antimicrobial agents cell wall inhibitors. penicillin penicillin is a group of antibiotics derived...
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ANTIMICROBIAL AGENTS
cell wall inhibitors
PenicillinPenicillin is a group of antibiotics derived from penicillium fungi. They include penicillin G, procaine penicillin, benzathine penicillin, and penicillin V. Penicillin antibiotics are historically significant because they are the first drugs that were effective against many previously serious diseases, such as syphilis, and infections caused by staphylococci and streptococci. Penicillins are still widely used today, though many types of bacteria are now resistant. All penicillins are B -lactam antibiotics and are used in the treatment of bacterial infections caused by susceptible, usually Gram-positive organisms.
Chemical structure of penicillins
Penicillin core structure, where "R" is the variable group is responsible for the activity of the drug, and cleavage of the beta-lactam ring will render the drug inactive.
Why are penicillins more effective against gram-positive organisms than gram-negative organisms?
The structure of the bacterial cell wall in gram-positive organisms contains only a layer of peptidoglycans attached to the inner membrane, and leaves the PBPs relatively exposed. In a gram-negative organisms, the drug must enter through pores (porin) in order to reach the inner space between the double membrane and attach to PBPs.
The cell envelope of gram negative bacteria
Mechanism of Action of penicillins Penicillins are bactericidal drugs. They act to inhibit cell wall synthesis by the following
steps:1. Binding of the drug to specific enzymes (penicillin-binding
proteins [PBPs]) located in the bacterial cytoplasmic membrane.
2. Inhibition of the transpeptidation reaction that cross-links the linear peptidglycan chain constitunts of the cell wal.
3. Activation of autolytic enzymes that cause lesions in the bacterial cell wall.
NB: Penicillins exert a bacteriocidal action on growing or multiplying germ.
Resistance to PenicillinsI. Production of b-lactamases This family of enzymes can inactivate penicillins by
hydrolyzing the b-lactam ring The production of b-lactamases is considered the principal
cause of bacterial resistance to b-lactam antibiotics Examples of bacteria that produce b-lactamases are
staphylococcus aureus and many strains of H. influenzae, Neisseria and Pseudomonas
II. The occurrence of modified penicillin-binding sites Modified PBPs have a lower affinity for b-lactam antibiotics, requiring
clinically unattainable concentrations of the drug to effect its
bactericidal activity Example: penicillin resistance in Streptococcus pneumoniae
(pneumococcus) is caused by altered PBPs
III. Decreased permeability to the drug Decreased penetration through the outer membrane prevents the drug
from reaching the target PBP This occurs with G-ve organisms, which have an outer membrane that
limits penetration of hydrophilic antibiotics. This is of particular
relevance in determining the extraordinary resistance of Pseudomonas
aeruginosa to most antibiotics.
Classification of Penicillins
Types of penicillin and their antimicrobial activity
Penicillins (e.g., penicillin G): These have greatest activity against gram–positive organisms, gram-negative cocci, and non-β-lactamase producing anaerobes. They are susceptible to β-lactamase
Antistaphylococal penicillins (e.g., nafcillin): These penicillins are resistance to staphylococcal β-lactamase. They are active against staphylococci, streptococci but not against enterococci, anaerobic bacteria, and gram negative cocci and rods.
Extended-spectrum penicillins (ampicillin and the antipseudomonal penicillins):These drugs retain the antibacterial spectrum of penicillin and have improved activity against gram-negative organisms. Like penicillin, however, they are relatively susceptible to hydrolysis by β-lactamase.
Pharmacokinetics Oral absorption of penicillins varies, depending on their stability
in acid, protein binding and adsorption to food stuffs in the gut. Penicillins can also be given by IV and IM injections. Penicillins are polar compounds and are not metabolized
extensively. They are usually excreted unchanged in the urine via glomerular filtration and tubular secretion; the latter process is inhibited by probenecid (this would prolong serum penicillin levels)
Because renal dysfunction will compromise the elimination of penicillin, dosages may need to be reduced in patients with renal insufficiency.
The plasma half-lives of most penicillins vary from 30 min to 1 hr. Most penicillins cross the blood brain barrier (BBB) only when
the meninges are inflamed.
