Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5200_Библиотеки_им_академика_М_И_Перельмана
.pdf
days of therapy. After discontinuation of therapy, these reactions are uniformly reversible. The most
commonlaboratoryabnormalityisanincreasedlevelofconjugatedbilirubin.
DrugInteractions
The CYP3A4 isoenzyme (responsible for the metabolism of many drugs) is significantlyinhibited by
quinupristin/dalfopristin.Close clinical or serum level monitoringofknownsubstratesoftheCYP3A4
enzymeisrecommended.
PLEUROMUTILINS
Lefamulin (Xenleta) belongs to a new class of agents known as the pleuromutilins. This class is
structurallyunrelatedtootheranti-infectiveagentsandisderivedfromthenaturallyoccurringtricyclic
pleuromutilin, which received its name from the edible mushroom, Pleurotus mutilus (now called
Clitophilus scyphoides). Lefamulinis a semisynthetic compound witha modification at the C-14 side
chain, which is largely responsible for its excellent pharmacokinetics and tissue distribution profile,
enhancedantimicrobialspectrum,andtheavailabilityofbothIVandoralformulations.
PharmacokineticsandPharmacodynamics
FollowingIVandoraladministration,lefamulinhasahalf-lifeofapproximately8hoursinpatientswith
community-acquiredbacterialpneumonia(CABP).Itis95%boundtoplasmaproteinsandhasavolume
ofdistributionof1.25L/kg.Table6.19providesdosinginformationforlefamulin.Thedoseinadultsis
150mgIV or 600 mgorallyevery12hours. Lefamulinisnotextensivelymetabolizedintheliver and
doesnotrequireadjustmentsforrenalinsufficiencyorthosewithmildtomoderatehepaticinsufficiency.
Nodataareavailableforpatientswithsevereliverdisease.Lefamulinisnotremovedbyhemodialysis.
Lefamulin is bactericidal against S. pneumoniae, H. influenzae, Neisseria gonorrhoeae, and
MycoplasmagenitaliumandbacteriostaticagainstS.aureus.
MechanismofActionandSpectrumofActivity
Lefamulin inhibits bacterial protein synthesis by binding to the peptidyltransferase center of the 50S
ribosomal subunitwithhigh affinityandspecificity ata unique binding site thatisdifferentthanother
antimicrobial classes. Lefamulin is active against many gram-positive, fastidious gram-negative, and
some anaerobic organisms and spirochetes. It is noteworthy that lefamulin activity possesses against
MRSA and VRE, as well as multidrug resistant strains of S. pneumoniae, N. gonorrhoeae, and M.
genitalium.
TABLE6.19
PleuromutilinDosages
Drug AdultDosages PediatricDosages
Lefamulin(Xenleta) 150mgIVq12hor600mgPOq12h
ClinicalUses
LefamulinisapprovedbytheFDAfortreatingCABPinadults.
AdverseEvents
Lefamulinisgenerallywelltolerated,withnauseaandabdominalupsetbeingthemostcommonadverse
effectsreportedafteroraladministrationandlocalinfusionreactionsmostcommonlyreported after IV
administration.Lefamulincanproduceaconcentration-dependentprolongationintheQTcinterval;thisis
morepronounced(~10msincreaseonaverage)afterIVadministration.
DrugInteractions
Lefamulin tablets are contraindicated with sensitive CYP3A4 substrates that prolong the QT interval
(e.g., pimozide) as this may result in increased plasma concentrations of these drugs, leading to QT
prolongation.
ConcomitantuseoflefamulinIVororaltabletswithstrongandmoderateCYP3A4inducersorP-gp
inducers should be avoided unless the benefit outweighs the risks. In addition, concomitant use of
lefamulintabletsshouldbeavoidedwithstrongCYP3AinhibitorsorP-gpinhibitors.Concomitantuseof
sensitiveCYP3Asubstrateswithlefamulintabletsrequiresclosemonitoringforadverseeffectsofthese
drugs(e.g.,alprazolam,diltiazem,verapamil,simvastatin,vardenafil).
