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ID test 1

Bugs n drugs

Adhesion Pathogens ability to attach to a host
Invasions Ability to enter a host
Evasions ability to escape host defenses Abscess formation, capsule formation, biofilm production Doubling time
Nerds Gram Positive: Enterococcus (VRE)and staph epi Gram Negative:Acinetobactor
Jocks Gram Positive: Streptococcus pyogenes Toxin production, adhesion, fast doubling time Streptococcus pneumoniae Encapsulated Gram Negative:Legionella pneumophila Pleomorphic, grows in water
Sterile areas of the body Lungs, liver, bile, pancreas, kidneys, uterus and CSF
Host defense mechanisms First line - Natural Physical Barriers Skin Mucous membranes Respiratory tract Intestinal tract Genitourinary tract Eye Second line - Immune system
What results on the skin from the breakdown or lipids into fatty acids? The acid mantle, ph 5-6 which is an inhospitable environment for bacteria
What immunoglobulins are contained in body cavity secrections? IGG and IGA
What antimicrobial defenses are contained in tears? IGA and lysozymes
What level of leukocytes found on a cbc indicates infection? (leukocytosis) >10- 12 k = leukocytosis
What is left shift? an increase in immature neutrophils (bands)
WHat temperatures are considered fever? >100.4 F > 38 C
Stain used to detect fungus and molds? Lactophenol cotton blue
Stain used to detect parasites trichrome
Stain used to detect cryptococcal only fungal infections India ink
what bacteria is an acid fast stain typically used to detect mycobacterium and nocardia
why do we need an acid fast attain? the cell wall is a thin layer of peptidoglycan but is mostly mycolic acid. the process makes the bacterial cell wal retain the red colored carbol fuschin
Which culture and sensibility test is measured with a zone of inhibition? Kirby Bauer test.
if the zone of inhibition is large is the good or bad for resistance and how is it measured? it is a good indicator of low resistance and is measure in millimeters
Which test uses two fold serial dilutions to determine the MIC of an organism? Broth dilution method.
The higher the number on a serial broth dilution means what with reference to resistance? The higher the number the more resistant the organism is to the antibiotic.
What increments do broth dilutions follow? 0.125, 0.25, 0.5, 1.0,2.0, 4.0, 8.0 ...
What testing method uses zone of inhibition to measure the MIC of an antibiotic? E-Test
What does MIC represent? The relationship between one bug and one drug.
Define pharmacodynamics The relationship between an antibiotic and a specific bug.
Why do we use pharmacodynamics? To determine specific drug potency or the differences in potency between drugs in the same class of antibiotics.
What is drug drug additivism? When one drug compliments another drug enhancing the effect from 1-2 IE 1+1=2
What is drug synergy? multiplicative increase in efficacy, I.E. 1+1=5
What is a static antibiotic? <3 log kill in 24 hours
What is a cidal drug? > 3 log kill in 24 hours
Gram Positive cocci in clusters Staph auer and staph epi
Gram positive in pairs or chains Step Pneumo, strep pyogenes (GAS), Strep agalactacie (GBS) Entero face, Enteor facalus
Gram positive bacilli Lysteria monocytogenes
Gram negative cocci in pairs and chains Neisseria and M. catt
Gram negative bacilli or rods (enterobactericiae) E coli and klebsiela serraatia, proteus, enterobacter, morganella
atypicals legionella, chlymadia and mycoplasma pneumo
anaerobes clostridium and bacteroides
staph A is resistant due to what? the MecA gene which produces the betalactamase penicillinase
two types of Strep MRSA? CA and HA
primary locations for HA MRSA skin 37%, respiratory 22%, UTI, 20 %
Primary locations for CA MRSA SKIN 70%
Agents used to treat MRSA Reliable – active against almost all MRSA – 100% Vancomycin, telavancin Linezolid Daptomycin Tigecycline Ceftaroline TMP/SMX Less reliable Doxycycline – 70% Clindamycin – 60%
aka for staph epi NERD coag neg strep or staph not epi
how to treat staph epi infections Reliable MRSA agents
common infections caused by staph epi? Catheter-related bloodstream infections Catheter-related urinary tract infections Skin/skin structure infections – cellulitis Prosthetic joint infections Prosthetic valve endocarditis
strep pneumo aka pneumococcus locations sinuses and skin
strep pneumo infections? Most Common Cause of: Community-acquired pneumonia Bacterial meningitis Can cause Sinusitis Otitis media Skin/skin structure infections Much much more
strep pneumo virulence level? Highly virulent JOCK
Strep pneumo defenxe system Encapsulation
Strep pyogenes is AKA as what? Group A strep (GAS) Flesh eating bacteria
Why is GAS both virulent and pathogenic? it is a toxin producer and casuse tissue necrosis
what is the primary t/Tx for GAS? Still sensitive to penicillin
Gas is the common cause of what infections? Strep throat Skin/skin structure infections Toxic Shock Syndrome
Common AKA for strep agalactiae? GBS
location for GBS normal vaginal flora in 40 % of women
when do we typically test for GBS During pregnancy
