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Microbiology - Bacteria > Chapter 9: Gram-negative rods: Enterics > Flashcards

Chapter 9: Gram-negative rods: Enterics Flashcards

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0
Q

What does EMB agar stand for?

A

Eosine Methylene Blue

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1
Q

What is the Gram stain and morphology of the enterics?

A

Gram-negative rods

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2
Q

What type of bacteria grow on EMB agar?

A

Gram-negatives

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3
Q

EMB agar inhibits the growth of which type of bacteria?

A

Gram-positives

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4
Q

True or False: Gram-positives can grow on EMB agar.

A

False

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5
Q

True or False: EMB agar inhibits the growth of Gram-positive bacteria.

A

True

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6
Q

True or False: Gram-negatives can grow on EMB agar.

A

True

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7
Q

True or False: EMB agar inhibits the growth of Gram-negative bacteria.

A

False

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8
Q

EMB agar is used to detect what type of Gram-negative bacteria?

A

lactose-fermenters

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9
Q

What color do lactose fermenters have when grown on EMB agar?

A

become deep purple to black

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10
Q

Lactose fermenting Gram-negative bacteria appear purple to black when grown on what growth media?

A

EMB agar

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11
Q

What type of bacteria appear purple to black when grown on EMB agar?

A

Gram-negatives: lactose fermenters

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12
Q

What bacteria appear purple on EMB agar with a metallic green sheen?

A

Escherichia coli

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13
Q

Escherichia coli colonies appear purple with a metallic green sheen when grown in what media?

A

EMB agar

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14
Q

What 2 main types of media inhibit the growth of Gram-positive bacteria (so only Gram-negative bacteria grow on it), and have indicators that change color in the presence of lactose fermentation?

A

1) EMB agar

2) MacConkey agar

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15
Q

What type of bacteria grow on MacConkey agar?

A

Gram-negatives

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16
Q

MacConkey agar inhibits the growth of what type of bacteria?

A

Gram-positives

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17
Q

True or False: Gram-positives can grow on MacConkey agar.

A

False

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18
Q

True or False: Gram-negatives can grow on MacConkey agar.

A

True

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19
Q

True or False: MacConkey agar inhibits the growth of Gram-negatives.

A

False

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20
Q

True or False: MacConkey agar inhibits the growth of Gram-positive bacteria.

A

True

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21
Q

What color do lactose fermenters have when grown on MacConkey agar?

A

Pink/purple

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22
Q

Lactose-fermenting Gram-negative bacteria appear pink/purple when grown on what growth media?

A

MacConkey agar

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23
Q

What components of MacConkey agar inhibit the growth of Gram-positive bacteria? (2)

A

1) bile salts

2) crystal violet

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24
Q

Which species of bacteria appear as pink colonies when grown on MacConkey agar? (5)

A

lactose fermenters: “Lactose is KEE - Test with MacConKEE’s agar”

1) Citrobacter
2) Klebsiella
3) E. coli
4) Enterobacter
5) Serratia (weak fermenter)

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25
Q

Which species of bacteria appear as pink colonies when grown on MacConkey agar? (5)

A

lactose fermenters: “Lactose is KEE - Test with MacConKEE’s agar”

1) Citrobacter
2) Klebsiella
3) E. coli
4) Enterobacter
5) Serratia (weak fermenter)

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26
Q

What are the 4 main groups of enterics?

A

1) Enterobacteriaceae
2) Vibrionaceae
3) Pseudomonadaceae
4) Bacteroidaceae

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27
Q

What are the 3 major surface antigens of the enteric bacteria?

A

1) O-antigen
2) K antigen
3) H antigen

-These major surface antigens differ slightly from bug to bug.

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28
Q

What is O-antigen?

A

most external component of LPS of Gram-negative bacteria (remember O for Outer)

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29
Q

What is K antigen?

A

capsule that covers the O antigen

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30
Q

What is H antigen?

A

makes up subunits of the bacterial flagella, so only bacteria that are motile will possess this antigen

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31
Q

What major surface antigen is the most external component of LPS?

A

O antigen

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32
Q

What major surface antigen is the capsule that covers the O antigen?

A

K antigen

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33
Q

What major surface antigen makes up the subunits of bacterial flagella?

A

H antigen

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34
Q

What type of diarrhea results when enteric bacteria bind to the intestinal epithelial cells but do not enter the cell (no cell invasion)? Mechanism?

A

Watery diarrhea without systemic symptoms (such as fever).
-Diarrhea is caused by the release of exotoxins, which causes electrolyte and fluid loss from intestinal epithelial cells or epithelial cell death.

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35
Q

What type of invasion by enteric bacteria results in watery diarrhea without systemic symptoms (such as fever)? Mechanism?

A

no cell invasion
-The bacteria bind to the intestinal epithelial cells but do not enter the cell. Diarrhea is caused by the release of exotoxins which causes electrolyte and fluid loss from intestinal epithelial cells or epithelial cell death.

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36
Q

Escherichia coli causes exhibits what type of cell invasion and results in what type of diarrhea?

