Antibiotic Classification & Mechanism

Author: Derek Moore

Topic updated on 04/14/13 9:49am

Overview of By Mechanism

Antibiotic Grouping By Mechanism
Cell Wall Synthesis	Penicillins Cephalosporins Vancomycin Beta-lactamase Inhibitors Carbapenems Aztreonam Polymycin Bacitracin
Protein Synthesis Inhibitors	Inhibit 30s Subunit Aminoglycosides (gentamicin) Tetracyclines Inhibit 50s Subunit Macrolides Chloramphenicol Clindamycin Linezolid Streptogramins
DNA Synthesis Inhibitors	Fluoroquinolones Metronidazole
RNA synthesis Inhibitors	Rifampin
Mycolic Acid synthesis inhibitors	Isoniazid
Folic Acid synthesis inhibitors	Sulfonamides Trimethoprim

Antibiotic Classification & Indications

Inhibits Cell Wall Synthesis
Penicillins (bactericidal: blocks cross linking via competitive inhibition of the transpeptidase enzyme)
Class/Mechanism	Drugs	Indications (Drug of Choice)	Toxicity
Penicillin	Penicillin G Aqueous penicillin G Procaine penicillin G Benzathine penicillin G Penicillin V	Strep. pyogenes (Grp.A) Step. agalactiae (Grp.B) C. perfringens(Bacilli)**	Hypersensitivity reaction Hemolytic anemia
Aminopenicillins	Ampicillin Amoxicillin	Above + ↑ Gram-negative: E. faecalis** E. Coli**	Above
Penicillinase-resistant-penicillins	Methicillin Nafcillin Oxacillin Cloxacillin Dicloxacillin	Above + PCNase-producingStaph. aureus	Above + Interstitial nephritis
Antipseudomonal penicillins	Carbenicillin Ticarcillin Piperacillin	Above + Pseudomonas aeruginosa**	Above
Cephalosporins (bactericidal: inhibits bacterial cell wall synthesis via competitive inhibition of the transpeptidase enzyme)
1st generation	Cefazolin Cephalexin	Staph. aureus Staph. epidermidis Some Gram-negatives: E. Coli Klebsiella	Allergic reaction Coombs-positive anemia (3%)
2nd generation	Cefoxitin Cefaclor Cefuroxime	Above + ↑ Gram-negative	Allergic Reaction ETOH Disulfiram reaction
3rd generation	Ceftriaxone Cefotaxime Ceftazidime Cefepime (4th generation)	Above + ↑ Gram-negative Pseudomonas	Allergic Reaction ETOH Disulfiram reaction
Other Cell Wall Inhibitors
Vancomycin (bactericidal: disrupts peptioglycan cross-linkage)	Vancomycin	MRSA PCN/Ceph allegies S. aureus S. epidermidis	Red man syndrome Nephrotoxicity Ototoxicity
Beta-lactamase Inhibitors (bactericidal: blocking cross linking)	Clavulanic Acid Sulbactam Tazobactam	S aureus S epidermis E.Coli Klebsiella	Hypersensitivity Reaction Hemolytic anemia
Carbapenems	Imipenem (+ cilastatin) Meropenem Doripenem Ertapenem	Broadest activity of any antibiotic (except MRSA, Mycoplasma)
Aztreonam	Aztreonam	Gram-negative rods Aerobes Hospital-acquired infections
Polymyxins	Polymyxin B Polymyxin E	Topical Gram-negative infections
Bacitracin	Bacitracin	Topical Gram-positive infections
Protein Synthesis Inhibition
Anti-30S ribosomal subunit
Aminoglycosides (bactericidal: irreversible binding to 30S)	Gentamicin Neomycin Amikacin Tobramycin Streptomycin	Aerobic Gram-negatives Enterobacteriaceae Pseudomonas	Nephrotoxicity Ototoxicity
Tetracyclines (bacteriostatic: blocks tRNA)	Tetracycline Doxycycline Minocycline Demeclocycline	Rickettsia Mycoplasma Spirochetes (Lyme's disease)	Hepatotoxicity Tooth discoloration Impaired growth Avoid in children < 12 years of age
Anti-50S ribosomal subunit
Macrolides (bacteriostatic: reversibly binds 50S)	Erythromycin Azithromycin Clarithromycin	Streptococcus H. influenzae Mycoplamsa pneumonia	Coumadin Interaction (cytochrome P450)
Chloramphenicol (bacteriostatic)	Chloramphenicol	H influenzae Bacterial Meningitis Brain absces	Aplastic Anemia Gray Baby Syndrome
Lincosamide (bacteriostatic: inhibits peptidyl transferase by interfering with amino acyl-tRNA complex)	Clindamycin	Bacteroides fragilis S aureus Coagulase-negative Staph & Strep Excellent Bone Penetration	Pseudomembranous colitis Hypersensitivity Reaction
Linezolid (variable)	Linezolid	Resistant Gram-positives
Streptogramins	Quinupristin Dalfopristin	VRE GAS and S. aureus skin infections
DNA Synthesis Inhibitors
Fluoroquinolones (bactericidal: inhibit DNA gyrase enzyme, inhibiting DNA synthesis)
1st generation	Nalidixic acid	Steptococcus Mycoplasma Aerobic Gram +	Phototoxicity Achilles tendon rupture Impaired fracture healing
2nd generation	Ciprofloxacin Norfloxacin Enoxacin Ofloxacin Levofloxacin	As Above +Pseudomonas	as above
3rd generation	Gatifloxacin	As above + Gram-positives	as above
4th generation	Moxifloxacin Gemifloxacin	As above + Gram-positives + anaerobes	as above
Other DNA Inhibitors
Metronidazole (bacteridical: metabolic biproducts disrupt DNA)	Metronidazole (Flagyl)	Anaerobics	Seizures Crebelar dysfunction ETOH disulfram reaction
RNA Synthesis Inhibitors
Rifampin (bactericidal: inhibits RNA transcription by inhibiting RNA polymerase)	Rifampin	Staphylococcus Mycobacterium (TB)	Body fluid discoloration Hepatoxicity (with INH)
Mycolic Acids Synthesis Inhibitors
Isoniazid	Isoniazidz	TB Latent TB
Folic acid Synthesis Inhibitors
Trimethoprim/Sulfonamides (bacteriostatic: inhibition with PABA)	Trimethoprim/Sulfamethoxazole (SMX) Sulfisoxazole Sulfadiazine	UTI organisms Proteus Enterobacter	Thrombocytopenia Avoid in third trimester of pregnancy
Pyrimethamine	Pyrimethamine	Malaria T. gondii

