Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
102 Cards in this Set
- Front
- Back
|
What are some aminopenicillins? |
Ampicillin (parenteral, PO) Amoxicillin (PO) |
|
|
What is the spectrum of activity of aminopencillin? |
gram positive gram negative cocci non-beta- lactamase producing anaerobes (just like PCN G) AND increased activity against: enterococcus, select gram neg. organisms like e.coli, H influenza, salmonella, proteus mirabilis |
|
|
What are the clinical uses of Aminopenicillin? |
infections caused by:
- Strep B (pharyngitis, tonsillitis, otitis media, sinusitis) - Enterococcus (endocarditis) and listeria (bacteremia/meningitis) - Prophylactic for neonatal group B strep disease and rheumatic fever |
|
|
what are some extended spectrum penicillins? |
Ticarcillin (parenteral) Piperacillin (parenteral) |
|
|
what is spectrum of activity of extended spectrum penicillin? |
it has the activity of aminopenicillin with expanded gram negative activity (ie. enterobacter, providencia, morganella, pseudomonas aeruginosa) |
|
|
What are clinical uses of extended spectrum penicillins? |
- gram negative infections c/b enterobacteria and P. aeruginosa (ie. bacteremias, Resp tract infections, intra-abdominal infection, UTI)
- Empiric therapy in pt with fever and neutropenia |
|
|
What is the function of B-lactamase inhibitors? |
-B-lactamases split the B-lactam bond that is required for activity.
-The B-Lactam inhibitor mimics/copies the B-lactams, binds to the enzymes, and inhibits their actions, thus expanding the spectrum of parent B-lactam antibiotic (to kill the organism) |
|
|
What are some combinations of B-lactam and B-lactamase inhibitors? |
- Amoxicillin/clavulanic acid (Augmentin) (PO) - Ampicillin/sulbactam (Unasyn) (IV) - ticarcillin/clavulinic acid (Timentin) (IV) - Piperacillin/tazobactam (Zosyn) (IV) |
|
|
What is the spectrum of activity of B-lactam/B-lactamase inhibitor combinations? |
- largely depends on the parent B-lactam - gram +, gram -, and anaerobic organisms - adds activity against B-lactamase producing organisms (ie. e. coli, H. influenza, m. cattarhalis, staph aereus) - broad spectrum agents - DOES NOT improve activity against MRSA, enterococci, streptococci |
|
|
what are the pharmacokinetics of penicillins? (Absorption and Distribution) |
Absorption - very variable, most are incompletely absorbed - dicloxacillin, ampicillin, amoxicillin are more acid-stable - PCN VK absorbed best on an empty stomach
Distribution - very well distributed into most body tissues - not optimal penetration into eye, brain, CSF or prostate in absence of inflammation - most are excreted by kidneys (high urinary concentration) - cross the placenta (Category B) |
|
|
what are the pharmacokinetics of penicillins? (Metabolism and Excretion) |
Metabolism - only semisynthetic PCNs are hepatically metabolized and excreted in bile. The rest are renal.
Excretion - rapidly excreted by the kidney (short half-lives, renal tubule secretion and glomerular filtration, dose should be adjusted in pt w/ renal dysfunction) - Probenecid: increase concentrations by blocking renal tubular secretion |
|
|
What are the adverse effects of penicillin? |
- hypersensitivity (anaphylaxis, rash) (this is the most common ADE) - increased/loose stool (diarrhea) - interstitial nephritis (rare) - CNS effects (seizures at high doses) - increased liver enzymes (mostly common w/ semi-synthetic PCNs) - high sodium load (PCN G, ticarcillin. caution in HF pt) - thrombocytopenia; decreased platelet aggression - thrombophlebitis when given IV/peripheral line |
|
|
How are the Cephalosporins' spectrum of activity classified? |
