CephalothinCefazolin (Ancef, Kefzol) CephapririnCephalexin (Keflex)other
Inhibit 30s SubunitAminoglycosides (gentamicin)TetracyclinesInhibit 50s SubunitMacrolidesChloramphenicolClindamycinLinezolid Streptogramins
Strep. pyogenes (Grp.A)**Step. agalactiae (Grp.B)**C. perfringens(Bacilli)**
Above + ↑ Gram-negative:E. faecalis**E. Coli**
MRSA**PCN/Ceph allegies**S. aureusS. epidermidis
S aureus**S epidermis**E.Coli**Klebsiella**
RickettsiaMycoplasmaSpirochetes (Lyme's disease)
Coumadin Interaction (cytochrome P450)
Bacteroides fragilisS aureusCoagulase-negative Staph & StrepExcellent Bone Penetration
Pseudomembranous colitisHypersensitivity Reaction
PhototoxicityAchilles tendon ruptureImpaired fracture healing
ThrombocytopeniaAvoid in third trimester of pregnancy
Bacillus anthracisBacillus cereusClostridium tetaniClostridium botulinumClostridium perfringensClostridium difficile
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Average 4.1 of 32 Ratings
What mechanism allows Staphylococcus epidermidis to adhere to surfaces and resist phagocytosis?
Creation of active efflux pumps
Methylation of 23s rRNA
Alteration of cell wall permeability
Select Answer to see Preferred Response
Staphylococcus epidermidis is a gram-positive bacteria that utilizes a glycocalyx/biofilm to adhere to orthopedic implants and other surfaces and resist phagocytosis.
The biofilm creates a well-protected environment where bacteria can proliferate and thrive essentially undetected by the host immune system. This leads to chronic infections of orthopedic implants that can go undetected for years.
Arciola et al note that S. epidermidis can colonize surfaces in a self-generated viscous biofilm composed of polysaccharides and that the ica genes found in 56% of S. epidermidis isolates were associated with their ability to produce biofilm.
Olson et al discuss the importance of polysaccharide intercellular adhesin (PIA), a substance produced by 50-60% of S. epidermidis strains, in the adherence of S. epidermidis to biomaterials through biofilm creation. PIA plays a critical role in initial adherence of S. epidermidis to biomaterials, biofilm maturation and aggregation.
Illustration A shows microscopy of Staphylococcus epidermidis, which is a gram-positive, coagulase-negative cocci. Illustration B is an overview of the different classes of organisms in microbiology.
Answer 1,2,4,5: Efflux pump production, hydrolysis of B-lactam drugs with beta-lactamase, alteration in cell wall permeability, and ribosomal alteration are mechanisms that Staphylococcus uses to resists antibiotics.
Arciola CR, Campoccia D, Gamberini S, Donati ME, Baldassarri L, Montanaro L.
Acta Orthop Scand. 2003 Oct;74(5):617-21. PMID: 14620986 (Link to Abstract)
Olson ME, Garvin KL, Fey PD, Rupp ME
Clin. Orthop. Relat. Res.. 2006 Oct;451:21-4. PMID: 16906069 (Link to Abstract)
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Average 3.0 of 7 Ratings
Which of the following antibiotic families inhibit bacterial DNA gyrase?
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.
Levine AM, DiBona JR.
J Am Acad Orthop Surg. 2002 Jan-Feb;10(1):1-4. PMID: 11809044 (Link to Abstract)
Average 3.0 of 15 Ratings
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?
Methicillin-resistant staphylococcus aureus
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.
Marcotte AL, Trzeciak MA.
J Am Acad Orthop Surg. 2008 Feb;16(2):98-106. PMID: 18252840 (Link to Abstract)
Average 3.0 of 14 Ratings
What is the mechanism of action of vancomycin?
inhibition of cell wall synthesis
increase cell wall permeability
interference with DNA metabolism
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, imipenem). (2) Increasing cell membrane permeability (Bacitracin). (3) Ribosomal inhibition (gentamycin, erythromycins, linezolid, tetracyclines). (4) interference with DNA metabolism (quinolones), and (5) antimetabolite action (Trimethoprim).
Which class of antibiotics inhibit early fracture healing through toxic effects on chondrocytes?
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.
Perry AC, Prpa B, Rouse MS, Piper KE, Hanssen AD, Steckelberg JM, Patel R.
Clin Orthop Relat Res. 2003 Sep;(414):95-100. PMID: 12966282 (Link to Abstract)
Huddleston PM, Steckelberg JM, Hanssen AD, Rouse MS, Bolander ME, Patel R
J Bone Joint Surg Am. 2000 Feb;82(2):161-73. PMID: 10682725 (Link to Abstract)
Average 2.0 of 14 Ratings
Rifampin is highly effective against phagocytized intracellular Staphylococcus aureus especially in combination with other antibiotics because of its:
High cell penetration
Structural similarity to penicillin
Structural similarity to vancomycin
Based on the choices above, rifampin works well synergistically with other antibiotics because of its high cell penetration.
Rifampin is a bactericidal antibiotic that blocks the function of RNA polymerase and subsequent RNA transcription. It is used to treat both staphylococcus and mycobacterium infections. Because of the high rate of cellular penetration, it is effective against intracellular phagocytized staphylococcus.
Darouiche et al. investigated the cellular penetration of seven antibiotics in cultured human umbilical vein endothelial cells. Lipophilic drugs such as minocycline, ciprofloxacin and rifampin had better cell penetration. Although rifampin was found to have limited killing activity, it potentiated the bactericidal activity of other antibiotics when used in combination.
Illustration A shows a schematic detailing the mechanism of rifampin’s bactericidal action.
Answer 1, 3, 4, 5: Rifampin is lipophilic, rendering its ability to cross the cell wall/membrane and exert its actions against RNA polymerase.
Darouiche RO, Hamill RJ.
Antimicrob Agents Chemother. 1994 May;38(5):1059-64. PMID: 8067738 (Link to Abstract)
Average 3.0 of 11 Ratings
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?
daptomycin 600 milligrams intravenous 2 hours prior to procedure
amoxicillin 4 grams oral 1 week prior to procedure
levaquin 500 milligrams oral 1 hour prior to procedure
trimethoprim-sulfamethoxazole 2 tablets double-strength oral 1 hour prior to procedure
cephalexin 2 grams oral 1 hour prior to procedure
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.
Average 2.0 of 26 Ratings
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:
Haemophilus influenza type B vaccination
Meningococcal group C vaccination
Lifelong prophylactic antibiotics
Hepatitis A vaccination
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.
Answers 1-4 are incorrect because they are recommended in splenectomy patients.
Davies JM, Barnes R, Milligan D.
Clin Med (Lond). 2002 Sep-Oct;2(5):440-3. PMID: 12448592 (Link to Abstract)
Gandhi RR, Keller MS, Schwab CW, Stafford PW.
J Pediatr Surg. 1999 Jan;34(1):55-8; discussion 58-9. PMID: 10022143 (Link to Abstract)
Average 1.0 of 58 Ratings
All of the following antibiotics function by interfering with protein synthesis by inhibiting ribosomes EXCEPT
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.
Average 3.0 of 21 Ratings
All of the following antibiotics function by interfering with cell wall synthesis EXCEPT
Cephalosporins (cefazolin), penicillins, vancomycin, and imipenem 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.
Mader JT, Wang J, Calhoun JH.
Instr Course Lect. 2002;51:539-51. PMID: 12064145 (Link to Abstract)