Bacteria Overview

Gram Postive Cocci
Staphylococcus	Staph. aureus MSSA MRSA Staph. epidermis Staph saprophyticus
Streptococcus	Strep pneumoniae Strep pyogenes (Group A) Strep agalacticae (Group B) Strep viridans Strep Bovis (Group D)
Enterococci	E. faecalis (Group D strep)
Gram Positive Bacilli
Spore Forming	Bacillus anthracis Bacillus cereus Clostridium tetani Clostridium botulinum Clostridium perfringens Clostridium difficile
Non-Spore Forming	Corynebacterium diphtheriae Listeria monocytogenes
Gram Negative Cocci
Neisseria	Neisseria meningitidis Neisseria gonorrhoeae
Gram Negative Bacilli
Enterics	Escherichia coli Salmonella typhi Salmonella enteridis Shigella dysenteriae Klebsiella pneumoniae Serratia Proteus Campylobacter jejuni Vibrio cholerae Vibrio parahaemolyticus/vulnificus Helicobacter pylori Pseudomonas aeruginosa Bacteroides fragilis
Respiratory bacilli	Haemophilus influenzae Haemophilius ducreyi Bordatella pertussis
Zoonotic bacilli	Yersinia enterocolitica Yersinia pestis Brucella Francisella tularensis Pasteurella multocida Bartonella henselae
Other	Gardnerella vaginalis
Other Bacteria
Mycobacteria	Mycobacterium tuberculosis Mycobacterium leprae MOTTS
Spirochetes	Borrelia burgdorferi Leptospira interrogans Treponema pallidum
Chlamydiaceae	Chlamydia trachomatis Chlamydophila Rickettsia Ehrlichia
Mycoplasmataceae	Mycoplasma pneumoniae Ureaplasma urealyticum
Fungus-like Bacteria	Actinomyces israelii Nocardia