ANTIANAEROBICAGENTS
Clindamycin
Clindamycin (Cleocin) has been used extensively in treating gram-positive and anaerobic bacterial
infections.Itwasfirstusedorallytotreatstreptococcalandstaphylococcalinfections,butitsoonbecame
thedrugofchoiceforanaerobicinfections.Thecombinationofclindamycinandgentamicin(Garamycin)
isstillfrequentlyusedintreatingmixedaerobicandanaerobicinfections.
PharmacokineticsandPharmacodynamics
Boththehydrochlorideandpalmitatehydrochloridesaltsofclindamycinarewellabsorbedandconverted
toactiveformsintheblood.Clindamycinreachesmosttissuesandbone,butitsdistributionintoCSFis
limited.Itis93%boundtoproteins.Thehalf-lifeisapproximately3hours.Clindamycinismetabolized
bytheliver,necessitatingdosageadjustmentinpatientswithliverimpairment(Table6.20).Hemodialysis
andperitonealdialysisdonotremoveclindamycintoasignificantextent.
MechanismofActionandSpectrumofActivity
Clindamycinbindstothe50Ssubunitofthebacterialribosomeandinhibitsproteinsynthesis.Itactsatthe
samesiteaschloramphenicolandthemacrolides.
TABLE6.20
AntianaerobicAgents:Dosages
Drug AdultDosages PediatricDosages
Clindamycin 150–450mgPOq6–8hor600mgIVq8h 10–30mg/kg/dPOdividedq6–8h
25–40mg/kg/dIVdividedq6–8h
Metronidazole 250–500mgPOq6–8hor500mgIVq6–12h 15–35mg/kg/dPO/IVdividedq6h
Note:Dosageadjustmentrecommendedforpatientswithliverdysfunction.
IV,intravenous.
ClinicalUses
Clindamycinis typicallyincludedinregimensforitsanaerobiccoverage inmixed infections andmay
also beusedintreatinggram-positiveinfections,toxoplasmosis, andPCPorincombinationwithother
agentstotreatPID.Inaddition,itisfrequentlyusedtoinhibittoxinproductionaspartofthetreatmentfor
staphylococcalorstreptococcaltoxicshock.
AdverseEvents
Themajor sideeffectassociatedwithclindamycinis diarrheaandassociatedC.difficile colitis. This
adverse eventisunrelatedtodoseandmayrangefromacute,self-limitingsymptomstolife-threatening
toxicmegacolon.PainatthesiteofIVadministrationmayoccur.
DrugInteractions
In rare cases, clindamycin use in combination with skeletal muscle relaxants has been reported to
potentiateneuromuscularblockade.
Metronidazole
Metronidazole (Flagyl) was first recognized for its antiprotozoal activity in treating Trichomonas
vaginalis infections. Subsequently, its utilityas anantianaerobic agentwasusedintreatingB. fragilis
infections. Metronidazole has become a treatment of choice for anaerobic infections and is part of a
numberofregimenstoeradicateHelicobacter pylori–associatedduodenalulcers. Metronidazole is no
longerafirst-linetreatmentoptionforadultswithC.difficilecolitis.
PharmacokineticsandPharmacodynamics
MetronidazoleiscompletelyabsorbedfromtheGItractafteroraladministration.Itpenetrateswellinto
mosttissues,withanapparentvolumeofdistributionof0.3to0.9L/kg.Itsbindingtoplasmaproteinis
minimal. The liver metabolizes metronidazole, and dosage adjustments are necessary in patients with
hepaticimpairment(Table6.20).Thehalf-lifeisapproximately6to9hours.Metronidazoleisremoved
byhemodialysisandperitonealdialysis.
MechanismofActionandSpectrumofActivity
Metronidazole is reduced to a toxic product that interacts with DNA, causing strand breakage and
resultinginproteinsynthesis inhibition.Metronidazolehasexcellentactivityagainstgram-positive and
gram-negativeanaerobes,H.pylori,andprotozoasuchasT.vaginalis.
