1. Learn mechanism of action, use and toxicity of trimethoprim/sulfamethoxazole.
2. Know mechanism of action, use, drug interactions and toxicity of fluoroquinolones.
3. Review use and toxicity of nitrofurantoin.
4. Be aware of use and toxicity of six TB drugs.
Structurally similar to folic acid.
Selective inhibitor of dihydrofolate reductase.
Weak base which becomes trapped in acidic environments e.g. prostate/vagina. FOr this reason can be used alone for UTI prostatic infections.
Trimethoprim inhibits bacterial dihydrofolic acid reductase (which converts dihydrofolic acid to tetrahydrofolic acid) the pathway of purine synthesis and thus DNA synthesis.
TMP and SMX are synergistic, blocking sequential steps in folate synthesis increasing bacterial activity.
Antimetabolite-drug that through chemical similarity is able to interfere with endogenous compound in cellular metabolism.
Sequential blockade-combined action of two drugs that inhibit sequential steps in pathway of bacterial metabolism.
Combination is bactericidal!!! = TQ.
Comes in fixed 80:400 mg or 160:800 mg dose. So like high and low dose.
Acetylated or glucuronidated in the liver then excreted in urine.
–Dose reduction in significant renal failure.
Gram positive (MRSA, listeria- even though drug of choice of listeria is ampicillin).
Gram negative (Stenotrophomonas, Haemophilus influenzae, Moraxella catarrhalis).
~30% e. coli resistant to TMP/SMX
—Overproduction of PABA
—Dihydropteroate synthase with low affinity for drug
—Decreased bacterial permeability
Nocardia, pneumocystis (fungi), Toxoplasma (parasite).
– Treatment and prophylaxisMRSA
-Treatment and prophylaxis
-Avoid empiric in complicated UTI since 30% of E. coli is resistant to TMP/SMX.
-Treatment and prophylaxis
-Assume cross-hypersensitivity among sulfa drugs
-Stevens-Johnson: Rash all over body. Very severe, can be fatal.2. Fever
-Anemia, neutropenia, thrombocytopenia. This is due to interference with folate metabolism.-Hemolysis in G6PD deficiency.
–Also displaces methotrexate and warfarin
Hyperkalemia due to blockade of the collecting tubule sodium channel by trimethoprim.
Crystalluria with acid urine with SMX.
TMP decreases the tubular secretion of creatinine. So will have falsely elevated creatine.
Similar to sulfa drugs. Inhibits folate synthesis.
Second line agent for PCP prophylaxis.
Used to treat leprosy.
Causes hemolysis in G6PD deficiency.
It prevents DNA uncoiling.
Synthetic fluorinated analogs of naldixic acid.
Block bacterial DNA synthesis by inhibiting DNA gyrase (gram negative)/topoisomerase IV (gram positive).
Like aminoglycosides, has post antibiotic effect!!! = TQ.
Dose adjustment for decreased creatinine clearance (except moxifloxacin which is metabolized by liver).
-Have to dose adjust for renal dysfunction.
-MSSA sensitive but MRSA tends to be resistant
-E Coli, Salmonella, Shigella, Campylobacter
-Resistance issues: campylobacter, gonorrhea
–NB: there is cross resistance
You can use them for a wide variety of conditions:
-Salmonella, shigella, toxigenic e. coli campylobacter
-Conveniently also covers legionella.Note this is a fluoroquinolone.
has anaerobic activity!!!! = TQ.Not indicated for UTI.
Headache, dizzy, insomnia.
Ciprofloxacin is most common cause of c. difficile. Also clindamycin.
Absorption inhibited by di/trivalent cation antacids (Calcium, Magnesium, Aluminum).
Also iron, zinc, milk.
Ciprofloxacin inhibits metabolism of theophylline.
Tendon rupture (risk factors age, renal insufficiency, corticosteroids).Avoid in children and pregnant women to avoid damage of growing cartilage.
Bacterostatic and cidal for many gram positive and negative bacteria but pseudomonas resistant as well as many proteus species.
No systemic levels. So will only have the drug in the urine!!! = TQ.
Drug concentrates in urine so can only use for simple UTI not in patients with pyelonephritis. Since the ABx doesn’t go into the blood.
Can use as treatment for cystitis since limited to the bladder.
Contraindicated in renal insufficiency.
Usage: UTI or UTI prophylaxis.
Adverse effect: pulmonary hypersensitivity.