Clinical Pharmacokinetics Penicillins are poorly lipid soluble and do not cross the
blood-brain barrier in appreciable concentrations unless it is inflamed (so they are effective in meningitis)
They are actively excreted unchanged by the kidney, but the dose should be reduced in severe renal failure
Clinical uses of the penicillins Penicillins are given by mouth or in more severe infections,
intravenously, and often in combination with other antibiotics. Uses are for sensitive organisms. Including for example:
Bactrial meningitis: benzylpenicillin Bone and joint infections: flucloxacillin Otitis media,Bronchitis, Pneumonia,Urinary tract infections: amoxicillin Gonorrhea: amoxicillin (plus probenecid) Syphilis: procaine benzyl penicillin Serious infections with pseudomonas aeruginosa: ticarcillin, pipracillin
treatment with penicillins is some times started empirically, if the likely causative organism is one thought to be susceptible to penicillin, while waiting the results of laboratory tests to identify the organism and determine its antibiotic susceptibility.
Clinical uses of penicillins
1. 1-Narrow-spectrum penicillinase-susceptible agents:
A. Penicillin G is the prototype of a subclass of penicillins that have a limited spectrum of antibacterial activity and are susceptible to beta-lactamases.
Used for therapy of infections caused by common streptococci, meningococci, gram-positive bacilli, and spirochetes.
Most strains of pneumococci are now resistant to penicillins (penicillin-resistant streptococci pneumoniae [PRSP] strains).
Most strains of staphylococcus aureus and a significant number of strains of neisseria gonorrhoeae are resistant via production of beta-lactamase.
B. Penicillin V is the acid resistant form of penicillin which is marketed as oral dosage form.
All oral penicillins are best given on an empty stomach to avoid the absorption delay caused by food.
Penicillin V is less active than penicillin G against Neisseria species. It is satisfactory substitute for penicillin G against Streptococcus pneumonia and S. pyogenes.
It is the first choice in the treatment of odontogenic infections.
C. Procaine penicillin G{ Depot form } (is a form of penicillin which is a
combination of benzylpenicillin and the local anaesthetic agent .This combination is aimed at reducing the pain and discomfort associated with
a large intramuscular injection ) is best suited to the single-dose outpatient treatment of very sensitive organisms (e.g., penicillin-sensitive N. gonorrhea and group A streptococci)
D. Benzathine penicillin is another long-acting preparation given IM. It is used for prophylaxis of rheumatic fever and for treatment of syphilis.
2. Very-narrow-spectrum penicillinase-resistant drugs: Methicillin is the prototype but rarely used owing to its
nephrotoxic potential in addition to Nafcillin and oxacillin.
Their primary use is in the treatment of known or suspected staphylococcal infections.
Methicillin-resistant (MR) staphylococci (S aureus [MRSA] and S epidermidis [MRSE]) are resistant to all penicillins and are often resistant to multiple antimicrobial drugs.
They are resistant to bacterial penicillinase. Nafcillin and the isoxazolyl penicillins (oxacillin,
cloxacillin, dicloxacillin) are lipophilic in nature, with a high degree of efficacy against staphylococcus.
3. Wider-spectrum penicillinase-susceptible drugs:
A. Ampicillin and amoxicillin (aminopenicillins) : These drugs has a wider spectrum of antibacterial activity than penicillin G and have improved activity against gram-negative organisms but remains susceptible to penicillinase.
Their clinical uses are similar to penicillin G as well as infections resulting from enterococci, Listera monocytogenes, Escherichea coli, Proteus mirabilis, Haemophilus influenzae, and Moraxella catarrhalis.
When used in combination with inhibitors of pencillinases (e.g., clavulanic acid), their activity enhanced.
In enterococcal and listerial infections, ampicillin is synergistic with aminoglycosides.
Amoxicillin may be given orally to pediatric and geriatric patients.
B. Piperacillin and ticarcillin (Anti-Pseudomonal Penicillins): These drugs have activity against several gram-negative
rods, including Pseudomonas, Enterbacter, and in some
cases Klesiella species. Most of these drugs have synergistic actions when used with
aminoglycosides in the treatment of systemic Pseudomonas. Piperacillin and ticarcillin are susceptible to penicillinase and
are often used in combination with penicillinase inhibitors
(e.g., tazobactam and clavulanic acid) to enhance their
activity. These antibiotics have a broader spectrum of gram-negative
activity than do the aminopenicillins, and include activity
against most strains of P. aeruginosa These antibiotics are used in the treatment of urinary tract,
lung, and bloodstream infections caused by ampicillin-
resistant enteric gram-negative pathogens.
