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gram negative Flashcards

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1
Q

location where klebsiella and serratia is present

A

large intestine soil and water

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2
Q

gram negative bacteria are in general which type of hemolysis? except?

A

usually non hemolytic except e coli which is beta hemolytic

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3
Q

explain the general feature of motility in gram negative bacteria, and the exception.

A

generally motile except klebsiella and shigella

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4
Q

serratia in nutrient agar has

A

red pigment

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5
Q

urease test for klebsiella and serratia

A

K: + and S: -

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6
Q

explain whether or not klebsiella and serratia is a fast or slow lactose fermenter and what kind of colonies do they form?

A

K: Fast lactose fermenter forms mucoid colonies due to capsule
S: Slow lactose fermenter = produces red-pigmented colonies

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7
Q

virulence factor of klebsiella

A

Pili for attachment
Polysaccharide capsule (mucoid)
Endotoxic and antigens

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8
Q

virulence factor of serratia

A

Non-capsulated

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9
Q

disease caused by klebsiella

A

UTI and pneumonia (makes currant-jelly
sputum with mucus and blood)
Bacteremia, necrosis, abscess formation,
antibiotic-related diarrhea (K oxytoca)

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10
Q

disease caused by serratia

A

Pneumonia (water contamination from respiratory therapy devices)
Endocarditis (injection drugs)

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11
Q

location of e coli

A

GI commensal flora

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12
Q

E coli in our GI commensal flora helps in

A

digestion, makes vitamin K2, makes biofilms
to prevent invasion of harmful bacteria like C difficile

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13
Q

fermentation of e coli

A

Ferments lactose (forms pink colonies on MacConkey) and glucose

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14
Q

virulence factors of e coli

A

Type 1 fimbriae for adhesion and siderophores: for acquiring iron for metabolism + LPS
endotoxin

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15
Q

enterohemorrhagic E.coli: what does the toxin do and clinical manifestation

A

Shiga-like toxin = inhibits 28s RRNA and 60s subunit = inhibits protein synthesis
dysentery, hemorrhagic colitis hemolytic uremic syndrome (HUS)
HUS: thrombocytopenia, hemolytic anemia and acute renal failure (Affects kidneys and blood
clotting)

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16
Q

Enteropathogenic E coli: causes and clinical manifestation

A

After attaching to brush border, enzymes flatten microvilli which reduces absorption
efflux of water = noninflammatory watery diarrhea

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17
Q

Enterotoxigenic E coli: causes and CM

A

Has fimbriae to attach to small intestine’s brush border (diarrhea).
Heat labile (CAMP-inducing) and heat stable (CGMP-inducing) toxins + water and ion release = noninflammatory diarrhea (doesn’t invade cells) also known as Traveler’s diarrhea

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18
Q

Enteroinvasive E coli: causes and CM

A

lyses phagosomes and replicates in cytoplasm with enzymes and
invades other nearby cells in the large intestine.
necrosis, inflammation = dysentery (inflammatory bloody mucus diarrhea)

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19
Q

Enteroaggregative E coli: causes and CM

A

cytotoxic production and enzymes produce mucus and biofilm
damages intestinal cells = bloody diarrhea (noninvasive)

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20
Q

Uropathogenic E coli: causes and CM

A
  • P pili attaches to urinary tract forming biofilm
    -Hemolysin is used to invade tissues and causes cystitis (inflamed bladder), pyelonephritis (inflamed kidneys) - UTI
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21
Q

what does E coli K1 do?

A

Has K1 capsular polysaccharide which binds with neuroreceptors = enters blood-brain
barrier = meningitis

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22
Q

Aside from other stereotypical patients, what is a special category of patient who are susceptible to E coli?