GBS is the most common cause of what? neonatal sepsis
E. Faece and E. facalis normal locations Gi tract, mouth and skin
which is more resistant, e faece or e. faecalis? In your Faeceium
common infections caused by E face twins? Nosocomial (hospital-acquired) Blood stream infections Endocarditis UTI Wound infections
How to treat AMP S and vanc S enterococcus infections? 1st line – penicillins Amp/amox/pen ± BLI, pip/taz, ticar/clav 2nd line – carbapenems
How to treat AMP R and Vanc S enterococcus infections Vancomycin
How to treat amd R and Vanc R enterococcus infections Linezolid Daptomycin Tigecycline
common carrier for listeria Food stuffs like queso fresco, hot dogs, raw unpasteurized foods, refrigerated patte's and smoked foods
who should avoid the foods that can carry listeria? Pregnant and imunocomprimised
two Neisseria species Meningitis and gonorrhoeae
Is Neisseria gonorrhoeae normal flora and what does is cause? NO, and gonorrhea
What does M catt commonly cause URTI'S: ottis media, laryngitis, sinusitis and pneumonia
Gram negative rod general rules Common bacteria in GI tract Just about any antibiotic with Gram-negative activity will have intrinsic activity Exceptions: Pseudomonas, Acinetobacter Antibiotic susceptibilities vary widely dependent upon resistance mechanisms
Gram negative rod treatment Empiric therapy:1st line = anti-pseudomonal beta-lactam if Pseudomonas or other resistant GN rods are suspected De-escalation (ASAP)with: 1st line = “narrowest spectrum” beta-lactam that is sensitive 2nd line = Amino, fq,severe allergy
two most common producers of ESBL (extended spectrum beta lactamase prodcuers) E-coli and klebsiela
Common producers of AmpC beta lactamase S-Serratia P-Proteus P-Pseudomonas A-Acinetobactor C-Citrobactor E-Enterobactor M- Morganella
What does AMP-C do? Makes the bacteria resistant to all beta lactams except Cefepime and carbapenems
What is the most common gram positive cause of HCAP? MRSA
What is the most common gram negative casue of HCAP? Pseudomonas
What types of HCA infections besides Pneumonia can pseudomonas cause? Blood stream infections, wound infections, post-op infections, UTI
Antibiotics active against pseudomonas Pip/tazo, Ticar/Clav, cefepime, ceftazadime, Imi, mero, dori, aztreonam, Aminoglycosides(AGT, FQ's (Cipro and levo), colistin
Where is acinetobactor typically found on hospital equipment
how long can acinetobactor live on inanimate objects 1 day to 2 weeks
why does acinetobactor have a high mortality rate? not due to virulence rather the severity of the illness the patient already has.
What infections does h flu cause? CAP Meningitis Sinusitis Otitis media Conjunctivitis
Why is h flu a JOCK? and how do we treat it? It is encapsulated and we vaccinate for it primarily.
Name all three encapsulated organisms N. meningitidis, S. pneumoniae, H. influenzae
What is associated with clostridium botulinum and what does it cause? Honey and home canned foods, paralysis due to toxin production
how do we treat clostridium botulinum? no abx must get antitoxin from cdc.
What is associated with clostridium tetani? Puncture wounds especially from a metal object
what happens when you get clostridium tetani infection? muscle spasms, spasma and nyperflexia due to toxin production
How do we treat clostridium tetani? penicillin, surgery and muscle relaxants and we vaccinate every ten years
What is caused by clostridium perfringens? Gas gangrene
how do we treat clostridium perfringens? antitoxins, surgery and hyperbaric chamber
what is associated with a clostridium difficile infection? CDAD, cdif associated DIARRHEA
Treatment for C-DIFF infection oral metronidazole or oral Vancomycin
Anti MRSA beta lactam ceftaroline
anti enterococcal beta lactams penicillin, amoxicillin, ampicillin, pip/tazo, ticar/clav and carbepenems
antipseudomonal beta lactams pip/tazo, ticar/clav, cefepime, ceftazadime, imi, meor, dori and aztreonam
anti anaerobic beta lactams amox/ clav, amp/sulbactam, pip/taz, ticar/clav, cefotetin, cefoxitin and carbapenems
volume of distribution of beta lactams? 0.7 l/kg, water is 0.6 L/Kg, they go everywhere water goes.
where do beta lactams fail to go? Bone and Variable to CSF
what pharmacodynamics parameters do beta lactams have? Time>mic: Penicillins= 50% Cephalosporins = 60-70% Carbepenems= 40%
When can we use cephalosporins and carbapenems when a patient has an allergy to penicillin? When the reaction is not anaphylactic
options if patient has a severe penicillin allergy? aztreonam and other non beta lactams
Penicillin ROA? V=po G= IV IM
PCN monitoring parameters Electrolytes and renal function, renal adjustment required
what is PCN unstable against? betalactamase and penicillinase producers
what does PCN treat? GAS, GBS and syphilis are the most common places in therapy for PCN.
ROA for naf and OXacillin IV
ROA for Dicloxcillin PO
monitoring parameters for NAF/OX and dicloxacillins? Hepatic enzymes, excreted hepatically, electrolytes: high NA
Are NAF, OX and diclox stable against penicillinase producers? Yes!
What is the place in therapy for NAF, OX and Diclox? DOC FOR MSSA INFECTIONS!!!!!