Adverse reactionsPenicillins are among the safest drugs, and blood levels are not monitored. However, the following adverse reactions may occur.1. Hypersensitivity :This is the most important adverse effect of the penicillins. The major antigenic determinant of penicillin hypersensitivity is its metabolite, penicilloic acid, which reacts with proteins and serves as a hapten to cause an immune reaction. Approxi mately five percent of patients have some kind of reaction, ranging from maculopapular rash (the most common rash seen with ampicillin hypersensitivity) to angioedema (marked swelling of the lips, tongue, and periorbital area) and anaphylaxis. Cross-allergic reactions occur among the β-lactam antibiotics. To determine whether treatment with a β-lactam is safe when an allergy is noted, patient history regarding severity of previous reaction is essential.
maculopapular rash
periorbital area
2. Diarrhea: This effect, which is caused by a disruption of the normal balance of intestinal microorganisms, is a common problem. It occurs to a greater extent with those agents that are incompletely absorbed and have an extended antibacterial spectrum. As with most antibiotics, pseudomembranous colitis may occur.
3. Nephritis: All penicillins, but particularly methicillin, have the potential to cause acute interstitial nephritis. [Note: Methicillinis therefore no longer available.]
4. Neurotoxicity: The penicillins are irritating to neuronal tissue, and they can provoke seizures if injected intrathecally or if very high blood levels are reached. Epileptic patients are particularly at risk. When indicated, dosage adjustments for patients with renal dysfunction further minimize the risk for seizure
5. Hematologic toxicities: Decreased coagulation may be observed with high doses of piperacillin, ticarcillin and nafcillin
(and, to some extent, with penicillin G).
6. Cation toxicity: Penicillins are generally administered as the sodium or potassium salt.
Toxicities may be caused by the large quantities of sodium or potassium that accompany the penicillin. For example, sodium excess may result in hypokalemia. This can be avoided by using the most potent antibiotic, which permits lower doses of drug and accompanying cations. Treatment with aqueous penicillin G has a high potassium load, which must be taken into account while monitoring electrolytes. The same is true for ticarcillin which has a high sodium load.
Summary of the adverse effects of penicillin
Cephalosporin antibiotics Cephalosporin antibiotics are beta-lactam antibiotics,
similar in structure and action to penicillin, were first isolated from “Cephalosporium” fungus.
Semisynthetic broad-spectrum cephalosporins have been produced, they vary in susceptibility to beta-lactamase.
First-generation cephalosporins are active predominantly against Gram-positive bacteria, and successive generations have increased activity against Gram-negative bacteria.
In general, the spectrum of activity of cephalosporins increases with each generation because of decreasing susceptibility to bacterial b-lactamases
Mechanism of action Cephalosporins are bactericidal and have the same
mode of action as other beta-lactam antibiotics (such as penicillins) but are less susceptible to penicillinases.
Cephalosporins disrupt the synthesis of the peptidoglycan layer of bacterial cell walls. The peptidoglycan layer is important for cell wall structural integrity.
These agents bind to penicillin binding proteins. Like penicillins, they must enter the cell wall through
porins and attach to penicillin-binding proteins (PBPs). The binding of the drug to these proteins mediates an inhibition of cell wall synthesis and leads to autolysis.
Classification The cephalosporins are derivatives of 7-aminocephalosporanic acid
and contain the beta-lactam ring structure. Many members of this group are in clinical use. They vary in their antibacterial activity and are designated
according to the order of their introduction into clinical use:
First generation such as: cefradine, cefalexin, cefazolin and cefadroxil
Second generation such as: cefuroxime, cefaclor, cefamandole, and cefoxitin.
Third generation such as: cefotaxime, ceftazidime, cefixime, ceftriaxone and cefoperazone.
1. Fourth generation such as :cefepime, cefpirome.
CeftarolineFifth generation such as :
7-aminocephalosporanic acid nucleus
Structure of some cephalosporins
Pharmacokinetics These agents are water soluble and relatively acid stable. Several cephalosporins are available for oral use, but most
are administered parenterally, intramuscularly (which may be painful) or intravenously.
After absorption, they are widely distributed in the body and some, such as cefotaxime,cefuroxime and ceftriaxone, cross the blood brain barrier.
Excretion is mostly via the kidney unchanged, largely by tubular secretion, but 40% of ceftriaxone is eliminated in the bile.
Most first- and second-generation cephalosporins do not enter cerebrospinal fluid even when the meninges are inflamed.
