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Enterobacteriaceae
Enterobacteriaceae
Enterobacteriaceae
Enterobacteriaceae
Enterobacteriaceae
Enterobacteriaceae
Enterobacteriaceae
Enterobacteriaceae
Enterobacteriaceae
Enterobacteriaceae
Enterobacteriaceae
Enterobacteriaceae
Enterobacteriaceae
Enterobacteriaceae
Enterobacteriaceae
Enterobacteriaceae
Enterobacteriaceae
Enterobacteriaceae
Enterobacteriaceae
Enterobacteriaceae
Enterobacteriaceae
Enterobacteriaceae
Enterobacteriaceae
Enterobacteriaceae
Enterobacteriaceae
Enterobacteriaceae
Enterobacteriaceae
Enterobacteriaceae
Enterobacteriaceae
Enterobacteriaceae
Enterobacteriaceae
Enterobacteriaceae
Enterobacteriaceae
Enterobacteriaceae
Enterobacteriaceae
Enterobacteriaceae
Enterobacteriaceae
Enterobacteriaceae
Enterobacteriaceae
Enterobacteriaceae
Enterobacteriaceae
Enterobacteriaceae
Enterobacteriaceae
Enterobacteriaceae
Enterobacteriaceae
Enterobacteriaceae
Enterobacteriaceae
Enterobacteriaceae
Enterobacteriaceae
Enterobacteriaceae
Enterobacteriaceae
Enterobacteriaceae
Enterobacteriaceae
Enterobacteriaceae
Enterobacteriaceae
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Enterobacteriaceae

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  • 1. Enterobacteriaceae Escherichia Salmonella
  • 2. Plan  Enterobacteriaceae  Escherichia  Salmonella
  • 3. Enterobacteriaceae ПОДЗАГОЛОВОК
  • 4. Enterobacteriaceae  Domain: Bacteria  Phylum: Proteobacteria  Class: Gammaproteobacteria  Order: Enterobacteriales  Family: Enterobacteriaceae
  • 5. Classification and morphology  Over 30 genera and 120 species  More than 95% of clinically significant strains fall into 10 genera and less than 25 species  Small Gram-negative non-sporeforming enteric bacilli  Capsule, slime layer, or neither  Possess fimbriae (pili)  Motile via peritrichous flagella except ShigellaShigella and KlebsiellaKlebsiella which are non-motile  Complex cell wall  Typically 1-5 μm in length
  • 6. Cultivation  All are aerobic but can be facultative anaerobic  Various nutrient media:  Ordinary: MPA, MPB  Special: SS-agar, Ploskirev, Levin, Endo, Kessler media, bismuth- sulfite agar, MacConkey agar and broth, fluorogenic selective broth  Differential: SDS-broth – for detection of lactose fermentation; Kligler agar – lactose, glucose, H2S; Hiss media; citrate agar; acitate agar etc.
  • 7. Cultivation  Colony morphology: moist, gray (except Serratia marcescansSerratia marcescans which appears red) smooth colonies on ordinary media  Some strains are beta hemolytic on blood agar
  • 8. Fermentative properties Most EnterobacteriaciaeEnterobacteriaciae: ferment glucose with acid production reduce nitrates (NO3 to NO2 or all the way to N2) are oxidase negative Biochemically and metabolically diverse; ferment glucose by the mixed acid pathway; Klebsiella, EnterobacterKlebsiella, Enterobacter and SerratiaSerratia utilize the butanediol pathway
  • 9. Antigenic Structure  plays an important role for some species in epidemiology and classification  K (capsular)K (capsular) antigens: capsular polysaccharide, particularly heavy in Klebsiella  H (flagellar)H (flagellar) antigens: flagellar proteins of motile genera and species; used for typing; absent in nonmotile genera (Shigella and Klebsiella)  O (somatic)O (somatic) antigens: O-specific polysaccharide side chain of lipopolysaccharide; used for typing
  • 10. Epidemiology  Some of the normal inhabitants of the small and large intestine included in Enterobacteriaceae  Found in soil, water and decaying matter  Are responsible for nosocomial infections (5-10% of all hospital infections)
  • 11. Pathogenesis & Immunity:  Endotoxin: important virulence factor with wide-ranging effects on host  Capsule: antiphagocytic  Antigenic phase variation: capability to alternately express or not express either capsule or flagella and thus avoid host immunity  Sequestration of nutritional factors, in particular, iron by production of siderophores which are extracellular iron-chelating compounds (e.g., enterobactin, aerobactin): iron is important compound for both host and pathogen and is limited in supply and thus must be competed for; much of iron in host body is sequestered in heme proteins (e.g., hemoglobin, myoglobin) and in iron-chelating proteins (e.g., transferrin, lactoferrin)