ROA for PIP/tazo and Ticar Clav? IV for both
Activity for Pip/tazo and ticar/clav? penicillinase producers, anaerobes, enterococcus and pseudomonas.
general rules about cephalosporin's increasing gram negative coverage with generations, no enterococcal or listeria activity, stable against penicillinase, not anaerobic activity except cefotetan and cefoxitin
1st gen cephs Cephalexin (Keflex)PO Cephazolin (Ancef) IV
1st gen cephs place in T/Tx? skin and skin stricture infections
1st gen excretion method Renal, monitor renal function
2nd gen cephalosporin's IV options? cefoxitin(Mefoxin)IV cefotetan (Cefotan)no longer produced
2nd gen spectrum GP, Gn anaerobes
2nd gen excretion method Renal, monitor renal fxn
2nd gen ceph PO option cefuroxime (Ceftin, Zinacef)
3rd gen cephalosporin's IV option Ceftriaxone (Rocephin)
3rd gen Ceph Po option cefixime (Suprax)
3rd gen monitoring parameters? excreted both renal and hepatic, only need dose adjustment if both are comprimised
3rd gen adverse rxns biliary sludging in pediatric patients
place in therapy for 3rd gen cpehs DOC for CAP with azithromycin
3rd generation ceph that is only excreted renally ceftazadime (Fortaz)
ceftazadime ( Fortaz) activity pseudomonal, gn and weak gp
what inactivates ceftazadime? ampC and betalactamase
4th gen ceph cefepime (Maxipime)
cefepime (maxipime) roa and monitoring parameters? IV and monitor renal fxn as excreted renally
cefepime (Maxipime) activity pseudomonal and active against ampc and betalactamase
cefepime (Maxipime) place in therapy Option for impiric T/Tx in HC associated infections
5th gen ceph ceftaroline (Teflaro)
ceftaroline (Teflaro) ROA and monitoring parameters IV and renal as it is excreted renally
Ceftaroline activity Resistant Gram-pos MRSA and MDR-S. pneumoniae, VRSA and linezolid-resistant SA, common gram negative organisms
what degrades ceftaroline (Teflaro)? Amp C and ESBL
Carbepenem activity (except ertapenem) Active against Pseudomonas sp. Active against Enterococcus sp. Active against anaerobes Stable against penicillinase Stable against ampC beta-lactamase Stable against ESBLs extended-spectrum beta-lactamases
Imipenem/cilastin brand name Primaxin
meropenem brand name Merem
doripenem brand name Doribax
imi/mero/ dori ROA and monitoring parameters IV and monitor renal fxn
Imi/mero and dori adverse rxn Seizures that are dosage based Pts with prior neurological issues at higher risk Stroke, epilepsy Risk of seizure: imipenem > meropenem > doripenem
What is the difference between ertapenem and the other three car Ertapenem does not cover pseudomonas so is not used for hospital patients. typically used for diabetic foot infections
what patients are more likely to have seizures when given carbapenems? people with past stroke, epilepsy and patients on dialysis
monobactam aztreonam (Azactam)
aztreonam (Azactam) roa and monitoring parameters IV and monitor renal rxn as excreted renally
Aztreonam activity stable against penicillinase and gram negatives
when do we use aztreonam? in the event of a severe bata lactam allergy and if desperate.
what cross reactivity does aztreonam (Azactam) have? if allergic to ceftazadime also allergic to aztreonam, same side chain
Concentration dependent antibiotics aminoglycosides, Daptomycin and bactrim
time dependent antibiotics all beta lactams and monobactams
auc/mic dependent antibiotics FQ's, macrolides, tetracyclines, linezolid, glycopeptides
amino glycosides gentamycin, tobramycin, amikacin
aminoglycoside spectrum gram negative and antipseudomonal, used in combo with beta lactams for gram positive infections for staph A, coag neg staph and enterococcus
aminoglycoside MOA? inhibit protein synthesis, binds 30 s subunit. has post antibiotic effect. cidal
aminoglycoside VD? Low, low tissue concentration, mostly stays in vasculature 0.2-0.3 l/kg, low abscess conc.
