Bugs and Drugs: Update on Antimicrobial Therapy

Bugs and Drugs: Update on Antimicrobial Therapy
KCNPNM 2014 Conference Bugs and Drugs: Update on Antimicrobial Therapy

Objectives Compare and contrast the antimicrobial drug classes
Understand the types of antimicrobial drug resistance that can occur Create treatment plans for which antimicrobial therapy can be managed successfully Related prudent use of antimicrobial therapy to quality metrics

Introduction The modern age of antibiotic therapeutics was launched in the 1930s with sulfonamides and the 1940s with penicillin Since then, many antibiotic drugs have been developed, most aimed at the treatment of bacterial infections These drugs have played an important role in the dramatic decrease in morbidity and mortality due to infectious diseases While the absolute number of antibiotic drugs is large, there are few unique antibiotic targets While antibiotics have played a role in decreasing infectious disease related deaths, improved sanitation and vaccine development are extremely important advances as well.

Nine Factors to Consider When Selecting an Antibiotic
Spectrum of coverage Patterns of resistance Evidence or track record for the specified infection Achievable serum, tissue, or body fluid concentration (e.g. cerebrospinal fluid, urine) Allergy Toxicity Formulation (IV vs. PO); if PO assess bioavailability Adherence/convenience (e.g. 2x/day vs. 6x/day) Cost

Principles of Antibiotic Therapy
Empiric Therapy (85%) Infection not well defined (“best guess”) Broad spectrum Multiple drugs Evidence usually only 2 randomized controlled trials More adverse reactions More expensive Directed Therapy (15%) Infection well defined Narrow spectrum One, seldom two drugs Evidence usually stronger Less adverse reactions Less expensive Compare and contrast directed and empiric therapy. Which therapy would you rather have if you were the patient? In most medical centers only 15-20% of therapy is directed leaving 85-80% as empiric. Why is this?

Why So Much Empiric Therapy?
Need for prompt therapy with certain infections Life or limb threatening infection Mortality increases with delay in these cases Cultures difficult to do to provide microbiologic definition (i.e. pneumonia, sinusitis, cellulitis) Negative cultures Provider Beliefs Fear of error or missing something Not believing culture data available “Patient is really sick, they should have ‘more’ antibiotics” Myth of “double coverage” for gram-negatives e.g. pseudomonas “They got better on drug X, Y, and Z so I will just continue those” Compare and contrast directed and empiric therapy. Which therapy would you rather have if you were the patient? In most medical centers only 15-20% of therapy is directed leaving 85-80% as empiric. Why is this?

To Increase Directed Therapy for Inpatients:
Define the infection 3 ways Anatomically, microbiologically, pathophysiologically Obtain cultures before starting antibiotics Use imaging, rapid diagnostics and special procedures early in the course of infection Have the courage to make a diagnosis Do not rely solely on “response to therapy” to guide therapeutic decisions; follow recommended guidelines If empiric therapy is started, reassess at hours Move to directed therapy (de-escalation or streamlining) Do not use “response to therapy” to guide therapy as the patient’s “response” is often not directly attributable to your antibiotic prescription.

To Increase use of Directed Therapy for Outpatients:
Define the infection 3 ways Anatomically, microbiologically, pathophysiologically Obtain cultures before starting antibiotics Often difficult in outpatients (acute otitis media, sinusitis, community-acquired pneumonia) Narrow therapy often with good supporting evidence Amoxicillin/clavulanate for AOM, sinusitis and CAP Penicillin for Group A Streptococcal pharyngitis Clindamycin or trimethoprim/sulfamethoxazole for simple cellulitis Trimethoprim/sulfamethoxazole or ciprofloxicin for cystitis

Is An Infection Present?