  • 12. Pathogenesis & Immunity:  Resistance to serum killing: many bacteria are inherently sensitive to nonspecific bloodborne components and to circulating complement and the resultant complement-mediated clearancecomplement-mediated clearance, but Enterobacteriaceae and other bloodborne pathogens can resist such killing  True pathogenic members of the Enterobacteriaceae may possess specific virulence features, which are unique to individual genera or species: Adhesins; ExotoxinsAdhesins; Exotoxins, (e.g., enterotoxins which act in the small intestine)
  • 13. Laboratory diagnostics  Specimens whether pus, tissue, sputum, fluids, rectal swabs, or feces should be cultured immediately or placed on special media to prevent overgrowth  Special isolation media: contain various substances including indicators, inhibitors, etc.  Media and tests to differentiate the genera of the family  Tests that divide species of the genera, e.g., patterns of acid production from various carbohydrates  Serological identification
  • 14. Escherichia ПОДЗАГОЛОВОК
  • 15. Species  Escherichia albertii  E. blattae  E. coliE. coli  E. fergusonii  E. hermannii  E. senegalensis  E. vulneris  The genus is named after Theodor Escherich, the discoverer of Escherichia coli.
  • 16. E. coli  Straight Gram“-” rods  Sizes: 0,4-0,6 x 2,0-6,0 mcm  Peritrichous flagella; motile. Some strains immobile  Microcapsula built from homopolimer of sialic acid
  • 17. Cultivation  Well adopted to any nutrient media. Can grow even on nutrient media with only glucoseglucose as a single organic substance.  Can grow with a presence of oxygen as well as in absence.  In anaerobic conditions uses fermentation with production of acid and gas, can use NO2, NO3 or fumaric acid as final electron acceptors.  Can grow in ordinary media with formation of S and R-form of colonies.  S-colonies are smooth, covex, shiny, semi-translucent, greyish.  On liquid media – diffuse turbidity and demersal sedimentation
  • 18. Cultivation  Optimum temperature for growth is 30-37 °C and the optimum pH value of medium up 7.2-7.5  growth becomes visible in the first two days  E. coli from cold-blooded animals grows at 22-37° C but not at 42- 43° C.
  • 19. Cultivation  Endo media – pink colonies with metal shining  Levin (eosin methylene blue) media – dark blue colonies  Ploskirev media – red colonies
  • 20. Fermentative properties  E. coli does not liquefy gelatin. It produces indole and hydrogen sulphide, and reduces nitrates to nitrites; ferments glucose, levulose, lactose, maltose, mannitol, arabinose, galactose, xylose, rhamnose, and occasionally saccharose, raffinose, dulcitol, salycin, and glycerin, with acid and gas formation. It also coagulates milk.  There are varieties of the bacteria which ferment saccharose, do not produce indole, have no flagella, and do not ferment lactose.  Can have decarboxylation of lysine, galactozidase present  Does not utilize citrates, urea,aenilallanin
  • 21. Antigenic structure  Close to 171 serogroups according to O-antigen. IndenticalClose to 171 serogroups according to O-antigen. Indentical chemical structure with all genus.chemical structure with all genus.  K-antigen has 3 types:K-antigen has 3 types: A, B, L.A, B, L. By B type there are more then 97By B type there are more then 97 variant.variant.  By H-antigen – more then 57 variants. Present only in flagellatedBy H-antigen – more then 57 variants. Present only in flagellated forms of E.coli.forms of E.coli.  K-antigens can mask O-antigens. Last can be revealed after boilingK-antigens can mask O-antigens. Last can be revealed after boiling  Formula for antigenic structure: for serogroup (O:K), for serovarFormula for antigenic structure: for serogroup (O:K), for serovar (O:K:H). Example: O111:B4:H6(O:K:H). Example: O111:B4:H6
