Infection and Antibiotics

Name factors that influence the development of infection:

• Poor approximation of tissue, hematoma/seroma, hypothermia, long operation (>2 hours), excessive local tissue destruction/necrotic tissue, low blood flow, foreign body, dead space, and strangulation of tissues by tight sutures

Most common nosocomial infection:

• Urinary tract infection (UTI)

How many colony-forming units (CFUs) are needed on urine culture to confirm a diagnosis of UTI?

• >100,000 CFU

Most common nosocomial infection causing death:

• Pneumonia

Overall most common organism in surgical wound infections:

• Staphylococcus aureus

Most common anaerobe in surgical wound infections:

• Bacteroides fragilis

When do wound infection classically arise?

• Postoperative day 5 to 7

Treatment for a wound infection:

• Remove sutures/staples, culture wound, examine to rule out fascial dehiscence, leave wound open and pack, start antibiotics

Bacteria that will cause wound infection and fever within 24 hours after surgery:

• Group A β-hemolytic Streptococcus and Clostridium perfringens

Organisms that can cause necrotizing soft tissue infections:

• Group A β-hemolytic Streptococcus and Clostridium perfringens

Usual organism to cause necrotizing fasciitis:

• Polymicrobial (anaerobes with gram-negative organisms)

Time period to wait before obtaining a CT scan to look for postoperative abscess:

• >POD no. 7 (otherwise abscess may look like normal post-op fluid collection)

Findings on CT scan to indicate abscess:

• Gas in fluid collection, fibrous ring surrounding fluid collection

Usual initial treatment for intraabdominal abscess:

• Percutaneous drainage

Most common bacteria to cause a line infection:

• Staphylococcus epidermidis

How many CFUs are needed from a central line culture to indicate line infection?

• >15 CFU

In what instance should a central line be changed over a guidewire?

• Fever without obvious external signs of infection (catheter tip culture should be sent)

A line changed over a guidewire can be left in place with what catheter tip culture result:

• <15 CFU from previous line culture

A line change over a guidewire should be discontinued and a new line should be placed at a new site with this culture result:

• >15 CFU from previous line culture

Term for blanching erythema from superficial epidermal/dermal infection:

• Cellulitis

Name the classic signs and symptoms of infection/inflammation:

• Rubor (redness), calor (heat), dolor (pain), tumor (swelling)

Most common pathogen to cause bacterial meningitis in a patient with cerebrospinal fluid rhinorrhea:

• Streptococcus pneumoniae

True or false: Prophylactic antibiotics have proven benefit to prevent bacterial meningitis in a patient with cerebrospinal fluid rhinorrhea?

• False. Prophylactic antibiotics have shown no proven benefit and may predispose to meninigitis with antibiotic-resistant bacteria.

Empiric treatment for a patient with cerebrospinal fluid rhinorrhea who develops bacterial meningitis:

• Vancomycin and an extended-spectrum cephalosporin (ceftriaxone, cefepime, or cefotaxime)

Term for infection/abscess formation in apocrine sweat glands:

• Suppurative hidradenitis

Name the locations at which suppurative hidradenitis may occur:

• Any site with apocrine glands: axilla, buttocks/perineum, and inguinal area

Most common organism involved in suppurative hidradenitis:

• Staphylococcus aureus

What is the treatment for suppurative hidradenitis:

• Antibiotics, incision and drainage, excision of skin for chronic infections

Microscopic finding associated with Actinomyces infection:

• Sulfur granules

Antibiotic of choice for Actinomyces infection:

• Penicillin G

Name clinical situations that require systemic antifungal therapy:

• Candida endophthalmitis, osteomyelitis, septic arthritis, and endocarditis, or any patient with a single positive blood culture from an indwelling intravascular catheter

Treatment for mucocutaneous candidiasis:

• Local clotrimazole or nystatin

Treatment for Candida isolated from a surgical drain:

• Nothing, most likely represents colonization

Mechanism of action of voriconazole:

• Prevents the production of ergosterol by acting as a selective inhibitor of the fungal cytochrome P-450 system

Mechanism of action of caspofungin:

• Inhibits the synthesis of an essential fungal cell wall component; β-(1-3)-D-glycan

Mechanism of action of amphotericin B:

• Increases permeability of the fungal cell membrane by binding ergosterol, which causes leakage of macromolecules and intracellular ions leading to cell death

True or false: Spontaneous bacterial peritonitis (SBP) is usually a polymicrobial infection?

