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Enteric Gram-Negative Rods ( Enterobacteriaceae )

Enteric Gram-Negative Rods ( Enterobacteriaceae ). no. white colonies pathogenic. yes. colored colonies (red) non-pathogenic. SS plate. lactose fermentation.

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Enteric Gram-Negative Rods ( Enterobacteriaceae )

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  1. Enteric Gram-Negative Rods (Enterobacteriaceae)

  2. no white colonies pathogenic yes colored colonies (red) non-pathogenic SS plate

  3. lactose fermentation • Mechanism: Non-pathogenic enteric bacilli can ferment lactose to produce acidic by-products while pathogenic enteric bacilli such as Shigella and Salmonella can not. • Media: SS-plate or EMB plate , TSI agar slants • Basic components:lactose and a pH indicator

  4. IMViC test Indole test Methyl red (MR) test Voges-Proskauer (VP) test         Citrate utilization test E. coli Enterobacter Aerogenes  

  5. Live in the intestinal tract of humans and animals anaerobes • opportunistic infection (E. coli) • septicemia • pneumonia • meningitis • urinary tract infections • human pathogens (Salmonella and Shigella) • community-acquired diseases • respiratory infections (Klebsiella pneumoniae) • urinary tract infection (E. coli and Proteus)

  6. E. coli causes urinary tract infections such as acute cystitis and pyelonephritis

  7. pili • capsule • enterotoxin: cause diarrhea and tissue damage • endotoxin

  8. H Ag (flagella) K/Vi Ag (capsule) somatic OAg(lipopolysaccharide)

  9. Escherichia coli Gram stain? Motility? lactose fermentation? Antigens? IMViC? Transmission route? virulence factors?

  10. Enteropathogenic E. coli (EPEC) Enterotoxigenic E. coli (ETEC) Enteroinvasive E. coli (EIEC) Enterohemorrhagic E. coli (EHEC) Enteroaggregative E.coli (EAggEC)

  11. Enteropathogenic E. coli (EPEC) • Commonly associated with infant diarrhea. • Characteristic lesion with destruction of microvilli without invasion • Clinical signs • Fever • diarrhea with non-bloody stools • Vomiting • nausea

  12. Cause "traveller’s diarrhea". • Two types of plasmid-encoded toxins are produced: • Heat labile toxins (LT), an adenyl cyclase which catalyze ATP to cAMP. • Heat stable toxins (ST), a guanyl cyclase to catalyze GTP to cGMP. cAMP/cGMP are the intracellular second messagers. The former increases the secretion of water and ions, and the latter inhibits ionic uptake. • Clinical signs • watery diarrhea • Fever • nausea Enterotoxigenic E. coli (ETEC)

  13. Enteroinvasive E. coli(EIEC) • Associated with elder children and adult diarrhea. • Without flagella • High virulence: a small number of EIEC can cause serious illness • Clinical signs • Acute inflammatory responses • tissue destruction • diarrhea with little fluid, a lot of blood and mucus containing polymorphonuclear cells

  14. Enterohemorrhagic E. coli(EHEC) • EHEC produces bacteriophage-mediated exotoxin. This toxin is called as Vero toxin (VT) because of its cytotoxicity to cultured Vero cells. • In children, the disease may be progressed to a systemic stage called as hemolytic uremic syndrome (kidney injury) with 10% death rate. • Clinical signs • serious abdominal pain • diarrhea which is initially watery but then becomes bloody

  15. Enteroaggregative E. coli (EAggEC) • It produces enteroaggregative heat-stable toxin (EAST) similar to the heat stable toxins of ETEC. • It produces mucous associated autoagglutinin which causes aggregation of the bacteria and formation of biofilm. • Clinical Signs • persistent, mucus-watery diarrhea • vomiting and dehydration in infants

  16. Shigella Gram stain? motility? Lactose fermentation?

  17. Classification • According to the difference of O antigen, Shigellastrains are divided into 4 groups: • S. dysenteriae • S. flexneri • S. boydii • S. sonnei

  18. Clinical findings • Most common cause of bacterial dysentery in human • characteristic blood and mucus stools • Due to specific S-IgA, only invades intestinal mucosa and never enters bloodstream. But the endotoxin can be absorbed into bloodstream to cause endotoxemia. • Can cause toxic dysentery in children, display systemic toxic symptoms but no enteric symptoms. Has a a high death rate.

  19. Virulent factors • pilus • endotoxin • exotoxin:Shigella dysenteriae can produce an exotoxin called as shiga-toxin which is simmilar to Vero toxin (VT) of EHEC. Shiga-toxin is enterotoxic, cytotoxic and neurotoxic. So the dysentery (痢疾) caused by this microbe is more serious than that by the other three groups.

  20. Control transmission Dysentery is treated with antibiotics. But multiple drug resistance mediated by plasmids are common in many Shigella strains.