Antibiotic Resistance Mechanisms

Bacteria develop ability to hydrolyze these drugs using β lactamase
- confers resistance to penicillin
- e.g. E. coli, Staph epidermidis, Pseudomonas aeruginosa, Klebsiella pneumoniae
- add β lactamase inhibitor e.g. clavulanic acid in amoxicillin-clavulanate (Augmentin)
Genetic mutation of mecA
- a bacterial gene encoding a penicillin-binding protein. New PBP has reduced affinity for antibiotics
- confers resistance to methicillin, oxacillin, nafcillin
- e.g. MRSA
Altered cell wall permeability
- confers resistance to tetracyclines, quinolones, trimethoprim and β lactam antibiotics
Creation of biofilm barrier
- provides an environment where offending bacteria can multiply safe from the hoste immune system
  - Salmonella
  - Staph epidermidis
Active efflux pumps
- confers resistance to erythromycin and tetracycline
- e.g. msrA gene in Staph
Altered peptidoglycan subunit (altered D-alanyl-D-alanine of NAM/NAG-peptide)
- confers resistance to vancomycin
- e.g. vancomycin resistant enterococcus (VRE)
Ribosome alteration
- erm gene confer inducible resistance to MLS (macrolide lincosamide streptogranin) agents via methylation of 23s rRNA
- demonstrate using D zone test
  - for inducible clindamycin resistance in Staph and beta hemolytic Strep

Penicillins

Mechanism
- interfer with bacterial cell wall synthesis
Subclassification and tested examples
- natural
  - penicillin G
- penicillinase-resistant
  - methicillin (Staphcillin)
- aminopenicillins
  - ampicillin (Omnipen, Polycillin)

Cephalosporins

Overview
- bactericidal
Mechanism
- disrupts the synthesis of the peptidoglycan layer of bacterial cell walls
  - does so through competitive inhibition on PCB (penicllin binding proteins)
  - peptidoglycan layer is important for cell wall structural integrity.
- same mechanicsm of action as beta-lactam antibiotics (such as penicillins)
Subclassification and tested examples
- first generation
  - cefazolin (Ancef, Kefzol)
- second generation
  - cefaclor (Ceclor)
- third generation
  - cefriazone (Rocephin)
- fourth generation
  - cefepime (Maxipime)

Fluoroquinolones

Mechanism
- blocks DNA replication via inhibition of DNA gyrase
Side effects
- inhibit early fracture healing through toxic effects on chondrocytes
- increased rates of tendinitis, with special predilection for the Achilles tendon.
  - tenocytes in the Achilles tendon have exhibited degenerative changes when viewed microscopically after fluoroquinolone administration.
  - recent clinical studies have shown an increased relative risk of Achilles tendon rupture of 3.7.
Subclassification and tested examples
- ciprofloxacin (Cipro)
- levofloxacin (Levaquin)

Aminoglycosides

Mechanism
- bactericidal
- inhibition of bacterial protein synthesis
  - work by binding to the 30s ribosome subunit, leading to the misreading of mRNA. This misreading results in the synthesis of abnormal peptides that accumulate intracellularly and eventually lead to cell death. These antibiotics arebactericidal.
Subclassification and tested examples
- gentamicin (Garamycin)

Vancomycin

Coverage
- gram-positive bacteria
Mechanism
- bactericidal
- an inhibitor of cell wall synthesis
Resistance
- increasing emergence of vancomycin-resistant enterococci has resulted in the development of guidelines for use by the (CDC)
- indications for vancomycin
  - serious allergies to penicillins or beta-lactam antimicrobials
  - serious infections caused by susceptible organisms resistant to penicillins (MRSA, MRSE)
  - surgical prophylaxis for major procedures involving implantation of prostheses in institutions with a high rate of MRSA or MRSE

Rifampin

Most effective against intracellular phagocytized Staphylococcus aureus in macrophages

Linezolid

Linezolid binds to the 23S portion of the 50S subunit and acts by preventing the formation of the initiation complex between the the 30S and 50S subunits of the ribosome.