• False. SBP is a monomicrobial infection.

Most frequent organism responsible for SBP:

• Escherichia coli followed by Klebsiella pneumoniae

True or false: SBP results from translocation of gut flora?

• False. It is thought to be from the combination of impaired bactericidal activity of ascitic fluid, abnormal host defense, and intrahepatic shunting, which leads to prolonged bacteremia.

The ascitic fluid protein concentration associated with 10-fold increased risk of SBP:

• <1 g/100 mL

Who should be admitted and treated for SBP?

• All symptomatic patients with a peritoneal fluid polymorphonuclear count of 250 to 500 cells/μL

Current antibiotic regime for SBP:

• Third-generation cephalosporin (cefotaxime)

What does cefotaxime not cover?

• Enterococci

Which is the most likely blood-borne organism to be transmitted after a hollow bore needle stick?

• Hepatitis B

Recommendation for a nonimmune health care worker exposed to hepatitis B:

• Begin hepatitis B vaccination series and give hepatitis B immunoglobulin within 7 days of the exposure

Recommendation for a health care worker vaccinated against hepatitis B but whose immune status is unknown and is exposed to a patient with active hepatitis B infection:

• Determine immune status. If anti-hep B antibody–positive—no intervention; If anti-hep B antibody–negative—hep B vaccine booster with hep B immunoglobulin

Prophylaxis for a nonimmune health care worker exposed to hepatitis C:

• No postexposure prophylaxis for hepatitis C

Method to diagnose and the treatment for lymphogranuloma venereum:

• Serologic testing and treatment with oral doxycycline 100 mg BID × 21 days

Name risk factors that increase the risk of transmission of HIV after percutaneous injury:

• Deep puncture injury, visible blood present on a sharp object causing injury, injury from object present within a blood vessel of the source patient, and injury involving a source patient with advanced HIV (CD4 count <50 cells/mm³)

Time period to start postexposure prophylaxis for HIV in a high-risk injury:

• Within 72 hours

Most common intestinal manisfestation of AIDS:

• Cytomegalovirus (CMV) colitis

Most common cause of upper gastrointestinal (GI) bleed in AIDS:

• Kaposi sarcoma

Most common cause of lower GI bleed in AIDS:

• CMV

Most common anorectal lesion in a patient with HIV:

• Anal condylomata

Normal CD4 count:

• 800 to 1200 cells/mm³

CD4 count associated with symptomatic disease:

• 300 to 400 cells/mm³

CD4 count associated with opportunistic infections:

• <200 cells/mm³

Prophylaxis is given to this organism when an HIV-infected patient has a CD4 count <200 cells/mm³:

• Pneumocystis carinii

Recommended prophylaxis for Pneumocystis carinii:

• Bactrim (trimethoprim/sulfamethoxazole)

Prophylaxis is given to this organism when an HIV-infected patient has a CD4 count <50 cells/mm³:

• Mycobacterium avium

Recommended prophylaxis for Mycobacterium avium:

• Azithromycin

Greatest known risk factor for the reactivation of latent tuberculosis infection:

• HIV infection

Recommended 4 drug treatments for patients with active pulmonary tuberculosis:

• Isoniazid, rifampin, pyrazinamide, and ethambutol for 2 months; if drug-susceptible and negative sputum cultures can complete treatment with isoniazid and rifampin for 4 months

Name bactericidal antimicrobial agents:

• Aminoglycosides, bactrim, β-lactams, carbapenems, cephalosporins, daptomycin, metronidazole, monobactams, nitrofurantoin, quinolones, vancomycin

Name bacteriostatic antimicrobial agents:

• Chloramphenicol, clindamycin, erythromycin, lincosamides, linezolid, macrolides, spectinomycin, sulfonamides, tetracyclines, trimethoprim

Mechanism of action of aminoglycosides:

• Interferes with ribosomal protein synthesis and disrupts cell wall cation homeostasis affecting the integrity of the bacterial cell membrane

Mechanism of action of bactrim:

• Sulfamethoxazole is an analogue of p-aminobenzoic acid and acts as a false-substrate inhibitor of dihydropteroate synthetase ultimately inhibiting the production of dihydropteroic acid.

