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MDSC 3312 MB > Enterobacteriaceae > Flashcards

Enterobacteriaceae Flashcards

1
Q

Natural Habitat

A

intestinal tract of humans and animals

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2
Q

What is the general morphology (gram, shape, requires O2)?

A

gram -ve facultative anaerobe bacilli

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3
Q

What are some examples of genera?

A

Escherichia, Shigella, Salmonella, Enterobacter, Klebsiella, Serratia, Proteu

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4
Q

Which ones are pathogenic and normal flora?

A

Normal flora- E.coli but may incidentally cause disease

Shigella and salmonella - pathogenic

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5
Q

Motility, flagella, spores, gram and morphology, capsule

A

Gram-negative bacilli, non-motile or motile by peritrichous flagella; non-sporing, some encapsulated

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6
Q

What are the colonies on media?

A

circular, convex, glistening or mucoid

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7
Q

Bacteria that loses capsules present

A

rough colonies that are flat, irregular & granular in appearance.

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8
Q

What is the unique ability of proteus?

A

swarming pattern

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9
Q

What are the pigments?

A

non-pigmented, although a few spp include strains that produce red, pink, yellow or blue pigments.

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10
Q

What antigens do the family have? Why is it useful?

A

the somatic (O) Ag, most have the flagellar (H) Ag and the capsular (K) Ag is seen in some spp.

classification of spp & may yield useful epidemiologic information

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11
Q

What do gram -ve bacteria produce?

A

bacteriocins - like bactericidal substances are active against some other strains of the same or closely related spp

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12
Q

Bacteriocin production is controlled by?

A

plasmid

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13
Q

E Coli produces

A

colicins

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14
Q

Marcescins

A

serratia

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15
Q

Pyocins

A

pseudomonas

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16
Q

What is used for typing?

A

Bacteriosin - producing strains are resistant to their own bacteriocin; Bacteriocins can be used for “typing” of organisms

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17
Q

When are endotoxins liberated? What do they consist of

A

O Ags /LPS consist of sugars & lipid A.

Present in the cell wall of G –ve bacilli, liberated when the bacterial cell lyses;

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18
Q

What does the endotoxin cause?

A

; responsible for many pathological effects during human infection with the organism

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19
Q

When are exotoxins liberated?

A

Proteins liberated extracellularly from the intact bacterium by a few spp, e.g. S. dysenteriae; toxignic strains of E. coli.

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20
Q

What is seen with glucose fermentation and lactose fermentation, what are the gases produced and the colour change?

A

glucose fermentation and lactose fermentation

GF-Organic acids such as lactic, formic & acetic acids are produced. Some spp also produce H2 & CO2 gas during glucose fermentation

Lactose- NLF, LF -PINK COLONIES IF LF

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21
Q

Differential and Selective Media

A

MacConkey (contains bile salts to inhibit G+ve)

Eosin methylene blue (EMB) agar commonly used

LF develop pink coloration in isolated colonies.

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22
Q

What are the biochemical tests?

A
  1. nitrate reduced to nitrite
  2. H2S production
  3. indole formation
  4. acetyl methyl carbinol from glucose
  5. liquefaction of gelatin
  6. citrate
  7. hydrolysis of urea
  8. decarboxylation of amino acids
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23
Q

Oxidase

A

negative

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24
Q

Strain identification

A

Bacteriophage typing
Bacteriocin typing
Plasmid analysis
Polypeptide analysis by polyacrylamide gel-electrophoresis

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25
Q

What is released when Enterobacteriaceae dies and lead to?

A

LPS can result in endotoxin shock in humans

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26
Q

What does the toxic lps consist of? What is responsible for the symptoms?

A

consists of lipid A, the core PS, and the O Ag. The lipid A moiety of LPS is responsible for most of the symptomatology associated with endotoxin shock.

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27
Q

What is responsible for the symptoms of endotoxin shock?

A

lipid A moiety

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28
Q

Epidemiology- who are affected?