Administration and fate of the cephalosporins
Therapeutic advantages of some clinically useful cephalosporins
Clinical uses of the cephalosporins Cephalosporins are used to treat infections caused by sensitive
organisms. As with other antibiotics, patterns of sensitivity vary geographically , and treatment is often started empirically.
Many different kinds of infection may be treated, including: Septicaemia (e.g., cefuroxime, cefotaxime) Pneumonia caused by susceptible organisms. Meningitis (e.g., ceftriaxone, cefotaxime) Billiary tract infection Urinary tract infection (especially in pregnancy or in patients unresponsive to other
drugs) Sinusitis (cefadroxil).
In general, first generation cephalosporin possess excellent activity against gram-positive aerobic bacteria and poor activity against gram-negative organisms.
First-Generation Cephalosporins Cefazolin (parenteral), cephalexin (the first oral cephalosporin)
and the long acting agent cefadroxil are examples of this subgroup.
They are active against gram-positive cocci, including staphylococci and common streptococci.
Many strains of E. coli and K. pneumonia are also sensitive. Clinical uses include treatment of infections caused by these
organisms and surgical prophylaxis in selected conditions. These drugs have minimal activity against gram-negative
cocci, enterococci, mithicillin-resistant staphylococci, and most gram-negative rods.
They distribute widely throughout the body, but do not penetrate well into the CSF (not used for meningitis).
Second-Generation Cephalosporins Drugs in this subgroup usually have slightly less activity
against gram-positive organisms than the first generation drugs but have an extended gram-negative coverage.
Marked differences in activity occur among the drugs in this subgroup.
Examples of clinical uses include infections caused by the anaerobe Bacteroids fragilis (cefotetan, cefoxitin) and sinus air, and respiratory infections caused by H influenzae or M catarrhalis (cefamandole, cefaclor).
They are more resistant to b-lactamase than the first-generation drugs.
Cefoxitin is active against gram-negative organisms and anaerobes.
Third-Generation Cephalosporins Characteristic features of third-generation drugs (e.g.,
ceftazidime, cefoperazone, cefotaxime) include increased activity against gram-negative organisms resistant to other beta-lactam drugs and ability to penetrate the blood brain barrier (except cefoperazone and cefixime).
Most are active against Providencia, Serratia marcescens, and beta-lactamase-producing strains of H influenzae, Neisseria.
Ceftriaxone and cefotaxime are currently the most active cephalosporins against penicillin resistant pneumococci (PRSP strains).
Individual drugs also have activity against Pseudomonas aeruginosa (ceftazidine) and B fragilis (cdftizoxime).
Fourth-Generation Cephalosporins Cefepime is more resistant to beta-lactamases produced by
gram-negative organisms, including Enterobacter, Haemophilus, Neisseria, and some penicillin resistant pneumococci.
Cefepime combines the gram-positive activity of first-generation agents with the wider gram-negative spectrum of third-generation cephalosporins.
Fourth-generation agents are particularly useful for the empirical treatment of serious infections in hospitalized patients when gram-positive microorganisms, Enterobacteriaceae, and Pseudomonas all are potential etiologies
Fifth-Generation Cephalosporins These are novel cephalosporins with activity against MRSA Example: Ceftaroline Ceftaroline, has been recently approved by the US FDA for the treatment
of acute bacterial skin and skin structure infections and community-
acquired bacterial pneumonia This antimicrobial agent binds to penicillin binding proteins (PBP)
inhibiting cell wall synthesis and has a high affinity for PBP2a, which is
associated with methicillin resistance. Ceftaroline is consistently active against multidrug-resistant Streptococcus
pneumoniae and Staphylococcus aureus, including methicillin-resistant
strains The drug is usually administrated intravenously at 600 mg every 12 h Ceftaroline has low protein binding and is excreted by the kidneys and
thus requires dose adjustments in individuals with renal failure
Adverse effects Allergy : cephalosporins cause a range of allergic reactions
from skin rash to anaphylactic shock. These reactions occur less frequently with cephalosporins than with penicillin.
Cross reactivity between penicillins and cephalosporins is incomplete (5-10%), so penicillin allergic patients are sometimes treated successfully with cephalosporin.
Patients with a history of anaphylaxis to penicillin should not be treated with a cephalosporin.
Drugs containing a methylthiotetrazole group (e.g., cefamandole, cefoperazone, cefotetan) may cause hypoprothrombinemia and disulfuram-like reactions with ethanol.