the spectrum of activity is classified by generation and there are 4. - 1st generation is most narrow and treats Gram + organisms - 4th generation has the broadest spectrum and treats Gram - organisms. - In general, compared to PCNs, cephalosporins are more stable to B-Lactamases and thus have a broader spectrum of activity |
|
|
What is the spectrum of activity of the Cephalosporins? |
- they have NO activity against: Enterococci, Listeria monocytogenes, and MRSA
- Mechanism of Resistance: destruction by beta-lactamases (they interfere with the cell wall building activity of bacteria by causing it to swell and burst) |
|
|
What are the pharmacokinetics of the cephalosporins? |
Absorption - varies but well-absorbed (more acid-stable compared to PCNs; can be taken on empty stomach) Distribution - Variable distribution and protein binding Excretion - via glomerular filtration and tubular secretion - high urinary concentrations - ceftriaxone and cefoperazone are exceptions (biliary) - Probenecid: increased conc by blocking renal tubule secretion - Variable half lives
|
|
|
What are the clinical uses of Cephalosporins? |
- 1st Generation: skin/soft tissue infection, UTI, surgical prophylaxis
- 2nd: skin/soft tissue infection, UTI, respiratory tract infection (cefuroxime works only for Resp infection), cefoxitin, cefotetan: OB/GYN, intra-abdominal/pelvic infections
- 3rd/4th: treat nastier infections: resp tract infection c/b S. pneumoniae, meningitis, UTI, intra-abdominal infection, pseudomonal infection, N. gonorrhoeae |
|
|
What are the adverse effects of cephalosporins? |
Hypersensitivity, painful IM administration, diarrhea, interstitial nephritis, CNS effects (seizures at high dose), biliary sludge, pseudolithiasis |
|
|
What is the spectrum of activity of Monobactam (Aztreonam)? |
Monobactam (Aztreonam) - only treats Gram - organisms such as enterobacteria or P. aeroginosa - does NOT treat Gram + or anaerobes |
|
|
What are the pharmacokinetics and clinical uses of Aztreonam? |
- Used IV only - Distribution: widely distributed, adequate CSF concentrations with inflamed meninges - Excretion: primarily renal; half-life: ~2 hrs - Pregnancy Category B - Adverse effects: rash is most common; some GI effects |
|
|
What should you know about the safety of Aztreonam? |
- Can be safely administered to patients with hypersensitivity to PCN or other B-lactams
- Gram negative coverage in pt with PCN allergy
- Gram negative coverage for various infections: UTI, resp tract, intra-abdominal infection, skin/soft tissue infection, meningitis, and covers p. aeruginosa |
|
|
What are the 4 carbapenems? |
- Imipenem (primaxin) - meropenem (merrem) - doripenem (doribax) - ertapenem (invanz) |
|
|
What is a key point to know about the carbapenems? |
They are used to treat serious infections caused by a wide range of bacteria.
Monitor for GI effects, serious diarrhea, dizziness, superinfection. |
|
|
what is the spectrum of activity of the carbapenems? |
- Often reserved for severe, antibiotic-resistant infections - gram +, gram -, and anaerobes - broadest activity/spectrum of all the beta-lactams (except ertapenem bc it lacks activity against p. aeruginosa, acinetobacter) - stable to most B-lactamases - no activity against MRSA, enterococcus faecium
|
|
|
What are the pharmacokinetics of the carbapenems? |
- given IV, IM only
Distribution: adequate penetration into inflamed meninges
Excretion: primarily renal (need renal dose adjustment due to seizure potential); half lives differ: average is 1-4 hours |
|
|
What should you know about the safety of carbapenems?