A

considered to be pathogenic
Patients with underlying disease, immunosuppression, mechanical or medical manipulation & other forms of debilitation are susceptible to infection

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29
Q

What are the effects of the LPS?

A

fever, hypotension, intravascular coagulation, alteration in circulating blood cells, metabolism, increase humoral immunity

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30
Q

Fever

A

a rise in body temp usually occurs within 30 min of exposure to LPS

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31
Q

Hypotension - small doses and large doses

A

Small amounts of LPS in blood stream cause decrease in BP in most people within 30min of exposure,

Large doses are lethal - can cause permanent & fatal hypotension.

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32
Q

Intravascular Coagulation

A

Exposure to LPS can result in depletion of clotting factors & serious bleeding may occur.

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33
Q

What is the alteration in blood cells?

A

neutropenia within minutes

leukocytosis, monoblasts and other immature cell types

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34
Q

LPS stimulates the release of?

A

macrophages to release IL-1 & lysosomal enzymes

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35
Q

Humoral immunity and LPS

A
  • LPS stimulates the proliferation of B lymphocytes & activates Complement.
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36
Q

Effects on Metabolism

A

hypoglycemia & hypoferremia

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37
Q

Pregnancy effects

A

LPS cause placental haemorrhage because it stimulates the release of serotonin. LPS (lipid A) has caused abortions in lab. animals after IV injection.

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38
Q

E coli- IMViC

A

Positive Indole and Methyl red

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39
Q

Klebsiella-IMViC

A

vp, citrate positive

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40
Q

Citrobacter IMViC

A

indole, methyl red, citrate positive

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41
Q

Produce pink colonies on MAC and ferment sugars with the production of acid and gas

A

Citrobavcter, enteroobacter, klesiella, eschericha

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42
Q

E.coli inhabits

A

Normal inhabitants of the intestine of man & animals.

Some cause disease in humans.

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43
Q

Morphology of E.coli

A

Gram-negative bacilli, motile, some strains are capsulated.

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44
Q

What are the colonies producesd by EColi on MAC? Aerobes/Anaerobes ?

A

Facultative anaerobes, grow on simple media,

On MacConkey medium, they produce rose-pink colonies due to LF.

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45
Q

IMViC E.coli

A

indole and methyl red positive

Vp and citrate- negative

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46
Q

E.coli ferments

A

ferment glucose, lactose, maltose, mannite, sucrose & salicin with production of acid and gas.

47
Q

Is e.coli invasive?

A

invasive or non-invasive

48
Q

Invasive E.coli

A

Nontoxigenic

Toxigenic- shiga like cytotoxin (inhibits protein synthesis)

49
Q

Non-invasive E.coli

A

enteropathogenic and enterotoxigenic

50
Q

Enteropathogenic

A

EPEC EHEC

51
Q

Enterotoxigenic

A

Heat labile and heat stable

52
Q

Heat labile

A

LT- increase CAMP

53
Q

Heat Stable

A

increase cGMP

54
Q

What is the antigenic structure of E.coli?

A

O and H Ags, many pathogenic E. coli possess K Ag.

Routine serotyping is done for E. coli possess O Ags with numerical designations. e.g. 26, 55, 111, 119, etc.

55
Q

Endotoxins E.coli

A

LPS (O Ags) - causes endotoxic shock.

56
Q

What are the enterotoxins for Ecoli and determined by?

A

exotoxins: 2 types are known which are genetically determined by plasmids.
LT - heat-labile
ST - heat stable

57
Q

What are the virulence factors for ecoli?

A

toxins and pili(adhesive factors)

58
Q

What are the pili adhesive factors for e.coli?

A

antigens (CFA) I, II and III enable the organism to adhere to mucosal cells detected by lectin binding or by mannose - resistant hem-agglutination of RBC.

59
Q

Typing for E.coli

A

Determination of O antigens

  1. Colicine typing
  2. Biotyping
  3. Phage typing for certain serogroups, e.g. O157
60
Q

What are the clinical infections of E.coli?