A

No cell invasion –> Watery diarrhea without systemic symptoms (such as fever)
Invasion of the intestinal epithelial cells –> Leukocytes and RBC in the stool, fever

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37
Q

Vibrio cholera exhibits what type of cell invasion and results in what type of diarrhea?

A

No cell invasion –> Watery diarrhea without systemic symptoms (such as fever)

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38
Q

What type of diarrhea results from enteric invasion of the intestinal epithelial cell? Mechanism?

A

Leukocytes in the stool (as well as fever); Red blood cell leakage into the stool.
-The bacteria have virulence factors that allow binding and invasion into cells. Toxins are then released that destroy the cells. The cell penetration results in a systemic immune response with local WBC infiltration (leukocytes in the stool) as well as fever. The cell death results in RBC leakage into the stool.

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39
Q

What type of invasion by enteric bacteria results in leukocytes in the stool, fever, and red blood cell leakage into the stool?

A

invasion of the intestinal epithelial cells.
-The bacteria have virulence factors that allow binding and invasion into cells. Toxins are then released that destroy the cells. The cell penetration results in a systemic immune response with local WBC infiltration (leukocytes in the stool) as well as fever. The cell death results in RBC leakage into the stool.

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40
Q

Shigella exhibits what type of cell invasion and results in what type of diarrhea?

A

Invasion of the intestinal epithelial cells –> Leukocytes and RBCs in the stool, fever

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41
Q

Salmonella enteritidis exhibits what type of cell invasion and results in what type of diarrhea?

A

Invasion of the intestinal epithelial cells –> Leukocytes and RBCs in the stool, fever

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42
Q

What type of diarrhea results from enteric invasion of the lymph nodes and bloodstream?

A
  • Abdominal pain
  • Diarrhea containing WBCs and RBCs
  • Systemic symptoms of fever, headache, and WBC elevation
  • Mesenteric lymph node enlargement
  • Bacteremia and sepsis
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43
Q

What type of invasion by enteric bacteria results in diarrhea containing WBCs and RBCs, systemic symptoms of fever, headache, and WBC elevation, mesenteric lymph node enlargement, bacteremia and sepsis?

A

invasion of the lymph nodes and bloodstream

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44
Q

Salmonella typhi exhibits what type of invasion and results in what type of diarrhea?

A

Invasion of the lymph nodes and bloodstream –> WBC and RBCs in the stool, fever, headache, WBC elevation, mesenteric lymph node enlargement, bacteremia, sepsis

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45
Q

Yersinia enterocolitica exhibits what type of invasion and results in what type of diarrhea?

A

Invasion of the lymph nodes and bloodstream –> WBC and RBCs in the stool, fever, headache, WBC elevation, mesenteric lymph node enlargement, bacteremia, sepsis

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46
Q

Campylobacter jejuni exhibits what type of invasion and results in what type of diarrhea?

A

Invasion of the lymph nodes and bloodstream –> WBC and RBCs in the stool, fever, headache, WBC elevation, mesenteric lymph node enlargement, bacteremia, sepsis

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47
Q

True or False: Escherichia coli is part of normal gut flora.

A

True

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48
Q

E. coli - reservoir?

A

humans: GI and urinary tract

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49
Q

How does Escherichia coli in the gut become pathogenic?

A

it acquires virulence factors in the gut via conjugation with plasmid exchange, lysogenic conversion, by temperate bacteriophages, and direct transposon mediated DNA insertion

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50
Q

Escherichia coli - Gram stain and morphology?

A

Gram-negative rods (like all Enterobacterieae family)

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51
Q

Escherichia coli - catalase?

A

catalase-positive (like all Enterobacterieae family)

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52
Q

Escherichia coli - metabolism?

A

facultative anaerobe (like all Enterobacterieae family)

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53
Q

Escherichia coli - oxidase?

A

oxidase-negative (like all Enterobacteriaceae family)

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54
Q

Escherichia coli - glucose?

A

Ferments glucose (like all Enterobacterieae family)

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55
Q

Escherichia coli - lactose?

A

lactose fermenter

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56
Q

E. coli - indole?

A

indole-positive (makes indole from tryptophan)

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57
Q

Escherichia coli - encapsulated?

A

yes

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58
Q

Escherichia coli - motility?

A

motile

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59
Q

E. coli - K-antigen?

A

yes - encapsulated

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60
Q

E. coli - H-antigen?

A

yes, has flagella (multiple)

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61
Q

E. coli - hemolysis on blood agar?

A

beta-hemolytic

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62
Q

Escherichia coli - color on MacConkey agar?

A

pink (it is a lactose fermenter)

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63
Q

E. coli - mucoid? (on MacConkey agar)

A

no

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64
Q

What major surface antigens does Escherichia coli possess? (O, K, H)?

A

O-antigen = LPS endotoxin
K antigen = capsule
H antigen = flagella

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65
Q

What virulence factors does Escherichia coli possess? (5)

A

1) fimbriae (pili) = colonization factor
2) siderophores
3) adhesins
4) capsule (K-antigen)
5) flagella (H-antigen)

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66
Q

Are all Escherichia coli species pathogenic?

