacin ABST’ SHOULD BE DONE • Ampicillin • Cotrimoxazole 2nd line • Ciprofloxacin/Ceftriaxone/Cefuroxime Gentamicin

  25. Meningitis • E coli and Gp.B Strept. are the leading causes for • meningitis in infants. • K1 antigen is responsible for meningitis • K1 cross reacts with the Gp.B capsular • polysaccharides of N meningitides.

  26. Pneumonia • 25% of gram -ve pneumonia with 50% mortality • Usually broncho pneumonia • High level of resistance to Ampicillin /Cotrimoxazole

  27. Klebsiella • K pneumoniae • Present in respiratory tract and feces of about 5% of • normal individuals. • Can cause bacterial pneumonia. • Produce extensive hemorrhagic necrotising consolidation of lungs.

  28. UTI and focal infections in debilitated pts. Hospital acquired infections due to K pneumoniae K oxytoca K rhinoscleromatis produces rhinoscleroma, condition with destructive granuloma of the nose and pharynx.

  29. Enterobacter aerogenus • Capsulated • Free living in the intestine • Cause UTI and sepsis. Serratia • Common opportunistic pathogen in hospital pts.

  30. Cause pneumonia, bacterimia, endocarditis. Often resist to aminoglycosides and penicillin. Treatment-Third generation Cephalosporines.

  31. Proteus • Pathogenic only when the bacteria leave the intestinal tract • Cause UTI, bacteremia, Pneumonia. • Ex.P vulgaris

  32. Proteus produce urease-Alkaline urine • Stone formation • Rapid motility of the organism facilitates the invasion • Morganella morganii isan important nosocomial pathogen. • Treatment-Penicillin,Aminoglycosides,Cephalosporines

  33. Diagnostic tests 1.Specimens-Urine, blood, pus, CSF, Sputum, stools 2.Smear 3.Culture blood agar Immunity is not satisfactory. Management No single specific therapy available Sulfonamides marked antibacterial effect Ampicillin on enterics Cephalosporines Fluoroquinolone Aminoglycoside

  34. ABST is essential Predisposing factors to be corrected surgically. Eg:Obstructions- UTI Perforated abdominal organs Diarrhoea fluid replacement Bacterimia Rapid Antibiotic therapy fluid replacement Treatment for DIC

  35. Travelers diarrhoea • Bismuth subsalicilate suspension inactivate • E coli toxin • Tetracycline as prophylaxis • Food and water sanitation

  36. SHIGELLA • Natural habitat intestinal tract of humans/other • primates • Exclusively of parasites of human or primates • BLOODY MUCOUS DYSENTRY

  37. Morphology and identification • Slender Gram -ve rods • Facultative anaerobes • All Shigellae ferment glucose not lactose • S sonnei ferments lactose also.

  38. Antigenic structure • Complex, there are more than 40 sero types based on their LPS of somatic O antigen • There are four gps based on somatic O • A • B • C • D

  39. Pathogenesis Infection almost always limited to GIT • Blood invasion is rare • Highly communicable

  40. Infective dose 103 Organisms (Salmonella & Vibrio 105-108) - pretty small • Invade mucosal epithelial cells by induced phagocytosis, • escape from phagocytic vacuole multiply and spread with in the cell and adjacent cells.

  41. Microabscess in the large intestine and terminal ileum-necrosis-ulceration -bleeding. • Formation of pseudomembrane in ulcerated areas lead to scarring

  42. Toxins • Endotoxins - after autolysis, causes diarrhoea and ulcers • Exotoxins - acts as a enterotoxin - acts on mucosa ---transudation of fluids -acts as neurotoxin - polyneuritis/coma/meningism

  43. Common pathogenic species • S dysenteriae (A) • S flexneri (B) • S boydii (C) • S sonnei (D)

  44. Shigella Glucose Acid only Acid and gas A,B (except type 6), C,D Sh. flexneritype 6 Mannitol Indole -ve Fermented Non-fermented Gps BCD GpA OVERLAPPING SPECIES = DIFFERENT TYPES Indole Lactose -ve B,C +ve at 3-8 days GpD Sh sonnei +ve Sh. dysenteriae 2,7,7 -ve Sh. dysen 1,3,4,5,6 Indole +ve -ve Sh, flexneri/Sh. boydii Sh. boydii

  45. Clinical features • Incubation period 1-2 days. • Sudden onset of • abdominal pain fever and • watery diarrhoea, • mucus and bloody stools. • fever diarrhoea subsides 2-5 days. • loss of water - dehydration. • Chronic carrier status may result.

  46. Animal pathogenicity • Oral administration Normally does not cause true dysenteric lesions Sh. flexneri 1010 sever dysentery in monkeys • IV administration 0.01mg Sh. dysenteriae sever diarrhoea in rabbits

  47. Dysentery carriers • There are healthy carriers in the community • This will happen after an attack • Will excrete in the bacilli intermittently for few weeks - small proportion can become persistent carriers

  48. LAB DIAGNOSIS Specimens - fresh stool/mucous flakes/rectal swabs/Blood/serum Microscopy pus cells /RBC/Macrophages

  49. Culture MacConkey agar - selective DCA S-S agar = selective Selenite F broth - for enrichment and transport Colourless on MacConkey

  50. Biochemical Citrate -ve Urease -ve H2S -ve Sh. sonnei KCN -ve Indole +ve MR +ve

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