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Flashcards in Micro Midterm1 Deck (463):
1

What color are gram positive bacteria on a typical gram stain?  What about gram negative?

Gram positive: blueish or purple; gram negative: pink

2

What shape are cocci bacteria?

Typically spherical, in clusters, pairs, or chains

3

Can all bacteria be visualized with the gram stain?

No, some need other stains e.g. spirochetes

4

Do bacteria have organelles?

No, they are prokaryotes

5

What is the outermost coat of the gram-negative cell wall?

A phospholipid membrane (there are two of them, one for the cell well and one that functions as the plasma membrane)

6

What is the cell wall of gram-positive bacteria made of?

Peptidoglycan: peptide cross links between polysaccharide chains

7

Are lipopolysaccharides characteristic of gram positive or gram negative bacteria?

Gram negative, as they integrate into the outer phospholipid membrane

8

Does Staphylococcus epidermidis normally cause disease on the skin?

No, it is benign.  Staph aureus is the more virulent strain that can cause acne and other skin infections.

9

Is the peptidoglycan layer of the cell wall thicker in gram positive or gram negative bacteria?

Gram positive bacteria have thicker peptidoglycan

10

Bacteria can be colonize or can cause disease. The ability to cause disease is determined by–  [...] factors–  Host factors–  Environmental factors

Bacteria can be colonize or can cause disease. The ability to cause disease is determined by–  Virulence (bacterial) factors–  Host factors–  Environmental factors

11

Bacteria can be colonize or can cause disease. The ability to cause disease is determined by–  Virulence (bacterial) factors–  [...] factors–  Environmental factors

Bacteria can be colonize or can cause disease. The ability to cause disease is determined by–  Virulence (bacterial) factors–  Host factors–  Environmental factors

12

Bacteria can be colonize or can cause disease. The ability to cause disease is determined by–  Virulence (bacterial) factors–  Host factors–  [...] factors

Bacteria can be colonize or can cause disease. The ability to cause disease is determined by–  Virulence (bacterial) factors–  Host factors–  Environmental factors

13

Besides direct damage caused by the organism, what can infectious disease symptoms manifest via?

The immune response mounted by the host

14

What is hemolysis as it relates to bacteria?

The pattern that the colonies form on a blood agar plate, related to their ability to break down blood cells

15

Is this α or β hemolysis?

β: halo like growth around streaks

16

What kind of typing is this?  Which side is positive?

Lancefield typing; left is positive

17

What are non-suppurative complications?

When the host response causes the clinical manifestations of the disease

18

What bacterium causes pharyngitis, cellulitis, impetigo, and necrotizing fasciitis?

Streptococcus pyogenes

19

Is Streptococcus pyogenes α or β hemolytic?

β hemolytic

20

What clinical manifestation is this?  What bacterium is immediately suspect?

Pharyngitis; Streptococcus pyogenes

21

What clinical manifestation is this? What bacterium is suspected?

Erypsipelas; Streptococcus pyogenes

22

What skin condition is this?  What bacterium is immediately suspect?

Impetigo; Streptococcus pyogenes

23

What does it mean to talk about suppurative complications of an infection?

Clinical manifestations directly caused by the organism itself; e.g., pharyngitis or a rash

24

Are acute rheumatic fever, glomerulonephritis, scarlet fever, and toxic shock suppurative or non-suppurative complications?

Non-suppurative

25

What does the word "suppurative" derive from (e.g. what does suppuration refer to?)

Pus formation

26

Is acute rheumatic fever more rare or less rare over the age of 30 than below?

It is very rare over 30

27

Does acute rheumatic fever associate with a preceding S. pyogenes throat infection, or a skin infection, or both?

Only throat infections

28

When a bacteria is said to belong to Group A, B, etc. what grouping system is being referenced?

The Lancefield grouping system

29

What is the Lancefield grouping system based on? Does it apply to α hemolytic or β hemolytic bacteria?

The carbohydrate composition of bacterial antigens in their cell walls; Lancefield only worked on β hemolytic bacteria

30

Clinical manifestations of acute rheumatic fever include:•  [...]•  Carditis (heart failure, new murmur,pericarditis)•  Sydenham’s chorea•  Erythema marginatum

Clinical manifestations of acute rheumatic fever include:•  Painful, migratory arthritis•  Carditis (heart failure, new murmur,pericarditis)•  Sydenham’s chorea•  Erythema marginatum

31

Clinical manifestations of acute rheumatic fever include:•  Painful, migratory arthritis• [...] (heart failure, new murmur,pericarditis)•  Sydenham’s chorea•  Erythema marginatum

Clinical manifestations of acute rheumatic fever include:•  Painful, migratory arthritis•  Carditis (heart failure, new murmur,pericarditis)•  Sydenham’s chorea•  Erythema marginatum

32

Clinical manifestations of acute rheumatic fever include:•  Painful, migratory arthritis•  Carditis (heart failure, new murmur,pericarditis)•  Sydenham’s [...]•  Erythema marginatum

Clinical manifestations of acute rheumatic fever include:•  Painful, migratory arthritis•  Carditis (heart failure, new murmur,pericarditis)•  Sydenham’s chorea•  Erythema marginatum

33

Clinical manifestations of acute rheumatic fever include:•  Painful, migratory arthritis•  Carditis (heart failure, new murmur,pericarditis)•  Sydenham’s chorea•  [...] marginatum

Clinical manifestations of acute rheumatic fever include:•  Painful, migratory arthritis•  Carditis (heart failure, new murmur,pericarditis)•  Sydenham’s chorea•  Erythema marginatum

34

What is the pathogenesis of post-streptococcal glomerulonephritis?

Antibodies, complement components react with streptococcal antigens to form immune complexes which deposit in the renal glomerulus

35

Does post-streptococcal glomerulonephritis most often affect children or adults?

Children

36

What are these clinical manifestations characteristic of?  Hint: this patient had a known exposure to Streptococcus pyogenes.

Scarlet fever

37

What toxins cause streptococcal toxic shock syndrome?

Pyrogenic exotoxins (SPEA, SPEB, SPEC)

38

If a patient is in shock and undergoing multi-organ system failure following a streptococcal infection, what syndrome may be occurring?

Streptococcal toxic shock syndrome

39

What do the exotoxins involved in streptococcal toxic shock bind to? What does this cause the release of?

T lymphocytes and class II MHC complexes of antigen-presenting cells; leads to massive cytokine release

40

Is Streptococcus agalactiae in group A or B?  Is it α hemolytic or β hemolytic?

Group B; β hemolytic

41

What bacterium is highly associated with neonatal sepsis and maternal sepsis, as well as soft-tissue infection in diabetics?

Streptococcus agalactiae

42

Are enterococcal species more resistant or less resistant to cephalosporins and β-lactam based drugs?

More resistant

43

Enterococcus can cause: •  [...]•  Biliary tract infection•  Peritonitis•  Bacterial endocarditis•  Nosocomial superinfection: particularly bacteremia

Enterococcus can cause: •  Urinary tract infection•  Biliary tract infection•  Peritonitis•  Bacterial endocarditis•  Nosocomial superinfection: particularly bacteremia

44

Enterococcus can cause: •  Urinary tract infection•  Biliary tract infection•  Peritonitis•  Bacterial [...]•  Nosocomial superinfection: particularly bacteremia

Enterococcus can cause: •  Urinary tract infection•  Biliary tract infection•  Peritonitis•  Bacterial endocarditis•  Nosocomial superinfection: particularly bacteremia

45

Enterococcus can cause: •  Urinary tract infection•  Biliary tract infection•  Peritonitis•  Bacterial endocarditis•  Nosocomial superinfection: particularly [...]