  • 22. Resistance  Relatively resistant  Can survive in water and soil for several monthes  Dies in 50 C during 60 min, 60 C – 15 min  Cab react to changes of chemical composition, pH, temperature and osmolarity and move to or from it.  Can change diameter of channels of external membrane to get bigger molecules or stop their absorbtion
  • 23. Ecology  E.coli can be pathogenic or conditionally pathogenic  Constant inhabitant of colon.  Produce there low-molecular peptides (cellular messengers), antagonistic low-molecular proteins – microcines, high molecular substances – colicines, vitamins etc.  Average content of E.coli in feces – 109 per 1 g  Decreased amount of E.coli (e.g. because of antibiotics) lead to disbacteriosis  Conditionally pathogenic E.coli in unusual location lead to formation of inflammatory process (kidneys, bladder, joints, internal organs), especially in low immunity status
  • 24. Pathogenesity  Pathogenic strains cause 2 types of infections: urinary infections, neonathal meningitis, gastroenteritis  Pathogenic E.coli that cause intestinal escherichiosis are called diarrheagenic  Uropathogenic strains cause 90% of urinary infections. 14 times more often in women.  Neonathal meningitis develops in 1 case per 3000-4000 of newborns. Majorly caused by K-1-antigenic bacteria.
  • 25. Diarrheagenic E.coli  Enterotoxigenic – cause cholera like diseases. 17 serogroups. Majorly O6:H16, O8:H9, O78:H11, O148:H28O6:H16, O8:H9, O78:H11, O148:H28. Alimentary and water transmission  Enteroinvasive – immobile, do not ferment lactose. Close to 9 serogroups. Cause dysentery like diseases. Majorly O124, O144,O124, O144, O152O152. Alimentary and water transmission. Can case hospital infection  Enteropathogenic – cause diarrhea in children of 1st year. Especially in cases of artificial feeding. Majorly O55, O111, O26,O55, O111, O26, O18O18. O55:H10, O111:H2 produce toxins simillar to Shigella
  • 26. Diarrheagenic E.coli  Enterohemorrhagic – bloody diarrhea (hemorrhagic colitis) with further complications (uremia syndrome, thrombocytopenic purpura). Majorly caused by O157:H7O157:H7. Source of infection: cattle and sheep. Transmitted by meat.  Enteroaggregative – make adhesion on epithelial cells with formation of conglomerates. Damages are caused because of toxins.  Diffuseadhesive - make adhesion on epithelial cells with their destruction. Majorly in children with immune pathology.
  • 27. Laboratory diagnostics  Specimens: feces, vomiting masses, pus, blood, material after autopsy, water, food products, washouts from hands.  Obtaining and identification of pure culture  Seeding on special nutrient media with further serologic identification  EIA and PCR for detection of enterotoxins
  • 28. Prophylaxis  Specific – not developed  Non-specific – sanitary-hygienic rules and control especially for water supply, food industry, food products.  Correct usage of antibiotics  Usage of liquid coli-protein phage for most common serogroups (also can be used for treatment)
  • 29. Treatment  For cholera like syndrome –rehydration with glucose-electrolyte solutions, oral antiseptics: nitrofurans, oxyquinolons  For desentery like syndrome – salt sulutions, nitrofurans, quinolones, fluoroquinolons, enterosorbents, probiotics, vitamins  For enteropathogenic E.coli - oral antiseptics, in severe cases antibiotics: polymyxines, aminoglycosides, cephalosporins of 3rd generation, fluoroquinolons, kanamycin; rehydration  For enterohemorrhagic – same. In severe cases can be inclusion of glucocorticoid hormones, plasmapheresis, hemodialysis  Septic forms – according general principles of treatment of sepsis including correction of disseminated intravascular coagulation (DIC) syndrome
  • 30. Salmonella ПОДЗАГОЛОВОК