Signs and Symptoms Increase in WBCs and a “left shift” Fever
Pain and Inflammation Hemodynamic changes Neurologic changes Gram stain

Overview Colonization Infection Where bacteria are supposed to reside
Bacteria are present but no signs and symptoms of infection Infection Where bacteria invade Bacteria are present and have often migrated to different organs to cause systemic infection Most likely to occur The intrinsic virulence of the particular organism The immune status of the host The quantity or load of the initial innoculant

Treat Bacterial Infection, not Colonization
Many patients become colonized with potentially pathogenic bacteria but are not infected Asymptomatic bacteriuria or foley catheter colonization Tracheostomy colonization in chronic respiratory failure Chronic wounds and decubiti Lower extremity stasis ulcers Chronic bronchitis Can be difficult to differentiate Presence of WBCs not always indicative of infection Fever may be due to another reason, not the positive culture

Treat Bacterial Infection, not Colonization Example: Asymptomatic Bacteriuria
≥105 colony forming units is often used as a diagnostic criteria for a positive urine culture It does NOT prove infection; it is just a number to state that the culture is unlikely due to contamination Pyuria also is not predictive on its own It is the presence of symptoms AND pyuria AND bacteriuria that denotes infection

Do Not Treat Sterile Inflammation or Abnormal Imaging Without Infection Example: Community-Acquired Pneumonia (CAP) CAP: often a difficult diagnosis X-rays can be difficult to interpret. Infiltrates may be due to non-infectious causes. Examples: Atelectasis Malignancy Hemorrhage Pulmonary edema Additional examples of non-infectious causes of pulmonary infiltrates: Heart failure, pulmonary embolism, pulmonary effusions, chronic fibrosis

Do not Treat Viral Infections with Antibiotics
Acute bronchitis Common colds Sinusitis with symptoms less than 7 days Sinusitis not localized to the maxillary sinuses Pharyngitis not due to Group A Streptococcus spp. Role of bacteria in acute bronchitis is minimal. Mostly due to viral infections of the upper airways including: influenza A and B, parainfluenza, coronavirus, rhinovirus, respiratory syncytial virus, and human metapneumovirus. Note: May want to make a point that acute bronchitis is different from acute exacerbations of chronic bronchitis which in some situations have better outcomes on antibiotics. Gonzales R, et al. Annals of Intern Med 2001;134:479 Gonzales R, et al. Annals of Intern Med 2001;134:400 Gonzales R, et al. Annals of Intern Med 2001;134:521

Culture and Sensitivity
Final identification of pathogen and effectiveness of antibiotics May not give appropriate information Patient previously taking antibiotics Culture not obtained properly Contamination Not time sensitive

Key Terms MIC = Minimal inhibitory concentration. Lowest concentration of antimicrobial that inhibits growth of bacteria. Commonly used in clinical lab MBC = Minimal bactericidal concentration. Concentration of an antimicrobial that kills bacteria. Used clinically only in special circumstances Breakpoint = The MIC that is used to designate between susceptible and resistant. Arbitrarily set by the laboratory

Breakpoint Susceptibility
Susceptible – pathogens with the lowest MICs and are most likely to be eradicated with antibiotic therapy Intermediate - ?? – Treatment may be successful if the antibiotic is used in higher doses or if the antibiotic has good penetration into the infection site Resistant – significantly higher MICs that will cause a less than optimal clinical outcome even if higher doses of the antibiotic are used

Concept of Breakpoint to Determine Susceptibility
EXAMPLE: Susceptibility testing for a single isolate of Pseudomonas aeruginosa Antibiotic MIC Breakpoint Susceptibility Ampicillin >16 8 Resistant Gentamicin 2 4 Susceptible Cephalothin N/A Cefepime 32 Cefotaxime 16 16/32 Intermediate Ceftazidime Aztreonam Ciprofloxacin Amp/Sulbactam Meropenem 4/8 Pip/tazo 32-64/128 -Breakpoint for intermediate resistance for meropenem is 4 and for piperacillin/tazobactam (pip/tazo) 32 -Pip/tazo is the better choice between the two -Ciprofloxacin is a poor choice even though the MIC is lowest of the three Determining the minimal inhibitory concentration of an antibiotic for a specific bacterial strain does not tell you if the antibiotic is susceptible or resistant. MICs are relative while susceptible and resistant are absolute determinations. For any bacteria/antimicrobial pair, susceptible vs resistant is determined by comparing the MIC to an arbitrarily designated “breakpoint”. If the MIC is lower than the breakpoint, the bacterium is considered susceptible. If it is higher, it is considered resistant. Breakpoint numbers are designated by committees of microbiologists and antimicrobial experts. Data on antimicrobial clinical efficacy, pharmacokinetics and achievable antibiotic concentrations in serum and tissue are used to determine this number. Because susceptibility is determined by comparing the MIC to the breakpoint and the breakpoint is different for each antibiotic, one cannot compare MICs between different antibiotics to determine efficacy or potency of antibiotic. This example shows this clearly for a Pseudomonas aeruginosa clinical isolate.