Enterococcus can cause: •  Urinary tract infection•  Biliary tract infection•  Peritonitis•  Bacterial endocarditis•  Nosocomial superinfection: particularly bacteremia

46

Are strep viridans species α hemolytic or β hemolytic?  How are they distinguished from pneumococci?

α hemolytic; distinguished from pneumococci with the optochin test, which strep viridans are not sensitive to

47

What is the major agent causing bacterial endocarditis?

Streptococci, in particular strep viridans

48

Can Staphylococcus aureus cause bacterial endocarditis?

Yes

49

Are streptococcal strains gram positive or negative?

Gram positive

50

S. mutans and S. sanguis are both streptococcal bacteremia that comprise what group?

Strep viridans, or α hemolytic streptococci

51

How many kinds of hemolysis are there for a bacterial culture on blood agar?  What are they?

Three: α, β, γ

52

Is Streptococcus pyogenes sensitive to bacitracin?  Does an antibody to M protein enhance immune response?

Yes, it is sensitive to bacitracin; yes, antibody to M protein is protective

53

What are three pyogenic consequences of streptococcus pyogenes infection?

Pharyngitis, cellulitis, impetigo

54

What does "pyogenic" mean?

Causes creation of pus

55

What genus do E. faecalis and E. faecium belong to?

Enterococcus

56

How are enterococci divided by Lancefield grouping?

They are divided into group D and non-group D

57

What streptococcal bacteria normally colonize the oropharynx?

Strep viridans

58

What bacterium most typically causes dental caries (cavities)?

S. mutans

59

What is the hardest genus of streptococcus to kill with antibiotics?

Enterococcus

60

What is a mnemonic for three common causes of S. pyogenes based on "PH"?

PHaryngitis to rheum PHever and glomerulonePHritis 

61

What is a mnemonic for rheumatic fever symptoms?

JONES:- Joints- Heart (is round like an O)- Nodules- Erythema marginatum (pink rings on the trunk)- Syndenham's Chorea (abnormal involuntary movement disorder)

62

Is Staphylococcus aureus gram positive or negative? Does it form chains or clusters?

Positive; clusters

63

Is S. aureus coagulase positive or negative?

Positive

64

What bacteria are these?

Staphylococcus aureus; clusters + gram positive

65

Virulence factors for S. aureus include [...], surface factors, and secreted proteins.

Virulence factors for S. aureus include biofilm, surface factors, and secreted proteins.

66

Virulence factors for S. aureus include biofilm, [...], and secreted proteins.

Virulence factors for S. aureus include biofilm, surface factors, and secreted proteins.

67

Virulence factors for S. aureus include biofilm, surface factors, and [...] proteins.

Virulence factors for S. aureus include biofilm, surface factors, and secreted proteins.

68

What protein in S. aureus correlates with virulence and binds to the Fc terminal of IgG inhibiting complement fixation? What else does this inhibit?

Protein A; phagocytosis

69

S. aureus can surround their cell walls with a [...] capsule, which inhibits opsonization.

S. aureus can surround their cell walls with a polysaccharide capsule, which inhibits opsonization.

70

S. aureus can surround their cell walls with a polysaccharide capsule, which inhibits [...].

S. aureus can surround their cell walls with a polysaccharide capsule, which inhibits opsonization.

71

What part of S. aureus is protein A integrated into?

The cell wall

72

Are coagulase positive staphylococci more or less virulent than coagulase-negative ones?

More virulent

73

Do staphylocci infections typically produce pus?

Yes

74

What is the primary host immune response to staphylococcus infection?

Primarily mechanical and in the epidermis, but opsonization and neutrophil phagocytosis are also significant

75

Can S. aureus cause skin and soft tissue infections? What about endocarditis? Septic arthritis?

Yes to all

76

What toxin does S. aureus produce that causes toxic shock syndrome?

TSST1

77

What bacteria produces an abscess like this?

S. aureus

78

Can impetigo be caused by S. aureus?

Yes

79

What color is the crust around impetigo lesions?

Golden

80

What is skin infection is this picture characteristic of?

Cellulitis, probably by S. aureus

81

What is this infection called? Is this the same as a stye? What bacterium is it associated with?

Chalazion; it is different from a stye (it is a cyst blocking a tarsal gland, not a sebaceous gland); S. aureus

82

What are these?

Microemboli associated with endocarditis

83

What are serious neurologic targets of metastatic infection caused by S. aureus?

Brain abscesses or spinal epidural abscess

84

Can S. aureus cause knee arthritis?

Yes, it can infect it causing septic arthritis

85

What does "nosocomial" mean?

Hospital-acquired (usually referring to an infection)

86

What does MRSA stand for?  What infection source is it associated with?

Methicillin-resistant Staphylococcus aureus; nosocomial infections

87

What bacteria commonly causes acute food poisoning?  How long does this illness last?

Staphylococcus aureus; 24 hours

88

How long is an S. aureus bacteremia usually treated?  What is the reasoning behind this?

4 weeks; undertreating a bacteremia can lead to the development of a resistant strain

89

How do you treat MRSA?

Synthetic cell-wall active penicillins: Oxacillin, nafcillin, cefazonin; or vancomycin

90

Does vancomycin work on gram positive or gram negative bacteria?

Gram positive

91

Is S. epidermidis coagulase positive or negative?

Negative

92

Does S. epidermidis typically cause any disease while inhabiting the skin?

No, but it is important in association with medical devices

93

What is the thick, multilayered slime created by S. epidermidis that covers catheters during invasion and protects it from antibiotics called?

Biofilm

94

What bacterium is associated with infections from intravascular devices?

S. epidermidis

95

What location of infection is S. saprophyticus commonly associated with?

Urinary tract infection

96

S. saprophyticus most likely has unique surface proteins that permit it to bind to which receptors in the genitourinary tract?

Mucosal receptors

97

Wha tis the mechanism of Vancomycin?

It inhibits bacterial cell wall synthesis by binding firmly to D-ala-D-ala of the peptidoglycan, preventing elongation and cross-linking

98

What are two mechanisms of resistance to vancomycin?

- Altered peptidoglycan binding site: D-ala-D-ala to D-ala-D-lactate- Thickened cell wall

99

Is vancomycin active against gram-positive or gram-negative bacteria or both?

Gram-positive

100

What is the drug of choice for treating MRSA and penicillin-resistant pneumococcus?

Vancomycin

101

What are two major toxic side effects of vancomycin?

Nephrotoxicity and hypersensitivity (red man syndrome or anaphylaxis)

102

Why is vancomycin given slowly?

To avoid histamine reactions resulting from rapid infusion, such as red man syndrome

103

Why might a pretreatment of antihistamine be used before a rapid infusion of vancomycin?

To avoid anaphylaxis or red man syndrome

104

Is vancomycin bactericidal or bacteriostatic?

Slowly bactericidal, mostly bacteriostatic

105

Does daptomycin act against gram-positive or gram-negative bacteria?

Gram-positive

106

What is the mechanism of daptomycin?

It binds the cytoplasmic membrane and causes rapid depolarization

107

Is daptomycin bactericidal or bacteriostatic?

Rapidly bactericidal

108

Does daptomycin have gram-negative activity?

No

109

What ion does daptomycin use to bind to the cytoplasmic membrane?

Ca++

110

If an enterococcus is vancomycin resistant, what cyclic lipopeptide antibacterial can be used?

Daptomycin

111

What is the interaction between daptomycin and pulmonary surfactant? Can daptomycin be used to treat pneumonias?

Pulmonary surfactant breaks it down; no

112

Does daptomycin have adverse musculoskelatal effects?

Yes, including myalgias, weakness, rhabdomyolysis, and cramps

113

What serum levels can be measured to monitor musculoskeletal adverse effects of daptomycin?