Splenectomy

Splenectomy patients or patients with functional hyposplenism require the following vaccines and/or antibiotics
- Pneumococcal immunization
- Haemophilus influenza type B vaccine
- Meningococcal group C conjugate vaccine
- Influenza immunization
- Lifelong prophylactic antibiotics (oral phenoxymethylpenicillin or erythromycin)

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Qbank (10 Questions)

TAG

(OBQ11.70) Which of the following antibiotic families inhibit bacterial DNA gyrase? Topic

Review Topic

1. Quinolones
2. Penicillins
3. Aminoglycosides
4. Macrolides
5. Sulfonamides

PREFERRED RESPONSE ▶

DISCUSSION: Quinolones are a class of antibiotics which act by inhibition of bacterial DNA gyrase. Penicillins interfere with bacterial cell wall synthesis. Aminoglycosides and macrolides interfere with bacterial protein synthesis by acting on the 30S and 50S ribosome subunits respectively. Sulfonamides interfere with bacterial folic acid metabolism.

Levine and DiBona review fluoroquinolones as a class of antibiotics and describe their potential beneficial and adverse effects in the treatment and prevention of musculoskeletal infections. While not frequently used in musculoskeletal infection, fluoroquinolones appear to be very effective in the treatment of osteomyelitis and infections involving prosthetic implants like hip and knee replacements.

REFERENCES:

1. Morris CD. Orthopaedic pharmacology and therapeutics. In: Einhorn TA, O'Keefe RJ, Buckwalter JA, eds. Orthopaedic Basic Science: Foundations of Clinical Practice. 3rd ed. Rosemont, IL: American Academy of Orthopaedic Surgeons; 2007:315-330.

2. Levine AM, DiBona JR. Fluoroquinolones. J Am Acad Orthop Surg. 2002 Jan-Feb;10(1):1-4. Review. PMID:11809044 (Link to Abstract)

Question Authors:

Patrick O'Donnell MD/PhD, John Badylak MD, Ben Taylor MD,

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(OBQ11.138) MecA is the bacterial gene which encodes for a penicillin-binding protein that alters the efficacy of beta-lactam antibiotics. Which of the following species of bacteria are known to produce mecA? Topic

Review Topic

1. Clostridium dificile
2. Clostridium tetani
3. Vancomycin-resistant enterococcus
4. Methicillin-resistant staphylococcus aureus
5. Streptococcus epidermidis

PREFERRED RESPONSE ▶

DISCUSSION: Methicillin-resistant Staphylococcus aureus is the most common carrier of the mecA gene. This gene may also be found in Staphylococcus aureus and Streptococcus pneumoniae species and provide penicillin resistance for these bacteria. None of the other listed bacteria are known to harbor mecA in their bacterial genome.

Marcotte and Trzeciak review community-acquired MRSA with specific focus on diagnosis and treatment. They discuss the differences between community-acquired and hospital-acquired MRSA. Specifically, they emphasize bacterial gene products like mecA which alter the bacterial susceptibility towards common antibiotics, and provide appropriate treatment options for common MRSA infections.

REFERENCES:

1. Gross JM, Schwarz EM. Infections in orthopaedics. In: Einhorn TA, O'Keefe RJ, Buckwalter JA, eds. Orthopaedic Basic Science: Foundations of Clinical Practice. 3rd ed. Rosemont, IL: American Academy of Orthopaedic Surgeons; 2007:299-314.

