anti infectives

• interfere w normal fcn of host
• produce toxin

• + blue
• - pink

• kill bacteria and completely eradicate
• use in immunocompromised
• good for hard to reach areas

• suppress growth, but don't kill
• depend on host immune system to completely eliminate bug

lowest concentration needed to completely suppress bacterial growth

treat with [x] well above MIC- rely on just reaching MIC

need to remain above MIC for a long time, so give over extended period of time, and look at trough levels

• PCN, Cephalosporins, Carbapenems
• MOA: weaken bacterial cell wall
• -bind to PCN binding protein on cell wall
• -inhibit enzyme(transpeptidase) needed for cell wall synthesis/integrity

• MOA: inhibit cell wall synthesis
• G+
• DOC for strep, if sensitive

• Nafcillin, oxacillin
• MOA: inhibit cell wall synthesis
• G+
• DOC: staph

• Ampicillin, Amoxiliccin
• MOA: inhibit cell wall synthesis
• G+, G-, Anaerobe
• *hypersensitivity rxn, non immunological rash (in pts w/ mono)

• Piperacillin
• MOA: inhibit cell wall synthesis
• G+,G-, anaerobes, pseudomonas

• B-lactamase resistant
• ___penem
• MOA: inhibit cell wall synthesis
• time dependent
• very broad spectrum
• 40% cross rxn w/ PCN
• G+, G-, Anaerobes, pseudomonas (except ertapenem)
• *imipinem --> lowers sz threshold

• MOA: inhibit cell wall synthesis
• 1st: mostly G+
• 2nd: G+, some G-
• 3rd: mostly G-
• 4th: G+, G-, pseudomonas
• Ceftriaxone, Cefotaxime, Cefepime: penetrate CSF
• 10% PCN cross rxn, less w/ each generation

• MOA: inhibits cell wall synthesis
• G-, pseudomonas
• limited pcn cross rxn

• MOA: inhibits cell wall synthesis
• G+, MRSA
• time dependent- adjust dose based on trough levels
• ADR: red man, nephrotoxic, ototoxic

aminoglycosides, tertracyclines, macrolides, clindamycin, linezolid, tygacil

• gent, tobramicin, amikacin
• MOA: inhibit protein synthesis
• G-, pseudomonas
• concentration dependent: use extended interval dosing (big dose once/day)
• get random level after 10 hrs, see how quickly level is falling
• post abx effect: residual activity after [] falls below MIC
• nephrotoxic, ototoxic

• ___cycline (doxy)
• MOA: inhibit protein synthesis
• G+, G-, atypical
• Oral absorption decreased by cations, antacids--> separata by 2 hrs
• ADR: photosensitivity, tooth development in peds

• Erythromycin, Clarithromycin, Azithromycin
• MOA: inhibit protein synthesis
• G+, G-, atypical
• CYP interactions- least w/ azith
• don't use with clinda

• class-macrolide
• MOA: inhibit protein synthesis
• G+, G-, atypical
• --> GI SE

• class- macrolide
• MOA: inhibit protein synthesis
• G+, G-, atypical
• --> QT prolongation

• class- lincosamide
• MOA: inhibit protein synthesis
• G+, G- anaerobes only
• can be used for community acquired MRSA, but not nosocomial 
• ADR: significant GI upset; commonly associated w/ C Diff!
• -PO dose less than IV dose b/c of ADR
• don't use w/ macrolides

• MOA: inhibit protein synthesis
• G+, MRSA
• ADR: thrombocytopenia, GI, HA
• weak MAOI, watch for serotonergic effects w/ other seroteonin agents

• class- glycylcycline
• MOA: inhibit protein synthesis
• G+, MRSA, G-
• ADR: n/v (premedicate), hypotension
• only for complicated skin, intra-abd infections

fluoroquinolones, Flagyl

• ____floxacin(cipro, levaquin,avelox)
• MOA: inhibit DNA replication
• action: G+ (minimal in cipro), G-, atypical
• ADR: QT pronlongation, tendonitis, CYP, CNS disturbances, phototoxic
• poor oral absorption w/ antacids, cations- separate by 2 hr