Creatinine phosphokinase

114

What is a protein synthesis inhibitor in gram-positive cocci that acts on...- Initiation?- Elongation?- Transpeptidation?

- Initiation: linezolid- Elongation: doxycycline- Transpeptidation: clindamycin

115

Are protein synthesis inhibitors for gram positive cocci bactericidal or bacteriostatic?

Bacteriostatic

116

What drug family do doxycycline, minocycline, and demeclocycline belong to? What is their mechanism?

Tetracycline; inhibitor against protein elongation

117

What dietary substance should not by consumed with doxycycline?

Dairy, because it forms nonabsorbable chelates with Ca++

118

Doxycycline binds to which tissues undergoing calcification?

Teeth and bones

119

Is doxycycline excreted in the urine? Metabolized in the liver?

Yes to both

120

What effect on teeth can occur with doxycycline?

Discoloration of teeth or stunting of growth

121

Does clindamycin affect enterococcal bacteria?

No

122

Does clindamycin affect aerobic or anaerobic bacteria?

Anaerobic

123

Can clindamycin treat an infection in the CNS?

No, it does not reach therapeutic levels in CSF

124

What are two side effects of clindamycin?

Rash and clostridium difficile colitis

125

What is the bioavailability of oral linezolid?

100%

126

What is the mechanism of linezolid?

Inhibits protein synthesis initiation in gram positive bacteria

127

What are three main safety concerns with linezolid?

Thrombocytopenia/neutropenia, metabolic acidosis, serotonin syndrome

128

What side effect of linezolid is characterized by mental status changes, fever, hypertension, tachycardia, hyperreflexia, myoclonus, and tremor?

Serotonin syndrome

129

Is hyperthermia a more severe toxicity finding than altered mental status?

Yes

130

What is the mechanism of trimethoprim-sulfamethoxazole?

It is a folic acid antagonist

131

How do humans acquire folic acid? How do bacteria acquire folate?

Humans ingest it; bacteria synthesize it

132

What synthesis process requires folate-derived cofactors in bacteria?

Synthesis of DNA and RNA

133

Are folic acid antagonists bacteriostatic or bactericidal?

Bacteriostatic

134

What is the drug of choice for treatment of Pneumocystis jirovecii and Nocardia?

TMP-SMX, a combo of sulfamethoxazole and trimethoprim

135

Can TMP-SMX reach the CSF?

Yes

136

Side effects of TMP-SMX include: [...], rashes, hemolytic anemia, and kernicterus (a bilirubin-induced brain dysfunction)

Side effects of TMP-SMX include: hypersensitivity, rashes, hemolytic anemia, and kernicterus (a bilirubin-induced brain dysfunction)

137

Side effects of TMP-SMX include: hypersensitivity, [...], hemolytic anemia, and kernicterus (a bilirubin-induced brain dysfunction)

Side effects of TMP-SMX include: hypersensitivity, rashes, hemolytic anemia, and kernicterus (a bilirubin-induced brain dysfunction)

138

Side effects of TMP-SMX include: hypersensitivity, rashes, hemolytic [...], and kernicterus (a bilirubin-induced brain dysfunction)

Side effects of TMP-SMX include: hypersensitivity, rashes, hemolytic anemia, and kernicterus (a bilirubin-induced brain dysfunction)

139

Side effects of TMP-SMX include: hypersensitivity, rashes, hemolytic anemia, and [...] (a bilirubin-induced brain dysfunction)

Side effects of TMP-SMX include: hypersensitivity, rashes, hemolytic anemia, and kernicterus (a bilirubin-induced brain dysfunction)

140

What six antibacterials can be used to treat MRSA?

Vancomycin, daptomycin, clindamycin, doxycycline, linezolid, TMP-SMX

141

What is the common mechanism for penicillin, cephalosporin, carbapenems, and monobactam?

They are inhibitors of peptidoglycan crosslinking

142

Which side is gram +, and which is gram -?

Left is gram + (thick peptidoglycan); right is gram - (two cell membranes)

143

What drug derived from mold acts on this crosslinking process in peptidoglycan?  What enzyme is being inhibited?

Penicillin; a transpeptidase

144

What is the most common method of resistance to penicillin?

Beta-lactamase, a gene that breaks penicillin down

145

Where does beta-lactamase cleave penicillin?

The beta-lactam four atom ring

146

Can plasmids contain multiple resistance factors?

Yes

147

What channels do β-lactams use to enter the peptidoglycan layer of gram negative bacteria?

Porin channels

148

What is the mechanism of vancomycin and bacitracin?

Both inhibit peptidoglycan synthesis

149

Do vancomycin and bacitracin inhibit peptidoglycan crosslinking?

No, they inhibit polymerization of the peptide to the polysaccharide chain

150

Are gram negative and gram positive bacteria equally susceptible to vancomycin treatment? Why or why not?

Gram negative are intrinsically resistant; vancomycin cannot cross the outer membrane

151

What do enterococci synthesize instead of the terminal D-ala-D-ala on peptidoglycan to prevent vancomycin from binding?

D-ala-D-lactic acid

152

What is another name for transpeptidases in bacteria named after the drug that affects them?

Penicillin-binding proteins

153

What class of drugs does erythromycin belong to? What is their mechanism? How is resistance generated?

Macrolides; they inhibit protein synthesis by acting on the bacterial ribosome; the 50S subunit is modified so the drug cannot bind

154

How can resistance to tetracyclins be generated by bacteria?

They actively transport it out of the cell

155

What is the mechanism of metronidazole?

It enters bacteria and is metabolized by bacterial enzymes that allow it to cause DNA damage

156

What are two antibiotics that are DNA-dependent RNA polymerase inhibitors?

Rifampicin and actinomycin D (the latter is only a laboratory reagent)

157

Why do folic acid antimetabolites like sulfonamides and trimethoprim have antibacterial activity?

Bacteria need to metabolize folic acid to synthesize nucleotides (humans can acquire them from the diet)

158

How might resistance to trimethoprim develop, unrelated to modifications in the target enzyme itself?

Overproduction of the target enzyme can prevent the inhibitor from sufficiently affecting folic acid metabolism

159

What is the best possible antibiotic-antibiotic interaction?

Synergy

160

Can aminoglycosides still kill bacteria without protein synthesis?

No

161

What antibiotic (whose mechanism is still unclear) is used against TB?

Isoniazid

162

Is the number of antibiotics discovered per year increasing or decreasing?

Decreasing

163

Why is it less profitable to build a new antibiotic than, for instance, a new anti-cholesterol drug?

Antibiotics are usually not taken chronically and so patients and hospitals will almost always spend less on them than other drugs

164

What experiment did Avery et al. perform in 1944 to show that bacterial virulence is a genetic property?

Virulent bacteria could be non-encapsulated and mixed with encapsulated non-virulent bacteria which would then be able to infect and kill mice

165

Are bacteria typically haploid or diploid?

Haploid

166

How do bacteria normally exchange genetic material with other cells, conferring antimicrobial resistance?

Plasmids

167

What is the spontaneous frequency of a mutation that knocks out or knocks in an operon in bacteria, per replication?

10-6

168

What are three methods of genetic exchange used by bacteria?

Transformation, conjugation, and transduction

169

Could mutations alone explain the rapidity at which bacteria acquire resistance to drugs?

No, the exchange of genetic material is also significant

170

Can all bacteria use transformation to take up DNA from the environment?

No

171

How is bacterial conjugation different from transformation?

During conjugation, an extension of the membrane from one bacterium to another (a pillus) whereby the cytoplasms of the two cells can mix allows genetic material to move from one cell to the other. Transformation involves uptake of extracellular DNA.