aminoglycoside PD's? Peak/concentration dependent killing
PD goal for AG's with gram negative infections? > or equal to 16 times the MIC
dosing for gent and tobramycin for gram negative infections? 5-7 mg /kg (IBW) q 24h
synergistic dosing for gent and tobramycin for gram positive infections? 1 mg/kg (IBW) q8h
aminoglycoside adverse reactions ototoxicity, nephrotoxicity, neuromuscular block and rash
aminoglycoside ROA all IV
gentamycin and tobramycin monitoring parameters renal dosage adjustment required troughs for traditional dosing <1-2 mcg/ml once daily dosing <1 mcg/ml gram negative peak >16x MIC
amikacin dosing? 15-20 mg/kg (IBW)q24
amikacin mooitoring parameters renal fxn, dosage adjustment required trough goal < 8 mcg/ml
levofloxacin spectrum GP, GN, Pseudomonas, anaerobe and atypical
moxifloxicin spectrum GP, GN, anaerobe and atypical
ciprofloxacin spectrum GN and pseudomonas
FQ MOA binds dna gyrase topoisomerase II stopping replication= gn ACTIVITY BINDS DNA GYRASE TOPOISOMERASE IV interferes with separation of dna molecules= GP activity
FQ VD High VD high concentrations found in kidneys, liver, bile and lungs serum> site in bone and csf
PD goals for FQ's GP pathogens MIC> 35 GN pathogens MIC> 125
FQ common adverse reactions? N/V/D, dizziness/ confusion (mostly in the elderly), dose related CNS with levo >750 mg dose, cations bind in stomach (oral only)
FQ uncommon adverse rxns with BBW? Joint symptoms BBW for arthralgias (swelling, tendon rupture)Risk factors: Age >60, BMI <30 kg/m2, concurrent use of glucocorticoids, women significantly more likely than men to develop rupture
Fq uncommon rxn non BBW photosensitivity and LFT elevation
cipro ROA and monitoring parameters? IV and PO and monitor renal fxn, dosage adjustment required
cipro place in therapy best po option for anti-pseudomonal T/Tx, used for UTI, 90% bioavailable
levo ROA and monitoring parameters IV and PO, monitor renal fxn dosage adjustment required, QT wave prolongation, glucose abnormalities
levo place in therapy CAP for patients with beta lactam allergy, antipseudomonal agent (secondary and a bad choice)
Moxifloxacin (Avelox) ROA and monitoring parameters IV and PO, QT wave prolongation and glucose abnormalities, excreted HEPATICALLY!
can moxi treat pseudomonas? NO, no antipseudomonal activity
Place in therapy for moxi CAP patients with beta lactam allergy
Macrolides Azithromycin, Clarithromycin and erythromycin
Macrolide spectrum GP, GN (non- rods) and atypical. Erythromycin has activity against 50% of CA-MRSA but azith and clarith have none
Macrolide MOA Binds 23s subunit of the 50 s subunit block exit of the growing chain inhibiting protein synthesis
Macrolide VD Serum < site: lymph and CSF
Macrolide PK AUC/MIC
Macrolide adverse rxn N/V/D and metallic taste
Macrolide drug interactions azith< eryht< clarith all interact with anything metabolized by the liver. most commonly aan inhibitor of the cyp450 system. most noteably with all is warfarin, theophylline, digoxin and cyclosporine
macrolide uncommon adverse reaxtions? Hearing loss – dose related Eosinophilia Transaminase elevation QT prolongation
eryth ROA and monitoring parameters IV and PO, Monitor LFT's, qt wave prolongation and drug interactions
place in therapy prokinetic gent, GBS prophylaxis in pregnant patients allergic to PCN
Azithromycin (Zithromax) ROA and monitoring parameters IV and PO. LFT's
Azithromycin (Zithromax)) place in therapy DOC for Chlamydia trichomonas DOC for CAP for out pts DOC for CAP for in pts + beta-lactam Common option for all upper respiratory tract bacterial infections (beta-lactams preferred) Sinusitis, otitis media, bronchitis
Clarithromycin ROA and monitoring parameters PO only and LFT's and drug interactions
tetracyclines doxycycline, tetracycline, minocycline and kinda tigecycline
TCN spectrum ALL have GP, gram negative non rods and atypical. Tigecycline has GN rods and anaerobes also
TCN MOA inhibits protein synthesis by binding the 30 s subunit blocking the attachment of trna to mrna
TCN VD High VD serum >site: Lung Sinus Gynecological tissue Bone Bile Periodontal tissue Serum>site: CSF
TCN adverserxn's N/V/D, photosensitivity and tooth staining (contraindicated in children<12
TCn drug interactions Cations bind in the stomach
tetracycline ROA and monitoring parameters IV and PO. renal and hepatic fxn, decrease frequency with CrCl <50 and avoid altogether in patients with severe hepatic dysfunction
tetracycline place in therapy treatment of h-pylori and acne
doxycycline (Vibramycin)and minocycline (Minocin)roa and monitoring parameters IV and PO and no adjustment for renal or hepatic dysfunction
place in therapy for doxy and mino Doxy - oral MRSA treatment option Mino – tx of MDR ancinetobacter infections Odd infections Anthrax Chlamydia Tick borne diseases
tigecycline (Tygacil) ROA and monitoring parameters IV and hepatic fxn, dose adjust if severe, pancreatic enzymes and N&V occurs in 33% of people