Nephrotoxicity has been reported especially with cefradine.
Other beta-lactam antibiotics This group of antibiotics include (in addition to
penicillins and cephalosporins):
I. Monobactams
II. Carbapenems
III. Beta-lactamase inhibitors (clavulanic acid, sulbactam, and tazobactam).
These are important therapeutic agents with a beta-lactam structure act as inhibitors of cell wall synthesis.
They developed to deal with beta-lactamase-producing gram-negative organisms resistant to penicillins.
Basic structure of four groups of beta-lactam antibiotics and clavulanic acid
I- Monobactams Monobactams are monocyclic β-lactam compounds
where in the β-lactam ring is alone and not fused to another ring (in contrast to most other β-lactams, which have at least two rings).
They work only against Gram-negative bacteria. Their spectrum of activity is limited to aerobic gram
negative rods (including pseudomonas). Unlike other beta-lactam antibiotics, they have no
activity against gram-positive bacteria or anaerobes. The only commercially available monobactam antibiotic
is aztreonam. Other examples of monobactams are tigemonam,
nocardicin A, and tabtoxin.
Astreonam The main monobactam is astreonam which is resistant
to most beta-lactamases that are produced by most gram-negative bacteria and is the only monobactam available in USA.
It is an inhibitor of cell wall synthesis, preferentially binding to a specific penicillin binding protein (PBP3).
Aztreonam is effective only against G-ve aerobic organisms such as pseudomonads, Neisseria meningitidis and Haemophilus influenzae. Has no activity against gram-positive bacteria or anaerobes.
it has antimicrobial activity directed primarily against the Enterobacteriaceae, including P. aeruginosa.
Structural features of imipenem and aztreonam
Pharmacokinetics Astreonam is poorly absorbed when given via the oral route,
so it must be administered intravenously every 8 hours in a dose of 1-2 g, providing peak serum levels of 100 mcg/mL.
The plasma half-life is 1-2 hours and is greatly prolonged in renal failure.
It penetrates well into the cerebrospinal fluid, and is eliminated unchanged via renal tubular secretion.
It has structural similarities to ceftazidime; hence its gram-negative spectrum is similar to that of the third generation cephalosporins.
It is generally well tolerated. Patients who are allergic to penicillins or cephalosporins appear not to react to aztreonam, with the exception of ceftazidime.
Side effects Aztreonam is relatively nontoxic, but it may cause
phlebitis, skin rash, and occasionally, abnormal liver function tests.
Unwanted effects are, in general, similar to those of other beta-lactam antibiotics, this agent does not necessarily cross-react immunologically with penicillin and its products, and so does not usually cause allergic reactions in penicillin sensitive individuals.
Thus, this drug may offer a safe alternative for treating patients who are allergic and unable to tolerate penicillins and/or cephalosporins.
Phlebitis is a general term to describe the inflammation of a vein. Very often, the inflammation is accompanied by formation of a clot (thrombus), which occludes the blood flow through the vein. This condition is known as thrombophlebitis or venous thrombosis
II- Carbapenems Carbapenems are a class of β-lactam antibiotics with a broad
spectrum of antibacterial activity. They have a structure that renders them highly resistant to most β-lactamases.
Carbapenems are one of the antibiotics of last resort for many bacterial infections, such as Escherichia coli (E. coli) and Klebsiella pneumoniae.
Recently, alarm has been raised over the spread of drug resistance to carbapenem antibiotics among these coliforms, due to production of the New Delhi metallo-β-lactamase, NDM-1.
There are currently no new antibiotics in the pipeline to combat bacteria resistant to carbapenems, and worldwide spread of the resistance gene is considered a potential nightmare scenario.
The following drugs belong to the carbapenem class: Imipenem, generally given as part of Imipenem/cilastatin
(FDA approval 1985) Imipenem can be hydrolysed in the mammalian kidney by
a dehydropeptidase enzyme to a nephrotoxic metabolite, and so is given with a dehydropeptidase inhibitor, cilastatin
Meropenem (FDA approval 1996) Ertapenem (FDA approval 2001, since approved for
multiple indications, ) Doripenem (FDA Approval 2007) Panipenem/betamipron (Japanese approval 1993) Biapenem (Japanese approval 2001)
Imipenem Imipenem is an intravenous β-lactam antibiotic developed in 1980
by Professor Bissar. It has an extremely broad spectrum of antimicrobial activity, being active against many aerobic and anaerobic gram-positive and gram-negative (including P. aeruginosa) organisms, It is very resistant to hydrolysis by most β-lactamases.Enterococcus faecium, methicillin-resistant strains of staphylococci, Clostridium difficile are resistant.
