Bacterial resistance, development

Of increasing concern is the development of mutant strains of tuberculosis that are resistant to many of the aiititubercular drug s currently in use. Bacterial resistance develops, sometimes rapidly, with the use of anti-tubercular drag s. Treatment is individualized and... 

The routine use of the macrolides is limited because bacterial resistance develops quickly following repeated exposure. There can be crossresistance between the drugs in this class. The mechanisms of resistance include decreased drug entry into bacteria, inability to bind to the SOS ribosomal subunit and the plasmid-mediated production of macrolide-destroying esterase. 

Bisphenols are composed of two phenolic groups connected by various linkages. Triclosan (Fig. 17.7J) is the most widely used. It is bacteriostatic at use-concentrations and has little anti-pseudomonal activity. It has been incorporated into medicated soaps, lotions and solutions and is also included in household products such as plastics and fabrics. There is concern about bacterial resistance developing to triclosan. 

Erythromycin can be used for patients who reqnire systemic antibiotics, but cannot tolerate tetracyclines, or who acqnire hacterial strains resistant to tetracyclines. The dosage is nsnally 1 g/day with meals to minimize gastrointestinal intolerance. Zinc combination products possibly enhance penetration of erythromycin into the pilosebaceous unit. Erythromycin s efficacy is similar to tetracycline, but it induces higher rates of bacterial resistance. - Development of erythromycin resistance by P. acnes may be rednced by combination therapy with BPO. 

Resistance to antimicrobial agents is of concern as it is well known that bacterial resistance to antibiotics can develop. Many bacteria already derive some nonspecific resistance to biocides through morphological features such as thek cell wall. Bacterial populations present as part of a biofilm have achieved additional resistance owkig to the more complex and thicker nature of the biofilm. A system contaminated with a biofilm population can requke several orders of magnitude more chlorine to achieve control than unassociated bacteria of the same species. A second type of resistance is attributed to chemical deactivation of the biocide. This deactivation resistance to the strong oxidising biocides probably will not occur (27). 

Resistance to Tetracyclines. The tetracyclines stiU provide inexpensive and effective treatment for several microbial infections, but the emergence of acquired resistance to this class of antibiotic has limited their clinical usehilness. Studies to define the molecular basis of resistance are underway so that derivatives having improved antibacterial spectra and less susceptibiUty to bacterial resistance may be developed. Tetracyclines are antibiotics of choice for relatively few human infections encountered in daily clinical practice (104), largely as a result of the emergence of acquired tetracycline-resistance among clinically important bacteria (88,105,106). Acquired resistance occurs when resistant strains emerge from previously sensitive bacterial populations by acquisition of resistance genes which usually reside in plasmids and/or transposons (88,106,107). Furthermore, resistance deterrninants contained in transposons spread to, and become estabUshed in, diverse bacterial species (106). 

That bacterial resistance predates the era of clinical use of antibiotics by several hundred millions of years is the recent result of genomic sequence data mining from antibiotic-producing microorganisms. These are supposed to be the inventors of antibiotic resistance genes which they had developed to protect themselves from the lethal action of their own antibiotics [4]. 

Because the natural penicillins have been used for many years, drug-resistant strains of microorganisms have developed, making the natural penicillins less effective than some of the newer antibiotics in treating a broad range of infections. Bacterial resistance has occurred within tire penicillins. Bacterial resistance is the ability of bacteria to produce substances that inactivate or destroy the penicillin. One example of bacterial resistance is tiie ability of certain bacteria to produce penicillinase, an enzyme that inactivates penicillin. The penicillinase-resistant penicillins were developed to combat this problem. 

Upper respiratory tract infection (URI) is a term that refers to various upper airway infections, including otitis media, sinusitis, pharyngitis, and rhinitis. Most URIs are viral and often selflimited. Over 1 billion viral URIs occur annually in the United States, resulting in millions of physician office visits each year.1 Excessive antibiotic use for URIs has contributed to the significant development of bacterial resistance. Guidelines have been established to reduce inappropriate antibiotic use for viral URIs.2 This chapter will focus on acute otitis media, sinusitis, and pharyngitis because they are frequently caused by bacteria and require appropriate antibiotic therapy to minimize complications. 

Monitoring the patient s clinical course is necessary to assess the effectiveness of therapy, detect the potential development of bacterial resistance, and determine outcome. 

Newer antimicrobials have not demonstrated superiority in the prevention of SSI and should be reserved for treatment only. Carbapenems, antipseudomonal penicillins, and third-or fourth-generation cephalosporins are not appropriate antibiotics for surgical prophylaxis. Overuse of these antibiotics may contribute to collateral damage and the development of bacterial resistance. 

Cefazolin or cefuroxime are appropriate for prophylaxis in cardiothoracic and vascular surgeries. In the case of 3-lactam allergy, vancomycin or clindamycin are advised. Debate exists on the duration of antimicrobial prophylaxis. The National Surgical Infection Prevention Project cites data that extending prophylaxis beyond 24 hours does not decrease SSI rates and may increase bacterial resistance.1 American Society of Health-System Pharmacists guidelines from 1999 allow for the continuation of prophylaxis for up to 72 hours.22 Duration of therapy should be based on patient factors and risk of development of an SSI. SSIs are rare after cardiothoracic operations, but the potentially devastating consequences lead some clinicians to support longer periods of prophylaxis. 

Still among the most frequently prescribed drugs, the antibiotic tetracyclines have decreased in popularity recently due to development of bacterial resistance in the clinic. The search for improved agents goes on. 

Abstract Resistance to modern antibiotics is currently a major health concern in treating infectious diseases. Abuse, overuse, and misuse of antibiotics in treating human illness have caused the pathogens to develop resistance through a process known as natural selection. The most common mechanism of resistance to -lactam antibiotics is the production of /3-lactamases, which destroy -lactam antibiotics before they reach the bacterial target. Over the last two decades, combination therapy involving treatment with a -lactam antibiotic and a /3-lactamase inhibitor has become very successful in controlling -lactamase-mediated bacterial resistance. Currently available inhibitors like... 

Bacterial resistance to conventional antibiotics has become a serious problem in infection control, and has led to intensive research efforts to develop an effective novel antimicrobial agent. Antimicrobial peptides have already played a crucial role in pharmaceutical research as biomedically useful agents or as lead compounds for drug development. More specifically, cyclic peptides have shown some potential as a possible new class of... 

Local treatment of skin and soft tissue infections with antibiotic-containing ointments or solutions should not be used because it leads to allergic reactions and rapid development of bacterial resistance. In settings where MRSA or resistant Enterobacte-riaceae (like ESBL s gram negative bacteria with extended spectrum beta lactames) or Pseudomonas spp. occur, the empiric use of vancomycin and a carbapenem can be necessary. The risk of transmission of these organisms should be minimalised by hygienic and isolation measures. 

Trimethoprim-sulfamethoxazole (TMP-SMX) was introduced as a fixed dose combination in 1968. Trimethoprim was added to sulfamethoxazole to synergisti-cally and sequentially inhibit bacterial synthesis of tetrahydrofolic acid. The combination was also designed to delay development of bacterial resistance. Sulfamethoxazole was selected in part because it is a congener of the frequently used sulhsoxazole but exhibits slower enteric absorption and urinary excretion. Sulfamethoxazole has a half-life similar to that of trimethoprim. 

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