Enterobacteriaceae Flashcards
(114 cards)
1
Q
Natural Habitat
A
intestinal tract of humans and animals
2
Q
What is the general morphology (gram, shape, requires O2)?
A
gram -ve facultative anaerobe bacilli
3
Q
What are some examples of genera?
A
Escherichia, Shigella, Salmonella, Enterobacter, Klebsiella, Serratia, Proteu
4
Q
Which ones are pathogenic and normal flora?
A
Normal flora- E.coli but may incidentally cause disease
Shigella and salmonella - pathogenic
5
Q
Motility, flagella, spores, gram and morphology, capsule
A
Gram-negative bacilli, non-motile or motile by peritrichous flagella; non-sporing, some encapsulated
6
Q
What are the colonies on media?
A
circular, convex, glistening or mucoid
7
Q
Bacteria that loses capsules present
A
rough colonies that are flat, irregular & granular in appearance.
8
Q
What is the unique ability of proteus?
A
swarming pattern
9
Q
What are the pigments?
A
non-pigmented, although a few spp include strains that produce red, pink, yellow or blue pigments.
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
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
12
Q
Bacteriocin production is controlled by?
A
plasmid
13
Q
E Coli produces
A
colicins
14
Q
Marcescins
A
serratia
15
Q
Pyocins
A
pseudomonas
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
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;
18
Q
What does the endotoxin cause?
A
; responsible for many pathological effects during human infection with the organism
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.
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
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.
22
Q
What are the biochemical tests?
A
- nitrate reduced to nitrite
- H2S production
- indole formation
- acetyl methyl carbinol from glucose
- liquefaction of gelatin
- citrate
- hydrolysis of urea
- decarboxylation of amino acids
23
Q
Oxidase
A
negative
24
Q
Strain identification
A
Bacteriophage typing
Bacteriocin typing
Plasmid analysis
Polypeptide analysis by polyacrylamide gel-electrophoresis
25
What is released when Enterobacteriaceae dies and lead to?
LPS can result in endotoxin shock in humans
26
What does the toxic lps consist of? What is responsible for the symptoms?
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.
27
What is responsible for the symptoms of endotoxin shock?
lipid A moiety
28
Epidemiology- who are affected?
considered to be pathogenic
Patients with underlying disease, immunosuppression, mechanical or medical manipulation & other forms of debilitation are susceptible to infection
29
What are the effects of the LPS?
fever, hypotension, intravascular coagulation, alteration in circulating blood cells, metabolism, increase humoral immunity
30
Fever
a rise in body temp usually occurs within 30 min of exposure to LPS
31
Hypotension - small doses and large doses
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.
32
Intravascular Coagulation
Exposure to LPS can result in depletion of clotting factors & serious bleeding may occur.
33
What is the alteration in blood cells?
neutropenia within minutes
| leukocytosis, monoblasts and other immature cell types
34
LPS stimulates the release of?
macrophages to release IL-1 & lysosomal enzymes
35
Humoral immunity and LPS
- LPS stimulates the proliferation of B lymphocytes & activates Complement.
36
Effects on Metabolism
hypoglycemia & hypoferremia
37
Pregnancy effects
LPS cause placental haemorrhage because it stimulates the release of serotonin. LPS (lipid A) has caused abortions in lab. animals after IV injection.
38
E coli- IMViC
Positive Indole and Methyl red
39
Klebsiella-IMViC
vp, citrate positive
40
Citrobacter IMViC
indole, methyl red, citrate positive
41
Produce pink colonies on MAC and ferment sugars with the production of acid and gas
Citrobavcter, enteroobacter, klesiella, eschericha
42
E.coli inhabits
Normal inhabitants of the intestine of man & animals.
| Some cause disease in humans.
43
Morphology of E.coli
Gram-negative bacilli, motile, some strains are capsulated.
44
What are the colonies producesd by EColi on MAC? Aerobes/Anaerobes ?