what is their pregnancy category? what are their ADEs? what kind of drug interactions do they have? |
- Pregnancy Category B: Mero, Erta, Dori Category C: Imi
- ADE: hypersensitivity, avoid in pt w/ PCN allergy, seizures, diarrhea inc. pseudomembranous colitis, N/V
- Drug Interactions: eleptogenic agents (ie tramadol, -quinolones) Valproic acid (increases seizure risk) |
|
|
What are some clinical uses for Carbapenems? list & explain three types of infections |
- serious and life threatening infections: very broad spectrum, bacteremia, sepsis, hospital assoc pneumonia, intra-abd infection, febrile neutropenia, Gram - meningitis
- polymicrobial infections: usually reserved for more resistant organisms. Ertrapenem is more narrow spectrum and may be useful for UTI, skin/soft tissue infection, pneumonia, bone/joint infection, GYN infection - suspected resistant organisms |
|
|
What does it mean when a B-lactamase enzyme hydrolyzes the B-lactam ring? |
It means it goes through a process of breaking down or splitting the bond of the B-lactam ring |
|
|
which of the following has the most gram- negative activity? A. Ceftriaxone (3rd generation IV ceph) B. Cefazolin (1st generation IV ceph) C. Cefuroxime (2nd generation IV/PO ceph) D. Cephalexin (1st generation PO ceph) |
A. Ceftriaxone (3rd generation IV ceph) |
|
|
Which of the following is the most important adverse effected associated with carbapenems? A. nephrotoxicity B. GI distress C. seizures D. bone marrow suppression |
C. seizures |
|
|
which of the following beta-lactams has the broadest spectrum? A. ampicillin/sulbactam (unasyn) B. cefazolin (1st generation ceph) C. penicillin D. imipenem (carbapenem) |
D. imipenem (carbapenem) |
|
|
Vancomycin: mechanism of action which stage does vancomycin interefere with? is vaccomycin bacteriostatic or bactericidal? |
glycopeptide antibiotic mechanism of action: - inhibits cell wall synthesis by inhibiting the second stage of the peptidoglycan synthesis (elongation) - beta- lactams different in that they inhibit 3rd stage - bactericidal activity |
|
|
vancomycin: spectrum of activity is it considered narrow or broad spectrum? it is the drug of choice for which infamous bacteria? |
gram positives only (Staphylococci, Streptococci, Enterococci) considered a narrow spectrum agent bc it only covers staph and strep but covers the spectrum of these bacteria
considered the drug of choice for MRSA
|
|
|
vancomycin: mechanisms of resistance what are the two main mechanisms vancomycin has for resistance? |
- alteration of the D- alanyl-D-alaine target - increased thickness of cell wall |
|
|
vancomycin: mechanisms of resistance alteration of the D-alanyl-D-alanine target |
enterococci (VRE) - D-alanyl-D-lacate or D-alanyl-D-serine - bind vancomycin poorly - mediated by the van gene |
|
|
vancomycin: mechanisms of resistance increased thickness of the cell wall |
- "trapping" of vancomycin - more prevalent with Staphylococci - "intermediate" susceptibility to vancomycin (VISA)
VISA= vanco intermediate staph aureus |
|
|
vancomycin pharmacokinetics/pharmacodynamics absorption |
poorly absorbed after oral administration oral administration produces high levels in gut lumen only use oral for treatment of c. diff for example because you will not get to the GI system with IV cannot use PO to treat systemic infection ONLY IV for systemic infection |
|
|
vancomycin pharmacokinetics/pharmacodynamics distribution |
distributes widely into various body fluids, including CSF with inflamed meninges it's a large molecule so once the meninges are not inflamed and gaps are smaller it cannot get in ~ 0.7 L/kg (total body water) - protein binding ~30- 55% - IV does not distribute to the GI tract |
|
|
vancomycin pharmacokinetics/pharmacodynamics excretion |
primarily via the kidney - glomerular filtration - dose adjust in patient with kidney dysfunction not removed effectively by conventional HD, yes with CRRT
is NOT removed via dialysis |
|
|
vancomycin pharmacokinetics/pharmacodynamics is it bactericidal or bacteriostatic? is it time or concentration dependent kill? |
- bactericidal - time dependent killing exposure above MIC |
|
|
vancomycin pharmacokinetics/pharmacodynamics therapeutic drug monitoring when do you take trough levels? when do you take peak levels? when are optimal troughs? |