2. Marcotte AL, Trzeciak MA. Community-acquired methicillin-resistant Staphylococcus aureus: an emerging pathogen in orthopaedics. J Am Acad Orthop Surg. 2008 Feb;16(2):98-106. Review. PMID:18252840 (Link to Abstract)

Question Authors:

Patrick O'Donnell MD/PhD, Dave Marcu MD, Ben Taylor MD,

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(OBQ08.275) What is the mechanism of action of vancomycin? Topic

Review Topic

1. inhibition of cell wall synthesis
2. increase cell wall permeability
3. ribosomal inhibition
4. interference with DNA metabolism
5. antimetabolite action

PREFERRED RESPONSE ▶

DISCUSSION: Vancomycin is an inhibitor of cell wall synthesis and is bactericidal for gram positive organisms. Antibiotics exert their effects via five basic mechanisms: (1) Inhibition of cell wall synthesis (cephalosporins, penicillins, vancomycin, imipenim). (2) Increasing cell membrane permeability. (3) Ribosomal inhibition (gentamycin, erythromycins, linezolid, tetracyclines). (4) interference with DNA metabolism (quinolones), and (5) antimetabolite action.

REFERENCES:

1. Einhorn TA, O’Keefe RJ, Buckwalter JA (eds): Orthopaedic Basic Science: Foundations of Clinical Practice, ed 3. Rosemont, IL, American Academy of Orthopaedic Surgeons, 2007, pp 315-330

Question Authors:

Paul D. Kim MD, Derek Moore, Patrick McCulloch MD,

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TAG

(OBQ06.87) Which class of antibiotics inhibit early fracture healing through toxic effects on chondrocytes? Topic

Review Topic

1. cephalosporins
2. quinolones
3. penicillins
4. macrolides
5. sulfonamides

PREFERRED RESPONSE ▶

DISCUSSION: Animal models have shown that quinolones inhibit early fracture healing through a toxic effect on chondrocytes. The study by Perry et al demonstrated that fracture calluses in the animals treated with quinolones showed a lower histologic grade as compared with control animals representing a less mature callus with the presence of more cartilage and less woven bone. The study by Huddleston et al demonstrated fracture calluses in the animals treated with ciprofloxacin showed abnormalities in cartilage morphology and endochondral bone formation and a significant decrease in the number of chondrocytes compared with the controls. None of the other antibiotics listed are known to have toxic effects on chondrocytes.

REFERENCES:

1. Perry AC, Prpa B, Rouse MS, Piper KE, Hanssen AD, Steckelberg JM, Patel R. Levofloxacin and trovafloxacin inhibition of experimental fracture healing. Clin Orthop 2003; 414: 95-100. PMID:12966282 (Link to Abstract)

2. Huddleston PM, Steckelberg JM, Hanssen AD, Rouse MS, Bolander ME, Patel R. Ciprofloxacin inhibition of experimental fracture healing. JBJS Am 2000; 82: 161-173. PMID:10682725 (Link to Abstract)

Question Authors:

Greg Galano MD, Derek Moore, Patrick McCulloch MD,

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(OBQ06.134) Rifampin is highly effective against phagocytized intracellular Staphylococcus aureus especially in combination with other antibiotics because of its: Topic

Review Topic

1. hydrophilic activity
2. high cell penetration
3. structural similarity to penicillin
4. structural similarity to vancomycin
5. beta-lactamase activity

PREFERRED RESPONSE ▶

DISCUSSION: Darouiche et al examined antibiotic penetration and bactericidal properties of antibioics and discovered that rifampin had the best cell penetration and concentration among the drugs studied (nafcillin, cefazolin, cefuroxime, vancomycin, minocycline, and ciprofloxacin). In general the lipophilic drugs (minocycline, ciprofloxacin, rifampin) were better able to penetrate the cells than the hydrophilic drugs (nafcillin, cefazolin, cefuroxime, vancomycin). Rifampin by itself exhibited poor killing activity despite high concentration; it did however, potentiate the effects of other antibiotics such as nafcillin, vancomycin, and minocyclin.

