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Vet Derm Review > Pharmacology - Antibiotics > Flashcards

Pharmacology - Antibiotics Flashcards

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1
Q

Bacteriostatic or bactericidal: beta-lactams

A

bactericidal

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2
Q

Mechanism of action: beta-lactams

A

bind and inhibit penicillin binding proteins which are needed to catalyze the cross-linking (transpeptidation) of the peptidoglycan layer of bacterial cell walls; When PBPs are inactivated by β-lactam antibiotics, bacterial enzymes that hydrolyze the peptidoglycan cross-links during cell wall remodeling continue to function, which breaks down the cell wall further. The accumulation of peptidoglycan precursors also triggers activation of cell wall hydrolases, with further digestion of intact peptidoglycan. The end result is bac- terial rupture.

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3
Q

Why do different beta-lactam antibiotics have different spectrums of activities?

A

bacteria possess multiple penicillin binding proteins, which vary in their affinities for different beta-lactams; inhibition of PBP1a and PBP1b leads to cell lysis, whereas inhibition of PBP2 results in rounded cells called spheroblasts. Drugs that produce rapid lysis (e.g., carbapenems) are the most bactericidal and have highest affinity for PBP1.

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4
Q

Mechanisms of resistance to beta-lactams?

A

Beta-lactamase production, altered penicillin binding proteins (e.g. PBP2a), exclusion of drugs that normally diffuse through porins to their site of action

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5
Q

Time or concentration-dependent: beta-lactams

A

time-dependent

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6
Q

T/F: Beta-lactamase inhibitors possess weak intrinsic antibacterial activity.

A

TRUE

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7
Q

Method of excretion: penicillins

A

rapid renal elimination - active drug is concentrated in the urine

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8
Q

MIC for gram-negative vs gram-positive bacteria: penicillins

A

Penicillin MICs are generally higher for gram- negative bacteria than gram-positive bacteria; therefore, higher penicillin dosages may also be needed for gram-negative bacte- rial infections.

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9
Q

What are cephalosporins derived from?

A

Acremonium

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10
Q

Spectrum of activity: Cephalosporins

A

As the generation increases, there is an increase in gram-negative spectrum, and fourth-generation drugs have truly broad-spectrum activity

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11
Q

T/F: Cephalosporins are resistant to extended-spectrum beta-lactamase.

A

False: extended-spectrum β-lactamase (ESBL) enzymes can hydrolyze even third-generation cephalosporins and present an important therapeutic challenge

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12
Q

Method of excretion: 1st generation cephalosporins

A

excreted unchanged in the urine

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13
Q

What third generation cephalosporins are approved for use in small animals?

A

ceftiofur, cefpodoxime proxetil, and cefovecin

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14
Q

Adverse effects: cephalosporins

A

GI signs, hypersensitivity reactions; false-positive results on test strips that use copper reduction for urine glucose detec- tion. Certain cephalosporins, such as cefotetan and ceftriaxone, may exacerbate bleeding tendencies due to vitamin K antago- nism.8 Reversible bone marrow suppression has been reported in dogs given high doses of ceftiofur, cefonicid, and cefazedone long-term

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15
Q

What is ceftiofur approved for in small animals?

A

urinary tract infections in DOGS

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16
Q

Mechanism of action: carbapenem

A

They penetrate the outer membrane of gram- negative bacteria more effectively than many other β-lactam antibiotics and bind to a variety of PBPs, which leads to rapid lysis of a broad spectrum of bacteria

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17
Q

Adverse effects: imipenem

A

Imipenem is degraded by dehydropeptidase-1, a brush border enzyme in the proximal renal tubules, which results in produc- tion of an inactive metabolite that is nephrotoxic. In order to prevent nephrotoxicity and maximize imipenem’s antibacterial activity, imipenem is administered with cilastatin, which inhib- its the dehydropeptidase-1 enzyme

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18
Q

Adverse effects: carbapenems

A

vomiting, nausea, and pain on injection. Neurologic signs, including tremors, nystagmus, and seizures, can occur following rapid infusion of imipenem-cilastatin or in animals with renal insufficiency. Imipenem must be administered slowly in intravenous fluids. Slow administration is not required for meropenem

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19
Q

Mechanism of action: glycopeptides

A

cyclic glycosylated peptide antimicrobials that inhibit the synthesis of peptidoglycan by binding to amino acids (d-alanyl-d-alanine) in the cell wall, preventing the addi- tion of new units

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20
Q

Antibiotic class: Vancomycin?