A

No! E. coli normally resides int he colon without causing disease. Only upon acquiring certain virulence factors does it cause disease.

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67
Q

What virulence factor of Escherichia coli is a colonization factor?

A

fimbriae (pili)

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68
Q

siderophore - function?

A

allows bacteria such as E. coli to obtain iron from human transferrin or lactoferrin

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69
Q

What bacterial virulence factor allows it to obtain iron from human transferrin or lactoferrin?

A

siderophore

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70
Q

Which E. coli virulence factor is responsible for cystitis and pyelonephritis?

A

fimbriae

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71
Q

Fimbriae (virulence factor) in E. coli causes what clinical diseases?

A

cystitis

pyelonephritis

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72
Q

What E. coli virulence factor is responsible for pneumonia and neonatal meningitis?

A

capsule (K antigen)?

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73
Q

The E. coli capsule (K antigen) is responsible for what clinical diseases?

A

pneumonia, neonatal meningitis

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74
Q

What E. coli virulence factor is responsible for septic shock?

A

LPS endotoxin

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75
Q

E. coli LPS endotoxin is responsible for what clinical disease?

A

septic shock

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76
Q

The presence of which organism is used to determine fecal contamination of bodies of water?

A

Escherichia coli

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77
Q

Virulent E. coli can cause what 5 diseases?

A

1) diarrhea
2) urinary tract infection
3) neonatal meningitis
4) Gram-negative sepsis, occurring commonly in debilitated hospitalized patients
5) pneumonia, also hospital-acquired

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78
Q

Death resulting from Escherichia coli is usually due to what?

A

dehydration

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79
Q

Which bacterium does Montezuma’s Revenge refer to?

A

Escherichia coli

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80
Q

What populations are at risk for E. coli diarrhea? (3)

A

1) infants worldwide - have not yet developed immunity
2) adults and children from developed countries traveling to underdeveloped countries since they have not developed immunity during their childhood (Montezuma’s revenge)
3) hospital patients

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81
Q

What are the 4 strains of Eschierichia coli?

A

1) ETEC - enterotoxigenic E. coli
2) EHEC - enterohemorrhagic E. coli
3) EIEC - enteroinvasive E. coli
4) EPEC - enteropathogenic E. coli

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82
Q

What form of diarrhea does ETEC cause? Mechanism?

A

Enterotoxigenic E. coli causes traveler’s diarrhea (rice watery stool just like cholera)
ETEC has pili (colonization factor) that help it bind to intestinal epithelial cells, where it releases exotoxins: heat labile and heat stable toxins. These exotoxins inhibit the reabsorption of Na+ and Cl- an stimulate the secretion of Cl- and HCO3- into the intestinal lumen. Water follows the osmotic pull of these ions, resulting in water and electrolyte loss. This produces a severe watery diarrhea.

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83
Q

What strain of E. coli is associated rice watery diarrhea (similar to cholera)? Mechanism?

A

Enterotoxigenic E. coli (ETEC)
ETEC has pili (colonization factor) that help it bind to intestinal epithelial cells (noninvasive), where it releases exotoxins: heat labile and heat stable toxins. These exotoxins inhibit the reabsorption of Na+ and Cl- an stimulate the secretion of Cl- and HCO3- into the intestinal lumen. Water follows the osmotic pull of these ions, resulting in water and electrolyte loss. This produces a severe watery diarrhea.

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84
Q

What strain of E. coli is associated with traveler’s diarrhea? Mechanism?

A

Enterotoxigenic E. coli (ETEC)
ETEC has pili (colonization factor) that help it bind to intestinal epithelial cells (noninvasive), where it releases exotoxins: heat labile and heat stable toxins. These exotoxins inhibit the reabsorption of Na+ and Cl- an stimulate the secretion of Cl- and HCO3- into the intestinal lumen. Water follows the osmotic pull of these ions, resulting in water and electrolyte loss. This produces a severe watery diarrhea (like rice water, similar to cholera).

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85
Q

What exotoxins does ETEC release? Mechanism of action?

A

-Heat-labile toxin (LT): increases cAMP (same as cholera toxin)
-Heat-stable toxin (ST): increases cGMP
These exotoxins inhibit the reabsorption of Na+ and Cl- an stimulate the secretion of Cl- and HCO3- into the intestinal lumen. Water follows the osmotic pull of these ions, resulting in water and electrolyte loss. This produces a severe watery diarrhea (like rice water, similar to cholera).

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86
Q

ETEC - invasion? inflammation?

A

no invasion or inflammation

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87
Q

Which strain of E. coli has clinical manifestations similar to cholera?

A

ETEC (enterotoxic E. coli) - releases heat labile toxin (LT) and heat stable toxin (ST)

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88
Q

What form of diarrhea does EHEC cause? Mechanism?

A

Dysentery/Bloody diarrhea (no pus in stool), no fever.
Enterohemorrhagic E. coli have pili colonization factor like ETEC that help it bind to intestinal epithelial cells, and secrete the powerful Shiga-like toxin (verotoxin) that has the same mechanism as Shigella toxin: it inhibits protein synthesis by inhibiting the 60S ribosomal subunit, which results in intestinal epithelial cell death. The diarrhea is bloody (hemorrhagic), accompanied by severe abdominal cramps, and is called hemorrhagic colitis.