• class- fluoroquinolone
• MOA: inhibit DNA replication
• minimal G+, G-, pseudomonas, atypical

• class- fluoroquinolone
• MOA: inhibit DNA replication
• G+, G-, pseudomonas at high doses, atypical

• class- fluoroquinolone
• MOA: inhibit DNA replication
• G+, G-, atypical, anaerobe

• class- fluoroquinolone
• MOA: inhibit DNA replication
• anaerobes
• good tissue penetration: CNS, Bone, abscess
• DOC for C diff, protozoans
• ADR: disulfiram rxn w/ EtOH, increased [coumadin]

• Bactrim (trimethoprim and sulfamethoxazole are both sulfonamides that block 2 different
• enzymes, always used together)
• MOA:folic acid metabolism inhibitor
• G+, G-, community acquired MRSA, PCP
• **Sulfa
• ADR: rash, bone marrow suppression, thrombocytopenia
• **avoid w/ G6PD deficiency 

Daptomycin, Colistin

• MOA: inhibit cell membrane synthesis
• G+: resistant infections only (MRSA, VRSA)
• also when MIC for vanc is really high
• concentration dependent- don't need to check levels
• inactivated by surfactant: can't use in lungs
• ADR: muscle pain, elevated CPK -monitor q wk
• -d/c if CPK> 10x, or>5x w/ s/s (xnormal limit)

• MOA: inhibit cell membrane synthesis
• G-
• good for multi drug resistant
• very nephrotoxic!

• vanc
• linezolid
• tigecycline (tygacil)
• daptomycin

• clindamycin
• bactrim

• Extended spectrum PCN (zosyn)
• Carbapenem (imi/mero, NOT erta)
• 4th gen cephalosporin (cefepime)
• Aztreonam
• Aminoglycosides (genta, tobra, amikacin)
• cipro
• levofloxacin (in high doses)
• colistin

• AminoPCN 
• -amox/clav (augmentin)
• -amp/sulb (unasyn)
• Extended Spectrum PCN (zosyn)
• Carbapenem
• Clindamycin
• Tygasil
• flagyl

• tetracycline (doxy, minocycline)
• macrolides (erythro, clarithro, azithro)
• Fluoroquinolones: cipro, levo, moxi

• class- Polyene
• MOA: target cell membrane ergosterol --> leaking cell contents
• broadest spectrum antifungal, but very toxic
• ADR: nephrotoxic (Mg/K wasting, low GFR, high SCr); infusion related chills/fever/rigors
• newer version less toxic

• class- Polyene
• MOA: target cell membrane ergosterol --> leaking cell contentsbroadest spectrum antifungal, but very toxic
• ADR: nephrotoxic (Mg/K wasting, low GFR, high SCr); infusion related chills/fever/rigors
• so toxic, cant use systemic, only topical

• MOA: target ergosterol synthesis
• good against candida
• good oral absorption
• 25 hr 1/2 life
• dose dependent CYP inhibitor: watch coumadin/dilantin

• MOA:target ergosterol synthesis
• clotrimazole, miconazole
• OTC/topical

• VFEND
• MOA: target ergosterol synthesis
• broad spectrum,
• very bioavailable (IV/PO), but poor urinary penetration
• DOC: aspergillosis
• ADR: visual disturbances
• CYP: substrate AND inhibitor
• avoid IV in renal probs

• MOA: converted to 5FU which inhibits fungal DNA synthesis (pyrimidine)
• limited spectrum, used with ampho B
• ADR: marrow suppression

• ___fungin
• MOA: inhibit cell wall synthesis- no interaction w/ human cells
• broad spectrum, only for systemic infections- but poor urinary penetration

• MOA: inhibit enzyme for ergosterol synthesis (allylamine)
• oral and topical
• AE: hepatotoxic w/ systemic use

azithromycin, vancomycin, zosyn

flagyl (used for c.diff)

• cipro
• macrobid - only gets into urine

- Avelox or Levequin (gram +, gram -, and atypicals)