59 YOF presents to urgicare with 4 day history of frequent and painful urination. She has had fever chills and flank pain for 2 days but no vomiting. Urine dip positive leukocyte esterase. Urine culture pending. She has had three UTIs over the past year treated with TMP/SMX. She has osteoporosis and takes a calcium supplement daily. The decision is made to treat her with an oral antibiotic.
Given her history what would be a reasonable empiric antibiotic choice?
Depending on the antibiotic choice are there potential drug interactions she should be counseled on?
-The question is ciprofloxacin vs. TMP/SMX.Depending on the antibiotic choice are there potential drug interactions she should be counseled on?
-Want to use ciprofloxacin, but need to have patient stop taking calcium for the duration of the treatment since ciprofloxacin interacts with calcium.
Isoniazid (INH) (cidal)
Pyrazinamide (PZA) (static)
Ethambutol (ETB) (static)
Mycobacteria grow slowly and thus antibiotics that are most active against growing cells are ineffective.
The lipid-rich mycobacterial cell wall is impermeable to many agents.
Mycobacteria are intracellular pathogens.
Mycobacteria easily develop resistance.
For this reason usually give four drugs at the same time.
Inhibits synthesis of mycolic acids (essential component of mycobacterial cell wall).
More rapid clearance by rapid acetylators
-Proportion of fast acetylators higher among those of Asian origin including Native Americans.
INH inhibits metabolism of carbamazepine, phenytoin (both of these are seizure drugs) and warfarin.
Always given with pyridoxine (vit. B6). Deficiency in vit. B6 can cause neuropathy.
Used to treat active TB (in combination with other drugs) or latent TB (as a solo agent for nine months).
-Mild increased asymptomatic transaminase increase in 10-20% of patient which does not require discontinuation of drug.
-Hepatitis in 1% with nausea, vomiting, jaundice; can be fatal.
-Risk greater in alocholics and possibly in pregancy/postparrtum.
–0.3% age 21-35
–1.2% of age 36-49
–2.3% of age >50Peripheral neuropathy and CNS toxicity:
-More likely to occur in slow acetylators, malnourished, alcoholic, diabetes, AIDS, uremia.
-Neuropathy due to relative pyridoxine deficiency.
-Turns urine, sweat, tears, contacts orange/Red.
-Drug interactions!!!-induces CYP450 (Revs up)Mnemonic: urine Red and Revs up.
Uses: Rifabutin similar but less drug interactions than rifampin so used as a substitute in HIV-infected.
Active against gram positive and gram negative cocci, mycobacteria.
-Staphylococcus (eradication of carrier state or osteomyelitis)
-Meningococcal/Haemophilus influenzae carrier (like cipro)
Nonnucleoside reverse transcriptase inhibitors
Ethambutol causes retrobulbar neuritis with red-green color blindness.
Contraindicated in young children since they cannot tell you if they have had change in sight.
Mnemonic E is for eye…
Streptomycin is first line bactericidal IV treatment for tuberculosis. THis is the only IV tx for TB.
-Recall with streptomycin can get ototoxicity and renal toxicity.
Amikacin used more for MDR and atypical mycobacteria.
-M. avium complex (MAC)
-M scrofulaceumClarithromycin often used. Recall this is also used for H. pylori.
A 45 year old homeless man presents to the ED with a two month history of weight loss, fever, night sweats and productive cough. He has lived in homeless shelters and prison. He drinks two pints of hard liquor daily and uses intravenous drugs. CXR shows right apical infiltrate. Patient is placed in respiratory isolation. Sputum shows acid fast bacilli and rapid HIV test is positive.
What drugs should be started for presumptive treatment of pulmonary TB?
Does the patient have a heightened risk of medication toxicity?
How will HIV infection influence his treatment?
-RIPEDoes the patient have a heightened risk of medication toxicity?
-Alcoholic -> liver disease.
How will HIV infection influence his treatment?
-Rifampin interacts with lots of medications, esp. those for HIV meds. So need to check. Could use Rifabutin.
1. Understand the mechanism of action, use, pharmacokinetics and toxicity of aminoglycosides.
2. Be aware of the use and toxicities of other protein synthesis inhibitors.
3. Recall that metronidazole and oral vancomycin treat C. difficile.
Macrolides and clindamycin.
Chloramphenicol, Linezolid and quinupristin/dalfopristin.
Active against gram negative enteric bacteria.
-Gram negative bacteremia.