  21. Salmonella Gram stain? Motility? Lactose fermentation? antigenic structures?

  22. More than 2000 serotypes based on antigenic difference • Infect human (enteric fever) • S. typhi • S. paratyphi A • S. schottmuelleri (S. paratyphi B) • S. hirschfeldii • Infect animal and human • S. choleraesuis • S. typhimurium • S. enteritidis

  23. Virulent factors • Vi antigen: consisted of capsular polysacchride. It resists phagocytosis and plays an important role during invasion of Salmonella. • endotoxin • enterotoxin

  24. Diseases • enteric fever (typhoid fever) • S. typhi • S. paratyphi A • S. schottmuelleri (S. paratyphi B) • S. hirschfeldii

  25. Enteric fever (typhoid fever) is the most serious form of salmonella infection which only occurs in human. • Carrier state is common • In untreated patients, the death rate is 7% to 14%. • Antibiotic therapy is essential, vaccines are not effective and not widely used.

  26. enteric fever development • The microbe initially invades intestinal mucosal epithelium and propagate at the local. • The microbe penetrates into the bloodstream to cause the first round of bacteremia with symptoms of fever, general discomfort and pain. • The microbe enters many organs such as liver, spleen, kidney, gall and marrow for further propagation. • The microbe penetrates into the bloodstream again to cause the second round of bacteremia with serious symptoms of high fever, swell of spleen and liver, rose-colored spots in skin, and tissue injury.

  27. enteric fever Diagnosis 1. Definitive diagnosis-bacteria culture Blood @ first week Stool and urine @ from the second week on Marrow can be considered because of its high and permanent positive results.

  28. enteric fever diagnosis • 2. Widal test • a quantitative agglutination test using the known O antigen of S.typhi , and H antigens of S. typhi and S. paratyphiA/B to detect specific serum antibodies. • For one single serum sample,The titers of anti-O antigen IgM  1:80 and/or anti-H antigen IgG  1:160. • For two serum samples that collected with an interval of 5~7 days, 4-fold increase in titers of specific antibody.

  29. Diseases • Gastroenteritis (food-poisoning) • S. choleraesuis • S. typhimurium • S. enteritidis

  30. Gastroenteritis (food poisoning): • It is the most commonSalmonella infection and usually transmitted from contaminated food. However, only a few of food poisoning-causing salmonella serotypes can produceenterotoxin.

  31. Diseases • Septicemia: commonly caused by • S. hirschfeldii • S. typhimurium • S. choleraesuis

  32. Septicemia: • Many Salmonella serotypes can cause septicemia. This disease is commonly found in children or adult with low immunity.

  33. Vibrio choleraeCholera

  34. Introduction • Cholera caused by Vibrio cholerae is characterized by profuse watery diarrhea and serious vomiting which results in extreme loss of fluid and electrolytes, shock and kidney prostration. If patients are untreated, the death rate is as high as 60%.

  35. Cholera: outbreak in India

  36. Introduction • There have been 8 great outbreaks in the world. • In 1991, a great outbreak (7th) started in Peru. There were more than a million patients in Central and South America. • In 1992, another great outbreak (8th) started in India and then spread to all parts of Asia. Not serotype O1 but O139 caused this outbreak.

  37. Classification • classical biotype • El Tor biotype Responsible for the 1st-6th great outbreaks Further typing O1 Responsible for the 7th great outbreak Responsible for the 8th great outbreak in 1992 O-antigen O139 non-O1/139 Cause cholera-like disease

  38. high pH (pH8.5-9.0) • TCBS (thiosulfate-citrate-bile-sucrose) agar plate

  39. Major virulent factors Flagellum:offers an ability to penetrate enteric mucus layer to reach the surface of host cells. Pilus:adhesion Cholera toxin:the most important virulent factor which induce electrolyte and water hypersecretion. This toxin is chromosomally encoded and its molecule contains subunits A and B.

  40. Pathogenesis of cholera toxin ◇Subunit B binds to its receptor (gangliosides) on the surface of epithelial cells and provides a channel allowing subunit A to enter host cell. ◇ Cellular proteinase lyses subunit A into peptides A1 and A2 Peptide A1 has activity of ADP-ribosylation to transfer ADP from NAD onto protein G which activates protein G ↓ Activated protein G induces cAMP overproduction ↓ A large number of cAMP induces electrolyte and water hypersecretion of cells

  41. the major cause of death… Dehydration!! (脱水) Replace fluid and electrolyte！！！ -most important treatment Antibiotics such as tetracycline additionally used

  42. Vibrio parahemolyticus • exists in raw sea-food and causes food poisoning in human • It is halophilic and optimal NaCl concentration in media is 3.5% • It produces hemolysin • Can be rapidly killed by acid (eg. acetic acid)

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