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89
Q

What strain of E. coli is associated with dysentery/bloody diarrhea (no pus in stool)? Mechanism?

A

Enterohemorrhagic E. coli (EHEC)
Enterohemorrhagic E. coli have pili colonization factor like ETEC that help it bind to intestinal epithelial cells, and secrete the powerful Shiga-like toxin (verotoxin) that has the same mechanism as Shigella toxin: it inhibits protein synthesis by inhibiting the 60S ribosomal subunit, which results in intestinal epithelial cell death. The diarrhea is bloody (hemorrhagic), accompanied by severe abdominal cramps, and is called hemorrhagic colitis.

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90
Q

What exotoxins does EHEC release? Mechanism of action?

A

Shiga-like toxin
Inhibits protein synthesis by inhibiting the 60S ribosomal subunit, which results in intestinal epithelial cell death. The diarrhea is bloody (hemorrhagic), accompanied by severe abdominal cramps, and is called hemorrhagic colitis.

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91
Q

EHEC - invasion? inflammation?

A

no invasion

toxin alone causes inflammation

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92
Q

What strain of E. coli is associated with hemorrhagic colitis? Mechanism?

A

Enterohemorrhagic E. coli (EHEC)
Enterohemorrhagic E. coli have pili colonization factor like ETEC that help it bind to intestinal epithelial cells, and secrete the powerful Shiga-like toxin (verotoxin) that has the same mechanism as Shigella toxin: it inhibits protein synthesis by inhibiting the 60S ribosomal subunit, which results in intestinal epithelial cell death. The diarrhea is bloody (hemorrhagic), accompanied by severe abdominal cramps, and is called hemorrhagic colitis.

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93
Q

What is the most common serotype of EHEC?

A

0157:H7

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94
Q

0157:H7 is the most common serotype of what strain of bacteria?

A

EHEC (enterohemorrhagic E. coli)

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95
Q

0157:H7 is associated with what clinical manifestation?

A

hemolytic uremic syndrome (HUS)

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96
Q

What strains of bacteria is commonly associated with HUS?

A

1) EHEC (enterohemorrhagic E. coli) 0157:H7
2) Shigella
(hemolytic uremic syndrome)

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97
Q

What is the triad of HUS?

A

(hemolytic uremic syndrome)

1) anemia
2) thrombocytopenia (decrease in platelets)
3) renal failure (uremia)

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98
Q

What syndrome is characterized by:

1) anemia
2) thrombocytopenia
3) acute renal failure (uremia)

A

HUS (hemolytic uremic syndrome)

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99
Q

What is the mechanism by which 0157:H7 EHEC causes hemolytic uremic syndrome (HUS)?

A

Microthrombi form on endothelium damaged by toxin –> Mechanical hemolysis (schistocytes formed), and decreased renal blood flow. –> Microthrombi consume platelets –> Thrombocytopenia.

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100
Q

What is the reservoir for EHEC, particularly 0157:H7 associated with HUS?

A

cattle - numerous outbreaks have occurred secondary to infected hamburger meat served at fast food chains

101
Q

EIEC - invasion? inflammation?

A

both

102
Q

What form of diarrhea does EIEC cause? Mechanism?

A

Dysentery/Bloody diarrhea (with pus in stool), and fever.
The main virulence factor is encoded in a plasmid shared by Shigella and E. coli, which gives the bacteria the ability to actually invade the epithelial cells. EIEC also produces small amounts of Shiga-like toxin. The host tries to get rid of the invading bacteria, and this results in an immune-mediated inflammatory reaction with fever. White blood cells invade the intestinal wall, and the diarrhea is bloody with white blood cells.

103
Q

What strain of E. coli is associated with dysentery/bloody diarrhea (with pus in stool) and fever? Mechanism?

A

EIEC.
The main virulence factor is encoded in a plasmid shared by Shigella and E. coli, which gives the bacteria the ability to actually invade the epithelial cells. EIEC also produces small amounts of Shiga-like toxin. The host tries to get rid of the invading bacteria, and this results in an immune-mediated inflammatory reaction with fever. White blood cells invade the intestinal wall, and the diarrhea is bloody with white blood cells.

104
Q

Which strain of E. coli has clinical manifestations similar to Shigella?

A

EIEC (enteroinvasive Escherichia coli) - has ability to invade intestinal epithelial cells and produces Shiga-like toxin.

105
Q

What exotoxins does EIEC release? Mechanism of action?

A

Shiga-like toxin
Inhibits protein synthesis by inhibiting the 60S ribosomal subunit, which results in intestinal epithelial cell death. The diarrhea is bloody (hemorrhagic), accompanied by severe abdominal cramps, and is called hemorrhagic colitis.

106
Q

Define cystitis.

A

infection of the bladder

107
Q

Define pyelonephritis.

A

infection of the kidney

108
Q

What bacteria is the most common cause of UTI?

A

E. coli

109
Q

UTI usually occurs in which populations?