Resistance

Introduction Since the first use of antibiotics in the 1930s and 1940s, bacteria quickly adapted and developed mechanisms to escape their effects Over the following decades, new antibiotics were developed to overcome resistance Since the 1990s, new antibiotic development has fallen sharply while bacterial resistance continues to increase Antibiotic resistance is responsible for countless human deaths and billions of dollars in healthcare expenses 70% of bacteria that cause healthcare-acquired infections are resistant to common antibiotics Understanding antimicrobial resistance, how bacteria become resistant to antibiotics and the factors that contribute to resistance will be extremely important for us to preserve these important drugs for the future. Antimicrobial resistance is not a new phenomenon; however, the current magnitude of the problem and the speed with which new resistance phenotypes have emerged elevates the public health significance of this issue to a crisis level

Antibiotic Use Leads to Antibiotic Resistance
Inpatient Agriculture Sources of antibiotic resistant bacteria are where antibiotics are used. Most of the resistant pathogens of significance arise in the acute or long-term care facility and the outpatient clinics. Depending on the source, different pathogens are pressured and transmitted. This talk focuses on antimicrobial use in humans. However, it is important to note that almost one half of all of the antibiotic used in North America are used in agriculture. This pressures resistance in food-borne pathogens such as salmonella, campylobacter, and less importantly enterococcus. Outpatient

Clearing Up Misconceptions
Misconception: Antibiotics are no longer effective because people who have taken the medication have developed a tolerance to the drug Truth: People do NOT develop a tolerance to drugs; the reason drugs no longer work is because the bacteria is no longer killed by the drug because they have become resistant to the effects

Factors that Promote Resistance
Exposure to antibiotics Prolonged courses Use of incorrect antibiotic Sub-therapeutic doses Treatment of viral infections Introduction of resistant organisms from outside the population Transfers from outside facilities Long-term care facilities are primary reservoirs of antimicrobial resistance Food sources (BSE, VRE, Hepatitis A, GI bugs) Mobile society (SARS) Tissue culture passage effect Spread from patient to patient (hand hygiene) Animal to human spread - agriculture Melinda

Reasons for Antibiotic Overuse : Conclusions from Eight Focus Groups
Patient Concerns Want clear explanation Green nasal discharge Need to return to work Physician Concerns Patient expects antibiotic Diagnostic uncertainty Time pressure Antibiotic Prescription Barden L.S. Clin Pediatr 1998;37:665

“As long as we expose bacteria to antibiotics, they will evolve resistance to them. The more exposure…the more rapidly resistance will occur” (National Institute of Allergy and Infectious Diseases, 2014)

Antibiotic Use Leads to Antibiotic Resistance
Resistant bacteria or their genetic determinates are selected when colonizing or infecting bacteria are exposed to antibiotics Resistant bacteria can then be transmitted between patients Highest risk patients: Immunocompromised Hospitalized Invasive devices (central venous catheters) Important concept is that antibiotics are the only drug that have direct public health consequences for persons other than the one who received the antibiotic

Antibiotic Mechanism of Action
Linezolid Daptomycin Daptomycin Daptomycin Daptomycin Daptomycin Daptomycin

Mechanisms Of Antibiotic Resistance
Can be related back to how the antibiotic works Bacteria are capable of becoming resistant through several mechanisms One or many mechanisms may exist in an organism Multidrug-resistant bacteria often have multiple mechanisms Genes encoding resistance may exist on plasmid or chromosome Alteration in Target Molecule Decreased Permeability

Mechanisms of Resistance
Antibiotic Degrading Enzymes Sulfonation, phosphorylation, or esterifictation Especially a problem for aminoglycosides β-lactamases Simple, extended spectrum β-lactamases (ESBL), cephalosporinases, carbapenemases Confer resistance to some, many, or all beta-lactam antibiotics May be encoded on chromosome or plasmid More potent in gram-negative bacteria Examples: S. aureus, H. influenzae, N. gonorrhoeae, E. coli, Klebsiella sp., Enterobacter sp., Serratia sp., other enteric bacteria, anaerobes