- trough concentrations: blood level prior to the next dose . usually just do troughs - peak levels (after administration of the drug) are not usually helpful. only do peaks when pt has osteomylitis or CNS infection - optimal troughs 10-20 mcg/mL closer to 15-20 for severe infection and/or if MIC 2 mcg/mL |
|
|
vancomycin clinical uses (3) |
1. resistant gram positive infections 2. gram- positive coverage in patients with PCN- allergy or intolerance 3. Clostrium difficle- associated diarrhea |
|
|
vancomycin clinical uses 1. resistant gram positive infections
|
- MRSA, methicillin- resistant S. epidermidis (MRSE) - PCN resistant S. pneumoniae |
|
|
vancomycin clinical uses 2. gram- positive coverage in patients with PCN- allergy or intolerance |
treatment surgical prophylaxis |
|
|
vancomycin clinical uses 3. Clostrium difficle- associated diarrhea what is an alternative to? |
PO ONLY IV does not achieve adequate gut concentrations alternative to metronidazole |
|
|
vancomycin safety what pregnancy category is it? ADE |
pregnancy category C - "red man syndrome" - nephrotoxicity - ototoxicity - neutropenia - skin rash |
|
|
vancomycin safety: ADE "red man syndrome" |
- infusion-related reaction - erythematous rash of head, face, neck, upper trunk with hypotension - histamine- mediated and related to rate of infusion decreased rate of infusion and/or administer antihistamine usually administer 1 g vancomycin over 1 hour - not an allergic reaction! |
|
|
vancomycin safety: ADE nephrotoxicity |
- associated with impurities in early preparations - now see w/ high dose and/or when used with other nephrotoxins
nephrotoxicity used to be attributed to impurities but now have to use higher doses as bugs get smarter and so have higher troughs-- can cause renal damage |
|
|
vancomycin safety: ADE otoxticity |
associated with very high peak concentrations |
|
|
upper respiratory tract infections |
- pharyngitis - otitis media - sinusitis - atypical pathogens |
|
|
upper respiratory tract infections: atypical pathogens (3) |
1. Legionella pneumophila: pneumonia 2. Mycoplasma pneumoniae: pharyngitis, bronchitis, pneumonia 3. Chlamydia pneumoniae: pharyngitis, sinusitis, bronchitis, pneumonia |
|
|
streptococcus pneumoniae: describe the bacteria |
gram-positive, alpha- hemolytic streptococcus |
|
|
streptococcus pneumoniae: what does it cause? |
- pneumonia - sinusitis - AOM - meningitis - bacteremia - osteomyelitis - septic arthritis - endocarditis - peritonitis - brain abscess
a lot of bugs can cause CNS infections |
|
|
streptococcus pneumoniae: where is it in normal flora? |
normal flora of nasopharynx in 5-10% of healthy adults, 20-40% in kids |
|
|
streptococcus pneumoniae: what does it have increasing resistance to? |
increasing resistance to penicillin alteration in penicillin- binding protein - no benefit of beta- lactamase inhibitor need higher doses of PCN/amoxicillin or alternative agents (eg 3/4th generation cephs, quinolone, vancomycin) |
|
|
pharyngitis: what is it usually? |
usually viral: - rhinorrhea - cough - hoarseness - conjunctivitis - diarrhea
|
|
|
pharyngitis: what if it's a bacteria? what is an exception? |
most bacterial cases are self-limiting BUT exception is group A strep - Strepococcus pyogenes (5-15%) - associated with rheumatic fever
|
|
|
pharyngitis: is susceptible to what? |
susceptible to penicillin > penicillin VK or amoxicillin suspension in children - penicillin G benzathine IM x 1 dose also an option |
|
|
Acute Otitis Media (AOM) what's the most common indication? what kind of bacteria are involved? |
the most common indication for antibiotic prescribing - Streptococcus pneumoniae (30-35%) - Haemophilus influenzae (20-25%) - Moraxella catarrhalis (10-15%) |
|
|
otitis media: - definition - 4 major classes |
inflammation of the middle ear 1. Acute Otitis Media (AOM) 2. Otitis Media with Effusion (OME) 3. Persistent Otitis Media 4. Recurrent Otitis Media |
|
|
otitis media: AOM (3) |
1. history of acute onset of signs & symptoms 2. presence of middle- ear effusion 3. signs & symptoms of inflammation |
|
|
otitis media: OME (3) |
1. chronic otitis media 2. presence of middle-ear effusion 3. few or no clinical manifestations of infection |
|
|
otitis media: Persistent Otitis Media (2) |
1. presence of AOM beyond 6 days of therapy 2. AOM recurrence within a few days after treatment discontinuation |
|
|
otitis media: Recurrent Otitis Media (2) |