-In synergistic combination with vancomycin or a penicillin for endocarditis.
Passive diffusion via porin channels through outer membrane.
Active transport across cell membrane into cytoplasm by an oxygen dependent process
–low extracellular pH and anaerobic conditions may inhibit transport.
–Transport may be enhanced by cell well active drugs such as PCN or vancomycin.
Binds to 30S subunit ribosomal protein inside cell and irreversibly inhibits protein synthesis.
This aminoglycosides are bactericidal due to miscoding of the peptide chain. So miscoding, not just blocking.
Minimal oral absorption so typically given IV (except neomycin, which cleanses bowel prior to surgery, not absorbed).
Dose based on weight and creatinine clearance. This makes the drug hard to dose, so people don’t use it often.
Traditionally aminoglycosides given 2-3 times daily in patients with normal renal function.
Partial removal by dialysis so given be given intermittently in dialysis patients for convenience.
Levels must be monitored in patients receiving higher doses for more than a few days or patients with rapidly changing renal function.
Intrathecal or intraventricular needed for high CNS penetration.
Aminoglycosides have concentration dependent killing and a post-antibiotic effect. = TQ.
Increased concentration kill a greater proportion of bacteria and at a more rapid rate vs. PCN/cephalosporins which have time-dependent killing-efficacy is related to time above minimum inhibitory concentration (MIC).
Antibacterial activity persists beyond the time when measurable drug is present. = TQ.
Ototoxic (may be irreversible). Hearing loss and balance problems.
Typically used in combination with other antibiotics especially beta lactams (e.g. treatment of pseudomonas, listeria or enterococcus).
Gram negative (sepsis, antimicrobial resistance).
Endocarditis (streptococcal, enterococcal, staphylococcal).
Covers staphylococcus and gram negatives (pseudomonas!!! = TQ, proteus, enterobacter, klebsiella, serratia, stenotrophomonas).
No anaerobic activity! = TQ.
Synergistic with beta lactams/vancomycin; usually used together with second agent.
Note this an aminoglycoside. It is in fact the most widely prescribed.
Note this an aminoglycoside.
Better against pseudomonas!!! = TQ.
E. faecium is resistant to tobramycin.
Available as inhaled solution used for pseudomonas lung infections in cystic fibrosis patients.
Streptomycin is first line IV treatment for tuberculosis!!! = TQ.
15% of gentamicin resistant enterococcus will be sensitive to streptomycin.
Note this an aminoglycoside.
Note this an aminoglycoside.
Used in gram negative infection resistant to gentamicin/tobramycin. = TQ.
–Amikacin often is resistant to plasmid-mediated inactivating enzymes (group transferases) that inactivate gentamicin/tobramycin.
Treats mycobacterial infections (atypical and multidrug resistant) = TQ. So it is like streptomycin.
Neomycin used as topical and bowel prep & hepatic encephalopathy.
Paromomycin is anti-parasitic.
Spectinomycin (similar to aminoglycosides) used to treat GC in PCN allergic but not commercially available.
Enterohepatic circulation results in high concentrations of tetracycline accumulating in the liver and bile.
Tetracycline is eliminated in the urine; others mostly biliary/fecal route.
Usage: MRSA, acne/rosacea, atypical pneumonia/community acquired pneumonia, chlamydia, Lyme disease and other borrelia, rickettsia, malaria prophylaxis, helicobacter pylori, vibrio. The point is that if you acquired it in the outdoors, you can treat it with tetracyclines.
-Demecyclocyline for SIADH (inhibits antidiuretic hormone in the renal tubule).
-Large volume of distribution
-Broad spectrum (characteristic of tetracycline family).
-Covers MRSA, VRE, anaerobes
-excluding Pseudomonas, Proteus, Providencia and Morganella.
Approved for treatment of skin and abdominal infection.
Poor urinary concentration (not for UTI).
Low bloodstream concentration (not for bacteremia).
Chelate with calcium and deposits in growing teeth and bone. Makes teeth yellow/grey. Thus, avoid in children and pregnancy.
Local irritation of gastrointestinal tract/esophageal irritation.
Dizzy, vertigo (with minocycline).
Nausea, vomiting (with tigecycline).
1. Erythromycin (derived from bacteria Streptomyces erythreus).
Semisynthetic derivatives of erythromycin:
Macrocyclic lactone ring, thus the class name macrolide.
Binds to 50S ribosomal RNA.