Facultative anaerobes, grow on simple media,
| On MacConkey medium, they produce rose-pink colonies due to LF.
45
IMViC E.coli
indole and methyl red positive
Vp and citrate- negative
46
E.coli ferments
ferment glucose, lactose, maltose, mannite, sucrose & salicin with production of acid and gas.
47
Is e.coli invasive?
invasive or non-invasive
48
Invasive E.coli
Nontoxigenic
| Toxigenic- shiga like cytotoxin (inhibits protein synthesis)
49
Non-invasive E.coli
enteropathogenic and enterotoxigenic
50
Enteropathogenic
EPEC EHEC
51
Enterotoxigenic
Heat labile and heat stable
52
Heat labile
LT- increase CAMP
53
Heat Stable
increase cGMP
54
What is the antigenic structure of E.coli?
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
Endotoxins E.coli
LPS (O Ags) - causes endotoxic shock.
56
What are the enterotoxins for Ecoli and determined by?
exotoxins: 2 types are known which are genetically determined by plasmids.
LT - heat-labile
ST - heat stable
57
What are the virulence factors for ecoli?
toxins and pili(adhesive factors)
58
What are the pili adhesive factors for e.coli?
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
Typing for E.coli
Determination of O antigens
2. Colicine typing
3. Biotyping
4. Phage typing for certain serogroups, e.g. O157
60
What are the clinical infections of E.coli?
Urinary tract infection
Diarrhea
Pyogenic infections – peritonitis , abscess, neonatal meningitis
Septicemia – septic shock
61
What is the commonest cause of UTI? Which type colonizers the area
Uropathogenic E.coli (E.coli common cause)
62
UTI
Uropathogenic E. coli colonize the vagina & periurethral region from where they ascend to the bladder or kidney causing cystitis or pyelonephritis.
63
E.Coli O157:H7 cause of
an emerging cause of foodborne (ground meat) and waterborne illness.
64
Which serotype causes traveller's diarrhoea and X?
ETEC- 06708
| watery and ranges from mild to sever cholera - may be fatal
65
Mechanism of ETEC
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
After toxins released, what happens?
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
EPEC is associated with
Certain serotypes e.g. O55, O111 cause outbreaks of neonatal diarrhoea in nurseries
68
How does EPEC act?
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
EIEC causes
Certain serotypes e.g. O124, O164 cause dysentery - like diarrhoea through invasion of intestinal epithelial cells
70
EHEC serotype produces
Certain serotypes e.g. O157. These strains produce verocytotoxin (VT).
71
EHEC cause
These strains cause haemorrhagic colitis which is severe form of diarrhoea with bloody discharge. Produce shiga toxin
72
Enterotoxigenic strains posses
colonising factor antigens
73
Enteropathogenic strains may produce
Some strains of enteropathogenic E. coli elaborate enterotoxin & produce verocytotoxin.
74
What is the effect on neonates, blood etc?
Neonatal meningitis: E. coli causes 40% of neonatal meningitis followed by group B streptococci.
4. It causes bacteraemia & endotoxic shock in immunocompromised host.
5. It causes hospital-acquired infections
75
What specimens are collected for Ecoli?
Specimen according to the site of infection e.g. urine, pus, stools, CSF etc.
76
After pathological materials are collected, what occurs?
Pathologic material is inoculated on MacConkey media; LF colonies are further identified by their morphology & biochemical reactions.
77
In the case of gastroenteritis, what is done/?
serological typing with E.coli anti-Osera
78
Detection of E.coli
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
E.coli resistant to
Extended-spectrum β-lactamase-producing Escherichia coli
80
Enterobacter found and similar to?
intestinal flora and similar to Klbsiela
81
Enterobacter positive for
motility, citrate, vp and produce gas from glucose
82
What does enterobacter cause?
UTI and sepsis
83
Small capsule Enterobacter
e aerogenes
84
Citrobacter is similar to? What is the deffrence? Antigenically imilar to?