A

glycopeptide

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21
Q

Bacteriostatic or bactericidal: glycopeptides

A

Bactericidal (vancomycin)

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22
Q

Mechanism of resistance to vancomycin?

A

Resistance to vancomycin results from bacterial alteration of the terminal amino acid to which vancomycin binds.

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23
Q

Adverse effects: vancomycin

A

histamine release after rapid infusion

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24
Q

Mechanism of action: fluoroquinolones

A

bind to DNA gyrase (AKA topoisomerase II) and topoisomerase IV – enzymes that cleave DNA during DNA replication. The result is disruption of bacterial DNA and protein synthesis

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25
Q

Why do gram-positive bacteria have higher MICs than gram-negative bacteria for fluoroquinolones?

A

DNA gyrase is the primary target for gram-negative bacteria and topoisomer- ase IV is the primary target for gram-positive bacteria. Because topoisomerase IV has a lower affinity than DNA gyrase for this group of drugs, higher MICs are observed for gram-positive bacteria compared to the Enterobacteriaceae

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26
Q

What is the only third generation fluoroquinolone approved for small animals?

A

pradofloxacin – approved for CATS in the US and dogs & cats in Europe

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27
Q

Mechanism of resistance to fluoroquinolones?

A

DNA gyrase mutations, decreased bacterial permeability, and increased drug efflux

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28
Q

T/F: Resistance to one fluoroquinolone predicts susceptibility to all fluoroquinolones.

A

True - with the exceptions of third- generation fluoroquinolones (such as pradofloxacin) and cipro- floxacin, which has higher in vitro activity against P. aeruginosa than other fluoroquinolones

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29
Q

Time or concentration-dependent: fluoroquinolones

A

concentration-dependent

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30
Q

What can affect absorption of fluoroquinolones when administered orally?

A

poor absorption occurs when they are complexed by divalent and trivalent cation-containing medications (e.g., antacids) and supplements (aluminum, calcium, iron, zinc).

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31
Q

Method of excretion: fluoroquinolones

A

Most fluoroquinolones are highly concentrated in the urine; Enrofloxacin is metabolized to ciprofloxacin, which is subsequently excreted in the urine. Approximately half of the administered dose of marbofloxacin and orbifloxacin is excreted as unchanged drug in the urine. In contrast, difloxacin is excreted primarily in bile, and little drug enters the urine.

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32
Q

Why can fluoroquinolones penetrate the prostate and respiratory secretions?

A

due to their lipophilicity

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33
Q

T/F: Fluo- roquinolones can attain high intracellular concentrations and can be used to treat infections caused by intracellular pathogens such as Mycoplasma spp. and some Mycobacterium spp.

A

TRUE

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34
Q

Adverse effects: fluoroquinolones

A

GI signs (anorexia, vomiting); Rapid IV administration can cause systemic hypotension, tachycardia, and cutaneous erythema, possibly as a result of histamine release.26 Neurologic signs, including tremors, ataxia, and seizures, can occur in dogs and cats treated with high doses of parenteral fluoroquinolones; cats can develop blindness resulting from acute retinal degeneration, manifested as bilateral mydriasis with tapetal hyperreflectivity when treated with high doses of enro

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35
Q

Why can enrofloxacin cause blindness in cats?

A

functional defect in a fluoroquinolone transport protein in the cat, with subsequent accumulation of photoreactive drug in the retina

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36
Q

Why can fluoroquinolones affect cartilage?