Active against gram POSITIVE organisms (pneumococci, streptococci, staphylcoccus, corynebacteria), mycoplasma, legionella, chlamydia, bordatella pertussis.
-Used to treat gastroparesis.Hepatotoxicity (particularly estolate).
-Inhibits cytochrome p450 increases theophylline, anticoagulants, cyclosporine.
-Increases digoxin level by increasing bioavailabilty.
Similar to erythromycin except more active against mycobacterium avium complex (MAC).
H. pylori!!!! = TQ.
Similar to erythromycin and clarithromycin but less GI upset and drug interactions.
Given this it is the most commonly used.
Slightly less active against gram positives and slight more active against haemophilus influenzae.
Active against chlamydia!!!!! = TQ, MAC, toxoplasma. These are the atypicals.
Half life is 3 days!
1 gm dose for chlamydia!!! = TQ
1200mg once weekly MAC prophylaxis
Zpak for community acquired pneumonia = TQ
19YOF presents to student health with 2 weeks of foul smelling vaginal discharge. No fever or abdominal pain but reports vaginal bleeding after intercourse. Unprotected vaginal intercourse with two men over past 6 months. Patient missed her last period. Pelvic exam positive for mucopurulent cervical discharge. No cervical motion tenderness. NAAT test sent for GC/CT. Urine pregnancy test sent. Pending results, decision made to treat for GC/CT.
What are the potential treatment options?
How does her potential pregnancy affect treatment decision?
-Ceftriaxone for gonorrhea and doxycycline or Azithromycin.How does her potential pregnancy affect treatment decision?
-No doxycycline to pregnant women due to cation chelating effect.
NOTE: this is NOT a macrolide. It just has a similar name.
A chlorine substituted derivation of lincomycin an antibiotic elaborated by streptomyces lincolnensis.
Binding site on 50s ribosome is identical to that of erythromycin.
-Prevents production of bacterial toxins. Such as in group A step.
Good bone penetration
Skin and soft tissue infections (streptococcus and MRSA)
-Gynecologic (pelvic abscess, septic abortion, bacterial vaginosis)
Second line for PCP or toxoplasmosis Rx
RashPredisposes to getting C. difficile.
Can get pseudomembranous colitis!!! = TQ.
What is the mechanism of chloramphenicol?
What is the spectrum of use?
Binds to 50S ribosomal subunit.
Used (cheap, OTC) in the developing world.
Broad spectrum, used for typhoid fever and meningitis.
Toxicity of idiosyncratic, irreversible and possibly fatal aplastic anemia!!! = TQ.
Gray baby syndrome (when higher doses of drug accumulates infants with vomiting, flaccidity, hypothermia and shock).
Inhibits protein synthesis, unique, binds to 23S ribosomal RNA of 50S subunit.
No cross resistance with other drug classes!!!! = TQ.
Active against gram positive organisms including staphylococci, streptococci, enterococci, gram positive anaerobic cocci and gram positive rods and MTB.
Used for vancomycin resistant e. faecium and MRSA.
PNA or skin infections.
Key point: it is used for resistant bacteria.
Thrombocytopenia, especially after two weeks administration (also anemia, neutropenia). It is then pancytopenia.
Serotonin syndrome with SSRI. Will cause more serotonin.
Optic neuritis, neuropathy.
Active against gram positive cocci including resistant streptococcus, pneumococcus, MSSA/MRSA and e. faecium. So used for resistant bacteria.
Same ribosomal binding site as macrolides and clindamycin (50S).
E. fecalis is intrinsically resistant probably because of an efflux pump.
Used for Rx of vancomycin resistant e. faecium (VRE) (bacteriostatic).
Infusion related toxicity- need central line.
Mechanism of action: disruption of electron transport chain.
Metabolized in liver.
Disulfiram/antabuse effect. -Can’t drink alcohol with it.
Antiprotozoal and antibacterial/anerobic activity.
Clostridium difficile!!!! = TQ
Brain abscess (in combination with ceftriaxone, which has good CNS penetration).
1. Understand beta-lactams and vancomycin are bactericidal by disrupting bacterial cell wall synthesis.
2. Know beta-lactams are a group of antibiotics with similar chemistry and side effects.
3. Recognize penicillins, cephalosporins, carbapenems and aztreonam as beta-lactams.
4. Distinguish among beta-lactams on the basis of antimicrobial activity, pharmacokinetics and adverse effects.
4. AztreonamBeta-lactam family shares:
-Mechanism of action
-Pharmacologic characteristics. e.g. most excreted in urine.