Extended Spectrum -lactamases
-lactamases capable of hydrolysing extended spectrum cephalosporins, penicillins, and aztreonam Most often associated with E. coli and Klebsiella pneumoniae but spreading to other bacteria Usually plasmid mediated Aminoglycoside, ciprofloxacin and trimethoprim-sulfamethoxazole resistance often encoded on same plasmid Has become a significant resistance determinate in acute and long-term care facility enteric pathogens ESBLs hydrolyze a number of different compounds, especially broad-spectrum cephalosporins, including penicillins. Usually susceptible to carbapenem antibiotics unless the organism also encodes a carbapenemase ESBLs are most often associated with E coli and Klebsiella Other pathogens can produce ESBLs as well Many different types of ESBLs (more than 170 species) have been described 31

Class A Carbapenemases
Most common in Klebsiella pneumoniae (KPC) Also seen in E. coli, Enterobacter, Citrobacter, Salmonella, Serratia, Pseudomonas and Proteus spp. Very often with multiple other drug resistance mechanisms, resistance profile similar to ESBL but also carbapenem resistant Became problem in New York City first in and is being increasingly recognized in Mid-Atlantic US. Spreading across species to other gram-negatives and enterobacteriaceae Emerging in long-term care facilities 32

Multidrug Resistant Gram-Negative Organisms
Development of resistance to multiple antimicrobial classes severely limits treatment options and the incidence of resistance is rising Proportion of isolates resistant to three antibiotic classes ranged from 10 to 60% for different gram-negative bacteria, while some are resistant to four antibiotic classes Resistant to 3 antibiotic classes Resistant to 4 antibiotic classes Pseudomonas aeruginosa 10% 2% Acinetobacter baumannii 60% 34% Klebsiella pneumoniae 15% 7%

Multidrug Resistant Gram-Negative Organisms
Widespread use of cephalosporins and beta-lactam combination antibiotics has led to extended-spectrum beta-lactamases (ESBLs), which are resistant to both classes Carbapenems have been the only effective agents for ESBLs Emergence of carbapenemases, such as Klebsiella pneumoniae carbapenemase (KPCs) are threatening carbapenems as the antibiotics of last resort Significant issue for many military personnel due to the high amount of Acinetobacter in the desert NO NEW ANTIBIOTICS ON THE HORIZON!!!

Decreased Permeability Pseudomonas spp. Affects many antibiotics including carbapenems Efflux Pumps Pseudomonas spp. (multiple antibiotics) Tetracyclines Macrolides

Target Alteration DNA gyrase Fluoroquinolones Many gram-negatives, S. pneumoniae Penicillin-binding protein Methicillin-resistant S. aureus (MRSA) Penicillin-resistant S. pneumoniae Gram positive cell wall Vancomycin Enterococcus spp.

Target Alteration (cont’d) Ribosome Tetracyclines Macrolides S. pneumoniae, Staphylococcus sp., N. gonorrhoeae, enteric gram-negative rods

Treatment Options for Common Infections

HA-MRSA Patients have multiple risk factors
Usually involves various types of infection Bacteremia Intravenous lines Pneumonia Skin and soft tissue infections Transmission is person to person Growth rate is slow Resistant to multiple antibiotics Need to make sure that patient has an infection

Antibiotic Therapy for HA-MRSA
Usually resistant to multiple antibiotics Resistant to penicillins and cephalosporins May be resistant to clindamycin and trimethoprim-sulfamethoxazole Drugs of choice include vancomycin, linezolid (Zyvox), daptomycin (Cubicin), or quinupristin-dalfopristin (Synercid)

CA-MRSA Risk factors not clearly identified other than more likely in a younger patient Des seem to be a correlation between sharing of close quarters Transmission is person to person Growth rate is fast The prevalence factor is PVL (panton-valentine leukocidin) and two major clones have been identified - makes this strain more virulent Resistant to beta-lactams, but sensitive to other agents