• carbapenems and zosyn
• (both cover G+/G-, and anaerobe)

vancomycin and zosyn

• rely on host polymerases for replication
• HBV
• Herpes

• DONT rely on host polymerase
• HAV, HCV
• flu
• HIV

• absorption: stick to cell w/ specific receptors
• penetration: fusion w/ plasma membrane or endocytosis (some can cross directly)
• uncoating
• viral genome replication
• maturation
• release--> lysis or budding (uses host cell membrane) carry to infect more cells

• IM
• for everyone >6 mos
• may have flu like s/s
• C/I egg allergy b/c grown in eggs

• nasal
• for ages 2-49
• not in peds, elderly, immunocompromised 
• may have flu like s/s
• C/I egg allergy b/c grown in eggs

• PO flu treatment- good absorption
• MOA: inhibit neuramidase- the enzyme necessary for replication
• use: w/in 2 days of symptom onset
• ADR: GI
• active against influenza a/b, swine flu

• inhaled flu treatment: mostly in oropharynx
• MOA: inhibit neuramidase- the enzyme necessary for replication
• use: w/in 2 days of symptom onset
• ADR: bronchospasm
• active against infuenza a/b

• Use: severe RSV pna in infants/peds; inhaled
• not recommended for routine use b/c of risk to healthcare workers administering the aerosol + not consistently effective
• *don't use w/ vents
• preg cat X

• use: RSV prevention in high risk Peds
• MOA: monoclonal antibody, prevents replication
• avail: IM
• very expensive, monthly dosing q month december-march

• infect epithelial mucose then travel up peripheral nerve to neuron where remains inactive
• symptomatic: cells transcribe lytic genes
• latent: transcribe "latency associated transcript" (LAT)

• use: HSV, Zoster, herpes encephalitis 
• Prodrug activated by viral phosphorelation w/ thymidine kinase- won't have any effect if cells don't have virus
• MOA: inhibits DNA synthesis (nucleoside analog)
• avail: IV, PO, topical
• ADR: phlebitis, nephrotoxic, neurotoxic
• -need adequate hydration to prevent renal crystals; also give slow infusion
• poor oral availability --> need high doses
• good distribution --> CSF

enzyme responsible for viral phosphorylation --> activate acyclovir

• use: HSV, shingles
• prodrug of acyclovir, with better PO absorption
• ADR: neutropenia, nephrotoxicity, HA, GI
• caution: TTP/HUS in immunocompromised

• use: shingles, genital HSV
• MOA: inhibits DNA synthesis
• avail: PO
• PK/PD: rapid and thorough absorption, hepatic metabolism
• ADR: GI, HA, dysmenorrhea

• denavir, abreva
• MOA: inhibit viral entry
• OTC

opthalmic HSV treatment

• Use: CMV retinitis, pneumoniis, colitis, viremia, and prophylaxis
• Avial: Iv, PO, occular implant, eye gel
• pk/pd: poor oral bioavailability
• ADR: thrombocytopenia, sterility (may be irreversible at high doses)
• terratogenic: avoid pregnancy for 90 days
• more broad spectrum than acyclovir --> more effective, but more marrow suppression
• monitor CBC weekly: stop if plt<25000 or ANC <500

• prodrug of gancyclovir w/ better bioavailability
• avail: PO
• ADR: thrombocytopenia, sterility (may be irreversible at high doses)
• terratogenic: avoid pregnancy for 90 daysmore broad spectrum than acyclovir --> more effective, but more marrow suppression
• monitor CBC weekly: stop if plt<25000 or ANC <500

• Use: CMV retinitis after failed 1st line tx
• MOA: inhibits viral DNA polymerase
• avail: IV 
• pk/pd:long 1/2 life
• ADR: nephrotoxic, neutropenia
• CI: pts on other nephrotoxics
• must give with probenacid to prolong exposure, prevent elimination