REFERENCES:

1. Darouiche RO, Hamill RJ. Antibiotic penetration of and bactericidal activity within endothelial cells. Antimicrob Agents Chemother. 1994 May;38(5):1059-64. PMID:8067738 (Link to Abstract)

Question Authors:

Paul D. Kim MD,

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TAG

(OBQ05.99) A 62-year-old man undergoes an uncomplicated total shoulder replacement 9 months ago. What is an appropriate choice of prophylactic antibiotics to be taken prior to dental work if he has no allergies? Topic

Review Topic

1. daptomycin 600 milligrams intravenous 2 hours prior to procedure
2. amoxicillin 4 grams oral 1 week prior to procedure
3. levaquin 500 milligrams oral 1 hour prior to procedure
4. trimethoprim-sulfamethoxazole 2 tablets double-strength oral 1 hour prior to procedure
5. cephalexin 2 grams oral 1 hour prior to procedure

PREFERRED RESPONSE ▶

DISCUSSION: Patients not allergic to penicillin should take 2 grams of Amoxicillin, Cephalexin, or Cephadrine, by mouth one hour prior to the dental procedure. IV antibiotics are very rarely used in dental offices. If allergic to penicillin, clindamycin would be the next best alternative.

REFERENCES:

1. Buckwalter JA, Einhorn TA, Simon SR (ed): Orthopaedic Basic Science: Biology and Biomechanics of the Musculoskeletal System, ed 2. Rosemont, IL, American Academy of Orthopaedic Surgeons, 2000, pp 239-259.

2. American Academy of Orthopaedic Surgeons Website. Advisory Statement: Antibiotic Prophylaxis for Dental Patients with Total Joint Replacement. Available at http://www.aaos.org/news/aaosnow/may09/cover2.asp

Question Authors:

Greg Galano MD, Guillem Lomas MD, John Badylak MD,

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(OBQ04.42) A splenectomy is performed in a 7-year-old boy following a motor vehicle accident. All of the following are recommended for long-term management EXCEPT: Topic

Review Topic

1. Pneumococcal vaccination
2. Haemophilus influenza type B vaccination
3. Meningococcal group C vaccination
4. Lifelong prophylactic antibiotics
5. Hepatitis A vaccination

PREFERRED RESPONSE ▶

DISCUSSION: All of the responses are correct except the need for Hepatitis A vaccine. Hepatitis A is a virus with tropism for hepatocytes which causes infection from fecal-oral contaminated food/water, and shows no increased rate of either infectivity or morbidity in patients with hyposplenism.

Basic recommendations for splenectomized patients include:
1. All splenectomized patients and those with functional hyposplenism should receive pneumococcal immunization.
2. Patients not previously immunized should receive haemophilus influenza type B vaccine.
3. Patients not previously immunized should receive meningococcal group C conjugate vaccine.
4. Influenza immunization should be given.
5. Lifelong prophylactic antibiotics are still recommended (oral phenoxymethylpenicillin or erythromycin). This is seemingly despite lack of good data demonstrating a role for lifelong chemoprophylaxis and the acknowledgement that long-term compliance may be problematic.

Davies et al review the current level of evidence supporting these guidelines for infection prevention in patients with hyposplenism. New to these guidelines are issues regarding occupational exposure and the use of the meningococcal group C and the seven-valent pneumococcal vaccine in non-immunized hyposplenic patients.

Gandhi et al evaluated their nonoperative management of blunt splenic injury in pediatric trauma care. They found compared to historical controls, children with blunt splenic injuries who were hemodynamically stable could be safely monitored with a protocol which required 4 days of inpatient care, 3 weeks of quiet home activities, and 3 months of light activity. This protocol seems to allow for safe return to unrestricted activity.

Incorrect Answer:
Answers 1-4 are incorrect because they are recommended in splenectomy patients.

REFERENCES:

1. Davies JM, Barnes R, Milligan D; British Committee for Standards in Haematology. Working Party of the Haematology/Oncology Task Force. Update of guidelines for the prevention and treatment of infection in patients with an absent or dysfunctional spleen. Clin Med. 2002 Sep-Oct;2(5):440-3. PMID:12448592 (Link to Abstract)

2. Gandhi RR, Keller MS, Schwab CW, Stafford PW. Pediatric splenic injury: pathway to play? J Pediatr Surg. 1999 Jan;34(1):55-8; discussion 58-9. PMID:10022143 (Link to Abstract)

Question Authors:

Patrick O'Donnell MD/PhD, Derek Moore, Ben Taylor MD, Mark Miller MD,

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(OBQ04.58) All of the following antibiotics function by interfering with protein synthesis by inhibiting ribosomes EXCEPT Topic