-Immunologic characteristics. If allergic to one, are allergic to all of them.
-Extended spectrum penicillins
All beta lactam antibiotics inhibit bacterial growth by interfering with the transpeptidation reaction of bacterial cell wall synthesis.
Beta lactam antibiotics bind to penicillin binding proteins.
Penicillin-binding protein (PBP) is an enzyme needed for cell wall synthesis located in the bacterial cytoplasmic membrane.
All Beta Lactams are Bactericidal.
Mnemonic: If it rhymes with ‘cillin, I know it’s killing.
Beta lactam antibiotics kill bacterial cells only when they are actively growing and synthesizing cell wall.
Recall: Bacteriostatic inhibits bacterial multiplication, resumes upon removal of the agent.
Bactericidal kills bacteria, effect is irreversible; the killed organism can no longer reproduce even upon removal of the agent.
1. Inactivation of antibiotic by beta lactamases.
2. Modification of target PBP.
3. Impaired penetration of drug to PBP.
Many hundreds of different beta lactamases.
Some, e.g. those produced by staphylococcus aureus prefer penicillin to cephalosporins (penicillinases) and thus maintain sensitivity to cephalosporins.
Others e.g. extended spectrum beta lactamases (ESBL) hydrolyze both PCN and cephalosporins.
Carbapenems are resistant to hydrolysis by penicillinases and cephalosporinases. So these are broad spectrum.
Altered PBP are basis of methicillin resistance in staphylococcus and penicillin resistance in pneumococci and enterococci.
Resistant organisms produce PBPs that have low affinity of binding beta lactam antibiotics.
Gram negative bacteria have outer cell wall membrane.
Beta lactam antibiotics cross outer membrane and enter gram negative organisms via outer membrane channels (porins).
Absence/decrease of proper channel impairs drug entry (e.g. pseudomonas).
Gram negatives may also produce efflux pump.
Penicillin G and Penicillin V are called natural penicillins because they can be purified directly from cultures of Penicillium mold.
They are susceptible to hydrolysis by beta lactamases.
Spectrum: gram positive organisms, gram negative cocci, and non beta lactamase producing anaerobes.
Ex: Streptococci (pyogenes, viridans).
Ex: Treponema pallidum (syphilis).
-Group A Streptococcal pharyngitis – strep throat.
Penicillin G is intravenous:
-Actinomyces; Clostridium perfringens, tetani; meningococcus; Pasteurella etc.
-Group A Streptococcal pharyngitis
-Erysipelas/CellulitisBenzathine penicillin IM yields prolonged blood levels.
-Daily IM Benzathine penicillin plus probenecid is an alternative treatment for neurosyphilis.
-Blood levels of penicillins can be raised by probenecid which impairs renal tubular secretion of penicillin.
–Probenecid is a uricosuric drugs used in gout.
–Promotes renal clearance of uric acid by inhibiting urate-anion exchangers in the proximal tubule that mediates urate reabsorption.
Nafcillin is the classic example of a semi-synthetic anti-staphylococcal, penicilllinase resistant PCN.
Mnemonic: Use Naf for staph!
Dicloxacillin is oral version of nafcillin.
Methicillin=older version of same type. This drug causes renal toxicity.
Metabolized by the liver and thus do not need to adjust for renal disease!
Drug of choice to treat Staphylococcus that is sensitive to methicillin (MSSA-methicillin sensitive staphylococcus aureus).
-75% of Staph epidermidis are methicillin resistant.
-covers streptococcus but not as good as natural PCN.
Use decreasing due to MRSA (MSSA-methicillin resistant staphylococcus aureus).
Indications: MSSA endocarditis or streptococcal cellulitis.
MRSA=Nafcillin resistant staphylococcus.
-Better activity against gram negatives because enhanced ability to penetrate gram negative outer membrane.
-Inactivated by many beta lactamases. So usually give with sulbactam or clavulanic acid. Or tazobactam for piperacillin.
-AmOxicillin give oral/PO better absorbed than ampicillin
Indications: urinary tract infection, otitis, sinusitis, bites.
Make sure to use for Listeria monocytogenes.
Ureidopenicillins AKA Antipseudomonal Penicillins. So want to use these ureidopenicillins for Pseudomonas infections.
Piperacillin-tazobactam commonly used.
Indication: Hospital-acquired infections.