172

As double-stranded DNA enters the bacterium during transformation, what happens to it?

One strand of it is degraded, and then it forms a triple-strand with genomic DNA

173

During conjugation of two bacteria, are the cell walls of each organism interrupted?

Yes

174

Can plasmids be exchanged during conjugation?

Yes, along with chromosomes

175

What structures allow transduction to occur between bacteria?

Bacteriophages

176

When bacteriophages add DNA to a bacterium, is it necessarily killed?

No, it is only killed in the lytic cycle, not the lysogenic cycle

177

What are phages capable of only the lytic cycle called?

Virulent

178

Can all phage species undergo the lytic cycle? What happens to the bacterium in this cycle?

Yes; it is killed

179

If bacteriophages create and replicate their own DNA during the lytic cycle, how could it be used to transfer host genetic material to another bacterium (transduction)?

Host genetic material (e.g. part of a chromosome) could be packaged by accident into a phage created within a bacterium, which goes on to inject it into another cell

180

What genetic studies can be facilitated by measures of cotransduction?

Linkage, or an estimate of how far apart two bacterial genes are to each other on a chromosome

181

What are DNA sequences that can jump from one position to another called?

Transposons

182

How long are insertion sequences (IS elements), a type of transposon? What is encoded by them?

1-3kb; a transposase protein that facilitates the transposition action, along with regulatory proteins

183

What are DNA elements that encode a site-specific recombinase along with its recognition region called?  What public health issue are they relevant for?

Integrons; multiple antibiotic resistance

184

What can destroy DNA that enters a bacterium?

Nucleases, or it can be inherently unstable and self-destruct

185

What type of recombination does RecA facilitate?

Homologous recombination

186

What is the most frequent cause of genetic variation in bacteria? How frequently does it occur per generation?

Homologous recombination, with a frequency of 10-1 to 10-2 per generation

187

Is plasmid transfer in bacteria more frequent per generation than transposition?

Generally more frequent

188

What was the first bacterial genome sequenced?

Haemophilus influenzae in 2003

189

Are aminoglycosides, fluoroquinolones and lipopeptides like daptomycin time-dependent or concentration-dependent?

Concentration-dependent

190

For concentration-dependent drugs, is a large bolus administered, or frequent smaller doses?

A large bolus

191

What is the minimum inhibitory concentration of an antibiotic/bacteria combination?

The lowest concentration that will inhibit the visible growth of bacteria in vitro

192

Can broth microdilution measure minimum inhibitory concentration (MIC)?

Yes

193

What method is microdilution (to measure minimum inhibitory concentration) based on?

Broth macrodilution

194

Is the epsilometer more or less accurate than broth macrodilution at measuring minimum inhibitory concentration (MIC)?

Less

195

Does Kirby Bauer disc diffusion produce the minimum inhibitory concentration of a drug-bacteria combination?

No

196

Is the zone size measured by Kirby Bauer proportional to bacterial resistance or susceptibility?

Proportional to susceptibility

197

Can an antibiotic be bactericidal against some organisms and bacteriostatic against others?

Yes, e.g., vancomycin

198

Would a person already severely ill from bacterial infection preferably receive a bactericidal or bacteriostatic agent?

Bactericidal

199

What is the identifying prefix for cephalosporin antibiotics?

Cef- or Ceph-

200

What are the four families of β-lactam antibiotics?

Penicillins, cephalosporins, carbapenems, and monobactams

201

Where is penicillin-binding protein located within a bacterium?

The cell membrane (the inner one, for gram-negative bacteria)

202

Do natural penicillins have activity against streptococci? What about staphylococci?

Yes against streptococci; usually not against staphylococci

203

Are there synthetic penicillins that act against staphylococci?

Yes

204

What penicillin is very completely absorbed after oral administration?

Amoxicillin

205

Which penicillin is not cleared renally?

Nafcillin

206

What diagnoses are penicillin still used for today?

Group A and Group B Strep, caused by S. pyogenes and S. agalactiae, respectively, and syphilis, caused by Treponema pallidum

207

What is the oral formulation of pencillin called? What is the IV forumation called?

Penicillin V - oral; penicillin G - intravenous

208

What bacteria causing skin infections is mostly resistant to penicillin because of the production of β-lactamases?

Staphylococcus aureus

209

Can anti-staphylococcal penicillins be cleaved by β-lactamases (penicillinases)?

Usually, no.

210

What are three anti-staphylococcal penicillins? What is  the route of administration?

NOD: Nafcillin, oxacillin, dicloxacillin; oral

211

Is methicillin still used clinically?

Usually no, because of nephrotoxicity

212

What common infection are NOD (Nafcillin, oxacillin, dicloxacillin) used to treat?

Skin or bloodstream infections with Staphylococcus aureus

213

What is another name for extended-spectrum penicillins?

Amino-penicillins

214

What are two extended-spectrum penicillins taken orally?

Ampicillin and amoxicillin

215

Do ampicillin and amoxicillin have gram-negative activity?

Yes, although Klebsiella is resistant

216

What penicillins have good activity against enterococci?

Amino-penicillins like ampicillin and amoxicillin

217

What is the drug of choice for listeria monocytogenes?

Amino-penicillins: ampicillin, amoxicillin

218

What should this 12 year old patient be tested for? What is the treatment for the common infection that results in this appearance of the tonsils?

Strep type A (S. pyogenes); it can be treated with penicillin or amoxicillin

219

Why is Mycoplasma resistant to penicillins?

It has no cell wall

220

What two penicillin resistance strategies can a gram-negative bacteria develop that a gram-positive bacteria cannot?

Change in the outer membrane porins, or an efflux pump in the outer membrane

221

What mutation commonly causes the resistance to penicillins seen in MRSA?

An alteration to penicillin-binding protein (transpeptidases) that decreases affinity for β-lactams

222

What is the point of a β-lactamase inhibitor?

It inhibits the β-lactamases that break down β-lactam antibiotics, so the β-lactam can inhibit transpeptidases

223

What class of drugs do clavulanic acid, sulbactam, and tazobactam belong to?

β-lactamase inhibitors

224

What three drugs can be combined with penicillins to increase gram-negative activity by inhibiting β-lactamases?

Clavulanic acid, sulbactam, and tazobactam

225

What does the sulbactam in an ampicillin-sulbactam combination do?

It inhibits β-lactamases that would break down the ampicillin

226

What does the clavulanic acid in the amoxicillin-clavulanic acid combination formulation do?

It is a β-lactamase inhibitor that inhibits breakdown of the amoxicillin

227

What are two common adverse reactions to penicillin that present as skin symptoms?

Hypersensitivity and rash

228

Can penicillins cause anaphylaxis?

Yes

229

Are rash and hypersensitivity reactions to penicillin common?  What other drug allergies can be suspected after such a reaction?

Yes; increased chance of reactivity to other β-lactams (cephalosporins, carbapenems) excepting monobactams

230

Almost 100% of patients with what viral infection develop a maculopapular rash to amoxicillin?

EBV-associated mononucleosis

231

What kidney-related adverse reaction can occur with penicillins? What antibiotic is no longer used because of this risk?

Nephritis (acute kidney injury); methicillin

232

What kind of colitis can result from penicillin administration?

Clostridium difficile colitis

233

How many generations of cephalosporins have been made?  What increases over the generations?

5; gram-negative activity

234

Can cephalosporins cross the blood-brain barrier?

Yes, after the 3rd and 4th generation

235

Do cephalosporins treat Enterococcus or Listeria?

No

236

Can cephalosporins treat MRSA?

Only the "5th" generation, ceftaroline

237

What is the 1st generation cephalosporin?  What is its oral formulation called?

Cefazolin; cephelexin is the oral formula

238

Can cefazolin be used against group A and group B strep, and S. viridans?