A

women, and hospitalized patients with catheters in the urethra

110
Q

What are symptoms of UTI? (3)

A

1) dysuria - burning on urination
2) having to pee frequently
3) feeling of fullness over the bladder

111
Q

What strain of E. coli causes diarrhea usually in children?

A

EPEC (enteropathogenic E. coli)

112
Q

What exotoxins does EPEC release? Mechanism of action?

A

No toxin is produced - bacterium adheres to apical surface, flattens villi, and prevents absorption, causing diarrhea, usually in children.

113
Q

E. coli - transmission? (4)

A

1) fecal-oral
2) migration up the urethra
3) colonization of catheters in hospitalized patients (Foley catheters, central lines, etc.)
4) aspiration of oral E. coli

114
Q

E. coli - treatment? (4)

A

1) cephalosporins (3rd generation: ceftriaxone) - for meningitis and sepsis
2) aminoglycosides
3) trimethoprim & sulfamethoxazole - for UTI
4) fluoroquinolones - for UTI

115
Q

Which strain of E. coli does not ferment sorbitol, thus distinguishing it from other E. coli strains?

A

EHEC (enterohemorrhagic)

116
Q

How can EHEC be distinguished from other E. coli strains?

A

EHEC (enterohemorrhagic E. coli) does not ferment sorbitol

117
Q

What bacteria is the most common cause of gram-negative sepsis?

A

E. coli, usually in debilitated patients.

118
Q

What form of diarrhea does EPEC cause? Mechanism?

A

Enteropathogenic E. coli
Diarrhea usually in children (Pediatrics).
No toxin is produced. Adheres to apical surface, flattens villi, prevents absorption.

119
Q

Klebsiella pneumoniae - Gram stain and morphology?

A

Gram-negative rods (like all Enterobacterieae family)

120
Q

Klebsiella pneumoniae - catalase?

A

catalase-positive (like all enterobacteriaceae family)

121
Q

Klebsiella pneumoniae - oxidase?

A

oxidase-negative (like all Enterobacteriaceae family)

122
Q

Klebsiella pneumoniae - metabolism?

A

facultative anaerobe (like all Enterobacteriaceae family)

123
Q

Klebsiella pneumoniae - indole?

A

indole-negative (cannot make indole from tryptophan)

124
Q

Klebsiella pneumoniae - encapsulated?

A

yes

125
Q

Klebsiella pneumoniae - motility?

A

non-motile

126
Q

Klebsiella pneumoniae - K-antigen?

A

yes, is encapsulated

127
Q

Klebsiella pneumoniae - glucose?

A

ferments glucose (like all Enterobacteriaceae family)

128
Q

Klebsiella pneumoniae - urease?

A

urease-positive (splits urea into NH3 and CO2)

129
Q

Klebsiella pneumoniae - H-antigen?

A

No, is not motile (no flagella)

130
Q

Klebsiella pneumoniae - lactose?

A

yes, ferments lactose

131
Q

Klebsiella pneumoniae - color on MacConkey agar?

A

pink/purple - it is a lactose fermenter

132
Q

Klebsiella - mucoid? (on MacConkey agar)

A

mucoid

133
Q

What major surface antigens does Klebsiella pneumoniae exhibit? (O, K, H)

A

O-antigen = LPS
K-antigen = encapsulated
(does not have flagella and is non-motile, so no H-antigen)

134
Q

What are the 4 A’s of Klebsiella pneumoniae?

A

Aspiration pneumonia
Abscess in lungs and liver
Alcoholics
di-A-betics

135
Q

Klebsiella pneumoniae infection can result in which clinical manifestations? (4)

A

1) (aspiration) lobar pneumonia, with bloody sputum
2) lung and liver abscess
2) nosocomial UTI
3) sepsis

136
Q

Klebsiella pneumoniae - transmission?

A

direct person-to-person contact: nosocomial infection is spread by healthcare workers or contamination of objects in the environment, such as catheters and ventilators

137
Q

What populations are particularly vulnerable to Klebsiella pneumoniae infection?

A

1) people in long-term healthcare settings
2) people with impaired immune defenses, especially alcoholics and diabetics
(uncommon in otherwise healthy people)

138
Q

Describe the pneumonia commonly associated with Klebsiella pneumoniae infection.

A
  • Lobar pneumonia (single lung consolidation)
  • Violent pneumonia that frequently destroys lung tissue, producing cavities
  • Thick bloody sputum that looks like red currant jelly, the color of the O-antigen
139
Q

Pneumonia with thick “red currant jelly” bloody sputum is associated with what bacterium?

A

Klebsiella pneumoniae

140
Q

Klebsiella pneumoniae - treatment?

A

1) third-generation cephalosporin (ceftriaxone)
2) ciprofloxacin (second-generation fluoroquinolone) for UTI
(poor prognosis despite antibiotic therapy)

141
Q

Proteus mirabilis - Gram stain and morphology?

A

Gram-negative rods (like all Enterobacteraceae family)

142
Q

Proteus mirabilis - catalase?

A

catalase-positive (like all Enterobacteriaceae family)

143
Q

Proteus mirabilis - metabolism?

