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Antimicrobial Resistance*: It’s Time to Reverse the Trend FREE TO VIEW

Joseph P. Lynch, III, MD, FCCP
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*From the University of Michigan Medical Center, Ann Arbor, MI.

Correspondence to: Joseph P. Lynch III, MD, FCCP, Professor of Internal Medicine, Division of Pulmonary and Critical Care Medicine, The University of Michigan Medical Center, 3916 Taubman Center, Ann Arbor, MI 48109

Chest. 2001;119(2_suppl):371S-372S. doi:10.1378/chest.119.2_suppl.371S
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The problem of antimicrobial resistance among clinically relevant pathogens continues to plague our hospitals. Between 20% and 60% of nosocomial infections are thought to be caused by antibiotic-resistant bacteria. Such infections increase patient morbidity and mortality rates and cause health-care costs to escalate. Critically ill patients in ICUs are particularly hard-hit by antimicrobial-resistant pathogens. These clever, single-celled organisms adapt to counteract our repertoire of antimicrobial artillery at a rate that exceeds our efforts to devise new strategies to thwart their attack.

While hospital-acquired pneumonia (HAP) is the second most frequent nosocomial infection, it is first in morbidity and mortality rates. Patients receiving mechanical ventilation in the ICU are particularly vulnerable to the effects of HAP. The pathogens that commonly cause “late-onset” HAP, including Pseudomonas aeruginosa and Acinetobacter, are highly resistant to a number of antimicrobials. This high-level resistance is associated with substantial mortality rates of approximately 30 to 50%.

This supplement issue was compiled to address the current state of antimicrobial resistance and its impact on the treatment of nosocomial infections, particularly HAP. In addition, the question of how to prevent further increases in the prevalence of antimicrobial-resistant bacterial pathogens is discussed. The supplement begins with an article by Dr. Ronald Jones (see page 397S), who provides an in-depth overview of the present patterns of antimicrobial resistance among nosocomial pathogens. Dr. Jones indicates that third-generation cephalosporins, such as ceftazidime, are likely to be ineffective against some nosocomial infections and may actually promote the development of resistance. He discusses other therapeutic options for treating antibiotic-resistant, Gram-positive and Gram-negative pathogens, such as β-lactam/β-lactamase inhibitors, the carbapenems, and cefepime.

My article (see page 373S) discusses the risk factors, causative pathogens, and current treatment options for HAP. It is clear that adequately timed and appropriate empiric therapy for HAP is the key to patient survival. Dr. Gerry San Pedro’s article (page 385S) critically reviews thepotential roles and limitations of invasive or noninvasive diagnostic tests in aiding physicians with their therapeutic decisions. At present, there is no strong evidence to show that adjusting antimicrobial therapy based on results of such tests significantly affects mortality rates due to HAP.

How can we make it easier for physicians to choose the correct empiric antimicrobial therapy for patients with HAP? Dr. Stanley Fiel provides a critical review of the guidelines (page 412S) set forth by the American Thoracic Society in 1996, and he discusses how newer agents fit into these guidelines. In addition, Dr. Fiel discusses the role of computer-assisted antibiotic management programs, based on surveillance of local antimicrobial-resistance patterns, in helping physicians select the most appropriate antimicrobial agent. Hospitals that have employed these computer-based programs have observed stabilization of antimicrobial resistance rates and reduced costs.

Klebsiella pneumoniae and Escherichia coli with extended-spectrum β-lactamases (ESBLs) and vancomycin-resistant enterococci (VRE) are some of the most problematic antibiotic-resistant pathogens. Dr. Louis Rice (page 391S) reviews the evolution of ESBLs and discusses how the overuse of third-generation cephalosporins, particularly ceftazidime, has promoted resistance among these organisms. Furthermore, Dr. Rice summarizes his clinical experience and recommendations regarding the substitution of piperacillin/tazobactam for ceftazidime to curb increases in ESBL-producing K pneumoniae. Use of this β-lactam/β-lactamase inhibitor reduced the prevalence of ESBL-producing K pneumoniae without increasing the degree of resistance to it.

Dr. Jan Patterson offers supporting evidence (see page 426S) that implicates the overuse of ceftazidime and vancomycin as causes for increased rates of ESBL-producing K pneumoniae and VRE. Concordantly, Dr. Patterson reviews intriguing data from her institution that demonstrate a decrease in ESBL-producing K pneumoniae and VRE on a shift in antibiotic utilization from ceftazidime to piperacillin/ tazobactan, in conjunction with infection-control guidelines. Dr. Rekha Murthy reports (page 405S) how her institution had a decrease in ESBL-producing K pneumoniae and VRE by restricting vancomycin utilization, discouraging broad-spectrum antibiotic use, and implementing a hospital-wide educational campaign about antimicrobial resistance.

Our understanding of the molecular mechanisms by which the host immune system fights bacterial infections has grown dramatically over the past decade. Subsequently, there has been increasing interest in using this knowledge to formulate therapies that may boost the immune response to pathogenic microorganisms. Dr. Steve Nelson (page 419S) reviews a series of interesting reports that illustrate how local cytokine expression in the lung may be modulated to improve treatment of pneumonia. Dr. Nelson also discusses how augmentation of the neutrophil response to infection via cytokine immunotherapy may promote increased antibiotic delivery to infected sites.

The tremendous increase in the number of antimicrobial-resistant pathogens over the past several decades is aresult of our overuse and misuse of antimicrobials. We have elevated the selective pressure to drive bacterial pathogens to resist antimicrobial agents, and we are now racing to develop methods and therapies to reverse the trend. However, until other therapeutic options become available, the key to reversing the trend in the next decade will entail careful and appropriate antibiotic selection, surveillance, and infection-control procedures.

Abbreviations: ESBL = extended-spectrum β-lactamase; HAP = hospital-acquired pneumonia; VRE =vancomycin-resistant enterococci




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