Antimicrobial spectrum of imipenem
Side effects Adverse effects of imipenem-cilastatin include gastrointestinal
distress, skin rash, and at very high plasma levels, CNS toxicity (confusion, encephalopathy, seizures).
There is partial cross-allergenicity with the penicillins. Therefore, Patients who are allergic to other b-lactam antibiotics may have hypersensitivity reactions when given imipenem.
Pharmacokinetics Imipenem is not absorbed orally. Both imipenem and
cilastatin have a t1/2 of about 1h. When administered concurrently with cilastatin, about 70% of it is recovered in the urine as the active drug. Dosage should be modified for patients with renal insufficiency
III- Beta-lactamase Inhibitors b-lactamase inhibitors in clinical use include clavulanic acid
(usually combined with amoxicillin Augmentin®), sulbactam (usually combined with ampicillin Unasyn®). These drugs bind irreversibly to b-lactamase, inactivating the
enzyme, restoring the original spectrum of activity to enzyme-susceptible antibiotics.
Clavulanic acid is a chemical similar in structure to penicillin, which acts as a substrate for penicillinase, thus inhibiting its action on penicillin.
Beta-lactamase inhibitors do not reduce the activity of beta-lactamase produced by Enterobacter, Citrobacter, Serratia, Psedomonas and Staph organisms.
b-lactamase inhibitors themselves do not have significant antibacterial activity.
Beta-lactamase inhibitors
The in vitro growth of Escherichia coli in the presence of amoxicillin, with and without clavulanic acid
Other Cell Wall or Membrane-active Agents Vancomycin is a glycopeptide antibiotic used in the
prophylaxis and treatment of infections caused by Gram-positive bacteria (e.g., S. pyogenes, S. pneumoniae).
Vancomycin was first isolated in 1953 at Eli Lilly, It is a naturally occurring antibiotic made by the soil bacterium Streptococcus orientalis species.
It is complex chemical compound and an example of a comparatively rare halo organic natural compound, containing two organically bonded chlorine atoms
Mechanism of action of vancomycin
Vancomycin acts by inhibiting cell wall synthesis. Vancomycin is a bactericidal glycoprotein that binds to the
D-Ala-D-Ala terminal of the nascent peptidoglycan pentapeptide side chain and inhibits transglycosylation.
This action prevents elongation of the peptidoglycan chain and interferes with crosslinking. The peptidoglycan is thus weakened, and the cell becomes susceptible to lysis.
Resistance in strains of enterococci (vancomycin-resistant enterococci [VRE]) and staphylococci (vancomycin-resistant S aureus [VRSA]) involves a decreased affinity of vancomycin for the binding site by 1000 times because of the replacement of the terminal D-Ala by D-Lactate.
Inhibition of bacterial cell wall synthesis by Vancomycin
Pharmacokinetics Vancomycin is poorly absorbed from the GIT. It can be administered orally to patients with pseudomembranous
colitis due to C difficile. Parenteral doses must be administered intravenously. Slow IV infusion (60-90 mins) is employed for treatment of
systemic infections or for prophylaxis. Inflammation allows the intravenous formulation to peneterate into
the meninges. However, it is often necessary to combine vancomycin with other
antibiotics, such as ceftriaxone for synergistic effect when treating meningitis.
Ninety percent of the drug is excreted by glomerular filtration. In the presence of renal insufficiency, unusual accumulation may occur.
Normal half-life of vancomycin is 6 to 10 hours.
Administration and fate of vancomycin
Antimicrobial spectrum Vancomycin has a narrow spectrum of activity and is effective
against gram-positive organisms. It has been lifesaving in the treatment of MRSA and MRSE
infections as well as enterococcal infections With the emergence of resistant strains, it is important to
curtail the increase in vancomycin-resistant bacteria by restricting the use of vancomycin to the treatment of serious infections such as: Management of infections due to methicillin-resistant staphylococci, including
pneumonia & endocarditis Management of severe staphylococcal infections in patients who are allergic
to penicillins and cephalosporins Management of known or suspected penicillin-resistant pneumococcal
infections.
Antimicrobial spectrum of vancomycin