A

facultative anaerobe (like all Enterobacteriaceae family)

144
Q

Proteus mirabilis - oxidase?

A

oxidase-negative (like all Enterobacteriaceae family)

145
Q

Proteus mirabilis - motility?

A

VERY motile (swarming)

146
Q

Proteus mirabilis - appearance on agar culture?

A

swarming: colonies swarm over entire culture plate rather than as distinct round colonies

147
Q

Proteus mirabilis - glucose?

A

glucose-fermenter (like all Enterobacteriaceae family)

148
Q

Proteus mirabilis - H-antigen?

A

yes, is motile (has flagella)

149
Q

Proteus mirabilis - lactose?

A

does not ferment lactose

150
Q

Proteus mirabilis - color on MacConkey agar?

A

yellow (does not turn pink) - is not a lactose fermenter

151
Q

Proteus mirabilis - toxins?

A

does not produce toxins

152
Q

Proteus mirabilis - indole?

A

indole-negative (does not make indole from tryptophan)

153
Q

Proteus mirabilis infection results in what clinical manifestations? (2)

A

1) UTI

2) bacteremia or sepsis

154
Q

Proteus mirabilis - capsule?

A

yes, encapsulated

155
Q

Proteus mirabilis - K-antigen?

A

Yes, it is encapsulated: large mucoid capsule and viscous colonies

156
Q

What does examination of the urine reveal in a patient with Proteus mirabilis infection?

A

alkaline urine (high pH), from splitting urine into NH3 and CO2

157
Q

What is the Weil-Felix test?

A

Uses antibodies against certain strains of Proteus mirabilis to diagnose Rickettsia infection. 3 strains of Proteus (OX-19, OX-2, OX-K) have cross-reacting antigens with some Rickettsia. Patient serum is mixed with these Proteus strains to determine whether there are antibodies in the serum that react with the Proteus antigens.

158
Q

What is the name of the test used to diagnose Rickettsia infection, based on cross-reactivity with Proteus mirabilis antigens?

A

Weil-Felix test

159
Q

Proteus mirabilis - treatment?

A

1) ampicillin

2) trimethoprim & sulfamethoxazole (for UTI)

160
Q

Proteus mirabilis - urease?

A

urease-positive (splits urea into NH3 and CO2)

161
Q

Enterobacter - Gram stain and morphology?

A

Gram-negative rods

162
Q

Enterobacter - catalase?

A

catalase-positive (like all Enterobacteriaceae family)

163
Q

Enterobacter - oxidase?

A

oxidase-negative (like all Enterobacteriaceae family)

164
Q

Enterobacter - glucose?

A

ferments glucose (like all Enterobacteriaceae family)

165
Q

Enterobacter - metabolism?

A

facultative anaerobe (like all Enterobacteriaceae family)

166
Q

Enterobacter - lactose?

A

lactose fermenter

167
Q

Enterobacter - urease?

A

urease-negative (cannot split urea into NH3 and CO2)

168
Q

Enterobacter - motility?

A

highly motile

168
Q

Enterobacter - H-antigen?

A

yes (has flagella) - is very motile

169
Q

Enterobacter - color on MacConkey agar?

A

pink/purple (it is a lactose fermenter)

171
Q

Enterobacter - mucoid? (on MacConkey agar)

A

no

172
Q

True or False: Enterobacter is part of normal gut flora.

A

True

173
Q

Enterobacter is associated with what clinical manifestations?

A

UTI and nosocomial infections

174
Q

Serratia - Gram stain and morphology?

A

Gram-negative rods

175
Q

Serratia - catalase?

A

catalase-positive (like all Enterobacteriaceae)

176
Q

Serratia - oxidase?

A

oxidase-negative (like all Enterobacteriaceae)

177
Q

Serratia - glucose?

A

ferments glucose (like all Enterobacteriaceae)

178
Q

Serratia - metabolism?

A

facultative anaerobe (like all Enterobacteriaceae)

179
Q

Serratia - lactose?

A

slow lactose fermenter

180
Q

Serratia - urease?

A

urease-negative (cannot split urea into NH3 and CO2)

181
Q

Serratia - motility?

A

motile

182
Q

Serratia - H-antigen?

A

yes (is motile) - has flagella

183
Q

Serratia marcescens produces what color pigment?

A

red pigment (think red maraschino cherries)

184
Q

Serratia is associated with what clinical manifestations?

A

UTI, wound infections, pneumonia

185
Q

Serratia can cause osteomyelitis in which high risk populations?

A

Diabetics and IV drug users

186
Q

Which Gram-negative bacteria are lactose fermenters?

A

E. coli
Klebsiella
Enterobacter
Serratia (slow)

187
Q

Which of the Gram-negative lactose fermenters are urease-positive?

A

Klebsiella

E. coli, Enterobacter, and Serratia are lactose fermenters that are urease-negative

188
Q

Shigella - Gram stain and morphology?

A

Gram-negative rods

189
Q

Shigella - catalase?

A

catalase-positive (like all Enterobacteriaceae family)

190
Q

Shigella - lactose?

A

non-lactose fermenter

191
Q

Shigella - appearance on MacConkey agar?