ClinicalUses
Metronidazole is typically included in regimens for its anaerobic coverage in mixed infections. In
addition,metronidazoleisthetreatmentofchoiceforbacterialvaginosisandtrichomoniasisandmaybe
usedtotreatC.difficilediarrheainpatientswhocannottolerateordonothaveaccesstovancomycinor
fidaxomicin.
AdverseEvents
Metronidazole is usuallysafe andwell tolerated. GIsideeffectssuchasnausea, vomiting,abdominal
pain,anda metallictastearemostcommon.Moreseriousbutrare effectsincludeseizures, peripheral
neuropathy, and pancreatitis. Seizures have been associated with high doses, whereas peripheral
neuropathyhasbeendocumentedinpatientsreceivingprolongedcoursesofmetronidazole.
DrugInteractions
Metronidazoleenhancestheanticoagulanteffectofwarfarin,resultinginaprolongedhalf-lifeofwarfarin.
Adisulfiram-likereactioncharacterizedbyflushing,palpitations,nausea,andvomitingmayoccurwhen
alcohol is consumed during metronidazole therapy. Metronidazole is an inhibitor of the CYP3A4
isoenzyme. It has the potential to interact with multiple medications. Additionally, phenobarbital,
phenytoin,andrifampinincreasethemetabolismofmetronidazole,whichmayresultintreatmentfailure.
A careful review of a patient’s medication list for drug interactions should be done before initiating
metronidazole.
MISCELLANEOUSANTIMICROBIALAGENTS
Chloramphenicol
Chloramphenicol has a wide spectrumof activityagainst gram-positive, gram-negative, and anaerobic
organisms.However,itsusehasbeenlimitedbyitstoxicityprofile,whichincludesgraybabysyndrome,
opticneuritis,andfatalaplasticanemia.Nonetheless,inselectedsituations,chloramphenicolremainsan
importantagent.
PharmacokineticsandPharmacodynamics
ChloramphenicolisavailableasanIVsuccinateester.Thedoseisbasedonageandindication(Table
6.21). The ester formulationis hydrolyzedin the bodyto the active drug.Chloramphenicol penetrates
wellintomosttissuesandbodilyfluids,includingtheCSF.Chloramphenicolreadilycrossestheplacenta
inpregnantfemales.Itisconjugatedintheliverandexcretedbythekidneyinaninactive,nontoxicform.
Theserumhalf-lifeis3to4hours.Chloramphenicolis25%to50%boundtoprotein.
TABLE6.21
MiscellaneousAgents:Dosages
Drug AdultDosages Pediatric
Dosages
Chloramphenicol Olderchildrenandadults:50–100mg/kg/dIVdividedq6h(max4,000mg
daily)Olderchildrenandadultswithmeningitis:75–100mg/kg/dIVdivided
q6h
–
Olderchildrenandadultswithmeningitis:75–100mg/kg/dIVdividedq6h –
Nitrofurantoin 50mgPOq6h(macrocrystal)or100mgPOq12h(macrocrystal
monohydrate)
5–7mg/kg/dPO
dividedq6h
Rifampin 600mgPOoncedailyor10–20mg/kgIVdaily 10–20mg/kgIV
generallyonce
daily
Notes:Chloramphenicolshouldbeusedwithcautioninpatientswithrenalimpairment,andserumconcentrationsshouldbemonitoredtoguide
dosingandpreventtoxicity.
Dosageadjustmentforrifampinisrecommendedforpatientswithliverdysfunction.
Nitrofurantoiniscontraindicatedinpatientswithacreatinineclearanceof<60mL/min.
IV,intravenous.
Serumlevelsarefrequentlymonitoredinhigh-riskpatients.Thetherapeuticrangeofchloramphenicol
is5to20mg/dL.Dose-relatedmyelosuppressiontypicallyoccursatserumlevelsexceeding25mg/dL.