1. 3 or more episodes of OM within a 6 month period 2. 4 or more episodes of OM within a 12 month period |
|
|
otitis media: risk factors - non- preventable - preventable |
risk factors 1. non-preventable - gender, ethnicity, family history, socioeconomic status, siblings - anatomic abnormalities, cochlear implants, immunodeficiency 2. preventable - social contacts, tobacco smoke exposure, environmental - bottle feeding, extended pacifier use |
|
|
otitis media: common causes (2) |
1. allergic: fall & winter seasonal allergies 2. viral: respiratory syncytial virus (RSV), Influenza A & B, Adenovirus |
|
|
otitis media: common pathogens (3) |
1. Streptococcus pneumoniae (25-50%) 2. Non-typeable Haemophilus influenzae (15-20%) 3. Moraxella catarrhalis (3-20%) |
|
|
otitis media: first line drug of choice |
amoxicillin |
|
|
otitis media: second line drugs in patients that do not respond |
amoxicillin/clavulanate 2nd or 3rd generation cephalosporin 70% of H. influenzae and 100% catarrhalis produce beta- lactamase |
|
|
OM: 2004 AAP AAFP Guidelines: Recommendation 1 |
clinicians should confirm a history of acute onset identify signs of middle-ear effusion evaluate for the presence of signs and symptoms of middle- ear inflammation |
|
|
OM: 2004 AAP AAFP Guidelines: Recommendation 2 |
if pain is present, recommend treatment to reduce pain |
|
|
OM: 2004 AAP AAFP Guidelines: Recommendation 3 |
observation for 28-72 observation without use of antibacterial agents in a child with uncomplicated AOM is an option for selected children based on diagnostic certainty, age, severity, assurance of follow up - observation 6 month - 2 year old if non- severe and uncertain dx - observation over2 years if non-severe, certain or uncertain dx
if a decision is made to treat with an antibacterial agent, the clinician should prescribe amoxicillin 80-90 mg/kg/day for most kids |
|
|
OM: 2004 AAP AAFP Guidelines: Recommendation 4 |
- if the patient fails to respond to the initial management option within 48-72 hours, AOM must be confirmed excluding other causes of illness - if confirmed in the patient initially managed with observation, the clinician should begin antibacterial therapy - if the patient was initially managed with an antibacterial agent, the clinician should change the antibacterial agent |
|
|
OM: 2004 AAP AAFP Guidelines: Recommendation 5 |
clinicians should encourage the prevention of AOM through reduction of risk factors |
|
|
OM: 2004 AAP AAFP Guidelines: Recommendation 6 |
there are no recommendations for complementary and alternative medicine (CAM) for treatment of AOM are made based on limited and controversial data |
|
|
amoxicillin & amoxicillin/clavulanic acid what is it used for? what is the preferred dose for kids? |
amoxicillin is the first line for AOM preferred dose for kids is 90 mg/kg/day |
|
|
amoxicillin & amoxicillin/clavulanic acid what is it effective against? what are the formulations (give examples) |
effective against beta lactamse producing strains of H. influenzae and M. catarrhalis
examples of formulations 1. augmentin ES 600 mg amox/ 42.9 mg clav acid per 5 mL) 2. AUGMENTIN 400 mg 3. Agumentin 125 3. Agumentin 250 |
|
|
amoxicillin & amoxicillin/clavulanic acid dosage |
keep clavulanic acid dosage < 10 mg/kg/day 90 mg/kg/day amox + 6.4 mg/kg/day clav
clav acid itself causes GI upset and diarrhea, give the least amount as possible |
|
|
otitis media: treatment cefdinir, cefuroxime, cefpodoxime dose: alterative: non- resistant: |
dose: all are Q12h, all for 5-10 days alterative for non-anaphylactic pencillin allergy non- resistant S. pneumoniae, Haemophilus, Moraxella |
|
|
otitis media: treatment ceftriaxone dose: alterative: coverage: |
dose: 50 mg/kg/day IM once a day x 1- 3 days alterative for penicillin allergy in severe infection coverage: S. pneumoniae, Haemophilus, Moraxella |
|
|
otitis media: treatment azithromycin dose: alterative: coverage: |
otitis media: treatment azithromycin dose: "huge" single dose or "high dose" x3 or 5 day regimen alterative for anaphylactic (type 1) penicillin allergy coverage: non-resistant S. pneumoniae, H. flu, Moraxella atypicals |
|
|
otitis media: treatment clindamycin dose: alterative: coverage: |
otitis media: treatment clindamycin dose: Q6-8H alterative for penicillin allergy after clinically defined treatment failure with other antimicrobials coverage: S. pneumoniae, anaerobes |
|
|
acute bacterial sinusitis why does it happen? is it viral or bacterial? symptoms? |