  • 31. Species  Salmonella bongoriSalmonella bongori  Salmonella enterica:Salmonella enterica:  S. enterica subsp. arizonaeS. enterica subsp. arizonae  S. enterica subsp. diarizonaeS. enterica subsp. diarizonae  S. enterica subsp. entericaS. enterica subsp. enterica :: over 2500 serovarsover 2500 serovars  S. enterica subsp. houtenaeS. enterica subsp. houtenae  S. enterica subsp. indicaS. enterica subsp. indica  S. enterica subsp. salamaeS. enterica subsp. salamae
  • 32. Salmonella bongori  Generally can be obtained from reptiles, can rarely occurs in dogs and birds  In pet animals can cause diarrhea, but mostly asymptomatic  In humans can be associated with diarrhea, fever, gastroenteritis in children less than 3 years old after an oral contact with animal feces
  • 33. Salmonella enterica subsp. enterica  Salmonella CholeraesuisSalmonella Choleraesuis  Salmonella DublinSalmonella Dublin  Salmonella EnteritidisSalmonella Enteritidis  Salmonella Gallinarum  Salmonella Hadar  Salmonella Heidelberg  Salmonella Infantis  Salmonella Paratyphi ASalmonella Paratyphi A  Salmonella Paratyphi BSalmonella Paratyphi B  Salmonella TyphiSalmonella Typhi  Salmonella TyphimuriumSalmonella Typhimurium  Salmonella Genru
  • 34. Cultivation  Morphology: similar to Escherichia  Facultative anaerobes  Well grow on ordinary media and media with yolk with temperature 7-45 C, pH 6-8  On Endo, Levin, Ploskirev media form 2-3 mm colorless, smooth, round, flat colonies (lack of lactose fermentation), on bismuth- sulfite agar – black colonies (H2S production)  Enriched media: yolk and selenite broth
  • 35. Biochemical properties  Ferment glucose, manitol and maltose with acid and gas  No fermentation of lactose, sucrose and salicin.  Citrate positive  Do not hydrolyze urea, produce H2S with exception of S. paratyphi A and S.choleraesuis
  • 36. Antigenic structure  O-antigen: 1-65, named according to numbers or letters  H-antigen: 2 types. First – specific, encoded by letters. Second – nonspecific, encoded by numbers  Some Salmonella have Vi-antigen (variant of K-antigen) – sensitive to phages, can give O-agglutinative properties
  • 37. Resistance  Relatively resistant  3 month survive in water and soil, 80-255 days in dust  pH 4-9  Store in frozen sausages – 3 month, meat and eggs – 1 year, vegetables and fruits – 5-10 days  Temperature: 56 C – 45-60 min, 100 C – immidiatly  5% phenol, 3% chloramine, 3% lysole kill in 2-3 min
  • 38. Typhoid fever  Caused by S.typhi (S.choleraesuis serovar typhi)  Also known as gastric fever, abdominal typhus, infantile remittant fever, slow fever, nervous fever
  • 39. Typhoid fever  Only human disease, source – sick or carrier  1000 microbes cause infection  Mechanism of transmission: fecal-oral  Rout of transmission: water, alimentary, contact  Major storage: milk, milk products, meat, jelly
  • 40. Pathogenesity  In the first week, the temperature rises slowly, and fever fluctuations are seen with relative bradycardia, malaise, headache, and cough. A bloody nose (epistaxis) is seen in a quarter of cases, and abdominal pain is also possible. There is a decrease in the number of circulating white blood cells (leucopenia) with eosinopenia and relative lymphocytosis; blood cultures are positive for Salmonella typhi or paratyphi. The Widal test (AT) is negative in the first week
  • 41. Pathogenecity  In the second week of the infection, the patient lies prostrate with high fever in plateau around 40 °C and bradycardia, classically with a dicrotic pulse wave. Delirium is frequent, often calm, but sometimes agitated. This delirium gives to typhoid the nickname of "nervous fever". Rose spots (rush) appear on the lower chest and abdomen in around a third of patients. Fever is that the fever usually rises in the afternoon up to the first and second week  The abdomen is distended and painful in the right lower quadrant. Diarrhea can occur in this stage: six to eight stools in a day, green, with a characteristic smell. Constipation is also frequent. The spleen and liver are enlarged (hepatosplenomegaly) and tender, and there is elevation of liver transaminases. The Widal test is strongly positive, with anti-O and anti-H antibodies. Blood cultures are sometimes still positive at this stage.