MechanismofActionandSpectrumofActivity
Chloramphenicolreversiblybindstothelarger50Ssubunitoftheribosome,therebyinhibitingbacterial
proteinsynthesis.Itisvariablybactericidal.
Chloramphenicolisactiveagainstgram-positiveandgram-negativeaerobesandanaerobesaswellas
atypicalorganisms,includingmycoplasma,chlamydia,andrickettsia.Itsgram-negativeactivityincludes
E.coli,Proteusspecies,andSalmonellaspeciesbutnotP.aeruginosa.
ClinicalUses
Neweragentshavereducedtheneedtousechloramphenicolintreatinginfection.However,itcanbeused
asanalternativeintreatingbacterialmeningitiswhenapatienthasalife-threateningpenicillinallergy.It
is alsouseful intreatingrickettsialdiseasessuchas RockyMountainspottedfever andtyphusfever in
patientsallergic totetracyclinesor inpregnantwomen.Chloramphenicol maybe usedintreatingVRE
infectionsaswell.
AdverseEvents
Themajoradverseeventsassociatedwithchloramphenicol are graybabysyndrome,blood dyscrasias,
and optic neuritis. Gray baby syndrome typically occurs in neonates and is manifested by vomiting,
lethargy, respiratory collapse, and death. It results from drug accumulation because neonates cannot
conjugate chloramphenicol. Two forms of hematologic toxicity may occur with chloramphenicol
administration. Dose-related bone marrow suppression has occurred in patients receiving doses
exceeding 4 g/d andat serumlevels exceeding25 mg/dL.Itmaypresentasacombinationofanemia,
leukopenia, andthrombocytopenia. Aplastic anemiais an idiosyncratic effectindependentof dose and
mayoccurweeksaftertherapywithchloramphenicol.Itisassociatedwithagreaterthan50%mortality
rateandoftennecessitatesbonemarrowtransplantation.Opticneuritisisamajorneurologiccomplication
andisassociatedwithlongcoursesofchloramphenicol.Thetoxicityinvolvesred-greencolorchanges
andlossof vision.Itmaybe reversibleorpermanent. GIsideeffects havebeenassociated withhigh
dosesofchloramphenicol.
DrugInteractions
ChloramphenicolismetabolizedbytheliverandisaninhibitoroftheCYP2C19andCYP3A4enzymes.It
prolongsthehalf-lifeofwarfarin,phenytoin,andcyclosporine.
Rifampin
Rifampinisamacrocyclicantibiotic usedina varietyofsettings,anditisa first-lineagentintreating
tuberculosis. It is typically combined with other antibiotics such as vancomycin in treating MRSA
infections.
PharmacokineticsandPharmacodynamics
Rifampin is completely absorbed after oral administration. It distributes into most tissues and fluids,
includingtheCSF.Thehalf-lifeofrifampinisapproximately3hours.Itismetabolizedbytheliverandis
notremovedbyhemodialysisorperitonealdialysis.Table6.21providesdosinginformation.
MechanismofActionandSpectrumofActivity
Rifampin suppresses initiation of chain formation for ribonucleic acid(RNA)synthesis in susceptible
bacteriabyinhibitingDNA-dependentRNApolymerase.Thebeta-subunitoftheenzymeappearstobethe
siteofaction.
Rifampin is extremely active against gram-positive cocci. It has moderate activity against aerobic
gram-negative bacilli. Neisseriameningitidis, Neisseria gonorrhoeae,andH.influenzaeare the most
sensitivegram-negativeorganisms.RifampinmaintainsactivityagainstM.tuberculosis.
ClinicalUses
Rifampiniscommonlyusedincombinationwithacellwall–activeagenttotreatserious,gram-positive
infectionsthatfailtorespondtoothercoursesoftherapy.Thiscombinationisusedforsynergisticactivity
and prevents rapid resistance development. It is the drug of choice for postexposure meningitis
prophylaxis against N. meningitidis and H. influenzae type B. Rifampin is a first-line agent in the
treatmentofM.tuberculosisinfection,anditisusedtotreatnontuberculousmycobacterialinfectionsas
well.