A

yellow (does not turn pink because not a lactose fermenter)

192
Q

Shigella - oxidase?

A

oxidase-negative

193
Q

Shigella - glucose?

A

glucose fermenter (like all Enterobacteriaceae family)

194
Q

Shigella - metabolism?

A

facultative anaerobe (like all Enterobacteriaceae family)

195
Q

Shigella - H2S production?

A

no

196
Q

Shigella - motility?

A

non-motile

197
Q

Shigella - H-antigen?

A

no (is non-motile, no flagella)

198
Q

How can Shigella be differentiated from E. coli?

A

Shigella does not ferment lactose, but E. coli does.

199
Q

How can Shigella be differentiated from Salmonella?

A

(Both are non-lactose fermenters)
Salmonella produces H2S, but Shigella does not.
Salmonella is motile, but Shigella is non-motile.

200
Q

True or False: Shigella is part of normal gut flora.

A

False! Shigella is NEVER considered part of the normal intestinal flora - it is always a pathogen.

201
Q

What are the 4 species of Shigella? Which is the most common? Most virulent?

A

1) S. dysenteriae
2) S. flexneri
3) S. boydii (India)
4) S. sonnei

S. dysenteriae is the most common and the most virulent (the others have decreased virulence because of the lack of toxin production)

202
Q

Does Shigella produce toxins?

A

yes - Shiga toxin (similar to Shiga-like toxin of EHEC and EIEC)

203
Q

Shiga toxin - mechanism?

A

Shigella (similar to EIEC) invades intestinal epithelial cells and releases Shiga toxin, which inactivates the 60S ribosome. The host tries to get rid of the invading bacteria, and this results in an immune-mediated inflammatory reaction with fever. White blood cells invade the intestinal wall, and the diarrhea is bloody with white blood cells.

204
Q

Shigella - reservoir?

A

humans only

205
Q

Why do patients with Shigella infection develop diarrhea?

A

Shigella invades the intestinal epithelial cells. The inflamed colon, damaged by the Shiga toxin, is unable to reabsorb fluids and electrolytes.

206
Q

Shigella causes what type of diarrhea?

A

Dysentery/bloody diarrhea with flecks of pus (white cells), and illness begins with fever.

207
Q

Shigella - transmission?

A

fecal-oral transmission

humans are the only reservoir for Shigella

208
Q

Shigella - treatment?

A

usually supportive in moderate cases, and usually include oral rehydration.

1) fluroquinolones for severe cases
2) azithromycin
3) trimetoprim & sulfamethoxazole

209
Q

Salmonella - Gram stain and morphology?

A

Gram-negative rods

210
Q

Salmonella - catalase?

A

catalase-positive (like all Enterobacteriaceae family)

211
Q

Salmonella - oxidase?

A

oxidase-negative

212
Q

Salmonella - lactose?

A

non-lactose fermenter

213
Q

Salmonella - glucose?

A

ferments glucose

214
Q

Salmonella - metabolism?

A

facultative anaerobe (like all Enterobacteriaceae family)

215
Q

Salmonella - H2S?

A

yes, produces H2S

216
Q

Salmonella - motility?

A

motile (has flagella and H-antigen)

like a salmon

217
Q

Salmonella - H-antigen?

A

yes, is motile (has flagella)

218
Q

Salmonella - capsule?

A

yes (Vi antigen) (just like the K antigen)

219
Q

Salmonella - K antigen?

A

yes, but it is called Vi antigen (for virulence)

220
Q

What is Vi antigen?

A

polysaccharide capsule of Salmonella that surrounds the O antigen, thus protecting the bacteria from antibody attack on the O antigen. Just like the K antigen, but called Vi (for virulence) antigen in Salmonella.

221
Q

What are the 3 groups of Salmonella serotypes?

A

1) Salmonella typhi
2) Salmonella cholerae-suis
3) Salmonella enteritidis

222
Q

Salmonella - reservoir?

A

Salmonella typhi - only found in humans
Non-typhi groups of Salmonella (S. cholerae-suis, S. enteritidis) - zoonotic (lives in the GI tracts of animals): pet turtles, chickens, uncooked eggs

223
Q

True or False: Salmonella is considered part of normal human gut flora.

A

False! Salmonella is NEVER considered part of the normal intestinal flora. It is always pathogenic. (like Shigella)

224
Q

Salmonella - transmission?

A

fecal-to-oral (contamination of food or water with animal feces in non-typhi groups; S. typhi is carried only by humans; non-typhi groups live in the GI tracts of animals)

225
Q

What 4 disease states can Salmonella cause in humans?

A

1) typhoid fever (enteric fever)
2) carrier state
3) sepsis (including osteomyelitis)
4) gastroenteritis (diarrhea)

226
Q

Is Shigella dysenteriae acid-labile or acid-resistant?

A

acid-resistant

227
Q

What size inoculum of Shigella is needed to cause clinical gastric symptoms?

A

small incoulum: 10-100 organisms

it is acid-resistant

228
Q

What size inoculum of Salmonella is needed to cause clinical gastric symptoms?

A

large inoculum: 200-1 million organisms

229
Q

How do Salmonella and Shigella differ in motility?