Review Topic

1. gentamycin
2. tobramycin
3. vancomycin
4. erythromycin
5. linezolid

PREFERRED RESPONSE ▶

DISCUSSION: Gentamycin and tobramycin are aminoglycosides that function by inhibition of bacterial protein synthesis via irreversible binding to ribosomal subunits. Erythromycin functions by binding to the 50s subunit of the bacterial 70s rRNA complex and thereby inhibits protein synthesis. Linezolid binds to the 23s portion of the ribosomal subunit and inhibits protein synthesis. In contrast, Vancomycin acts by inhibiting proper cell wall synthesis and does not inhibit the ribosome.

REFERENCES:

1. Buckwalter JA, Einhorn TA, Simon SR (eds): Orthopaedic Basic Science: Biology and biomechanics of the musculoskeletal system, ed 2. Rosemont, IL, American Academy of Orthopaedic Surgeons, 2000, pp 239-259

Question Authors:

Paul D. Kim MD, Derek Moore, Patrick McCulloch MD,

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(OBQ04.190) All of the following antibiotics function by interfering with cell wall synthesis EXCEPT Topic

Review Topic

1. Cefazolin
2. Penicillin G
3. Vancomycin
4. Imipenem
5. Gentamicin

PREFERRED RESPONSE ▶

DISCUSSION: Cephalosporins (cefazolin), penicillins, vancomycin, and imipenim function by interfering with cell wall synthesis. Gentamicin, an aminoglycoside, functions by inhibiting ribosomes and protein synthesis and does not affect cell wall synthesis.

The reference by Mader et al. is an instructional course lecture that reviews the different mechanisms of antibiotics and their indications in musculoskeletal infections.

Illustration A is a table showing common mechanisms of antibiotics.

Illustrations: A

REFERENCES:

1. Buckwalter JA, Einhorn TA, Simon SR (eds): Orthopaedic Basic Science: Biology and Biomechanics of the Musculoskeletal System, ed 2. Rosemount, IL, American Academy of Orthopaedic Surgeons,

2. Mader JT, Wang J, Calhoun JH: Antibiotic therapy for musculoskeletal infections. Instr Course Lect 2002;51:539-551 PMID:12064145 (Link to Abstract)

Question Authors:

Derek Moore, Patrick McCulloch MD, John Badylak MD, Mark Miller MD,

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Evidence & References Show References

Level of Evidence 3 (Retrospective Cohort Study or Case-Control Study)

Gandhi RR, Keller MS, Schwab CW, Stafford PW. Pediatric splenic injury: pathway to play? J Pediatr Surg. 1999 Jan;34(1):55-8; discussion 58-9. PMID:10022143 (Link to Abstract)

Level of Evidence 5 and Other Journal Articles (includes Case Reports, Expert Opinions, Personal Observations, and Biomechanic Studies)

Arciola CR, Campoccia D, Gamberini S, Donati ME, Baldassarri L, Montanaro L. Occurence of ica genes for slime synthesis in a collection of Staphylococcus epidermidis strains from orthopedic prosthesis infections. Acta Orthop Scand. 2003 Oct;74(5):617-21. PMID:14620986 (Link to Abstract)
Olson ME, Garvin KL, Fey PD, Rupp ME. Adherence of Staphylococcus epidermidis to biomaterials is augmented by PIA. Clin Orthop Relat Res. 2006 Oct;451:21-4. PMID:16906069 (Link to Abstract)
Levine AM, DiBona JR. Fluoroquinolones. J Am Acad Orthop Surg. 2002 Jan-Feb;10(1):1-4. Review. PMID:11809044 (Link to Abstract)
Marcotte AL, Trzeciak MA. Community-acquired methicillin-resistant Staphylococcus aureus: an emerging pathogen in orthopaedics. J Am Acad Orthop Surg. 2008 Feb;16(2):98-106. Review. PMID:18252840 (Link to Abstract)
Davies JM, Barnes R, Milligan D; British Committee for Standards in Haematology. Working Party of the Haematology/Oncology Task Force. Update of guidelines for the prevention and treatment of infection in patients with an absent or dysfunctional spleen. Clin Med. 2002 Sep-Oct;2(5):440-3. PMID:12448592 (Link to Abstract)

