How do broad spectrum antibiotics work

Antibiotics are strong drugs. They fight the infections caused by bacteria. So the U. Centers for Disease Control and Prevention CDC is now urging hospitals to cut back on the drugs when they are not needed. This can happen if you have an infection that may be serious, like pneumonia. The human body hosts trillions of microbes, with an estimated 10, bacterial species living in and on the surface of our bodies.

No two people — not even twins — have identical combinations of bacteria microbiomes , which begin to develop at birth, particularly if we were born through the microbe-rich birth canal. For a long time, scientists focussed only on infection-causing pathogenic bacteria and thought that non-pathogenic bacteria were, at best, unimportant.

However, microbial cells outnumber our human cells by about ten to one and scientists are now beginning to understand that they play a significant role in our wellness, especially within the immune and digestive systems. In digestion, for example, there are bacteria that feed on foods that we cannot digest with our human cells alone.

The waste products of these bacteria are nutrients for our human systems. Probiotics refer to live microorganisms thought to have beneficial effects, and popular knowledge of this has led to a surge in probiotic use; however, other bacteria have harmful effects, especially when they overpopulate specific areas of our bodies. Infection with pathogenic bacteria can happen following an injury, when common external bacteria enter the human body through the bloodstream, or by contamination with unfriendly microorganisms that produce toxic by-products, as in many cases of food poisoning.

Antibiotics do not usually affect human cells, which is why we can ingest them safely for use as a medicine. However, like all medicines, some people may react or have side-effects from antibiotics as well.

Some antibiotics attack a wide range of bacteria broad-spectrum antibiotics , while researchers develop others to only attack specific pathogenic strains narrow-spectrum antibiotics.

There are antibiotics that work only against bacteria that need oxygen aerobic and others that work against bacteria that live in the absence of oxygen anaerobic. When you swallow an antibiotic pill or liquid, it enters your digestive tract and is absorbed into the blood stream just as nutrients are from food.

From there, it circulates throughout the body, soon reaching its target area, where pathogenic bacteria are causing an infection. In some situations, such as when an infection is especially severe, physicians might administer antibiotics via injection intravenously, directly into the bloodstream. With certain skin infections, the most effective way to get the antibiotic to the pathogenic organisms quickly is to apply it directly to the infection as a topical cream or ointment.

Your physician chooses a particular antibiotic and its route of administration based on a number of factors, such as the exact type and extent of infection. Yow, MD. Author Affiliations Houston. Access through your institution. Add or change institution. Save Preferences. Privacy Policy Terms of Use. Access your subscriptions. Free access to newly published articles. Nausea and vomiting occurred more frequently in tigecycline- versus comparator-treated patients in phase 3 studies.

Pancreatitis and hepatotoxicity have been reported rarely. Tigecycline inhibits bacterial protein synthesis by binding to the 30S ribosomal subunit and exhibits bacteriostatic activity against a broad range of pathogenic aerobic and anaerobic bacteria, including MRSA, VRE, MDR-A. Similar to colistin, tigecycline efficacy in the treatment of MDR-Gram-negative infection has not been well-established in controlled clinical trials.

Both treatment success and failure, primarily in association with bacteremia, pulmonary, and intra-abdominal infection have been reported. In , the FDA issued a drug safety communication warning that pooled analysis of phase 3 and 4 clinical trials revealed increased all-cause mortality associated with tigecycline use. This was primarily observed among patients with ventilator-associated pneumonia VAP , where more deaths occurred in tigecycline- versus imipenem-treated patients.

Interestingly, in vitro synergy between colistin and vancomycin for clinical isolates of MDR-A. Other novel agents in preclinical study include compounds such as: efflux pump inhibitors, outer membrane synthesis inhibitors, metallo-beta-lactamase inhibitors, lipopolysaccharide synthesis inhibitors, and unique inhibitors of the 50S ribosomal subunit.

The management of infection with MDR-Gram-negative bacilli is perhaps the most daunting challenge. With the widespread emergence of carbapenem-resistant organisms, clinicians have turned to agents such as colistin and tigecycline with increasing frequency.

Largely abandoned decades ago due to the availability of effective and less toxic alternatives, questions related to the efficacy and safety of colistin remain given a poor understanding of optimal dosing, confusion with existing dosage recommendations, and ongoing reports of resistance. Tigecycline resistance has also become problematic and its use in the setting of bacteremia is particularly controversial given that maximum serum concentrations may not exceed the organism MIC.

Whether or not increased doses would serve to improve efficacy without compromising safety is unknown. Inherent microbiologic limitations also exist given that tigecycline has no useful activity against P. In an outcomes assessment of patients infected with carbapenem-resistant Klebsiella pneumoniae, it is sobering to note that treatment with at least one active antibiotic was not associated with patient survival. Rather, adjunctive measures such as debridement, drainage, or catheter removal represented the only therapeutic intervention associated with a mortality benefit.

This highlights not only the importance of source control when possible, but also the dire need for new antibiotics with reliable clinical efficacy against MDR-Gram-negative pathogens. Effective agents for the treatment of VRE infection have been welcome additions to the antimicrobial armamentarium in the last decade and have been useful in outbreaks.

However, linezolid-resistant enterococci have emerged in both the presence and absence of increased linezolid consumption. A linezolid-resistant S. Combination therapy has achieved clinical cure in many cases and remains an area of active investigation. The optimal management of patients experiencing treatment failure with vancomycin and daptomycin nonsusceptible strains of S. Given that prolonged therapy is often required, linezolid use may be limited by toxicity.

Further study is needed to define the role of telavancin or ceftaroline in this setting. Apart from guidelines for therapeutic drug monitoring of vancomycin, no agent-specific guidelines exist, nor are there formal recommendations for the management of infections due to VRE and multidrug-resistant Gram-negative bacilli. A consensus statement from the European carbapenem-non-susceptible Enterobacteriaceae CNSE Working Group identified antibiotic policy as one of ten areas for improvement in the response to these organisms.

Noting the contribution of antibiotic overuse and misuse to the selection of CNSE from commensal flora, antibiotic diversification and de-escalation, particularly with respect to carbapenems, fluoroquinolones, and third-generation cephalosporins were recommended. Infect Control Hosp Epidemiol.

Infect Dis Clin N Am. French, GL. Int J Antimicrob Agents. Epidemiol Infect. Rice, LB. J Infect Dis. Clin Infect Dis. Isturiz, RE. N Engl J Med. December 10, Louis, MO: Forest Pharmaceuticals. Antimicrob Agents Chemother.