AdverseEvents
ThemostcommonsideeffectsassociatedwithrifampinareGIdistress(nausea,vomiting,anddiarrhea),
headache, and fever.Rifampinchanges bodilyfluids suchas sweat, saliva, and tears to a red-orange
color.Hepatotoxicityisrare,buttheriskincreaseswhenitisadministeredincombinationwithisoniazid.
Liver functionshouldbemonitored while patientsreceive rifampin. Anemiaorthrombocytopeniaalso
hasbeenreported.
DrugInteractions
Rifampinisa potentinducer ofhepaticCYPdrugmetabolismandprecipitates manydruginteractions.
Rifampin increases the clearance of agents such as antiarrhythmics, azole antifungals, clarithromycin,
estrogens,moststatins,warfarin,andmanyHIVmedications.Acarefulreviewofthepatient’smedication
listfordruginteractionsshouldbedonebeforeinitiatingrifampin.
Nitrofurantoin
Nitrofurantoin is an antimicrobial agent used only for treating and preventing urinary tract infections.
Nitrofurantoin has been used in the United States since 1953 and still remains very effective. It is a
syntheticnitrofuran-compoundderivative,aclassthatalsoincludesfurazolidone,availableinEurope.
PharmacokineticsandPharmacodynamics
Followingoraladministration,nitrofurantoinisrapidlyabsorbed.Thebioavailabilityofnitrofurantoinis
approximately40%to50%.Absorptioncanbeenhancedwithfood.Nitrofurantoinserumconcentrations
arelow,withaserumhalf-lifeoflessthan30minutes.Forthisreason,nitrofurantoinshouldnotbeused
for complicated urinary tract infections or in patients for whom a concern of bacteremia exists.
Nitrofurantoin undergoes renal elimination. Inadequate urinary concentrations are achieved in patients
with renal insufficiency;thus, thedrugis ineffective. Itiscontraindicated inpatientswitha creatinine
clearanceoflessthan60mL/min.Table6.21providesdosing
MechanismofActionandSpectrumofActivity
The exact mechanism of nitrofurantoin is poorly understood. The drug does inhibit several bacterial
enzymes,whichresultsinimpairedbacterialcellwallsynthesis.
Nitrofurantoinhasadequateantimicrobialcoverageagainstcommonorganismsthatcauseurinarytract
infections such as E. coli, Citrobacter species, Staphylococcus saprophyticus, E. faecalis, and E.
faecium.NitrofurantoinfrequentlycoversstrainsofVRE.Resistancehasincreasedagainstsometypesof
bacteria,suchasEnterobacterandKlebsiellaspecies.
ClinicalUses
Nitrofurantoinisonlyusedforthetreatmentandprophylaxisofuncomplicatedurinarytractinfections.As
mentionedearlier,itshouldnotbeusedforcomplicatedurinarytractinfectionssuchaspyelonephritis.
AdverseEvents
Themostcommonsideeffectsofnitrofurantoinincludenauseaandvomiting.Nitrofurantoinmaycausea
harmless yellow-brown discoloration of urine. Allergic reactions are rare. Pulmonary reactions
(pulmonaryinfiltrates,pneumonitis,pulmonaryfibrosis)andhepaticeffects(hepatitis,hepaticnecrosis)
have been reported in rare cases, usually associated with long-term use. Additionally, peripheral
neuropathyhasbeenassociatedwithlong-termuseinpatientswithrenalfailure.
DrugInteractions
Nitrofurantoinisnotassociatedwithsignificantdruginteractions.
ANTIMICROBIALRESISTANCE
There are multiple mechanismsbywhichbacteriaformor acquire antibiotic resistance.Sometypesof
resistance occur naturally, while others are acquired from another strain of bacteria. Additionally,
resistancecansometimesbeinducedduringantibiotictreatment.Table6.22summarizesthemostcommon
resistancemechanisms.