Textbooks

Review of Orthopaedics, 6th Edition, Mark D. Miller MD, Stephen R. Thompson MBBS MEd FRCSC, Jennifer Hart MPAS PA-C ATC, an imprint of Elsevier, Philadelphia, Copyright 2012
AAOS Comprehensive Orthopaedic Review, Jay R. Leiberman. Published by American Academy of Orthopaedic Surgeons, Rosemont IL. Copyright 2009
Orthopaedic Knowledge Update 10, John M Flyn. Published by American Academy of Orthopaedic Surgeons, Rosemont IL. Copyright 2011
Hoppenfeld SP. Surgical Exposures in Orthopaedics: The Anatomic Approach. Lipponcott, Williams, and Wilkins, Philadelphia, PA, Copyright 2009
Orthopaedic In-training Examination (OITE) Questions 2004-2012, American Academy of Orthopaedic Surgeons, Rosemont IL. Copyright 2004-2012
Self-Assessment Examination (SAE) Questions 2004-2012, American Academy of Orthopaedic Surgeons, Rosemont IL. Copyright 2004-2012
Morris CD. Orthopaedic pharmacology and therapeutics. In: Einhorn TA, O'Keefe RJ, Buckwalter JA, eds. Orthopaedic Basic Science: Foundations of Clinical Practice. 3rd ed. Rosemont, IL: American Academy of Orthopaedic Surgeons; 2007:315-330.
Gross JM, Schwarz EM. Infections in orthopaedics. In: Einhorn TA, O'Keefe RJ, Buckwalter JA, eds. Orthopaedic Basic Science: Foundations of Clinical Practice. 3rd ed. Rosemont, IL: American Academy of Orthopaedic Surgeons; 2007:299-314.

Undefined

Einhorn TA, O’Keefe RJ, Buckwalter JA (eds): Orthopaedic Basic Science: Foundations of Clinical Practice, ed 3. Rosemont, IL, American Academy of Orthopaedic Surgeons, 2007, pp 315-330
Perry AC, Prpa B, Rouse MS, Piper KE, Hanssen AD, Steckelberg JM, Patel R. Levofloxacin and trovafloxacin inhibition of experimental fracture healing. Clin Orthop 2003; 414: 95-100. PMID:12966282 (Link to Abstract)
Huddleston PM, Steckelberg JM, Hanssen AD, Rouse MS, Bolander ME, Patel R. Ciprofloxacin inhibition of experimental fracture healing. JBJS Am 2000; 82: 161-173. PMID:10682725 (Link to Abstract)
Darouiche RO, Hamill RJ. Antibiotic penetration of and bactericidal activity within endothelial cells. Antimicrob Agents Chemother. 1994 May;38(5):1059-64. PMID:8067738 (Link to Abstract)
Buckwalter JA, Einhorn TA, Simon SR (ed): Orthopaedic Basic Science: Biology and Biomechanics of the Musculoskeletal System, ed 2. Rosemont, IL, American Academy of Orthopaedic Surgeons, 2000, pp 239-259.
American Academy of Orthopaedic Surgeons Website. Advisory Statement: Antibiotic Prophylaxis for Dental Patients with Total Joint Replacement. Available at http://www.aaos.org/news/aaosnow/may09/cover2.asp
Buckwalter JA, Einhorn TA, Simon SR (eds): Orthopaedic Basic Science: Biology and biomechanics of the musculoskeletal system, ed 2. Rosemont, IL, American Academy of Orthopaedic Surgeons, 2000, pp 239-259
Buckwalter JA, Einhorn TA, Simon SR (eds): Orthopaedic Basic Science: Biology and Biomechanics of the Musculoskeletal System, ed 2. Rosemount, IL, American Academy of Orthopaedic Surgeons,
Mader JT, Wang J, Calhoun JH: Antibiotic therapy for musculoskeletal infections. Instr Course Lect 2002;51:539-551 PMID:12064145 (Link to Abstract)

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Antibiotic Classification & Mechanism

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