Mnemonic (P is for pip & pseudomonas)!
5-8% of patents state they have an allergy to penicillin.
1. Have have anaphylaxis (IgE, type 1 hypersensitivity reaction). This includes hives.
2. Can have rash.
-Ampicillin causes rash with patients that have EBV. EBV causes mono.
-Antibiotic associated diarrhea vs. clostridium difficile.
4. Seizure especially with decreased creatinine clearance. All beta-lactam antibiotics can produce seizure.
5. Interstitial nephritis (classically associated with methicillin).
6. Neutropenia (with nafcillin)/hemolytic anemia/thrombocytopenia.
Intravenous (IV) Cefazolin.
Oral (PO) Cephalexin.
Indication: skin infection, surgical prophylaxis (IV)
Streptococcus pyogenes (not enterococcus),
Staphylococcus (not MRSA),
some GNR (some e. coli, klebsiella and proteus mirabilis).Pro Tip: In general, cephalosporins have increasing gram negative activity as generation # increases.
Intravenous (IV) Cefoxitin, Cefotetan, Cefuroxime.
Oral (PO) Cefaclor.
IV surgical/gynecological infections
PO Otitis media
some gram positive cocci, s
ome gram negative rods (e. coli, klebsiella, proteus, haemophilus influenzae)Cefoxitin and cefotetan active against anaerobes e.g. Bacteroides fragilis.
Indication: bacterial meningitis (ceftriaxone/cefotaxime since ceftriaxone has good CSF penetration), gonorrhea.
gram positive cocci (e.g. penicillin-resistant pneumococcus, streptococcus viridans)haemophilus influenzae,
meningococci, gram negative rods (no anaerobes, enterococcus, listeria)
Avoid use with enterobacter due to development of resistance.
More resistant to hydrolysis by chromosomal beta lactamases produced by enterobacter.
Usage: Hospital acquired infections, neutropenic fever.
Cross reactivity 5-10% so need to avoid in patients with a history of anaphylaxis to penicillin.
Cephalosporins that contain a methylthiotetrazole group (cefmandole, cefmetazole, cefotetan, cefoperazone) cause hypoprothrombinemia and bleeding as well as disulfiram/antiabuse effect (this is that you will feel sick when take with alcohol).
Imipenem, meropenem, doripenem, ertapenem.
Imipenem aka “Gorillapenem” because of WIDE spectrum pseudomonas, gram positives, anaerobes (not enterococcus faecium, MRSA/SE, C. diff, Burkholderia, Stenotrophomonas)
Key here is wide spectrum.
All carbapenems are cleared renally.
Treatment of choice for enterobacter.
Indication: febrile neutropenia.
-May cross react with penicillin allergic (10%).-Imipenem may causes seizures especially in patients with renal failure.
Spectrum: Gram negative rods ONLY (klebsiella, serratia, pseudomonas)
Indication: urinary tract infection.
No cross reactivity with other Beta-lactams
Safe in penicillin allergic = TQ.
Vancomycin is a glycopeptide.
Inhibits cell wall synthesis by binding to D-Alanyl-D-Alanine portion of peptidoglycan precursor.
-Vancomycin resistant enterococcus and Staphylococcus aureus have modified D-Ala-D binding site of the peptidoglycan
Bactericidal but less efficient killer than penicillins.
-Staphylococcus aureus, staphylococcus epidermidis, streptococcus (pyogenes, viridans, pneumococcus), clostridium, some enterococcus)Indication: MRSA/E (Staphylococcus aureus or epidermidis), (catheter-related infection), clostridium difficile, meningitis due to highly PCN resistant pneumococci, enterococcus (in synergy with an aminoglycoside).
Clostridium difficile is the only indication for oral vancomycin; otherwise IV is used.
Note: Vancomycin is renally cleared.
-Caused by release of histamine
-Prevented by prolonging infusion time
-Can give antihistamines2. Can cause ototoxicity and nephrotoxicity esp. with aminoglycosides.
-Active against vancomycin-resistant enterococci and staphylococcus aureus
-Can cause myopathy; monitor creatinine phosphokinase
-Inactivated by lung surfactant. So it won’t work in the lung.
-cross-reactivity among them
-that they are bactericidal cell wall agents
-Know that penicillin treats syphilis
-Know that piperacillin covers pseudomonas
-Know ceftriaxone is the core empiric treatment of meningitis and gonorrhea
-Recognize “red man” syndrome