1.Themostcommontypeofresistanceisbacterialenzymeproduction.Forexample,bacteriafrequently
produceenzymesthatdisruptbeta-lactamantibiotics,alteringthestructuresotheycannotbindtothe
PBPs. There are hundreds of different types of these enzymes known as beta-lactamases. Some
enzymes have activity only against penicillins (penicillinases), whereas others, such as extendedspectrum beta-lactamases, can render almost all beta-lactam antibiotics ineffective. Separate from
beta-lactamases,bacteriaalsoproduceenzymesthatcanalterthechemicalstructureorinactivatethe
drug. This can occur with aminoglycosides, chloramphenicol, macrolides, streptogramins, and
tetracyclines.
2.Resistancecanoccurasthebacteriaaltertheirowncellmembranes,notpermittingantibioticstoenter
thebacteria.Anexampleofthisislossofporinsonthegram-negativebacterialcelloutermembrane.
Specifically, withbeta-lactam antibiotics,lossofthese porinsalterstheabilityoftheantimicrobial
agenttoenterthecell.
3.Athird,commonmechanismofresistanceistheactivationofeffluxpumpsthatexpelantibioticsoutof
theintracellular space backacrossthecellmembrane.Thispreventsantibioticsfromacting attheir
intracellulartargetsite.Thisisacommonmechanismofresistancewithclassessuchastetracyclines
andmacrolides.
4. A fourth type of resistance is alteration of the antibiotic’s target site of action. This occurs with
macrolides,amongotherclasses,whenmutationsaltertheribosomalbindingsite.Theantibioticdoes
notbindas wellor at allto theribosomeanymore.Similarly, VREisa resultofalteredcellwall
precursors. Plasmid-mediated resistance results in a modified peptidoglycan precursor that binds
vancomycin,preventingitfrombindingtoitsintendedtargetsite.
5.Afifthtypeofresistanceisalterationoftargetenzymes.Forexample,theFQsworkbyinhibitingthe
enzymesDNAgyraseandtopoisomeraseIV.Mutationstoavarietyofdifferentchromosomesonthese
enzymescanreducetheefficacyoftheFQs.
6. Last, overproduction of target enzymes can result in resistance. The best example of this is with
sulfonamides and TMP. SMX–TMP works by inhibiting folic acid synthesis by inhibiting the
dihydropteroate synthetase and dihydrofolate reductase enzymes, respectively. These enzymes are
requiredforbacterialfolicacidsynthesis.Excessproductionofthesetwoenzymesinsomestrainsof
bacteriacanrendertheantibioticineffective.
Aspecificarea ofinterestinantimicrobialdevelopmentistargetingthepreventionoforovercoming
drugresistance.
TABLE6.22
AntimicrobialResistance
ANTIMICROBIALSTEWARDSHIP
Overuse of antibiotics is well documented and has led to increased resistance to various strains of
bacteria worldwide. Some examples of drug-resistant bacteria include extended-spectrum betalactamases against E.coli and Klebsiella, carbapenem-resistant Klebsiella, FQ-resistant gonococcus,
MRSA, and vancomycin-intermediate S. aureus. The IDSA and Centers for Diseases Control and
Preventionhavedevelopedcoreprinciplesfortheimplementationofantimicrobialstewardshipprograms
for both the inpatient and the outpatient settings. These guidelines stress the importance of a
multidisciplinaryteamapproachtoimprovingantibioticuse,withafocusonensuringthatthebestdrug,at
thebestdoseandduration,isprescribedtopatients.
CASESTUDY1
J.G., a 55-year-old man, is started on daptomycin for methicillin-resistant Staphylococcus aureus
(MRSA)bacteremiaandpresumptiveendocarditis.Hismedicationsincluderivaroxaban,atorvastatin,
andlorazepam.