Yes

239

Are cephalosporins affected by β-lactamases?

No, they are not β-lactam drugs

240

Is cefazolin more active against gram-positive or gram-negative bacteria?

Gram-positive

241

Can cefazolin be used for UTIs and skin infections?

Yes

242

Do cephalosporins have similar adverse reactions as penicillin?

Yes

243

What is the cross-reactivity of cephalosporins with people that have penicillin allergies?  Should they be used in a patient that has had hives in reaction to penicillin?

About 1-10%; no

244

If a patient who has a history of IV drug abuse has high fevers and a methicillin susceptible S. aureus infection, what are some reasonable treatments?

Anti-staphylococcal penicillins: NafcillinCephalosporins: CefazolinThese will kill methicillin-susceptible S. aureus, and both drugs are unaffected by penicillase (most S. aureus harbors penicillase)

245

Besides age and allergies, what else should be evaluated before prescribing β-lactam or cephalosporin antibiotics?

Kidney function

246

If a skin infection has gram positive cocci that are identified as β hemolytic, what bacterium related to the one causing strep throat should be suspected?

S. pyogenes

247

What are examples of non-suppurative consequences of a S. pyogenes infection?

Scarlet fever, acute rheumatic fever, glomerulonephritis

248

Are penicillins bacteriostatic or bactericidal?

Bactericidal

249

What potential problem when treating abscesses with oral antibiotics, assuming the right one was prescribed at the right dosage and the organism is susceptible?

Distribution of the drug into the abscess, since the neutrophils surrounding the abscess can block access of the antibiotic to the area with the most bacteria

250

When the serum C3 complement level is measured as low, what does this indicate?

It has been consumed (broken down to C3b and C3a), so the immune system was exposed to an antigen that activated the complement pathway (alternatively: there is a C3 deficiency, but this is rare)

251

Acute rheumatic fever is most often associated with streptococcal strains rich in what protein?

Protein M

252

Are streptococcal strains rich in M protein more or less virulent?  Why?

They are relatively resistant to phagocytosis and multiply quickly in tissues

253

What exotoxin is secreted by extra-virulent S. pyogenes that causes necrotizing fasciitis?  What life-threatening syndrome can this exotoxin cause?

Superantigen, which hyperactivates T cells; it can cause toxic shock syndrome

254

What is the course of treatment for necrotizing fasciitis?

Aggressive surgical debridement, and secondarily, IV antibiotics

255

Which researcher on tuberculosis developed postulates that led to a new understanding of infectious disease and a Nobel?

Robert Koch

256

What is the property of tuberculosis bacteria's cell wall that makes it resistant to disinfectants and traditional stains?

It is lipid rich

257

What is the major component of mycobacterium's cell wall?

Mycolic acid

258

Why do mycobacteria clump together?

Hydrophobicity of the cell wall

259

Are mycobacteria motile? Are they spore-forming?

No to both

260

What is the gram staining of mycobacteria?

Gram null to weakly gram positive

261

What kind of staining, also called Ziehl-Neelsen or Kinyoun, reveals mycobacteria?

Acid fast staining

262

Of the four Runyon classes of mycobacteria, which grows fastest?

Runyon class IV

263

Is mycobacterium tuberculosis in a Runyon class?  If so, which one?

No, it is not in a class.

264

Do mycobacteria encourage or discourage phagocytosis by immune cells?  What happens to a phagosome containing a mycobacteria?

Phagosome formation is encouraged; phagosome maturation is blocked, so the bacterium can survive

265

What fusion event is inhibited after phagocytosis of mycobacteria to allow them to survive?

Phagosome-lysosome fusion is inhibited

266

What immune proteins that normally surround intruders to aid in their destruction are rendered ineffective by mycobacterium?

Antibody and complement proteins

267

Is the incidence of TB in the United States among native-born persons still declining?

Yes

268

Approximately what fraction of the world's population carries mycobacterium tuberculosis?

One third

269

The spread of what disease in the 1980's led to an uptick in tuberculosis infection?

HIV/AIDS

270

What can a tuberculosis patient do to expose other people to the bacterium, besides blood-to-blood contact?  Can TB bacilli remain infectious in the air?

Coughing, sneezing, speaking, or singing; yes, it can remain suspended in the air for several hours

271

During the primary infection process for mycobacterium tuberculosis, is there a host immune response?

No, the bacteria replicate freely in alveolar macrophages

272

What channels does the tuberculosis bacterium use to spread after infection of the alveoli?

Lymphatics and bloodstream

273

What immune response (humoral or cell-mediated) contains the primary infection by TB? What histological immune structures form in the lungs during the killing of the bacilli?

Cell-mediated immune response; granulomas

274

Within caseating centers of granulomas, does TB replicate faster or slower? Why?

Slower; because of the lower pH and the anoxic environment.

275

In 90% of patients, what is the endpoint of primary tuberculosis?  Is it symptomatic?

Latent tuberculosis; usually it is not

276

Is latent tuberculosis contagious?

No

277

What is the common test for latent TB infection?  What is a requirement for this test, without which it will return a false negative?

PPD (the tuberculin skin test); you need a functional immune system

278

How long does it take for delayed hypersensitivity reactions to tuberculins to be detectable by a PPD after the initial infection?  How long are the tuberculins implanted in the skin before reading?

6-8 weeks; 48-72 hours

279

What is a more sensitive assay for past exposure to tuberculosis bacterium?  How does it work?

Interferon γ release assay; it is an ELISA test that detects release of interferon γ from sensitized patients after incubation with two peptides from TB

280

What is the standard approach to latent tuberculosis?

Chest x-ray, sputum analysis, and Isoniazid for 9 months

281

What are the common presenting symptoms of active tuberculosis?

Cough, hemoptysis (bloody cough), night sweats, anorexia, weight loss

282

Can tuberculosis infect tissues besides the longs?

Yes, including the bones, lymph nodes, brain, GI tract...

283

What is common in HIV patients with tuberculosis infections?

It spreads to other tissues quickly, e.g., the fingers

284

What is visible on a CT scan of the lungs of most tuberculosis patients?

Nodules (they can be bilateral or unilateral and in any lobe, as the following CT shows)

285

What is the mnemonic for the 4-drug regimen to treat active tuberculosis?

RIPE:- Rifampin- Isoniazid- Pyrazinamide- Ethambutol

286

Which part of the bacterium does isoniazid act upon?

The cell wall

287

What dietary warning is given to people on prolonged isoniazid for tuberculosis infection?

Do not consume alcohol

288

What is the mechanism of Rifampin? Is it bactericidal or bacteriostatic?

It inhibits DNA-dependent RNA polymerase in mycobacteria; bactericidal

289

What is the primary adverse effect of Rifampin? Why?

Hepatotoxicity; it induces hepatic cytochrome p450 enzymes

290

What is the primary adverse affect of isoniazid, requiring a dietary warning?

Hepatotoxicity

291

Production of what component of mycobacterium is inhibited by isoniazid?  Is it bacteriostatic or bactericidal?

Mycolic acid synthesis, the main component of the cell wall; bactericidal

292

Is pyrazinamide bacteriostatic or bactericidal? What globally common infection is it used to treat?

Bacteriostatic; tuberculosis

293

What does ethambutol inhibit that makes it a good treatment for tuberculosis?  Is it bacteriostatic or bacteriocidal?

Cell wall polysaccharide synthesis

294

What is the primary adverse effect of ethambutol?

Optic neuritis

295

Are certain strains of TB resistant to isoniazid and/or rifampin?

Yes

296

What can be used to supplement treatment for MDR or XDR tuberculosis?

Other antibacterials: streptomycin, linezolid, fluoroquinolones, kanamycin, ...