tigecycline (tygacil) place in therapy MRSA treatment alternative MDR S. pneumoniae treatment alternative VRE treatment alternative Pt with multiple antibiotic allergies Carbapenemase producing pathogens
Lincosamides clindamycin (Cleocin)
Glycopeptides Vancomycin, televancin (Vibativ)
Oxazolidinones Linezolid (Zyvox)
Lipopeptides Daptomycin (Cubicin)
clindamycin (Cleocin Spectrum GP: MRSA/ staph, strep no entero. anaerobes:Bacteroides sp. Peptostreptococcus sp. Fusobacterium sp. NO clostridium activity
clindamycin MOA Binds 50 s subunit inhibiting protein synthesis
clindamycin VD Medium 0.6-1.2 l/kg can be found in Bone (osteomyoletis), sputum (can be used for pneumonia), tissue and sinus tract Not good in CSF
clindamycin PD? Unknown
clindamycin adverse effects N/V/D which is dose limiting, considered the major cause of CDAD,
clindamycin max dosing? max oral dose is 450 mg q6h max IV dose 600-900 mg q6-8h
clindamycin ROA IV and Po
clindamycin place in therapy DOC for GAS infection with PCN patients with PCN allergy and anaerobic infections
Bactrim spectrum GP, MRSA, GN no GAS or enterococcus
Bactrim MOA Dna inhibition through PABA (sulfameth) and dihydrofolic acid (trimetho)
Bactrim VD? medium, limited data, UTI, pneumonia, joint infections and skin/stricture infections
Bactrim PD Concentration dependent both static and cidal
Bactrim common adverse reactions Dermatologic: Rash Urticaria Gastrointestinal Loss of appetite N/V Renal Elevation in SrCr w/o ↓ in GFR Interstitial nephritis Crystalluria Hyperkalemia
Bactrim serious adverse reactions Hematologic: Agranulocytosis Aplastic anemia Hepatic Hepatic necrosis Fulminant liver failure Immune hypersensitivity reaction Rash Erythema Multiforme Stevens-Johnson syndrome Toxic epidermal necrolysis
Bactrim ROA and monitoring parameters IV and PO, Renal dose adjustment if renal dysfunction, K+ and LFT's
Bactrim place in therapy UTI's, PCP prophylaxis in HIV patients with a cd4 count <50, MRSA skin infections
Linezolid (Zyvox) spectrum GP, MRSA and enterococcus, including resistant strep pneumo and VRE. Also mycobacterium avium, TB and nocardium
Linezolid (ZYvox) MOA prevent the formation of 30s and 50 s subunits into the 70s subunits
linezolid (ZYvox) VD Medium 0.5-1.0 l/kg. serum , sites: lung phagocytes and tissues serum> site: CSF
linezolid PD AUC/MIC
linezolid (ZYvox) common adverse rxn's thrombocytopenia >14 days of therapy neutropenia >28 days of therapy
linezolid serious adverse reactions Lactic acidosis, peripheral neuropathy > 28 days of T/Tx, optic neuropathy > 28 days of T/Tx, serotonin syndrome
linezolid (Zyvox) ROA and monitoring parameters IV and PO 100% bioavailability. Monitor CBC
linezolid (Zyvox) place in therapy MRSA pneumonia MRSA skin infections Vancomycin resistant Enterococcus (VRE) infections Alternative therapy for Mycobacterium and Nocardia infections
Vancomycin and televancin spectrum All GP, MRSA and enterococcus
Vanco and televancin MOA cell wall inhibitor, binds d-ala d-ala blocking cross linking process
vanco tissue VD medium VD 0.6-0.7, serum < site, none Serum > site Lung, Tissue and CSF
vanco and televancin PD AUC/MIC maybe time/mic still being debated
vanco trough goals 15-20 mcg/ ml
vanco dosing 15 mg/kg q 8-12 often dose 1g q12
vanco adverse common adverse reactions infusion reaction (redman syndrome) slow th rate of infusion Nephrotoxicity: trough and duration related
vanco rare adverse reactions ototoxicity related to peak dose, neutropenia and thrombocytopenia
televancin common adverse reactions Hematologic: Thrombocytopenia Nephrotoxic CNS: Insomnia, psychiatric disorder, headache GI: Metallic/soapy taste, N/V/D GU: Foamy urine
televancin rare adverse reactions transient hearing loss and qt wave prolongation
Vanco ROA and monitoring parameters IV nd PO (Po only for CDAD infections Monitor: serum trough concentrations and SCr levels
vanco place in therapy first line option for all MRSA infections with a possible exception for Pneumonia. Tied with metronidazole for CDAD infections
televancin ROA and monitoring parameters IV monitor SCr, platlets and K+
Daptomycin (Cubicin) spectrum GP, MRSA and enterococcus
Daptomycin (Cubicin) MOA cell wall inhibitor
Daptomycin (Cubicin) VD Low, 0.1-0.2 l/kg minimal data, not appropriate for CSF infections Distributes to the lugs but is bound by surfactant so is useless in pneumonia.
Daptomycin (Cubicin) PD Peak dependent killing, rapidly cidal peak dependent to prevent regrowth
Daptomycin common adverse reactions myalgias and myocitis
Daptomycin rare adverse reactions rhabdo and renal failure secondary to rhabdo
Daptomycin (Cubicin) ROA and monitoring parameters IV Monitoring parameters: Creatinine kinase – prior to start then weekly SrCr – dose adjustments in renal failure
Daptomycin (Cubicin) place in therapy Secondary therapy for: MRSA bacteremia, endocarditis and skin and skin stricture infections
Rifampin spectrum GP, MRSA and enterococcus and mycobacterium like TB and avium...