Antibiotic Therapy for CA-MRSA
When the infection is skin/ soft tissue, incision and drainage of area may be needed Usually resistant to the beta-lactams (penicillin and cephalosporins) Usually sensitive to clindamycin, trimethoprim-sulfamethoxazole, minocycline, doxycycline May be beneficial to add Rifampin for synergistic effect Also sensitive to vancomycin, daptomycin, and linezolid, although these agents are not first-line

Acute Pharyngitis One of the four most common episodic clinic visit
May be viral or bacterial 40% of children with pharyngitis have Group A Streptococcal pharyngitis Most commonly affected ages of 5 to 12 years Not usually seen in children under age 3 Only 5-15% of adult cases of acute pharyngitis are caused by group A beta-hemolytic streptococcal (GABHS)

Acute Pharyngitis Treatment No antibiotics when viral!
Treatment with antibiotics usually last for 7 to 10 days Penicillin Amoxicillin or amoxicillin/ clavulanate Second or third generation oral cephalosporin Macrolide Penicillin is recommended for initial treatment of GABHS No resistance seen in the United States yet Fluoroquinolones are NOT appropriate

Rhinosinusitis Most cases are viral Bacterial - often atypicals
Less than 10% are bacterial Resolves in about 7 days Bacterial - often atypicals Double-sickening – symptoms last longer than 7 days Nasal congestion Cough - often worse at night due to drainage Facial pain - above or below the eyes that worsens when patient leans forward Toothache - if maxillary sinuses are involved Headache Purulent drainage, although nasal discharge alone is not a good predictor of a bacterial infection Clear to yellow to green High fever – 102 or higher

Pharmacologic Treatments
Regardless of whether the etiology is infectious, allergic, or irritant, treatment should focus on relieving obstruction and establishing drainage Analgesics Decongestants Antihistamines Corticosteroids Mucolytics Antibiotics

Antibiotics Rhinosinusitis is the fifth most common diagnosis for which an antibiotic is prescribed First need to be sure that the infection is bacterial – most are viral and not bacterial Want to use antibiotics with good coverage of atypicals and gram-positive organisms, as well as good penetration into the sinus cavity Usually need to treat for 10 to 14 days If chronic sinusitis, may need to consider 3 to 4 weeks of antibiotics, especially if surgery may be required

Antibiotics For milder infections
Penicillins, such as amoxicillin/clavulanate Doxycycline May not be as effective due to increasing resistance among pneumococci Second or third generation cephalosporins Macrolides For more serious infections Amoxicillin/ clavulanate (high dose) Quinolone with antipneumococcal activity, such as levofloxacin PQRS Measure

Treatment Options for OM
Studies have shown that the symptoms of OM spontaneously resolved in 80% of children at 2 to 7 days. (Otalgia – endpoint) More likely to be bacterial if child has siblings or attends day care Ibuprofen or acetaminophen are the best options for pain control Analgesic ear drops can also provide symptomatic relief Some controversy over the use of decongestants, although fluid accumulating behind the ear drum is often a contributing factor

Treatment Options for OM
Antibiotics Amoxicillin or Amoxicillin/ clavulanate Second or third generation cephalosporin Macrolide PQRS Measure

Pneumonia Common lower respiratory tract infection that causes inflammation of the lung parencyma Pneumonia – sixth leading cause of death The defense mechanisms of the lung usually help to prevent passage of foreign materials Disease states, such as COPD Age Smoking Immunization! Pneumococcal vaccination will help to decrease incidence and severity of susceptible strains of pneumonia

CAP vs HCAP HCAP - Healthcare-associated pneumonia
Acquired in an environment, such as a hospital, residing in a nursing home, receiving home health care, or dialysis Usually caused by very different organisms MRSA Gram-negative organisms CAP - Community-acquired pneumonia Streptococcus pneumoniae More than 15% of S. pneumoniae are highly resistant to penicillin and increasingly resistant to macrolides and cephalosporins Hospital Core Measure