A

they inhibit proteoglycan synthesis and chelate mag- nesium

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37
Q

What adverse effect has been reported in dogs treated with >10 mg/kg of pradofloxacin?

A

myelosuppression

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38
Q

T/F: Fluoroquinolones inhibit some cytochrome p450 enzymes.

A

True – occurs with theophylline in dogs (decreases metabolism of theophylline)

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39
Q

Bacteriostatic or bactericidal: metronidazole

A

bactericidal

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40
Q

Mechanism of action: metronidazole

A

Metronidazole diffuses into bacterial cells as a prodrug and is activated in the cyto- plasm. Once within the cell, the nitro group of metronidazole preferentially accepts electrons from electron transport proteins such as ferredoxin. A short-lived nitroso free radical is thus gen- erated that damages DNA. The intermediate compounds then decompose into non-toxic, inactive end products.

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41
Q

Mechanism of resistance to metronidazole?

A

reduced drug uptake and decreased reduction activity

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42
Q

Clinical use of metronidazole in dogs and cats?

A

anaerobic bacterial and protozoal infections

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43
Q

How is metronidazole metabolized? How is it excreted?

A

by the liver - metabolites and intact drug are excreted in the urine

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44
Q

Adverse effects: metronidazole

A

neurotoxicity, which tends to occur with high doses (>30 mg/kg/day) or in animals with hepatic dysfunction.

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45
Q

Can metronidazole increase or decrease cyclosporine levels?

A

increase - inhibits hepatic microsomal enzymes

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46
Q

Bacteriostatic or bactericidal: rifamycins

A

bactericidal

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47
Q

Mechanism of action: rifamycins

A

inhibit the beta-subunit of DNA-dependent RNA polymerase –> impaired RNA synthesis

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48
Q

Mechanism of resistance to rifampin?

A

single mutation that leads to an altered RNA polymerase that does not effectively bind rifampin.

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49
Q

Clinical use of rifampin in small animals?

A

One of the major advantages of rifampin is its high degree of lipid solubility, which provides the degree of intracellular pen- etration required for treatment of infections caused by intracel- lular bacteria such as Mycobacterium spp. and Brucella canis infections. Rifampin has been used to treat bartonellosis in com- bination with doxycycline; MRS infections

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50
Q

How is rifampin metabolized? How is it excreted?

A

metabolized by the liver –> active metabolites are excreted in bile and to a lesser extent in the urine

51
Q

Adverse effects: rifampin

A

vomiting, anorexia; red-orange color to the urine and, to a lesser extent, tears, saliva, the sclera, and mucous membranes; increased serum liver enzymes and hepatopathy

52
Q

What effect can rifampin have on co-administered drugs?

A

can increase the clearance of many drugs – thereby decreasing their efficacy; due to induction of hepatic microsomal enzymes and efflux proteins (such as P-glycoprotein)

53
Q

Mechanism of action: trimethoprim

A

inhibits bacterial dihydrofolate reductase

54
Q

Mechanism of action: sulfonamides

A

chemical analogs of para-aminobenzoic acid and competitively inhibit the incorporation of PABA into dihydropteroic acid by the enzyme dihydropteroate synthetase –> decreased folic acid synthesis

55
Q

Bacteriostatic or bactericidal: trimethoprim-sulfonamides

A

When administered separately, each drug is bacteriostatic, but the combination is bactericidal

56
Q

Mechanism of action: trimethoprim-sulfonamides

A

act synergistically to inhibit folic acid metabolism by bacteria; combination interferes with purine and therefore DNA synthesis

57
Q

Why do trimethoprim-sulfonamides only affect bacterial purine synthesis?

A

because folic acid is of dietary origin in animals

58
Q

Mechanism of resistance to trimethoprim-sulfonamides?