E.coli except citrate +ve and antigenically to salmonella
85
Citrobacter in pathogenic in
It is seen as opportunistic pathogen in immunocompromised individuals
86
What does Citrobacter cause?
Causes UTI, sepsis, wound infection, osteomyelitis in elderly hospitalized patients.
Cases of neonatal meningitis
87
Citrobacter species
C freundii, koseri
88
Klebsiella inhabitants and habit
inhabitants of the intestine & respiratory tract.
| Are saprophytes in soil & water, some cause disease in man
89
Klebsiella morphology
Gram-negative bacilli, non motile and capsulated.
90
Klebsiella ferments
They ferment glucose, lactose, maltose, mannite, sucrose & salicin with production of acid & gas.
91
Klebsiella IMViC
indole -ve, VP +ve & MR -ve, IMViC -- ++
92
Klebsiella Typing
Antigenic analysis of the capsular PS which comprise the large capsule typical of this genus.
2. Klebicine (bacteriocine) typing
93
FRIEDLANDER's BACILLUS causes
lobar penumonia, hospital acquired infections e.g UTO
94
K.pneumoniae isolated from
pneumoniae can be isolated from the oropharynx or GIT (feces) of about 5% of healthy people
95
Rhinoscleroma caused by
K.rhinoscleromatis causes rhinoscleroma which is a granulomatous lesion (chronic granuloma) of the nose & throat /oropharynx.
96
K ozane
atrophic rhinits
97
K oxytoca
UTI, RTI, wound sepsis
98
Extended-spectrum β-lactamase-producing Klebsiella is due to
```
Associated with multidrug resistance
– Increased virulence
– Positive selection
– Adoptive strategies
– Vertical and horizontal transmission
```
99
What species produces red colonies ? Where are they located and morphology?
Serratia marcescens is a gram-negative motile rod found in soil & water most strains produce red colonies
100
The non-pigmented Serratia strains cause?
pulmonary infection (pneumonia), UTI, bacteremia & endocarditis particularly as cross-infection in hospitalized patients and narcotic addicts.
101
S marcescens resistant to and can be treated by?
S. marcescens is multiple resistant to penicillins & aminoglycosides
Infections can be treated with 3rd generation cephalosporins
102
Proteus habitat and morphology
intestine, when ut leaves the intestine causes disease
Gram-negative bacilli very pleomorphic (variable in length) and highly motile.
103
UTI
proteus mirabilis
104
Which proteus species causes nosocomial infections?
. Proteus vulgaris: nosocomial infections
105
Culture characteristics of proteus and on MAC agar
They grow on nutrient agar producing a spreading growth "swarming". Proteus forms colourless colonies on MacConkey agar
106
What differentiates proteus from salmonella and shigella?
They are urease positive (i.e. decompose urea rapidly with liberation of ammonia), a property which differentiate them from salmonella & shigella,
107
Indole, ferment, gas Proteus
Indole negative,
ferment glucose with production of acid & gas,
produce H2S.
Lactose is not fermented
108
What arethe antigenic structures of Proteus?
Proteus possess O & H antigens.
109
How can rickettsial diseases be diagnosed/?
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
What is the typing proteus?
Serotyping
2. Bacteriocine typing
3. "Dienes" phenomenon: Inhibition of swarming by dissimilar strains of Proteus mirabilis.
111
What is the treatment of proteus?
Proteus are highly resistant to antibiotics
| Sensitivity tests should be done before treatment
112
P mirablis is resistant to? Others are to?
P. mirabilis is inhibited by penicillin
| Other members: aminoglycosides & cephalosporins
113
Proteus mirabilis causes
uti,Often isolated from mixed flora of wounds, burns, pressure sores, chronic discharging ears.
3. Septicaemia
114
With UTI caused by proteus, there is an increased risk of?
Urinary urea is "split" by the bacterial urease to produce ammonium salts: this results in alkaline urinary pH & an increased risk of urinary calculi