Rifampin MOA DNA damage, inhibits transcription of dna to rna
interesting kinda unique parts of Rifampin MOA Intracellular Penetrates biofilms Able to kill bacteria in stationary phase All intra-cellular antibiotics should share this attribute
rifampin VD HIGH 1.5-2.0l/kg: Concentrates in: [serum] ≤ [site] Abscess Bile Stomach wall Ascites Liver Other sites of distribution: [serum] > [site] Bone CSF Lung
Rifampin PD AUC/MIC
Rifampin common adverse reactions abnormal skin, sweat saliva, tear and urine colors, range from orange to brown, Increased LFT's
Rifampin ROA and monitoring parameters? IV and PO Monitoring parameters:Renal function – dose change in renal failure Hepatic function Q 2 weeks DRUG INTERACTIONS – potent inducer of 3A4
Rifampin place in therapy First line for mycobacterium like TB, used in combination for treatment of staphylococcal and enterococcal infections Foreign material – hip, catheter, heart valve
Drugs Rifampin is CI with? Fosamprenavir Lopinavir Saquinavir Tipranavir Voriconazole
Is Rifampin an inducer or inhibitor of the cyp 450 system? Potent inducer, always check for interactions before giving Rifampin
Colistin spectrum strictly gram negative activity against pseudomonas
which gram negatives is Colistin not active against? Proteus sp. Serratia marcescens Moganella morganii Neisseria sp. Moraxella catarrhalis Providentia sp. Helicobacter pylori
Colistin MOA electrostatic displacement of CA and Mg from membrane lipids causing cell membrane degredation
Colistin VD Low, 0.3- 0.5 l/kg tissue= serum binds to liver kidneys, brain, heart, muscle, lungs and placenta for up to 5 days. CSF 25% of serum level
Colistin PD Peak dependent killing
Colistin adverse reactions Nephrotoxicity, dizziness, seizures, tingling, Inhalation route: Bronchospasms Acute respiratory failure Respiratory tract paralysis
Colistin ROA and monitoring parameters IV monitor SCr and mental status changes
Colistin place in therapy MDR pseudomonas and acinetobactor infections...the only drug that is succeseptable inhalation used for PNA and colonization in intubated patients
Nitrofurantoin spectrum GP, GN, MRSA and enterococcus
Nitrofurantoin MOA DNA damage, attacks ribosomal proteins, DNA, respiration, pyruvate metabolism and other intracellular components
Nitrofurntoin VD Unknown, 50% excreted in urine (25% unchanged) and 50 % in bile, if kidney gfr low then less in urine. CrCl between 30-60 = CI
Nitrofurantoin PD Peak dependent killing
Nitrofurantoin adverse reactions Hematologic: Hemolytic anemia Eosinophilia Hepatic: Cholestatic jaundice syndrome Hepatic necrosis Immune hypersensitivity reaction Neurologic: Neuropathy Respiratory: Interstitial lung disease Pulmonary fibrosis
Nitrofurantoin ROA and monitoring parameters PO monitor SCr to determine appropriate patients
Nitrofurantoin place in therapy UTI's only, especially in pregnant patients (DOC)
Metronidazole spectrum Anaerobes only
Metronidazole MOA DNA damage systemic: Reduced metronidazole interacts with DNA to cause a loss of helical structure, strand breakage, and resultant inhibition of nucleic acid synthesis and cell death
Metronidazole VD (tissue) medium 0.5-1 l/kg [Tissue] ≈ [Serum] Female GU tract – pelvic tissue, uterus, etc. Peritoneal fluid Bone Pancreas Colorectal tissue [CSF] = 50-75% of serum
Metronidazole PD Peak dependent killing
Metronidazole adverse reactions gastro, some neurological like seizures, Leukopenia and disulfiram like reactions avoid ETOH during and for 48 H post T\Tx
Metronidazole ROA and monitoring parameters IV, PO, topical and vaginal monitoring parameters...none listed
Metronidazole place in therapy? DOC for CDAD infections, bacterial vaginitis, vaginal protozoal infections, other protozoal infections like giardia
quinupristin/dalfopristin spectrum GP, MRSA, enterococcus, GN rods and atypicals
Quinupristin/dalfopristin MOA binds 50 s subunit inhibiting protein synthesis
Quinupristin/dalfopristin VD LOW 0.45 for q and 0.25 for D, [Tissue] > [Serum] Kidney Liver Spleen Salivary glands WBC [Tissue] < [Serum] Skin/soft tissue Does not cross BBB or placenta
Quinupristin/dalfopristin PD AUC/MIC
Quinupristin/dalfopristin adverse reactions thrombophlebitis, injection site rxns, Conjugated hyperbilirubinemia, Arthralgia Myalgia
Quinupristin/dalfopristin ROA and monitoring parameters iv Hepatic transaminase elevation Dose adjustment in severe hepatic dysfunction Bilirubin increases
chloramphenicol spectrum GP, MRSA, enterococcus, GN rods and atypicals
Chloramphenicol MOA Inhibits transpeptidation prohibiting protein synthesis on 70s subunit
Chloramphenicol VD Medium: Concentrates in: [serum] ≤ [site] Kidney Liver Other sites of distribution: [serum] > [site] CSF – 50% of serum
Chloramphenicol adverse reactions Grey baby syndrome, fatal in newborns and toddlers, neurotoxicity, aplastic anemia (usually fatal occurring months post therapy),
Chloramphenicol ROA and monitoring parameters IV, OT and OP, rarely used, baseline cbc q 2 days during therapy