A

Urinary tract infection
Diarrhea
Pyogenic infections – peritonitis , abscess, neonatal meningitis
Septicemia – septic shock

61
Q

What is the commonest cause of UTI? Which type colonizers the area

A

Uropathogenic E.coli (E.coli common cause)

62
Q

UTI

A

Uropathogenic E. coli colonize the vagina & periurethral region from where they ascend to the bladder or kidney causing cystitis or pyelonephritis.

63
Q

E.Coli O157:H7 cause of

A

an emerging cause of foodborne (ground meat) and waterborne illness.

64
Q

Which serotype causes traveller’s diarrhoea and X?

A

ETEC- 06708

watery and ranges from mild to sever cholera - may be fatal

65
Q

Mechanism of ETEC

A

The organism adheres to intestinal epithelium through the pili or colonization factors. Then they liberate enterotoxins LT and ST.
The ST toxin cause diarrhoea by stimulating guanyl cyclase in intestinal mucosal cells.

66
Q

After toxins released, what happens?

A

The heat labile/LT toxin bind to receptors of intestinal mucosa & other cells, activates membrane-bound adenyl cyclase  Increased intracellular concentrations of cyclic adenosine monophosphate (cAMP) cause the active excretion of electrolytes, which carry large amounts of water with them.

67
Q

EPEC is associated with

A

Certain serotypes e.g. O55, O111 cause outbreaks of neonatal diarrhoea in nurseries

68
Q

How does EPEC act?

A

mainly by adhering tightly to intestinal mucosa resulting in loss of microvilli & cupping of cells around the bacteria. Thus preventing the normal functions of absorption & secretion

69
Q

EIEC causes

A

Certain serotypes e.g. O124, O164 cause dysentery - like diarrhoea through invasion of intestinal epithelial cells

70
Q

EHEC serotype produces

A

Certain serotypes e.g. O157. These strains produce verocytotoxin (VT).

71
Q

EHEC cause

A

These strains cause haemorrhagic colitis which is severe form of diarrhoea with bloody discharge. Produce shiga toxin

72
Q

Enterotoxigenic strains posses

A

colonising factor antigens

73
Q

Enteropathogenic strains may produce

A

Some strains of enteropathogenic E. coli elaborate enterotoxin & produce verocytotoxin.

74
Q

What is the effect on neonates, blood etc?

A

Neonatal meningitis: E. coli causes 40% of neonatal meningitis followed by group B streptococci.

  1. It causes bacteraemia & endotoxic shock in immunocompromised host.
  2. It causes hospital-acquired infections
75
Q

What specimens are collected for Ecoli?

A

Specimen according to the site of infection e.g. urine, pus, stools, CSF etc.

76
Q

After pathological materials are collected, what occurs?

A

Pathologic material is inoculated on MacConkey media; LF colonies are further identified by their morphology & biochemical reactions.

77
Q

In the case of gastroenteritis, what is done/?

A

serological typing with E.coli anti-Osera

78
Q

Detection of E.coli

A

by enterotoxigenic strains can be detected in animal models, or by ELISA & by passive latex agglutination.
Gene probe may be used to detect the gene for toxin production

79
Q

E.coli resistant to

A

Extended-spectrum β-lactamase-producing Escherichia coli

80
Q

Enterobacter found and similar to?

A

intestinal flora and similar to Klbsiela

81
Q

Enterobacter positive for

A

motility, citrate, vp and produce gas from glucose

82
Q

What does enterobacter cause?

A

UTI and sepsis

83
Q

Small capsule Enterobacter

A

e aerogenes

84
Q

Citrobacter is similar to? What is the deffrence? Antigenically imilar to?

A

E.coli except citrate +ve and antigenically to salmonella

85
Q

Citrobacter in pathogenic in

A

It is seen as opportunistic pathogen in immunocompromised individuals

86
Q

What does Citrobacter cause?

A

Causes UTI, sepsis, wound infection, osteomyelitis in elderly hospitalized patients.
Cases of neonatal meningitis

87
Q

Citrobacter species

A

C freundii, koseri

88
Q

Klebsiella inhabitants and habit

A

inhabitants of the intestine & respiratory tract.