• Use: resistant HSV/VSV/CMV
• MOA: inhibit dna/rna polymerase
• avail: IV
• ADR: nephrotoxic, chelates cations --> lyte/mineral imbalances- need to replace
• dose limiting toxicity: need aggressive pre hydration; usually in 2nd wk

B, C, D

• (interferon alpha)
• Use: chronic HCV, HBV
• MOA: blocks viral entry, protein synthesis, viral assembly, and release
• avail: subQ, IV
• dose: 3x/week
• ADR: neutropenia
• contraindicated in pregnancy, men w/ pregnant partners

• (interferon alpha)
• Use: chronic HCV, HBV
• MOA: blocks viral entry, protein synthesis, viral assembly, and release
• avail: subQ, IV
• dose: 1x/week (lasts longer than intron A, but has worse SE)
• ADR: neutropenia
• contraindicated in pregnancy, men w/ pregnant partners

• use: chronic HCV- in combo w/ interferon alpha
• MOA: unknown/nucleotide analog
• avail: po
• ADR: hemolytic anemia, neutropenia
• pregnancy category X

• HCV1 protease inhibitor
• quicker, but have to use w/ interferon/ribavarin
• PK: inhibit CYP
• ADR: neutropenia, anemia, GI, alopecia, arthralgia

• HCV1 protease inhibitor
• quicker, but have to use w/ interferon/ribavarin
• PK: inhibit CYP
• ADR: anemia, rash

• use: HBV, HIV
• MOA: NRTI
• avail: PO
• ADR: nephrotoxic, lactic acidosis
• avoid in HIV b/c can --> NRTI resistant HIV b/c of low doses used to tx HBV

• use: HBV
• MOA: NRTI
• avail: PO
• ADR: lactic acidosis

• use: HBV, HIV (different dosing)
• MOA: NRTI
• avail: PO
• ADR: pancreatitis, lactic acidosis
• best tolerated NRTI

• use: chronic HBV
• MOA: inhibits DNA polymerase and viral replication
• avail: PO
• no risk of HIV resistance

RNA --> dna --> incorporated into host cell

CDR <200

development of HIV antibodies --> tests +

• 2 NRTS + NNRTI/PI/II
• for pts with OI, pregnancy, CDR 350-500, age>50

• binding and fusion: via CCR5 receptor (later shifts to CXCR4)
• reverse transcription: RNA converted into  DNA
• Integration: Viral dna intergrates into host dna
• transcription: production of viral proteins
• viral rna/proteins move to cell surface --> budding: new, immature virus break free 
• maturation: protease cuts protein chain --> working virus

• backbone of HIV tx
• MOA: nucleoside/tide analogs incorporated into viral dna
• ADR: can be taken up by mitochindra --> can't reproduce --> lactic acidosis

• NRTI
• Use: HIV in pregnancy- starting 14 wks, and infant for 6 wks
• only NRTI avail IV
• ADR: bone marrow suppression

• NRTI (not used as much)
• ADR: pancreatitis, peripheral neuropathy
• give on empty stomach b/c absorption decreased by food

• NRTI (not used as much)
• ADR: peripheral neuropathy

• NRTI 
• have to test for hypersensitivity w/ HLAB*5701. r/t genetic variation, can be fatal. usually presents in 1st 6 wks of tx

• NRTI
• (not the same tenofovir as for hep)

• NRTI
• ADR: hyperpigmentation of palms and soles

• MOA: binds to and inhibits reverse transcriptase (same effect as nrti, but different action)
• PK: metabolized by and induce CYP
• ADR: severe rash
• very prone to resistance, one you fail one (viral load not decreasing) fail whole class

• MOA: NNRTI-binds to and inhibits reverse transcriptase
• 1st line tx
• PK: metabolized by and induce CYP
• ADR: CNS symptoms- give at night
• terratogenic

• MOA: NNRTI-binds to and inhibits reverse transcriptase
• PK: metabolized by and induce CYP
• generally well tolerated
• only use in HIV1 resistant to other ARVs

• MOA: NNRTI-binds to and inhibits reverse transcriptase
• PK: metabolized by and induce CYP
• ADR: hepatitis
• not active against HIV2