A

plasmid-mediated production of altered dihydrofolate reductase or dihydropteroate synthetase, with reduced binding affinities; overproduction of dihydrofolate reductase or PABA by bacteria, reduced bacterial permeability to trimethoprim-sulfonamides

59
Q

What species of bacteria is intrinsically resistanct to TMS antibiotics?

A

enterococci

60
Q

What is the primary difference between trimethoprim-sulfadiazine and trimethoprim-sulfamethoxazole?

A

sulfadiazine is more water soluble and is excreted in the urine in an unchanged formula; sulfadiazine is the veterinary formula

61
Q

Why can TMS penetrate the prostate?

A

trimethoprim is a weak base and is able to penetrate the blood-prostate barrier

62
Q

How is TMS metabolized? How is it excreted?

A

both trimethoprim and sulfonamides are metabolized to some extent by the liver; both active drug and inactive metabolites appear in the urine

63
Q

Are the adverse effects of TMS due to the trimethoprim or sulfonamide?

A

primarily caused by the sulfonamide component

64
Q

Adverse effects: TMS

A

GI signs (vomiting), KCS, fever, polyarthritis, cutaneous drug eruptions, IMTP, IMHA, hepatitis, pancreatitis, meningitis, interstitial nephritis, glomerulonephritis, aplastic anemia, reversible hypothyroidism

65
Q

What breed of dog is more susceptible to adverse effects of TMS? Why?

A

Doberman pinschers - inability to detoxify certain sulfonamide metabolites; Samoyeds and miniature schnauzers are also more susceptible to adverse effects

66
Q

What formulation of TMS is approved for use in dogs?

A

ormetoprim-sulfadimethoxine

67
Q

Aminoglycosides with names that end in -mycin are derived from what?

A

Streptomyces spp.

68
Q

Aminoglycosides with names that end in -micin are derived from what?

A

Micromonospora

69
Q

Mechanism of action: aminoglycosides

A

bind electrostatically to the bacterial outer membrane and displace cell wall Mg2+ and Ca2+, which normally link adjacent LPS molecules; binding is greater in gram-neg bacteria b/c of a greater presence of an outer membrane; result is disrupted cell permeability –> bacterial cell takes up aminoglycoside molecules and they become trapped irreversibly within the cytoplasm (this is an oxygen-dependent process => anaerobes are resistant); once within the cell, aminoglycosides bind to the 30S subunit of the bacterial ribosome –> which results in decreased protein synthesis

70
Q

What organisms are intrinsically resistant to aminoglycosides? Why?

A

anerobes –uptake of aminoglycosides into the cytoplasm is an oxygen-dependent process

71
Q

Mechanism of resistance to aminoglycosides?

A

enzymatic modification of the drug by bacteria; reduced drug uptake by bacteria

72
Q

T/F: Resistance to one aminoglycoside predicts susceptibility to all aminoglycosides.

A

False - resistance to one aminoglycoside does not imply resistance to others

73
Q

Why don’t aminoglycosides penetrate the prostate?

A

they are very water soluble and poorly lipid soluble – penetrate tissue fluids well, but do not penetrate tissues dependent on lipid diffusion (prostate, brain, eye, CSF)

74
Q

How are aminoglycosides metabolized? How is it excreted?

A

excreted unchanged by the kidney in urine

75
Q

Bacteriostatic or bactericidal: aminoglycosides

A

bactericidal

76
Q

Time or concentration-dependent: aminoglycosides

A

concentration-dependent

77
Q

Adverse effects: aminoglycosides

A

nephrotoxicity, ototoxicity, neuromuscular blockable

78
Q

What is the mechanism of nephrotoxicity of aminoglycosides?

A

apoptosis and necrosis of renal tubular epithelial cells, direct damage to the glomerulus; can accumulate in renal tissue

79
Q

What are risk factors for aminoglycoside-induced nephrotoxicity?