• Trimethoprim interferes with dihydrofolate reductase inhibiting the synthesis of tetrahydrofolic acid.

Mechanism of action of β-lactams:

• Interferes with cross-linking of peptidoglycan (primary component in the cell wall of a Gram-positive bacteria) by covalently binding to and inactivating a bacterium's transpeptidase enzymes

What are carbapenems?

• A class of β-lactam antibiotics that are highly resistant to β-lactamases with a broad spectrum of antibacterial activity

The only β-lactams capable of inhibiting L,D-transpeptidases:

• Carbapenems

Mechanism of action of cephalosporins:

• Disrupt the synthesis of the peptidoglycan layer of the bacterial cell wall

Mechanism of action of daptomycin:

• Binds to the membrane and causes rapid depolarization resulting in a loss of membrane potential leading to inhibition of protein, DNA, and RNA synthesis, resulting in bacterial cell death

Mechanism of action of metronidazole:

• Once taken up by anaerobes, it is nonenzymatically reduced by reacting with reduced ferredoxin, resulting in the production of toxic products, which are taken up into bacterial DNA and form unstable molecules.

Mechanism of action of nitrofurantoin:

• Rapid reduction of nitrofurantoin inside the bacterial cell by flavoproteins (nitrofuran reductase) leads to multiple reactive intermediates that attack DNA, pyruvate metabolism, respiration, ribosomal proteins, and other macromolecules within the cell

Mechanism of action of quinolones:

• Inhibits bacterial DNA gyrase and topoisomerase IV, leading to inhibition of DNA replication and transcription

Mechanism of action of vancomycin:

• Prevents incorporation of N-acetylmuramic acid and N-acetylglucosamine peptide subunits into the peptidoglycan matrix (major structural component of Gram-positive cell wall)

Mechanism of action of chloramphenicol:

• Inhibits peptidyl transferase activity by binding to A2451 and A2452 residues in the 23S rRNA of the 50S ribosomal subunit, thus preventing peptide bond formation and protein synthesis

Mechanism of action of clindamycin:

• Inhibits ribosomal translocation by binding preferentially to the 23S rRNA of the large bacterial ribosome subunit, thus preventing protein synthesis

Mechanism of action of erythromycin:

• Interferes with aminoacyl translocation (prevents transfer of tRNA bound at A site of rRNA complex to P site) and inhibits protein synthesis by binding to the 50S subunit of the bacterial 70S rRNA complex

Mechanism of action of lincosamides:

• Causes premature dissociation of the peptidyl-tRNA from the ribosome by binding to the 23S portion of the 50S subunit of bacterial ribosomes

Mechanism of action of linezolid:

• Binds to the 23S portion of the 50S subunit and prevents the formation of the initiation complex (30S and 50S subunits of the ribosome, tRNA, and mRNA)

Mechanism of action of spectinomycin:

• Binds to the 30S ribosomal subunit and disrupts protein synthesis

Mechanism of action of sulfonamides:

• Competitive inhibitor of the enzyme dihydropteroate synthetase

Mechanism of action of tetracyclines:

• Prevents the docking of aminoacylated tRNA by binding the 30S ribosomal subunit, which interacts with 16S rRNA

The only tissue that cefazolin does not penetrate well:

• Central nervous system

What are the appropriate vancomycin peak and trough values?

• Peak 20 to 40 μg/mL and trough 5 to 10 μg/mL

What are the appropriate gentamicin peak and trough values?

• Peak 5 to 10 μg/mL and trough <1 μg/mL

Mechanism of acquired vancomycin resistance:

• Alteration to the terminal amino acid residues of the NAM/NAG peptide subunits that vancomycin binds

Name the 3 known mechanisms of fluoroquinolone resistance:

1. Efflux pumps that decrease intracellular quinolone concentration

2. Plasmid-mediated resistance genes that produce proteins, which bind to and protect DNA gyrase

3. Decreased binding affinity from mutations at key sites in DNA gyrase or topoisomerase IV

Usual mechanism of penicillin resistance:

• Plasmids that code for β-lactamase

Mechanisms for aminoglycoside resistance:

• Enzymatic modification (most common), reduced uptake or decreased cell permeability, and altered ribosome-binding sites