• MOA: NNRTI-binds to and inhibits reverse transcriptase
• PK: metabolized by CYP.
• Only NNRTI that doesn't induce CYP
• absorption better in acidic environment, avoid acid suppressants

• MOA: NNRTI-binds to and inhibits reverse transcriptase
• PK: metabolized by and induce CYP
• ADR: qt prolongation
• take w/ food to enhance absorption

• MOA: inhibits cleaving of viral proteins- last step in maturation
• OK: inhibit CYP
• ADR: metabolic syndrome (DM 2 mos after starting tx), increased bleeding risk

• MOA: PI- inhibits cleaving of viral proteins- last step in maturation
• *booster to help decrease exposure to S-T-D

• Saquinivir
• Tipranavir
• Darunavir 
• need to be used w/ ritonavir b/c metabolized extensively by liver

• MOA: PI- inhibits cleaving of viral proteins- last step in maturation
• oral solution contains EtOH caution disulfram rxn w/ flagyl

• MOA: PI- inhibits cleaving of viral proteins- last step in maturation
• ADR: nephrolithiasis, hyperbilirubinemia
• (stones don't impair kidney fxn, resolve w/ hydration)

• MOA: PI- inhibits cleaving of viral proteins- last step in maturation
• needs to be used w/ ritonavir

• MOA: PI- inhibits cleaving of viral proteins- last step in maturation
• ADR: dose limiting diarrhea

• MOA: PI- inhibits cleaving of viral proteins- last step in maturation
• ADR: GI
• avoid in sulfa allergies
• C/I: pregnancy, <4yr, renal/heaptic probs, flagyl/disulfiram

• MOA: PI- inhibits cleaving of viral proteins- last step in maturation
• requires acidic environment for absorption
• ADR: jaundice, PR prolonged (2nd AV block)
• less hyperlipidemia

• MOA: PI- inhibits cleaving of viral proteins- last step in maturation
• ADR: severe hepatitis, intracranial hemorrhage
• *Sulfa allergy
• needs to be used w/ ritonavir
• can adapt to changes in protease: used when Resistant to other PIs

• MOA: PI- inhibits cleaving of viral proteins- last step in maturation
• used when resistant to other PIs
• Sulfa allergy
• needs to be used w/ ritonavir

• MOA: integrase inhibitor
• use: treatment experienced pts w/ multi resistant virus

combo only for treatment-naive pts

• MOA: fusion inhibitor- blocks receptor
• use: treatment experienced pts w/ multi resistant virus w/ CCR5 
• CYP metabolism

Emtricitabine + tenofovir

truvada (Emtricitabine + tenofovir)+ efavirenz (sustiva- nnrti)

• occupational: 2 NRTI (+ PI)
• non occupation: 2 NRTI+ sustiva or kaletra

lopinavir + ritonavir

2 NRTI + kaletra or sustiva or viramune

• can be latent for a long time- activate when immunocompromised
• mostly in lungs, but can disseminate

• RIPE
• rifampin and Isoniazid X 6 mos
• Pyrazinamide and Ethambutol only for 1st 2
• (4 drugs for 2 months, then 2 drugs for 4 months)

resistant to INH and Rifampin

• use: active/latent TB
• MOA: uknown
• ADR: dose related peripheral neuropathy (supplement w/ pyroxidine)
• hepatotoxic (monitor LFT monthly)- risk inc w/ age

• Use: Active/latent TB
• MOA: inhibit bacterial RNA polymerase
• ADR: hepatotoxic (more s/s than INH), red-orange body fluids

• use: MAC (mycobacterium avium complex) prophylaxis/tx, TB
• MOA: inhibit bacterial RNA polymerase
• ADR: GI, body fluid discoloration

• use: active TB
• MOA: unknown
• ADR: hepatotoxic, hyperuircemia (r/t renal excretion of uric acid- not gout)

• Use: active TB, disseminated MAC, 
• MOA: supresses incorporation of mycolic acid into cell wall
• ADR: optic neuritis (resolves)