A

older age, reduced renal function, concomitant liver disease, dehydration, sodium depletion, hypokalemia, concurrent administration of nephrotoxic drugs (NSAIDs, furosemide, cyclosporine)

80
Q

What is the mechanism of ototoxicity of aminoglycosides?

A

damage to the cochlear or vestibular apparatus – cochlear toxicity results from damage to the hair cells of the organ of Corti, whereas vestibular toxicity results from damage to hair cells at the tip of the ampullae cristae

81
Q

Why should aminoglycosides be avoided in an animal with myasthenia gravis?

A

aminoglycosides have the potential to cause neuromuscular blockade – can exacerbate clinical signs of myasthenia gravis

82
Q

Mechanism of action: chloramphenicol

A

binds to the 50S subunit of the bacterial ribosome –> inhibits bacterial protein synthesis

83
Q

Spectrum of activity: chloramphenicol

A

broad-spectrum: gram-pos and gram-neg, anaerobes, some rickettsial pathogens

84
Q

Mechanism of resistance to chloramphenicol?

A

porin mutations, drug efflux, or production of chloramphenicol acetyltransferase enzymes (inactivate the antibiotic)

85
Q

T/F: Resistance to one chloramphenicol derivative predicts susceptibility to all derivatives.

A

TRUE

86
Q

Why can chloramphenicol penetrate the prostate?

A

highly lipid soluble – diffuses to tissues with barriers such as the CNS and the eye

87
Q

How is chloramphenicol metabolized? How is it excreted?

A

metabolized by glucuronidation in the liver, inactive metabolites excreted by the kidney

88
Q

Adverse effects: chloramphenicol

A

aplastic anemia in humans; GI signs (anorexia, hypersalivation, vomiting); reversible bone marrow suppression; drug-drug interactions; hindlimb weakness

89
Q

T/F: The macrolides and lincosamides are chemically related.

A

False - but possess similar mechanisms of action, resistance, and antimicrobial activity

90
Q

Mechanism of action: macrolides

A

inhibit protein synthesis by binding to the 50S subunit of bacterial ribosomes

91
Q

Mechanism of action: lincosamides

A

inhibit protein synthesis by binding to the 50S subunit of bacterial ribosomes

92
Q

Why can macrolides and lincosamides concentrate intracelullarly in leukocytes?

A

they are weak bases - can concentrate in the relatively acidic interior of leukocytes

93
Q

What is different about azithromycin compared to other macrolides?

A

it is an azalide – contains nitrogen

94
Q

T/F: Resistance to one macrolide predicts susceptibility to all macrolides.

A

True - susceptibility to erythromycin often predicts susceptibility to other macrolide antimicrobial drugs

95
Q

Mechanism of resistance to macrolides?

A

decreased bacterial permeability (gram-neg bacteria), alteration in target site, increased drug efflux, enzymatic inactivation of certain macrolides by bacterial esterases

96
Q

What enzyme confers high-level resistance to azithromycin, clarithromycin, and clindamycin?

A

methylase enzyme –> results in alteration in the target site through production of a ribosomal methylase that adds a methyl group to the 50S subunit RNA, preventing the macrolide from binding to the ribosome

97
Q

Bacteriostatic or bactericidal: macrolides

A

bacteriostatic

98
Q

Spectrum of activity: macrolides

A

gram-positive&raquo_space; gram-negative

99
Q

How are macrolides metabolized? How is it excreted?

A

excreted in high concentrations in bile, followed by enterohepatic circulation, eliminated in feces

100
Q

How can a macrolide be effective even if its serum concentration is less than the MIC?

A

because of its prolonged tissue retention, serum concentrations of azithromycin do not reflect tissue concentrations – intracellular concentrations of azithromycin are 10- to 100-fold those in serum (concentrations are considered bactericidal)

101
Q

Primary indication for macrolides in small animals

A

mycobacteria, bartonella (combined with rifampin); babesia, cytauxzoon (combined with atovaquone)

102
Q

Primary indication for clindamycin in small animals

A

gram-postive bacteria; anaerobic bacterial infections, toxoplasma, neospora

103
Q

Adverse effects: erythromycin

A

vomiting, anorexia, nausea –> due to stimulation of receptors of the GI hormone motilin –> increases GI smooth muscle activity; poorly absorbed orally –> produces diarrhea due to changes in GI flora

104
Q

What effect can azithromycin and erythromycin have on co-administered drugs?