Are saprophytes in soil & water, some cause disease in man

89
Q

Klebsiella morphology

A

Gram-negative bacilli, non motile and capsulated.

90
Q

Klebsiella ferments

A

They ferment glucose, lactose, maltose, mannite, sucrose & salicin with production of acid & gas.

91
Q

Klebsiella IMViC

A

indole -ve, VP +ve & MR -ve, IMViC – ++

92
Q

Klebsiella Typing

A

Antigenic analysis of the capsular PS which comprise the large capsule typical of this genus.

  1. Klebicine (bacteriocine) typing
93
Q

FRIEDLANDER’s BACILLUS causes

A

lobar penumonia, hospital acquired infections e.g UTO

94
Q

K.pneumoniae isolated from

A

pneumoniae can be isolated from the oropharynx or GIT (feces) of about 5% of healthy people

95
Q

Rhinoscleroma caused by

A

K.rhinoscleromatis causes rhinoscleroma which is a granulomatous lesion (chronic granuloma) of the nose & throat /oropharynx.

96
Q

K ozane

A

atrophic rhinits

97
Q

K oxytoca

A

UTI, RTI, wound sepsis

98
Q

Extended-spectrum β-lactamase-producing Klebsiella is due to

A 
Associated with multidrug resistance
– Increased virulence
– Positive selection
– Adoptive strategies
– Vertical and horizontal transmission
99
Q

What species produces red colonies ? Where are they located and morphology?

A

Serratia marcescens is a gram-negative motile rod found in soil & water most strains produce red colonies

100
Q

The non-pigmented Serratia strains cause?

A

pulmonary infection (pneumonia), UTI, bacteremia & endocarditis particularly as cross-infection in hospitalized patients and narcotic addicts.

101
Q

S marcescens resistant to and can be treated by?

A

S. marcescens is multiple resistant to penicillins & aminoglycosides
Infections can be treated with 3rd generation cephalosporins

102
Q

Proteus habitat and morphology

A

intestine, when ut leaves the intestine causes disease
Gram-negative bacilli very pleomorphic (variable in length) and highly motile.

103
Q

UTI

A

proteus mirabilis

104
Q

Which proteus species causes nosocomial infections?

A

. Proteus vulgaris: nosocomial infections

105
Q

Culture characteristics of proteus and on MAC agar

A

They grow on nutrient agar producing a spreading growth “swarming”. Proteus forms colourless colonies on MacConkey agar

106
Q

What differentiates proteus from salmonella and shigella?

A

They are urease positive (i.e. decompose urea rapidly with liberation of ammonia), a property which differentiate them from salmonella & shigella,

107
Q

Indole, ferment, gas Proteus

A

Indole negative,
ferment glucose with production of acid & gas,
produce H2S.
Lactose is not fermented

108
Q

What arethe antigenic structures of Proteus?

A

Proteus possess O & H antigens.

109
Q

How can rickettsial diseases be diagnosed/?

A

Certain types of proteus (proteus OX19, OXK, OX2) share antigens with Rickettsiae and are used as diagnostic Ags in the serological diagnosis of rickettsial diseases (Weil-Felix agglutination tests).

110
Q

What is the typing proteus?

A

Serotyping

  1. Bacteriocine typing
  2. “Dienes” phenomenon: Inhibition of swarming by dissimilar strains of Proteus mirabilis.
111
Q

What is the treatment of proteus?

A

Proteus are highly resistant to antibiotics

Sensitivity tests should be done before treatment

112
Q

P mirablis is resistant to? Others are to?

A

P. mirabilis is inhibited by penicillin

Other members: aminoglycosides & cephalosporins

113
Q

Proteus mirabilis causes

A

uti,Often isolated from mixed flora of wounds, burns, pressure sores, chronic discharging ears.
3. Septicaemia

114
Q

With UTI caused by proteus, there is an increased risk of?

A

Urinary urea is “split” by the bacterial urease to produce ammonium salts: this results in alkaline urinary pH & an increased risk of urinary calculi

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