297

Why are multiple antibiotics administered concurrently to eradicate a TB infection in a patient?

To prevent development of a resistant strain

298

What is the most significant gram-negative microbe in the GI tract?

E. coli

299

Can E. coli cause neonatal sepsis or meningitis?

Yes

300

There are 3 important surface antigens on E coli. How are they named?

O, H, and K

301

In the strain serotype E. coli O157:H7, what is the meaning of the second part of this name?

It refers to surface antigens O and H

302

When a patient complains of dysuria and changes in frequency of urination, a UTI is suspected.  What is significant about a co-presentation with flank pain and cost-vertebral angle tenderness?

An upper UTI may be suspected as opposed to a lower UTI. This might include e.g. pyelonephritis

303

What is the most common cause of UTIs?

E. coli

304

What does dysuria mean?

Painful urination

305

Which pili on E. coli allows certain strains to adhere to the urinary epithelium?

P-pili

306

What is the typical IV therapy for pyelonephritis?

Fluroquinolones (e.g. Ciprofloxacin) or ceftriaxone

307

What is the typical course of treatment for a lower UTI?

Fluoroquinolones, ceftriaxone, or trimethoprim-sulfamethoxazole

308

What is the typical cause of "traveler's diarrhea"?

E. coli, caused by a lack of immunity to bacteria in the local water

309

ETEC, EPEC, EIEC, EHEC, STEC, and EAEC are all strains of...

Diarrhea-causing E. coli

310

In enterotoxigenic E. coli, is the mucosa of the GI tract disrupted?

No

311

What long structures surround E coli, mediating its attachment to various surfaces?

Pili

312

Which pili mediates adhesion of ETEC to the GI tract?

CF pili

313

What other microbial toxin is the Heat Labile Toxin of ETEC similar to?

Cholera toxin

314

What enzyme is stimulated by Heat Labile Toxin and what doe sthis cause?  What organism secretes this toxin?

Adenylate cyclase, causing export of Na+, K+, and water into the GI lumen (diarrhea); enterotoxigenic E. coli (ETEC)

315

What enzyme is stimulated by Heat Stable Toxin, released by enterotoxigenic E. coli?

Guanylate cyclase

316

Enterotoxigenic E. coli secretes two toxins abbreviated LT and ST. What are their full names?

Heat labile toxin and heat stable toxin

317

What does the stimulation of guanylate cyclase by heat stable toxin cause? What organism secretes it as an exotoxin?

Secretion of Cl-, HCO3- and water; ETEC (enterotoxigenic E. coli)

318

What organism causes hemolytic-uremic syndrome (HUS)?

Enterohemorrhagic E. coli

319

How is enterohemorrhagic E. coli acquired?

Consumption of raw beef, food contaminated by animal feces, or animal contact

320

What is the hallmark symptom of enterohemorrhagic E. coli infection?

Bloody diarrhea

321

What are two common abbreviations for the organism that causes hemolytic uremic syndrome?

EHEC or STEC, both referring to enterohemorrhagic E. coli

322

What toxin is produced by EHEC that triggers hemolytic uremic syndrome?

Shigatoxin

323

What is the best way to test for EHEC infection?

Test for Shiga toxin in the stool

324

Can sorbital agar reliably identify EHEC?

It can only identify the O157:H7 strain—it will not identify other strains of EHEC

325

Where are the typical genomic locations for virulent factors of E. coli strains, like exotoxins?

Phages, plasmids, or pathogenicity islands

326

What does enteroinvasive E. coli cause (EIEC)?

Dysentery

327

When E. coli is suspected for a case of dysentery, what can be used on the stool to diagnose it?

A stool smear to reveal WBCs

328

Is there disruption of the mucosa in EIEC?

Yes, bacteria invade the enterocytes (enteroinvasion)

329

What do enteroaggregative E. coli form on the wall of the GI epithelium?

A biofilm, inhibiting proper absorption across the intestinal membrane

330

Why is bacterial neonatal sepsis and meningitis treated with ampicillin in addition to cefotaxime?

Cefotaxime is for E. coli, but the ampicillin is intended to kill listeria, another top bacterial etiology for these symptoms

331

What is notable about the strains of E. coli that cause nosocomial infections?

They are typically resistant to many antibiotics

332

Is meningitis more common in children or adults?

Children under 2 years of age

333

Removal of what organ can cause in increase in risk for meningitis?

Spleen

334

How is neisseria meningitidis transmitted?

Respiratory droplets, which is why it is more likely to cause epidemics in overcrowded conditions

335

What is "meningococcus" an abbreviation for?

Neisseria meningitidis

336

What does N. meningitidis secrete to allow survival in the respiratory tract?

IgA protease

337

What is the function of the pili on N. meningitidis in the respiratory tract, besides conjugation?

Attachment to the respiratory epithelium

338

What is the capsule of N. meningitidis made of?

Polysaccharides

339

What form of endotoxin is secreted by N. meningitidis that can cause sepsis?

Lipooligosaccharide

340

What is the defining feature of the rashes caused by meningococcemia?

They are all non-blanching

341

Which serogroup of N. meningitidis has no vaccine? Why not?

Serogroup B, because it has a polysaccharide capsule similar to human sialic acid

342

Is LOS different from LPS? If so, how?

Yes; they are a subtype of LPS present in bacteria that colonize mucosal surfaces not bathed in bile, such as N. meningitidis

343

What is the difference with the conjugate vaccine for meningitis as opposed to the polysaccharide vaccine?

The conjugate vaccine has proteins, which are more immunogenic

344

Does N. meningitidis produce β-lactamases?

No

345

What can be used to treat N. meningitidis?

Penicillin works, but ceftriaxone is more common

346

Empiric treatment of bacterial meningitis in adults when nothing is seen on gram stain consists of what drugs?

Ceftriaxone (against meningococcus, Haemophilus and pneumococcus), vancomycin (against β-lactam pneumocci), and sometimes ampicillin (against Listeria monocytogenes)

347

Is Listeria gram positive or negative?  What is its shape?

Gram positive; rod (bacillus)

348

What is the motility style of Listeria?

Tumbling, end over end

349

Which age groups does Listeria affect?  What other population is particularly at risk?

Infants and the elderly (bimodal); the immunocomprised, such as pregnant women

350

Is ceftriaxone used to treat L. monocytogenes?

No, ampicillin is more reliable

351

What can be used to prevent spread of meningitis to those in close contact?

Chemoprophylaxis

352

What is a nickname for N. gonorrhoeae?

Gonococcus

353

What is the difference in the capsule between N. meningitidis and N. gonorrhoeae?

N. gonorrhoeae does not have a true polysaccharide capsule

354

What is the energy source for N. gonorrhoeae in culture? Is this different from N. meningitidis?

Glucose only; yes, N. meningitidis can also use maltose

355

What part of N. gonorrhoeae makes development of a vaccine difficult?

Antigenic variability of the pili

356

Is the age distribution of N. gonorrhoeae infections modal or bimodal?

Modal, with the highest range around 15-25 years of age

357

What inflammatory disease can be caused by chronic N. gonorrhoeae infection?

Pelvic inflammatory disease

358

Which diagnostic tool is used most often in clinical practice for gonococci?

DNA amplification probes

359

What is the mainstay of therapy for N. gonorrhoeae? Do they have β-lactamase? What co-infection is assumed?

Cephalosporins, e.g., ceftriaxone; yes; Chlamydia

360

When a patient presents with respiratory symptoms, and a cultured bacterium grows on chocolate agar and with VX factor, what organism is suspected?

Haemophilus influenzae

361

Is the present vaccine for Haemophilus influenzae a polysaccharide vaccine or a conjugate vaccine?