Macrolide-Resistant S
Macrolide-Resistant S. pneumoniae Prevalence is Increasing in US – 2000 to 2005 While Penicillin, cephalosporin and fluoroquinolone resistance has decreased in the US, likely due to introduction of the conjugate pneumococcal vaccine and prudent antibiotic use macrolide resistant continued to increase in the later 2000s. One possible reason being that macrolide use, especially azithromycin, continued to increase in the US from 2000 to 2005 Prevalence is increasing, but incidence is decreasing. We have seen a huge drop in incidence with PCV7 and expect further decreases with PCV13. Jenkins S. et al Emerg Infect Dis. 2009;5:1260 Hicks L et. Al. Emerg Infect Dis. 2010;16:896

Empiric Treatment - Outpatients
Macrolide (azithromycin, clarithromycin) Doxycyline If S. pneumoniae is thought to be the causative organism, then a penicillin or cephalosporin would be the drug of choice provided there is no resistance Also starting to see resistance to macrolides If resistance is an issue, may need to use a quinolone

Empiric Treatment - Inpatients
Necessary to cover both typical and atypical pathogens Ampicillin/Sulbactam plus a Macrolide Newer Fluoroquinolone – high dose, short course Third-generation Cephalosporin plus a Macrolide s With structural lung disease a regimen with activity against Pseudomonas should be considered, such as a Third or Fourth generation Cephalosporin plus a Fluoroquinolone If aspiration pneumonia is suspected, Metronidazole or Clindamycin can be added In treating pneumococcal pneumonia that is highly resistant, an IV fluoroquinolone, vancomycin, or linezolid may need to be added to the regimen. Early gram-stain may be helpful for choosing antibiotics Core Measure

Treatment Options for Bronchitis
No antibiotics! Increase hydration Expectorants/ Antitussives Antipyretics Albuterol ? If antibiotics are considered Macrolides or doxycycline for atypical coverage Second generation cephalosporins Amoxicillin/clavulanate (high dose) Quinolones when compromised lung function

C. Diff Treatment Decreasing the use of antibiotics that most often lead to C diff infections by 30% could lead to 26% fewer infections Quinolones Beta-lactams Extended spectrum cephalosporin In 23% of patients, C difficile-associated disease will resolve within 2 to 3 days of antibiotic discontinuation Avoid anti-motility agents Hospital HAC Measure

C. Diff Treatment Infection can be treated with either metronidazole or oral vancomycin for 10 to 14 days Likely to take 2 to 4 days before the diarrhea stops Vancomycin should only be used if treatment failure to metronidazole, patient is pregnant, or known resistant strain Oral agents preferred but may use IV metronidazole if patient cannot tolerate oral therapy

New Strain of C diff Increased rates of C diff-associated disease with more severe symptoms and an increase in mortality has been seen Meta-analysis showed a 23% annual increase in hospitalizations from C diff-associated disease from 2000 through 2005 along with a 35% increase in deaths A new strain of C diff has been found that appears to be more virulent, produces greater quantities of toxin A and B, and is resistant to current therapies Cause may be changes in antimicrobial usage Treatment – metronidazole or vancomycin Fidoxamicin Fecal transplant

Fecal Transplant Gaining more acceptance
No standard administration approach Most often enema/ colonoscopy although can be administered through NG tube Stool slurry that needs to be used immediately from donor Success is measured through resolution of symptoms and absence of relapse within 8 weeks

UTI Organisms E. coli causes 80% of all community-acquired UTIs and about half of UTIs in the hospital E. coli has become increasingly resistant to TMP-SMX to where it is no longer a first line agent for complicated UTI or pyelonephritis Beta-lactams are associated with about a 40% resistance rate for E. coli Other pathogens include gram-negative rods, such as Proteus, Klebsiella, and Enterobacter Although the quinolones are used for complicated UTIs, more resistance is being seen with Enterococci Nitrofurantoin has low resistance, but has little use beyond the urinary tract because of poor tissue perfusion

Summary of Asymptomatic Bacteriuria Treatment
Treat symptomatic patients with pyuria and bacteriuria Don’t treat asymptomatic patients with pyuria and/or bacteriuria Define the symptomatic infection anatomically Dysuria and frequency without fever equals cystitis Dysuria and frequency with fever, flank pain, and/or nausea and vomiting equals pyelonephritis Remember prostatitis in the male with cystitis symptoms Remove catheters!!! SCIP Measure PQRS Measure Hospital HAC Measure Note: The two scenarios in which the treatment of asymptomatic bacteriuria is appropriate are: pregnancy and patients undergoing a urologic procedure for which bleeding is anticipated.