Selective pressure Survival of the fittest bugs
Mechanisms of antibiotic resistance Intrinsic (lack of drug target)or Acquired resistance
alteration of the antimicrobial agent ESBL, AMP-c beta lactamase alters the drug before it can reach the target
Acquired antibiotic resistance: Mutation in the target site Changes in the target molecule occur as a result of spontaneous mutation, resulting in decreased affinity of the target for the antimicrobial Ex: PBP alteration to PBP2a
Acquired antibiotic resistance: Decreased accumulation Decreased uptake Ex: Porin channel modifications Porin channels only in Gram-negative bacteria Increased efflux Ex: Efflux pumps – may be nonspecific, effluxing multiple antimicrobials and/or other cellular ingredients
how is staph A resistant to penicillin? >95 % resistant by producing beta lactamase
Define MRSA and why it is resistant Presence of the mecA gene, encodes penicillin-binding protein 2a (instead of PBP 2) Alteration of binding site confers resistance to ALL beta-lactams (except ceftaroline) 50/50 MSSA to MRSA
How are VISA (vanc intermediate SA) and GISA (glycopeptide SA) resistant? Thickened cell wall increasing the number of D-ala-D-ala targets, preventing adequate drug concentration from reaching binding sites at cell wall
How is VRSA resistant Resistant mechanism: Plasmid mediated transfer of vanA gene vanA gene codes for D-ala-D-lactate leaving no binding site for vancomycin
How is VRE (vanc resistant enterococcus) resistant? vanA gene vanA codes for D-ala-D-lactate leaving no binding site for vancomycin
gram negative amp C Beta-lactamase MOA? Chromosomally mediated (mostly), can be spread to other bacteria via plasmids Confers clinical resistance to most beta-lactams Exceptions: cefepime and carbapenems Beta-lactamase inhibitors (tazobactam, sulbactam, clavulanate) NOT effective
What are the common amp-C beta -lactamse producers? S;serratia P; proteus, pseudomonas A; Acinetobactor C; Citrobactor E; Enterobactoer M; Morganella
Define ESBL -lactamases capable of hydrolyzing penicillins, cephalosporins, monobactams Inhibited by clavulanic acid in vitro – NOT CLINCIALLY RELEVANT
Common ESBL producers? Klebsiella pneumoniae Escherichia coli Less common ESBL producers Pseudomonas aeruginosa Proteus mirabilis
ESBL MOA Plasmid mediated so can be easily transferred between bacteria species Plasmids often contain genes coding for other resistance mechanisms against AG, chloramphenicol, sulfonamides, trimethoprim, TCN, FQs End result: multi-drug resistant pathogen
Treatment of choice for ESBL's? Carbepenems and Non--lactams – ONLY if susceptible AND non-life threatening infections (UTI or pyelonephritis)
Define KP carbepenemase First associated with Klebsiella, but all Enterobacteriaceae and Pseudomonas have been associated with carbapenmase production KPC is plasmid mediated Bacteria with KPC enzymes inactivate all beta-lactams
Agents most likely to be active against carbepenemase producers? Colistin, amikacin, rarely tigecycline
In what patients do mold infections most commonly occur? imunocomprimised patients
What are the most common mold infections? aspergillus and mucorales both have very high mortality rates
most common site of aspergillus infection? Pulmonary
most common site of mucorales infections? nose, mouth, sinus – invade up into brain
Where and whom do Fusarium mold infection effect Immunocompetent – superficial Nail infections Kertitis Immunosuppressed – invasive Nose/mouth/sinus Pulmonary Skin
where do candida yeast infections occur? Normal flora of GI tract Superficial infections Skin, mouth (thrush), esophagitis, UTI, genital Invasive infections (systemic) Intra-abdominal, bloodstream infections
How are dimorphic endemic fungi unique? Ability to cause disease in a healthy host Association with a specific ecologic niche in the environment Demonstration of temperature dimorphism (mold in the environment at a temperature of 25°–30° C and yeast at body temperature
how do dimorphic endemic enter the body and what do they cause? Enter host via respiratory system, initially causes pulm infections, can spread systemically
Name the polyenes Amphotericin B Nystatin
Name the triazoles Fluconazole Itraconazole Voriconazole Posaconazole
Name the Echinocandins Caspofungin Micafungin Anidulafungin
Name the "other" antifungal 5-FC (flucytosine)
Amphotericin spectrum and ROA Mold – not as good as vori or posa Yeast – not as good as azoles Dimorphic
Nystatin ROA and spectrum Yeast – cutaneous or mucocutaneous infections aka superficial infections
Polyene MOA Cell membrane inhibitor Binds to ergosterol in the fungal cell membrane, forms pores, leaking Na, K, and Ca, depolarizing cell
Ampho B adverse rxns Infusion related – chills/rigors, fever, tachypnea Nephrotoxicity Electrolyte depletion
Ampho B PD Peak dependent killing
Ampho B Lipid-associated formulations created to decrease ADRs AmBisome – liposomal – tolerated best - $$$ Amphotec Abelcet