  • 42. Pathogenecity  In the third week of typhoid fever, a number of complications can occur:  Intestinal haemorrhage due to bleeding in congested Peyer's patches; this can be very serious but is usually not fatal.  Intestinal perforation in the distal ileum: this is a very serious complication and is frequently fatal. It may occur without alarming symptoms until septicaemia or diffuse peritonitis sets in.  Encephalitis  Neuropsychiatric symptoms (described as "muttering delirium" or "coma vigil"), with picking at bedclothes or imaginary objects.  Metastatic abscesses, cholecystitis, endocarditis and osteitis  The fever is still very high and oscillates very little over 24 hours. Dehydration ensues, and the patient is delirious (typhoid state). One third of affected individuals develop a macular rash on the trunk.  Platelet count goes down slowly and risk of bleeding rises.
  • 43. Immunity  Strong and long term  Up to 1 week – antibodies to O-antigen, decreases after disease  Anti-H – long term circulation, also present in vaccinated  Anti-Vi – in carriers
  • 44. Laboratory diagnostics  1st week – seeding of blood on enriched media (yolk and selenite broth ) → Endo, Levin, Ploskirev media → identification by biochemical and serological tests  Vi-phages – for detection of source  Since 3rd week – seeding from blood positive only in 3-40%  1st week – positive seeding of feces in 1-15%, after 3rd -4th week – 75%, after 8th week – 10 %, after year – 3%  Since 2nd week – passive hemagglutination test with O, H, Vi antigens (test positive in titer not less 1:200), agglutination test (Widal test), ELISA
  • 45. Prophylaxis  Specific: TABte vaccine (typhus, paratyphus A,B, tetanus) and spirit typhus vaccine enriched with Vi-antigen  Give to adults, children from 5 years and people who will travel to endemic zones, medical stuff, military men  1 subcutaneous injection with 0,5 ml. Antibodies appears after 2-3 weeks. Immunity - not less then 3 years  In epidemic cases: dry typhoid bacteriophage  Nonspecific: early detection and treatment of sick persons, detection of carriers among workers of food services and markets, sanitary control of water sources, hygienic rules in cooking
  • 46. Treatment  Rehydration  Antibiotics: in sporadic cases - fluoroquinolones, 3rd generation cephalosporins  In epidemic areas (multiresistant causative agent): ceftriaxone, azithromycin  Surgery: in case of complications  Prognosis: without treatment fatal: 10-47% cases, with treatment: less than 1%
  • 47. Salmonellosis  Salmonella Choleraesuis  Salmonella Dublin  Salmonella Enteritidis  Salmonella Typhimurium
  • 48. Pathogenesity  Sources: chickens, turkeys, ducks, pigs, cows, dogs, cats, rats, parrots, turtles  Oral transmission with contaminated food (eggs, subproducts, liver) or beverages; very rare: by blood thrombocyte transfusion or usage of contaminated fibroscopes  Infective dose: 1 mln – 100 mln bacteria  Infected people excrete Salmonellae with feces from 3 days to 3 weeks, sometimes to 1 year
  • 49. Pathogenesity  Incubation period: 2-72 hours  Gastro-intestinal form: acute beginning with abdominal pain, liquid defecations with mucus and blood, vomiting (rare intensive and long term)  Temperature: 38-39 C  Duration:2-5 days  In typhoid form: 10-14 days with enlargement of spleen and liver, sometimes rush  Septic form: clinical signs of sepsis  Fatal cases: less than 1%, mostly children, old people  Can lead to bacteremia, Salmonella can reach bones, joints, pleura etc
  • 50. Immunity  Mostly related with sIg A  Weak, specific to serovars  Blood antibodies only witness of infectious process
  • 51. Laboratory diagnostics  Specimen: vomiting masses, washouts from stomach, feces, bile, urine, blood  Bacteriological investigation: similar to other Salmonella  Serological tests: passive hemagglutination test, agglutination test, ELISA with pair sera method
  • 52. Prophylaxis  Specific: among agricultural animals and birds  Nonspecific: prevention of spreading of infection among agricultural animals and birds, sanitary control of farms and food industry, storage and cooking of food.
  • 53. Treatment  Rehydration therapy  Antibiotics: nitrofuranes, fluoroquinolones

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