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ENTEROBACTERIACEAE

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B.Enterotoxigenic E coli ( ETEC) ... B. Enteritis/Enterocolitis. C. Systemic infections. Sources of in infection. contaminated water ... – PowerPoint PPT presentation

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Title: ENTEROBACTERIACEAE


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

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 in infants of
  • 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 called VETEC ( 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 is an important nosocomial
    pathogen.
  • Treatment-Penicillin,Aminoglycosides,Cephalosporin
    es

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 ma
rked antibacterial effect Ampicillin on
enterics Cephalosporines Fluoroquinolone Aminoglyc
oside
34
ABST is essential Predisposing factors to be
corrected surgically. EgObstructions- 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. flexneri type 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
51
  • Slide agglutination
  • Use of polyvalent antisera of three gps (ABC) and
    of gp D
  • Monovalent antisera is being used when ve for
    polyvalent

52
  • Treatment
  • Ciprofloxacin,Ampicillin,Tetracyclin,Trimethoprim
  • Sulfamethoxasole, Chloramphenicol
  • Transmission by food, fingers, feces, flies.

53
Salmonella Pathogenic when acquired through
oral route. Transmitted from animals animal
products. Produce A. Enteric
fever B. Enteritis/Enterocolitis
C. Systemic infections
54
  • Sources of in infection
  • contaminated water
  • contaminated dairy products
  • shellfish
  • dried or frozen eggs
  • meat and meat products of infected animals
  • Household pets

55
  • Morphology
  • vary in length.
  • motile with peritrichous flagellae.
  • never ferment lactose or sucrose
  • Usually produce H2S, survive freezing in water.
  • Resist chemicals.

56
Antigenic structure Antigens O H K - Vi Ag
invasiveness
57
  • Classification - Complex -
  • Kauffmann White Scheme
  • Ex S typhi
  • S. paratyphi A/B India and Asian
  • S. choleraesuis
  • S. typhimurium
  • S. enteritidis
  • SO MANY OTHER SPECIES

58
Toxin
  • LPS - endotoxin

59
  • Pathogenesis
  • Almost always enter orally with contaminated
  • S. typhi/S. parathyphi A/B - in humans
  • Majority of Salmonella infect animals man is the
    secondry host
  • food and drink.

60
  • Infective dose 105-108 - high
  • Resist infection by the host via
  • gastric acidity, normal flora ,Local
    immunity.

61
  • Enteric fever (Typhoid fever)
  • Important pathogen - S typhi/
  • S. paratyphi A/B/C
  • Fever/ malaise/ headache /constipation
    bradycardia / myelgia occur.

62
  • INCUBATION STAGE
  • Incubation period 10-14 days
  • Faecal oral route
  • Most of the cells will get killed
  • ID should be high
  • Reach the duodenum
  • Multiply in alkaline medium
  • adhere to villi
  • to the sub mucous coat
  • will be phagocytosed by Macro and Neutro

63
  • Virulent bacilli resist intracellular killing and
    multiply
  • Enters the mesenteric lymhnodes and multiply
    there and then to the blood (primary bacteraemia)
    1-7 days
  • bacilli will be cleared by MPS in the
    liver/spleen/bone marrow/lungs/lymhnode

64
  • SEPTICAEMIC STAGE
  • Primary bacteraemia - where bacilli will be
    multiply in the cells of MPS
  • 10th day parasitised cells undergo necrosis leads
    to seondry bacteramia, results in clinical
    symptoms thats about on the 14th day after the
    ingestion
  • some bacilli lyse and release endotoxins
  • bacteraemia and toxaemia causes fever and other
    signs

65
  • STAGE OF LOCALIZATION
  • Bacteraemia-gall bladder/liver/spleen/bone
  • bacilli can be discharge into the intestine from
    the gall bladder and cause inflammation of the
    Payers patches in the intstine and lymphoid
    follicles
  • Necrosis/sloughing---ulcers--haemorrhage

66
  • Severe mental clouding
  • headache
  • anorexia -cannot eat
  • High fever (Step ladder pyrexia)
  • spleen and liver enlargement
  • Splenohepatomagaly
  • Rose spots (1-2mm) on skin of chest and abdomen
    2nd and 3rd week

67
  • bacilli appear during 2nd and the 3rd week in
    stools - diagnostic
  • 4th week in urine - diagnostic
  • The disease lasts 4 to 5 weeks
  • WBC normal or low
  • Treatment - chloramphenicoal

68
  • Complications
  • Intestinal hemorrhage perforation
  • Hyperplasia and necrosis of Payers paches
  • Hepatitis, focal liver necrosis
  • gall bladder inflammation
  • bone ,lungs and other organs can be affected.

69
Bacteremia with focal lesions Commonly
associated with S cholerasius Blood culture ve
70
  • LABORATORY DIAGNOSIS
  • 1. Isolation of the bacteria
  • 2. Demonstration of antibodies
  • 3. Demonstration of circulating antigens
  • 4. Blood picture

71
  • Isolation of bacteria
  • Specimens - stools/urine/blood
  • Blood culture - before giving chloramphenicol
  • - repeat the culture
  • - 80-90 ve 1st week up to10days
  • - ve during relapses
  • - can culture bone marrow ve
  • 1-2 days after drug therapy ?
    good
  • -

72
  • When blood culturing is done there is diluting of
    the drug
  • Stool and urine culture
  • Stools - during the second and third week
  • Urine - during the third and the fourth week,
    less frequently ve than stools
  • Repeated culture is necessary when blood
    culture is -ve

73
  • Blood (5 - 10 ml)
  • BHI
  • Incubate 37 0C
  • Subculture
  • (18-24hrs/every 2nd day for 7days)
  • MacConkey
  • Stools and urine first should be cultured in
    enrichment media

74
  • Serological test
  • Detection of antibodies to H and O antigens
  • Widal test
  • Antibodies appear at the end of the first week
  • Rises during the 3rd week of the enteric fever
  • Two specimens are taken at interval of 7 to 10
    days

75
Interpretation of Widal test
  • 1. Antibody appears at the end of 1st week/rises
    during 2nd and 3rd/steady at the 4th week then
    decline
  • 2. Four fold rise of both H and O antibody in an
    interval of 7 - 10 days (between 1st and the 3rd
    week is highly significant)

76
  • Treatment
  • Antimicrobials - Ampicillin
  • TrimethoprimSulfamethoxasole
  • 3rd generation Cephalosporines

77
  • Paratyphoid fever
  • Fever is milder, shorter period
  • IP is short

78
  • Enterocolitis
  • Common manifestation of Salmonella
  • Common pathogen is S typhimurium
  • 8-48 hrs after ingestion
  • nausea/ headache/ vomiting and profuse
    diarrhoea,
  • low grade fever Resolution 2-3 days.
  • Inflammatory lesions in bowel are present

79
  • Bacterimia rare
  • Blood culture -ve
  • Stools remain ve for sometime after recovery

80
Diagnosis 1.Faeces, vomitus, food stuffs
(mainly a single source) 2. Convalescent serum
often agglutinates the suspension of casual
serotype
81
  • Prevention and control
  • Sanitation
  • Thorough cooking
  • Carriers should not handle food
  • Vaccination not successful long-term.
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