A

Diabetics (+ glucose in urine promotes E. coli colonization)

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23
Q

describe E coli’s resistance

A

Highly resistant to antibiotics due to bacterial conjugation

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24
Q

Pathogenic species of citrobacter

A

Citrobacter freundii, koseri and braakii

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25
Q

location of citrobacter

A

Colon and environment

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26
Q

tests for citrobacter

A

-indole, + methyl red, -VP, +citrate (-+-+)

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27
Q

citrobacter is fast or slow lactose fermenter

A

slow

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28
Q

where does citrobacter colonize

A

CNS, oral cavity, GIT, respiratory tract

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29
Q

Disease caused by citrobacter

A

Sepsis, meningitis, necrotizing fasciitis (koseri), brain
abscesses, UTI, respiratory tract, in bones

MeN Rent BUS

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30
Q

Yersinia enterocolitica is lactose or non lactose fermenter

A

Non-Lactose fermenter

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31
Q

Yersinia enterocolitica fermentation

A

sucrose + glucose

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32
Q

Yersinia enterocolitica is oxidase positive or negative

A

Negative

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33
Q

Mode of transmission for Yersinia enterocolitica

A

GIT of domesticated
animals (pigs, puppies)
contaminated milk and
water (fecal-oral route)

34
Q

Virulence factors of Yersinia enterocolitica

A

Psychrophilic (cold): milkand water
Surface proteins: adherence to GIT
Yersinia outer proteins (yops): affects phagocytosis)
Yersiniabactin: ironbinding protein
Urease: buffers stomachacid
Heat-stable enterotoxin = +CGMP = -NaCl =diarrhea
(Like ETEC)

35
Q

Patients who are susceptible to Yersinia enterocolitica

A
  1. Liver disease
  2. Hemochromatosis (iron overload)
  3. Children’s with weak immunity
36
Q

Patients who are susceptible to Y. Pestis

A

black death (soft tissue abscesses)

37
Q

Disease caused by Yersinia enterocolitica

A

yersiniosis (GIT infection)

38
Q

Symptoms of yersiniosis

A

Fever, bloody/ non-bloody diarrhea, nausea,
pain in right lower quadrant (like appendicitis), soft tissue abscess

39
Q

Campylobacter jejuni is thermophilic or halophilic

A

Thermophilic (42 degree)

40
Q

Campylobacter jejuni is a lactose or non lactose fermenter

A

Non lactose

41
Q

Fermentation of Campylobacter jejuni

A

Non-fermenting

42
Q

Campylobacter jejuni is oxidase + or -

A

+ve

43
Q

Mode of transmission of Campylobacter jejuni

A

Raw chicken, dirty water,
raw milk (fecal-oral route)

44
Q

Virulence factor of C jejuni

A

Flagellum: Invade intestinal epithelia = mucosal inflammation = bloody diarrhea

45
Q

Patients who are susceptible to C jejuni

A

Long-term use of
antacids,
immunocompromised,
people with HLA-B27
gene are more likely to
develop reactive arthritis
after infection due to
antibodies

46
Q

Disease caused by C jejuni

A

Guillaine-barre syndrome: which is a autoimmune neuropathy (paralysis)

47
Q

Symptoms of Guillaine-barre syndrome

A

Very bloody diarrhea,
fever, nausea, vomiting

48
Q

Motility of Vibrio cholerae

A

Highly motile (darting)

49
Q

Vibrio cholerae is thermophilic or halophilic

A

Halophilic

50
Q

Vibrio cholerae are lactose or non lactose fermenters

A

Non lactose

51
Q

Fermentation of Vibrio cholerae

A

Sucrose + glucose

52
Q

Vibrio cholerae is oxidase + or -

A

+ve

53
Q

Source of disease for Vibrio cholerae

A

Saltwater, contaminated
water (crowded living
areas)
Fecal-oral route

54
Q

Virulence factor for cholera

A

Cholera toxin (AB): binds
with G protein to prevent
GTP hydrolysis = activates
adenylyl cyclase = +
CAMP and + Cl = fluid
moves to intestine

55
Q

Patients who are susceptible to cholera

A

Immuno-compromised patients in developing countries and people who lives in crowded environment

56
Q

Disease caused due to cholera

A

Watery diarrhea with mucus (20-30 times) – rice-water-like stool Which can lead to Hypovolemic shock - death

57
Q

Symptoms of rice water stool

A

Nausea, abdominal pain

58
Q

Motility of Helicobacter pylori

A

Very motile (many flagella)