1.Whichofthefollowingistruefordaptomycin?
a.ItiseffectiveagainstMRSAandvancomycin-resistantenterococci(VRE).
b.Itworksbydisruptingbacterialcellwallsynthesis.
c.Hecanbeconvertedtooraltreatmentassoonashiswhitebloodcellcountdecreases.
d.Thrombocytopeniaoccursinasmallpercentageofpatients.
Answer:a.
2. About 1 week later, J.G. complains of lower extremity muscle aches and pains. Which of the
followingisaprobablereasonforthesesigns/symptoms?
a.Daptomycinisknownforcausingflu-likesymptoms.
b.Daptomycinisinteractingwiththerivaroxaban,leadingtoadeepveinthrombosis.
c.J.G.’sinfectionisgettingworseandvancomycinneedstobeaddedtotheregimen.
d.Atorvastatinisinteractingwiththedaptomycin,creatingarhabdomyolysis-likesyndrome.
Answer:d.
Afewexamplesofwaystoimproveantibioticuseincludeinfectiousdiseasespecialistoversightofthe
use ofspecificantimicrobials, theuseofrapiddiagnostics andevidence-based prescribing,theuseof
pharmacokinetic-pharmacodyamic-guided dose optimization, antibiotic streamlining, and de-escalation
andtheuseofvaccinesandotherinfectionpreventionprinciples.
Bibliography
*Starredreferencesarecitedinthetext.
Aloisamy,S.,Abdul-Mutakabbir,J.C.,Kebriaci,R.,etal.(2020).Evaluationoferavacycline:Anovelfluorocycline.Pharmacotherapy,40(3),
221–238.
Barber,K.,Bell,A. M.,Wingler,M.J. B.,etal.(2018).Omadacyclineentersthering:Anewantimicrobialcontender.Pharmacotherapy,
38(12),1194–1204.
Barlam,T. F., Cosgrove, S. F., Abbo,L. M., et al. (2016). Implementing an antibiotic stewardship program: Guidelines by the Infectious
DiseasesSocietyofAmericaandtheSocietyforHealthcareEpidemiologyofAmerica.ClinicalInfectiousDiseases,62(10),e51–e77.
Bonomo, R. A. (2019). Cefiderocol: A novel siderophore cephalosporin defeating carbapenem-resistant pathogens. Clinical Infectious
Diseases,69(7),S519–S520.
Burdette, S. D., & Trotman,R. (2015). Tedizolid: The first once-dailyoxazolidinone class antibiotic. Clinical Infectious Diseases, 61(8),
1315–1321.
CDC. (2019).Core Elementsof Hospital AntibioticStewardshipPrograms.Atlanta,GA:USDepartmentof Health andHuman Services,
CDC.Availableathttps://www.cdc.gov/antibiotic-use/core-elements/hospital.html
Cho,J.C.,Crotty,M.P.,White,B.P.,etal.(2018).Whatisoldisnewagain:Delafloxacin,amodernfluoroquinolone. Pharmacotherapy,
8(1),108–121.
Coggins,M.D.(2019).Fluoroquinoloneantibioticrisks.Today’sGeriatricMedicine,9(5),6.
*Craig,W.A.,&Vogelman,B.(1987).Thepostantibioticeffect.Annalsofinternalmedicine,106,900–902.
Doi,Y.(2019a).Ertapenem,imipenem,meropenem,doripenemandaztreonam.InG. L. Mandell,J. E. Bennett,R.Dolin,& M. J. Blaser
(Eds.),Principlesandpracticeofinfectiousdiseases(9thed.).Philadelphia,PA:Elsevier.
Doi,Y.(2019b).Penicillins.InG.L.Mandell,J.E.Bennett,R.Dolin,&M.J.Blaser(Eds.),Principlesandpracticeofinfectiousdiseases
(9thed.).Philadelphia,PA:Elsevier.
*FDAdrugsafety communication: FDAadvises restrictingfluoroquinolone antibiotic use for certainuncomplicatedinfections; warnsabout
Соседние файлы в папке Библиотека им академика М.И. Перельмана