- inflammation from viruses, allergy, pollution, or other irritation - viral 20- 200x more common than bacterial - sx > fever, facial swelling, maxillary tooth or facial pain, purulent nasal discharge |
|
|
acute bacterial sinusitis causes? drugs of choice |
S. pneumoniae, H. influenzae, M. catarrhalis drugs of choice: Amoxicillin --> amoxicillin/clavulanate |
|
|
Acute Bacterial Meningitis (ABM) cause |
inflammation of the membranes surrounding the brain & spinal cord, including the dura, arachnoid & pia matter
extends throughout the subarachnoid space around the brain, spinal cord, and ventricles |
|
|
Acute Bacterial Meningitis (ABM) risk factors |
- extremes of age - crowded conditions - sinusitis - otitis media - CSF leak - CSF shunt - recent neurosurgical procedure - brain abscess - terminal complement deficiency - splenectomy - sickle cell disease - alcoholism, cirrhosis |
|
|
Acute Bacterial Meningitis (ABM) presentation |
- headache, fever, meningismus + altered MS - nuchal rigidity: stiff neck is a problem of forward flexion only; resistance to lateral flexion, rotaion, or extension must be due to some other etiology - patterns of presentation - purpura, petechiae associated with N. menigitidis - seizures occur in 20-30% - kerning sign: flex knee & hip to 90 then extend to knee --> pain in hamstrings - brudzinski sign: flexing neck --> involuntary hip & knee flexion |
|
|
Acute Bacterial Meningitis (ABM) patterns of presentation |
- insidious development of symptoms over 1 or several days - acute, fulminant disease over several hours |
|
|
ABM: pathophysiology & risk |
- pathogens reach the CNS either by hematogenous spread or direct extension - virulence factors - once bacteria reach CSF they multiply quickly due to lack of host defenses - gram stain (+) in 60-90% - culture (+) in 70-85% - false (-) may occur in partially treated patients |
|
|
ABM: pathophysiology & risk virulence factors |
- IgA proteases allow bacteria to adhere to nasopharyngeal mucosa - capsule inhibits phagocytosis & complement- mediated bactericidal activity |
|
|
ABM: pathophysiology & risk gram stain (+) in 60-90% |
in patients who received an antibiotic 40-60% (+) |
|
|
ABM: pathophysiology & risk culture (+) in 70-85% |
in patients who received an antibiotic 40-60% (+) |
|
|
ABM: lumbar puncture if dx is certain? if dx is uncertain? |
- if DX highly suspect, do CSF & blood cultures before neuro-imaging - if DX uncertain, repeat CSF in 8- 12 hours |
|
|
ABM: pathophysiology & risk patients with neuro findings or papilledema brain abscesses? |
usually have dx other than ABM LP performed after imaging!
with brain abscess, subdural empyema, subdural hematoma or cerebral hemorrhage, LP may be catastrophic |
|
|
ABM: pathophysiology & risk LP contraindications |
underlying skin diagnosis significant bleeding disorder |
|
|
ABM: pathophysiology & risk WBC? % polymorphonuclear leukocytes (PMN) glucose protein why may protein be high? |
WBC > 1000 (vs 0-5) % PMNs 90 (vs 0-15) glucose < 40 (vs 45-65) protein > 150 (vs 20-45) protein may be a bit higher of traumatic brain injury (b/o RBCs in CSF) |
|
|
ABM: microbiology |
mimics what is causing the URI |
|
|
ABM: treatment what do you give and when? LP? |
- antibiotics within 30 minutes of presentation - vancomycin + ceftriaxone + ampicillin - if LP must be must be delayed, obtain a blood culture and immediately start antibiotics |
|
|
ABM: treatment what should therapy cover? |
therapy should cover: - S. pneumoniae - H. influenzae - N. meningitidis - Listeria monocytogenes |
|
|
ABM: treatment if there is significant immunosuppression? |
h/o CSF leak, recent neurosurgery, head trauma, potential line sepsis, therapy should also cover gram negative rods and S aureus |
|
|
ABM: treatment when is LP repeated? |
only when pt fails to improve |
|
|
meningitis (community-acquired) age: 19-50 etiology: empiric treatment: |
meningitis (community-acquired) age: 19-50 etiology: S. pneumoniae, N. meningitidis empiric treatment: cefotaxime/ ceftriaxone/meropenem + vancomycin |
|
|
meningitis (community-acquired) age: >50 years, alcoholism, impaired immunity etiology: empiric treatment: |
meningitis (community-acquired) age: > 50 years, alcoholism, impaired immunity etiology: S. pneumoniae, Listeria monocytogenes empiric treatment: Ampicillin + cefriaxone/ cefotaxime + vancomycin OR
|