Conjugate

362

Does the Haemophilus genus cause any STDs?

Yes, chancroid, by Haemophilus ducreyii. It is characterized by painful fluid-filled lesions on the genitals

363

What can Moraxella catarrhalis cause? Is it gram negative, or gram positive? Is it anaerobic or aerobic?

Otitis, sinusitis, and pneumonia (particularly with underlying emphysema); gram positive; aerobic

364

What is the gram negative coccobacillus that causes whooping cough?

Bordetella pertussis

365

Which vaccine was built to eliminate Bordetella pertussis?

DPT: diphtheria, pertussis, tetanus

366

Are incidents of pertussis on the rise or declining since the introduction of the DPT vaccine?

They are still rising

367

What capsulated bacterium produces a purpuric, petechial rash?

N. meningitidis

368

How many capsule serogroups of N. meningitidis are there?  Does the vaccine cover all of them?

13; no, the vaccine covers 4 of the most common

369

What is the vaccine protecting against Haemophilus influenzae called?

HiB vaccine

370

Are N. gonorrhoeae susceptible to quinolones?

No, resistance has developed

371

What is used to combat B. pertussis in severe cases of whooping cough?

Azithromycin

372

What type of organisms is the spleen an important defense organ for?

Encapsulated organisms, e.g. N. meningitidis and Listeria

373

Can fats and sugars within the outer membrane of a gram negative bacterium trigger a fatal response?

Yes, because of inflammation

374

What is notable about this CT that is suggestive of S. pneumoniae?

The infection is well contained to one lobe

375

What is the hemolysis pattern of S. pneumoniae?  Is it optochin sensitive or resistant?  Does it have a Lancefield antigen?

α hemolysis; optochin sensitive; no Lancefield antigen

376

How is S. pneumoniae transmitted? What is colonized transiently that leads to no symptoms in most adults? Is smoking a risk factor?

Through droplets; the nasopharynx; Yes

377

What is the distribution of ages for S. pneumoniae infection? What other significant risk factor must be considered, which e.g. asplenia could contribute to?

Very young and very old; immunosuppression

378

Besides age, immunosuppression, and smoking, what are two other risk factors for S. pneumoniae infection?

CSF leaks and cochlear implants

379

How many serotypes of S. pneumoniae exist?

Over 90

380

Did a vaccine for pneumococcus exist in 1998?

No

381

What is serotyping of S. pneumoniae based on? Are antibodies against these molecules protective?

The capsular polysaccharide; Yes

382

Do symptoms of S. pneumoniae present acutely or chronically compared to a TB patient?

Acutely

383

What are nuchal rigidity, Kernig and Brudzinsky signs all indicative of?

Meningitis

384

What infection with a high mortality can cause fever, photophobia, headache, and altered mental status?

Meningitis

385

Can S. pneumonia cause bacteremia, sinusitis, and peritonitis?

Yes

386

What type of antibody can prevent adherence of S. pneumoniae, preventing infection?

Secretory IgA (sIgA)

387

What is the main virulence factor of S. pneumoniae?

The capsule

388

What is binding of the pneumococcus to an epithelial cell mediated by?

Adhesins

389

What can pneumococci secrete to defeat secreted IgA and adhere to epithelial cells anyway?

IgA protease

390

Which pathway for complement activation is inhibited by the capsule of S. pneumoniae?

The alternate pathway

391

What bacterium contains pneumolysin?  Where is it stored in the bacterium? What is its function?

S. pneumonia; in the cytoplasm; it lyses phagocytic cells

392

Which system unrelated to the capsular specific antibodies is critical for clearing S. pneumoniae from the bloodstream?

The lymphoreticular system of the spleen

393

Why is the spleen more important for clearing capsulated organisms?

Phagocytosis by neutrophils is less efficient, so filtration in the spleen is a more significant way for these organisms to be cleared

394

What class of drugs is used to treat S. pneumoniae?  How does resistance usually present?

β-lactams; resistance is usually from altered penicillin binding proteins

395

Do clavulinic acid or sulbactam help β-lactam treatment of S. pneumoniae that are becoming β-lactam resistant? Why or why not?

No; they are β-lactamase inhibitors, but this is not the typical way that resistance develops in S. pneumoniae

396

Can you overcome the weak binding of β-lactams to PBP's in somewhat resistant S. pneumoniae by increasing the dose?

Sometimes, yes

397

Which β-lactams are most often used against S. pneumoniae?

Amoxicillin, ampicillin, cefotaxime and ceftriaxone

398

Why is ceftriaxone particularly effective against S. pneumoniae, particularly with regard to preventing serious complications?

It can get into the CSF, and does well against the three most common causes of bacterial meningitis

399

What cause of meningitis is not covered by cephalosporins?

Listeria monocytogenes

400

Can ceftriaxone be administered orally? Can vancomycin be administered orally?

No to both

401

How is ceftriaxone excreted?

Biliary ducts

402

How is cefotaxime excreted?  Does it have a shorter or longer half-life than ceftriaxone?

Kidneys; shorter half-life (8h) compared to ceftriaxone (12-24h)

403

What do fluoroquinolones inhibit causing bacterial death? Which fluoroquinolone cannot be used against respiratory infections?

Bacterial topoisomerase and DNA gyrase, thereby inhibiting DNA synthesis; Ciprofloxacin has no activity against gram positive organisms and thus is not indicated for respiratory infections (where S. pneumoniae is suspect)

404

What athletic activity is dangerous during administration of fluoroquinolones?

Weight lifting and running, because of the adverse effect of tendonitis and/or tendon rupture

405

If S. pneumoniae is resistant to β-lactams, what antibiotic can be used?  Is it active against gram negatives, gram positives, or both?

Vancomycin

406

What is the empiric treatment for bacterial meningitis?

Vancomycin and ceftriaxone, which both reach the CSF and in conjunction combat β-lactam sensitive and resistant gram positive and gram negative bacteria

407

What oral treatment is given for pneumococcal pneumonia?

Amoxicillin and/or azithromycin, and levofloxacin

408

If an IV drug user comes in and reports symptoms indicating bacterial pneumonia, what else must be suspected?

Immunodeficiency, e.g. AIDS

409

What would otitis media or sinusitis with a suspected bacterial cause be treated with?

Amoxicillin (oral)

410

Why isn't the pneumovax vaccine immunogenic in children under 2?  What vaccine is given to them instead, and why does that one work better?

It is a purified capsular polysaccharide antigen, which children of this age will not recognize as foreign (it is a T-cell independent antigen); the PCV-13 (Prevnar-13) vaccine has the polysaccharide conjugated to a diphtheria toxoid (T-cell dependent antigen), which the immune system will recognize as foreign at this age

411

After recommendation of the PCV7 vaccine in 2000, did rates of S. pneumoniae decrease in children, or across all age groups? What is this phenomenon called?

All age groups; herd immunity

412

What are environmental sources of pseudomonadaceae?

Soil, water, plant material, and environmental surfaces

413

What is this bacterium, which grows aerobically in immunocompromised hosts, particularly within burn injuries?

Pseudomonadaceae (gram negative bacilli)

414

Does P. aeruginosa ferment lactose?

No (right), which is different from E. coli (left)

415

Does Pseudomonas produce oxidase?

Yes

416

What can render a host particularly susceptible to Pseudomonas infections?

Neutropenia (e.g. by chemotherapy), severe burns, diabetes/foot ulcers, cystic fibrosis

417

What kind of Pseudomonas infection is most likely to manifest in a neutropenic patient?

Bacteremia or sepsis

418

What risk factors for P. aeruginosa infection associate a respiratory infection?

Cystic fibrosis or mechanical ventilation

419

What organism is associated with "hot tub folliculitis"?