A

Salmonella is motile (has flagella, H-antigen); Shigella is not.

230
Q

How do Salmonella and Shigella differ in H2S production?

A

Salmonella produces H2S; Shigella does not.

231
Q

How do Salmonella and Shigella differ in infective dose?

A

Shigella infects with 10-100 organisms (it is acid resistant); Salmonella infects with 200-1 million organisms (it is acid labile).

232
Q

What populations are at high risk of Salmonella infection?

A

1) young children
2) elderly
3) immunosuppressed populations

233
Q

Salmonella - urease?

A

negative

234
Q

Salmonella - indole?

A

negative

235
Q

What disease can Salmonella typhi cause? Symptoms?

A

Typhoid fever. Symptoms begin 1-3 weeks after exposure.

1) fever and headache
2) abdominal pain: either diffuse or localized to the right lower quadrant over the terminal ileum (often mimicking appendicitis)
3) hepatosplenomegaly (as inflammation of involved organs occurs),
4) and the patient may develop “pea-soup” DIARRHEA or constipation
5) and ROSE SPOTS on the abdomen (a transient rash consisting of small pink marks seen only on light-skinned people)

236
Q

What microbe causes a disease characterized by the following symptoms:

1) fever
2) abdominal pain that is either diffuse or localized to the right lower quadrant (mimicking appendicitis)
3) hepatosplenomegaly
4) rash: rose spots on the abdomen
5) “pea soup” diarrhea

A

Salmonella typhi (typhoid fever)

237
Q

What is the treatment for typhoid fever?

A

Salmonella typhi - treat with fluoroquinolone (ciprofloxacin)
Also ceftriaxone, trimethoprim-sulfamethoxazole, or azithromycin.

238
Q

What is the treatment for Salmonella typhi infection?

A

Typhoid fever - treat with fluoroquinolones (ciprofloxacin)

Also ceftriaxone, trimethoprim-sulfamethoxazole, or azithromycin

239
Q

Describe the carrier state of Salmonella typhi.

A

Some people recovering from typhoid fever (like Typhoid Mary) become chronic carriers, harboring Salmonella typhi in their GALLBLADDERS and excreting bacteria for years. These people are not actively infected and do not have any symptoms, but can still spread the bacteria to others.

240
Q

What Salmonella serotype is associated with salmonella-related sepsis (infects lungs, brain, or bones)?

A

Salmonella choleraesuis

241
Q

Which Salmonella serotype is associated with osteomyelitis (bone infection), especially in sickle cell anemia patients?

A

Salmonella choleraesuis

242
Q

What subpopulation is particularly prone to salmonella (choleraesuis)-related osteomyelitis (bone infection)?

A

sickle cell anemia patients

243
Q

Why are sickle cell anemia patients particularly prone to Salmonella (choleraesuis) osteomyelitis (bone infection)?

A

Salmonella is encapsulated with the Vi capsule. Our immune system clears encapsulated bacteria by opsonizing them with antibodies, and then macrophages and neutrophils in the spleen (reticulo-endothelial system) phagocytose the opsonized bacteria. Patients who are asplenic (from trauma or sickle-cell disease) have difficulty clearing encapsulated bacteria and are more susceptible to Salmonella infections.

244
Q

What is the treatment for Salmonella choleraesuis infection?

A

Vigorous and prolonged antibiotic therapy: (same as typhoid fever): treat with fluoroquinolones (ciprofloxacin)
Also ceftriaxone, trimethoprim-sulfamethoxazole, or azithromycin

245
Q

What is the treatment for Salmonella osteomyelitis?

A

Vigorous and prolonged antibiotic therapy: (same as typhoid fever): treat with fluoroquinolones (ciprofloxacin)
Also ceftriaxone, trimethoprim-sulfamethoxazole, or azithromycin

246
Q

Does infection with Salmonella choleraesius involve the GI tract (as in S. typhi and S. enteritidis?

A

No - causes sepsis (osteomyelitis)

247
Q

Which Salmonella serotypes are associated with GI symptoms?

A

S. typhi and S. enteritidis (but not S. choleraesius)

248
Q

What is the most common type of Salmonella infection?

A

diarrhea (gastroenteritis) - can be caused by any of hundreds of serotypes of nontyphoidal Salmonella.

249
Q

Is Salmonella an intracellular or extracellular microbe?

A

Both - it is facultative intracellular: it lives within macrophages in lymph nodes, and can live in the gallbladder for years

250
Q

Describe the clinical presentation caused by Salmonella enteritidis serotypes (non-typhi types).

A

Nausea, abdominal pain
Diarrhea that is either watery (cholera-like toxin) or, less commonly, contains mucus and trace blood (ileal inflammation).
Fever occurs in about half of patients.

251
Q

What is the treatment for Salmonella gastroenteritis?

A

fluids and electrolyte replacement. Symptoms usually resolve after 2-7 days, but patients will continue to excrete bacteria for months following infection.
Antibiotics do not shorten the course of the disease and do cause prolonged bacterial shedding in the stool.

Microbiology - Bacteria (15 decks)

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