Antibiotic Resistance in Elderly and How to Prevent It

Many studies have shown that antibiotic drugs are often prescribed unnecessary or inappropriate. Drugs for elderly (geriatric drugs) has certainly contributed to the growing problem of bacterial resistance to antibiotics in the elderly. As a group, elderly patients in hospitals and long-term care facilities are the main beneficiaries of antibiotics. One consequence is the promotion of the strain and the distribution of microorganisms resistant to antibiotics.

The nature and origin of antibiotic resistant organisms in hospitals and long-term care facilities have been carefully considered in a recent publication. Information on the antibiotic resistance strength for the elderly population residing in hospitals and long-term care facilities is probably the most reliable available. As in the review paper, bacteria that are resistant to antibiotics of the main concerns of geriatricians:

1) lactam-resistant organisms, especially in Gram pneumococci resistant to penicillin and negative aerobic bacteria resistant to third generation cephalosporins,
2) l-resistant enterococci ‘vancomycin and
3) quinolone-resistant Gram-negative and Gram-positive.

Altered penicillin-binding proteins that is enzymes in the final phase of the bacterial cell wall involved, with low affinity for penicillin, are responsible for resistance to this antibiotic. Other organizations known for its resistance to lactam antibiotics in the elderly, certain types of staphylococcus (some resistant to all penicillins, cephalosporins and carbapenems) and enterococci resistant to all cephalosporins, penicillin lack of significant protein links.

Enzymes known-lactamases are largely responsible for the ability of bacteria resistant to cephalosporins. Lactamases many parts of the spectrum (ESBL) will lead us out how the corresponding genes on plasmids encoding TEM-1 encoded in combination with intestinal bacteria. TEM-1 is responsible for nearly three quarters of the plasmid-bound-lactamase resistance leaders in the world. The presence of these enzymes can lead to the development of resistance to penicillin, cephalosporins, and cephamycins-lactamase. It should be noted that resistance to lactams after the entry is limited to antibiotics can occur and low affinity of penicillin binding proteins and destruction by-lactamases.

Drug ffflux pumps to restrict the entry of bacteria to antibiotics have a major problem in antibiotic treatment. Leading to inadequate accumulation of antibiotics in bacterial cells to be effective. The formation of transport proteins that bind and inactivate the antibiotic or accompanies the bacterial cell, antibiotics to prevent the achievement of critical importance. Tet B plasmid encoded, while chromosomal resistance to tetracycline mediation observed in some bacteria such as Proteus.

Quinolone antibiotics like ciprofloxacin and nalidixic acid gyrase binding to DNA (topoisomerase type II) in Gram-negative bacteria and topoisomerase IV in Gram-positive bacteria, thereby interfering with the reproductive DNA. The resistance to these antibiotics occurs in May due to mutations in bacterial topoisomerases, reduced permeability of the membrane of Gram-negative bacteria, proteins or active efflux carrier. Vancomycin is a glycopeptide that interferes with the formation of the cell wall of Gram-negative bacteria.

There are four known phenotypes of vancomycin-resistant enterococci), two (Van Van A and B associated with an high resistance to the antibiotic. These two phenotypes are easily movable elements and plasmid transposon. Vancomycin-resistant enterocci be introduced more frequently hospitals and long-term care facilities accepting patients who acquired resistant organisms in hospitals.

In this brief analysis of antibiotic resistance in the elderly, a word for full implementation in the classroom. These genetic data on resistance plasmids (plasmid R), are largely responsible for the resistance of bacteria to existing antibiotics. There are collections of bacteria, antibiotics have been placed before the Ad plasmids identified, but most of these plasmids lack of evidence of resistance to antibiotics. This should mean that the resistance to existing antibiotics harbors pathogenic bacteria display appeared as a plasmid plasmids by acquisition of resistance transposons. Among them, who teach multiple antibiotic resistances in elderly differ in containing transposons. Some resistance transposon unique set of factors.