A

can increase the concentration of other drugs – inhibit p450 enzymes

105
Q

Mechanism of action: linezolid

A

binds to the 50S subunit of the bacterial ribosome and prevents formation of the initiation complex for protein synthesis –> this is a unique mechanism because other protein synthesis inhibitors interfere with polypeptide extension

106
Q

Mechanism of resistance to linezolid?

A

modification of the drug’s target site (extremely rare because several step mutations are necessary before resistance can occur)

107
Q

Bacteriostatic or bactericidal: linezolid

A

bacteriostatic

108
Q

Adverse effects: linezolid

A

inhibits type A monoamine oxidase –> can interact with serotonin reuptake inhibitors; bone marrow suppression

109
Q

What antibiotics have a mechanism of action that interferes with bacterial protein synthesis?

A

tetracyclines, linezolid, macrolides, lincosamides, chloramphenicol, aminoglycosides

110
Q

What antibiotics have a mechanism of action that interferes with cell wall synthesis?

A

beta-lactams (penicillins, cephalosporins, monobactams, carbapenems), glycopeptides

111
Q

What antibiotics have a mechanism of action that interferes with nucleic acid synthesis?

A

fluoroquinolones, metronidazole, rifamycins, trimethoprim-sulfonamides

112
Q

Bacteriostatic or bactericidal: tetracyclines

A

bacteriostatic

113
Q

Time or concentration-dependent: tetracyclines

A

time-dependent

114
Q

Spectrum of activity: tetracyclines

A

gram-positive, gram-negative, anaerobes, atypical and intracellular pathogens such as spirochetes, Mycoplasma spp., rickettsiae

115
Q

Mechanism of action: tetracyclines

A

inhibit bacterial protein synthesis by binding to the 30S subunit

116
Q

T/F: Both macrolides and tetracyclines inhibit bacterial protein synthesis, therefore resistance to one class implies resistance to the other.

A

False - have different binding sites; tetracyclines bind to 30S ribosomal subunit, macrolides bind to the 50S ribosomal subunit

117
Q

What is unique about doxycycline and minocycline compared to other tetracyclines?

A

longer-acting and more lipophilic; have anti-inflammatory and immunomodulatory properties that result from inhibition of inducible nitric oxide synthase and proinflammatory cytokines such as TNF-alpha

118
Q

Mechanism of resistance to tetracyclines?

A

porin mutations that exclude tetracyclines from the bacterial cell, increased drug efflux (mediated by the tetK gene); tetM confers resistance to all tetracyclines

119
Q

A bacteria with the tetK gene may still be susceptible to what tetracyclines?

A

minocycline (tetM confers resistance to all tetracyclines)

120
Q

Which is more lipophilic: minocycline or doxycycline?

A

minocycline, it is also better absorbed orally

121
Q

How are tetracyclines eliminated?

A

concentrated in bile; sufficient drug is excreted in the urine to permit treatment of UTIs

122
Q

Adverse effects: tetracyclines

A

vomiting, decreased appetite, nausea, diarrhea; esophagitis and esophageal strictures in cats (doxycycline hydrochloride); interfere with bone growth; hepatic failure and renal tubular necrosis

123
Q

Why should tetracyclines not be given with food? What tetracycline is an exception to this rule?

A

administration with food can lead to significantly reduced drug absorption because of extensive binding with divalent and trivalent cations in the GI tract; doxycycline can be administered with food - does not have an affinity for cations

124
Q

What tetracycline should be avoided in dogs and cats with renal failure?

A

doxycycline

Vet Derm Review (44 decks)

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