59
Q

(Helicobacter pylori) lactose or non lactose fermenting

A

Non lactose

60
Q

Fermentation of Helicobacter pylori

A

Glucose

61
Q

(Helicobacter pylori) oxidase + or -

A

+ve

62
Q

Source of contamination of Helicobacter pylori

A

Humans (endogenous)

63
Q

Virulence factor of Helicobacter pylori

A

Flagella: adherence to gastric epithelial cells
Adhesins: adherence
Mucinase: degrades mucous layer of stomach
Urease: neutralizes stomach acid Stays under mucosal
layer causing inflammation + gastrin & -somatostatin
release

64
Q

susceptibility of H pylori

A

Underdeveloped
crowded areas
Genetic predisposition

65
Q

Disease caused by H pylori

A

Chronic gastritis, gastric carcinoma or MALT lymphomas, peptic ulcer disease

66
Q

Symptoms of H pylori disease

A

Epigastric pain,
dyspepsia, GI bleeding

67
Q

Describe the things that are similar between Pseudomonas aeruginosa and Acinetobacter baumannii: lactose and sugar fermenting, ways the infections could be acquired.

A

non-lactose fermenters (colorless), doesn’t ferment sugars (pink in TSI)
Wound infections and in hospitals

68
Q

Metabolism of Pseudomonas aeruginosa

A

Aerobic but can grow anaerobically if nitrate is present

69
Q

Where would you find Pseudomonas aeruginosa

A

Environment, human feces and throats (ubiquitous) =
Grape-like odor and blue-green sheen from pyocyanin
production (seen in tissue infections and sputum as well)
Normally found in skin and
respiratory tract (moist

70
Q

Acinetobacter baumannii is aerobic or anaerobic

A

Aerobic

71
Q

Acinetobacter baumannii is found in

A

Normally found in skin and
respiratory tract (moist
environments) – abnormal to be
found in sterile places (blood)

72
Q

Hemolysis of Pseudomonas

A

Beta hemolysis

73
Q

Hemolysis of Acinetobacter

A

Nonhemolytic (except A hemolyticus)

74
Q

Motility of pseudomonas and acinetobacter

A

PM: motile (flagella)
AB: non motile (twitching fimbriae)

75
Q

Catalase positive or negative for PM and AB

A

Both catalase +ve

76
Q

Oxidase - or + for PM and AB

A

PM: +ve
AB: -ve

77
Q

Virulence factor of PM

A

LPS (endotoxins)
Pili: attachment
Alginate secretion (exopolysaccharide capsule):
mannuronic and glucuronic acids = antiphagocytic + form
biofilms (inside and also on artificial medical devices
Exotoxin A (AB): catalyzes ribosylation of EF2 which
inhibits protein synthesis = cell death
Exoenzyme S (T3 secretion): affects cytoskeleton and
signaling pathways = apoptosis
Elastase: affects ECM by hydrolyzing elastin and can
degrade IgA and IgG = tissue damage

78
Q

Disease caused by PM

A

Respiratory (pneumonia), UTIs (catheterization)
osteomyelitis, ecthyma gangrenosum – skin
endocarditis - heart
diarrhea, enteritis, enterocolitis - GIT
conjunctivitis, keratitis – eyes

79
Q

Disease caused by AB

A

Ventilator-associated pneumonia
UTIs
Soft tissue infections
Bacteremia via IV catheters

PUS B

80
Q

People who are susceptible to PM

A

Patients with cystic fibrosis
burn wounds
low neutrophil levels
immunocompromised

81
Q

Neutropenic patients experience (PM)

A

Infarcts, alveolar necrosis, bacteremia, aggressive
pneumonia (Can lead to respiratory failure)

82
Q

PM community acquired infection

A
  1. Hot tub folliculitis (infected hair follicles due to dirty water)
  2. otitis externa (swelling and pain of outer ear) – can lead tocellulitis and mastoid osteomyelitis if untreated (in diabetics)
  3. Osteomyelitis (S aureus also): after puncture wound (nail) /trauma to head can cause meningitis

microbiology (3 decks)

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