Ampho B place in therapy First line for Cryptococcus neoformans meningitis Systemic candida infections - back up option when azoles or echinocandins fail
Nystatin place in therapy Topical powder for mild skin infections Swish and spit for thrush and mild esophagitis
Fluconazole ROA and spectrum IV, PO All yeast except C. krusei Dimorphic
Itraconazole ROA and spectrum PO Yeast Mold – itra < vori < posa Dimorphic
Voriconazole ROA and spectrum IV and PO Yeast Mold – itra < vori < posa Dimorphic
Posaconazole ROA and spectrum PO Yeast Mold – itra < vori < posa Dimorphic
Azole MOA Cell membrane inhibitor Inhibit the fungal cytochrome P-450 inhibiting synthesis of ergosterol. Depletion of ergosterol in the cell membrane and accumulation of toxic intermediate sterols, causing increased membrane permeability
Itraconazole PK problems unpredictable concentrations Solution – best absorbed on empty stomach Capsules – best absorbed with food (soda/cola best)
Voricanazole PK issues IV formulation in sulfobutylether-beta-cyclodextrin (SBECD) – renally cleared Used to be contraindicated in CrCl < 50 ml/min – SBECD can cause renal vacuoles at high doses (really high doses)
Posaconazole PK issues unpredictable concentrations High fat food will double absorption Taken 4 xs daily to maximize absorption – even though 35 hr t ½
Azole ADR's Hepatic – transaminase elevation, GI – N/V DI – CYP 3A4 inhibitors Voriconazole – vision changes – blurred, color changes (blue), photophobia
Fluconazole place in therapy First line for systemic Candidal infections First line for moderate/severe skin infections
Itraconazole place in therapy Oral option for dimorphic/endemic fungi
Voriconazole place in therapy First line for Aspergillus and other mold infections
Posaconazole place in therapy Option for Aspergillus First line for Mucormycosis infections
Echinocandin ROA and spectrum IV Yeast – all Candida sp. NO Cryptococcus Mold – Aspergillus sp. only
Echinocandin Mechanism of Action Cell wall inhibitor, Inhibits 1,3-beta glucan synthase resulting in an weak cell wall
Echinocandin ADR's and PD Almost none Some histamine release during infusion No hepatic or renal issues PD= Peak dependent killing
Echinocandin place in therapy Candidal systemic infections First line tx option – tied with fluconazole Aspergillus Combination tx with voriconazole
5-fluorocytosine (5-FC) ROA and spectrum PO Yeast Only used in combo with ampho B for Cryptococcus infections
5-fluorocytosine (5-FC) MOA DNA/ RNA inhibitor, 5-FU is phosphorylated and incorporated into RNA where it causes miscoding and halts protein synthesis.
5-fluorocytosine (5-FC):PD ADR and monitoring parameters PD - % T > MIC ADRs In pts with renal dysfuntion: Heme: leukopenia, thrombocytopenia GI: enterocolitis Death Monitor serum concentrations – goal < 100 mcg/ml
Cyclovir PO only options Valacyclovir, famciclovir and valganciclovir
Cylovir iv and po options acyclovir and ganciclovir
topical cyclovir option penciclovir
when a cyclovir has VAL in the front what does that mean? an increase in bioavailability
Cyclovir MOA inhibit dna synthesis
cyclovir PD AUC/MIC
Acyclovir, valacyclovir, famciclovir adverse reactions Malaise, HA Nephrotox, crystaluria at high IV doses
Ganciclovir, valganciclovir adverse reactions Neutropenia Dose limiting side effect – causes early discontinuation of treatment often Occurs > 7 days of tx Thrombocytopenia Nephtrotox
cyclovir monitoring parameters SCR for all and CBC for val and ganciclovir
Acyclovir and valacyclovir place in therapy First line treatment for HSV and VZV Oral acyclovir dosed 4 xs daily Valacyclovir dosed BID – better compliance
Famciclovir place in therapy Oral option for HSV
Penciclovir place in therapy Topical option for HSV 1 ***no topical treatments have shown dramatic impact on duration of blisters/ulcers (Abreva – docosanol, Zovirax – acyclovir
Ganciclovir and valganciclovir place in therapy First line for CMV or resistant HSV and VZV
Foscarnet MOA, PK/PD MOA: DNA inhibitor PK D – medium E – renal
Foscarnet Adverse Reactions Narrow therapeutic range Nephrotoxicity Azotemia, protenuria, ATN ATN – acute tubular necrosis Dose limiting ADR Occurs > 7 days of treatment Electrolyte chelator of divalent cations Mg, K, Ca, P CNS – HA, seizure, hallucinations
Foscarnet Monitoring SrCr CBC Chem 7, BMP, renal panel Electrolytes – Ca, Mg, P
Foscarnet Place in Tx CMV infections when: Ganciclovir resistant Ganciclovir induced-neutropenia Treatment of resistant herpes viruses HHV 6, 7
Cidofovir MOA, PK Inhibits DNA synthesis PK D – medium E – renal
Cidofovir Adverse Reactions Nephrotoxicity Proteinuria, azotemia, glycosuria, metabolic acidosis Contraindicated in CrCl < 55 ml/min Neutronpenia
Cidofovir monitoring SrCr CBC
Cidofovir Place in Tx CMV infections when: Resistant to ganciclovir Ganciclovir induced-neutropenia Treatment of resistant herpes viruses HHV 6, 7
Created by: btrain67



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