Treatment Options for UTIs
Antibiotic Duration Uncomplicated UTI TMP-SMX or Nitrofurantoin 3 days Uncomplicated UTI in Older Women TMP-SMX 7 days Uncomplicated UTI with Suspected Resistant Organisms Quinolone (ciprofloxacin) 3 – 7days UTI in Pregnancy Amoxicillin/ clavulanate or Second Generation Cephalosporin or Nitrofurantoin 7 – 10 days Complicated UTI (Outpatient) Quinolone 10-14 days Complicated UTI (Inpatient) Third Generation Cephalosporin or Carbapenem days

Treatment Options for UTIs
Antibiotic Duration Pyelonephritis Quinolone plus Aminoglycoside or Third Generation Cephalosporin or Antipseudomonal Penicillin 7 – 14 days, up to 21 days Hospital-Acquired UTI Quinolone or Carbapenem or 10-14 days

Pearls for Antibiotics

Key Points for Antibiotics
Carbapenems Not all agents are the same Ertapenem – not as broad spectrum Doripenem – concern about use in pneumonia Use carefully due to the development of carbapenases Clindamycin Good choice for CA-MRSA Psedomembraneous colitis Daptomycin Should not be used for pneumonia Watch for myositis

Fluoroquinolones Same effect either PO or IV Starting to see more issues with resistance Watch for tendon issues Not indicated for children under the age of 16 Linezolid Should be reserved for when resistance to vancomycin is present Thrombocytopenia – more common after 10 days of therapy Potential serotonin syndrome?

Metronidazole Same effect either PO or IV Potential for several adverse reactions’ GI Watch for disulfiram-like reaction with alcohol Penicillins Use may be limited because of resistance Addition of other agents to help combat resistance Rifampin Should not be used as monotherapy because quick development of resistance Used in combination with other antibiotics in the treatment of CA-MRSA for synergistic effect Change in secretions to red-orange

Sulfa Several potential drug-drug interactions Lots of potential adverse reactions Watch for hypersensitivity reactions Tetracyclines Drug-drug and drug-food interactions Contraindicated in pregnancy and in children under age 16 Vancomycin IV for MRSA only PO for C diff only Watch renal function and monitor trough levels

Antimicrobial Stewardship

What Is Antimicrobial Stewardship?
Antimicrobial stewardship is a mutlidisciplinary approach for rational antibiotic therapy Must be based on evidence-based guidelines Must be based on data Must apply to all practitioners

Core Actions to Prevent Antibiotic Resistance
Preventing infections Prevent the spread of resistance Tracking and surveillance Improve antibiotic prescribing through stewardship Development of new antibiotics and new diagnostic tests for resistance bacteria

Principles of Antibiotic Stewardship
Re-evaluate, de-escalate or stop therapy at hours based on diagnosis and microbiologic results Re-evaluate, de-escalate or stop therapy with transitions of care (e.g. ICU to step-down or ward) Do not give antibiotic with overlapping activity Do not “double-cover” gram-negative rods (i.e. Pseudomonas sp.) with 2 drugs with overlapping activity Make sure that all prescriptions/orders for antibiotics have the appropriate dose, duration, and indication

Principles of Antibiotic Stewardship
Limit duration of surgical prophylaxis to <24 hours perioperatively Use rapid diagnostics if available (e.g. respiratory viral PCR) Prevent infection Use good hand hygiene and infection control practices Remove catheters Consult infectious disease Use of biomarkers of inflammation (e.g. procalcitonin) is an emerging area in antibiotic stewardship

Conclusion Antibiotics clearly save lives
Poor prescribing of antibiotics are putting patients at unnecessary risk Adverse reactions Development of resistant organisms Every time an antibiotic is prescribed If at all possible, order recommended cultures before antibiotics are given Make sure an indication, dose, and expected duration are part of the prescription order Reassess within 48 hours and adjust antibiotic or discontinue if warranted Pay for performance indicators

Questions? Thank You! Melinda Joyce

Bugs and Drugs: Update on Antimicrobial Therapy

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