P. aeruginosa

420

What is the clinical (not genetic) marker of cystic fibrosis, which relates especially to P. aeruginosa?

They present with chronic lung infections and inflammation

421

With chronic infection by P. aeruginosa in cystic fibrosis patients, what are the two typical infections that precede it? Does the mucoid P. aeruginosa precede the non-mucoid, in the sequence of infections or the other way around?

S. aureus and H. influenzae; non-mucoid is typically first

422

Are cephalosporins useful against Pseudomonas aeruginosa? What about carbapenems?  Monobactams? Fluoroquinolones?

Yes to all, with various resistance factors seen in the wild

423

What two organisms (excepting P. aeruginosa) are linked to catheter-associated bacteremia and ventilator-associated pneumonia?

Burkholderia cepacia and Stenotrophomonas maltophilia

424

What classes of bacteria are aminoglycosides useful for treatment? Are they usually used as primary or secondary therapy?

Gram negative, aerobic bacteria, e.g. P. aeruginosa; usually secondary to another antibiotics

425

What is the basic structure of an aminoglycoside?

Amino sugar linked to a central hexose

426

What are the host cell entry, CSF, and tissue penetration characteristics of aminoglycosides?  Why is this?

All are poor; they are polycationic and highly polar

427

What is the mechanism of action of aminoglycosides?

Interference with bacterial protein synthesis (initiation, see the A pathway here)

428

What is the most common mechanism of resistance to aminoglycosides?

Drug modification (acetylation or adenylation of parts of the drug by the bacterium)

429

What kind of antibiotic is kanamycin? Is it currently administered?

Aminoglycoside; no longer used

430

What is a common topical aminoglycoside?

Neomycin

431

What class of drugs are streptomycin, gentamicin, tobramycin, and amikacin?

Aminoglycosides

432

What are four aminoglycosides that can be administered intramuscularly?  Are oral forms available?

Streptomycin, gentamicin, tobramycin, and amikacin; no

433

What are the main adverse toxicities of aminoglycosides?

Nephrotoxicity and ototoxicity, along with neuromuscular blockade

434

Important agents of nosocomial infection include:– [...] (e.g., RSV, Parainfluenza, Influenza, Adenovirus)– Methicillin-resistant Staphylococcus aureus– Vancomycin-resistant Enterococcus faecium– Multiresistant Gram-negative bacilli– Clostridium difficile

Important agents of nosocomial infection include:– Respiratory Viruses (e.g., RSV, Parainfluenza, Influenza, Adenovirus)– Methicillin-resistant Staphylococcus aureus– Vancomycin-resistant Enterococcus faecium– Multiresistant Gram-negative bacilli– Clostridium difficile

435

Important agents of nosocomial infection include:– Respiratory Viruses (e.g., RSV, Parainfluenza, Influenza, Adenovirus)– [...]-resistant Staphylococcus aureus– Vancomycin-resistant Enterococcus faecium– Multiresistant Gram-negative bacilli– Clostridium difficile

Important agents of nosocomial infection include:– Respiratory Viruses (e.g., RSV, Parainfluenza, Influenza, Adenovirus)– Methicillin-resistant Staphylococcus aureus– Vancomycin-resistant Enterococcus faecium– Multiresistant Gram-negative bacilli– Clostridium difficile

436

Important agents of nosocomial infection include:– Respiratory Viruses (e.g., RSV, Parainfluenza, Influenza, Adenovirus)– Methicillin-resistant Staphylococcus aureus– [...]-resistant Enterococcus faecium– Multiresistant Gram-negative bacilli– Clostridium difficile

Important agents of nosocomial infection include:– Respiratory Viruses (e.g., RSV, Parainfluenza, Influenza, Adenovirus)– Methicillin-resistant Staphylococcus aureus– Vancomycin-resistant Enterococcus faecium– Multiresistant Gram-negative bacilli– Clostridium difficile

437

Important agents of nosocomial infection include:– Respiratory Viruses (e.g., RSV, Parainfluenza, Influenza, Adenovirus)– Methicillin-resistant Staphylococcus aureus– Vancomycin-resistant Enterococcus faecium– [...] bacilli– Clostridium difficile

Important agents of nosocomial infection include:– Respiratory Viruses (e.g., RSV, Parainfluenza, Influenza, Adenovirus)– Methicillin-resistant Staphylococcus aureus– Vancomycin-resistant Enterococcus faecium– Multiresistant Gram-negative bacilli– Clostridium difficile

438

Important agents of nosocomial infection include:– Respiratory Viruses (e.g., RSV, Parainfluenza, Influenza, Adenovirus)– Methicillin-resistant Staphylococcus aureus– Vancomycin-resistant Enterococcus faecium– Multiresistant Gram-negative bacilli– [...] difficile

Important agents of nosocomial infection include:– Respiratory Viruses (e.g., RSV, Parainfluenza, Influenza, Adenovirus)– Methicillin-resistant Staphylococcus aureus– Vancomycin-resistant Enterococcus faecium– Multiresistant Gram-negative bacilli– Clostridium difficile

439

What two major classes of gram-negative bacilli are associated with nosocomial infections?

Enterobacteriaceae and Pseudomonodaceae

440

What units are most at risk for nosocomial infections?

Burn units, NICU, MICU/SICU, and oncology

441

What is the mean attributable cost to the hospital of a nosocomial bloodstream infection?

$36k

442

What standard precaution must be taken by all hospital workers with all patients to prevent nosocomial infections?

Hand hygiene

443

How long should we wash our hands with soap and water or Purell to prevent nosocomial infections?

>15 seconds

444

What is the usual suspect for "typical" pneumonia?

Streptococcus pneumoniae

445

Is there a productive cough and copious sputum with typical or atypical pneumonia?

Typical pneumonia

446

What extrapulmonary symptoms typically manifest in atypical pneumonia?  Do most patients seek medical care?

Muscle aches and headache, low fever; most do not

447

Is an elevated WBC more indicative or typical or atypical pneumonia?

Typical

448

What are the three major suspect bacteria for atypical pneumonia?

Mycoplasma pneumoniae, Chlamydophila pneumoniae, and Legionella

449

What is the incubation period of M. pneumoniae?

2-3 weeks

450

How is M. pneumoniae transmitted?  Can it spread between people across a room?

Respiratory droplet; no, it requires close contact

451

What structural feature makes M. pneumoniae an unusual bacterium?

It lacks a cell wall

452

What is the shape of M. pneumoniae?  Is it visible on a gram stain?

Short and rod-shaped; invisible on gram stain

453

Is M. pneumoniae easy to grow quickly in culture?

No, it has a long doubling time (6h)

454

Why was M. pneumoniae initially assumed to be a virus, in 1918?

It could pass through filters that only viruses could pass through

455

What is the age distribution of typical M. pneumoniae infections?

Unimodal, around adolescents and young adults

456

Do most patients survive M. pneumoniae infection without treatment?

Yes

457

Does M. pneumoniae grow inside or outside of cells?

Inside of them

458

What blood cell abnormality is a risk factor for Mycoplasma pneumoniae?

Sickle cell

459

Why does sickle cell predispose patients to M. pneumoniae?

Cold-agglutinins produced by polyclonal T cells and B cells during the immune response to M. pneumoniae bind to the I antigen on the RBC surface area, which is smaller for patients with sickle cell

460

What skin manifestation is associated with M. pneumoniae?

Erythema multiforme

461

Can M. pneumoniae cause meningitis?

Yes

462

Where in the respiratory tract does M. pneumoniae infection start?

Usually in the upper part, but it can spread anywhere within the tract

463

Is a cold-agglutinin test useful in diagnosing M. pneumoniae?

No, it is not sensitive or specific enough