Wednesday, 15 April 2020

Why is antibiotic resistance a problem?

antibiotic resistance


This enzyme is most important about natural products. Through which antibiotic resistance new antibiotics can be developed for the health of human life. Human health It was widely believed that there would no longer be a risk of serious bacterial infection. Bacterial diseases such as leprosy, pneumonia, others were being cured by the administration of antibiotics - compounds that kill bacteria in which they thrive without harming the human host. These have become increasingly resistant to "surprise drugs", as pathogenic bacteria cause many deaths that were once successful.

Which almost disappeared from developed countries, even tuberculosis is referred to worldwide as XDR extremely drug-resistant which is virtually untreated. A major XDR-TB is on the verge of becoming a global health crisis. There has been a drastic reduction in resources for the development of new antibiotics in this pharmaceutical industry.

This change of action is attributed by the pharmaceutical industry

(1) Antibiotics are only taken for a short period of time for chronic conditions such as diabetes - lack of financial incentives.

(2) New antibiotics with a relatively short lifespan in the market as bacteria become resistant to each successive product. 

(3) The most effective antibiotics are being widely used and as a last resort if other medicines are not successful.

The idea of ​​the formation of non-institutions for the new development has been widely considered by many antibiotics.

The action of antibiotics specifically targets enzymes that most antibiotics derive from natural products in the development of bacterial resistance, which is manufactured by microorganisms to kill other microorganisms. Bacteria have been shown to be weak in many ways.

These include the following:

1. Enzymes are involved in the synthesis of the bacterial cell wall 

Penicillin and its derivatives, such as methicillin, are structural analogs of the substrate of the peptidases of Tran that catalyze the final cross-linking reactions that toughen the cell wall. If these reactions do not occur, a rigid cell wall does not succeed in developing. Penicillin is an irreversible inhibitor of transpeptidases; The antibiotic is in the active site of these enzymes, forming a covalently bound complex that cannot be degraded. Vancomycin, an antibiotic originally derived from Borneo, was derived from a microorganism living in soil samples by inhibiting peptization of Tran by binding to the peptide substrate of the enzyme transpeptidase. Trans peptidase typically, the substrate terminates in a D-melanin-D-allene dipeptide.

To become vancomycin-resistant, a bacterial cell must synthesize an alternative terminus that does not bind the drug, a rounding process requiring several new enzymatic activities. Vancomycin antibiotics in which bacteria are able to develop minimal resistance and thus are given last resort when other antibiotics are not successful. Vancomycin-resistant to many pathogenic bacteria including Staphylococcus aureus has emerged in a few years. Aureus skin and nasal passages are relatively harmless, the organism causing life-threatening infections that develop in hospitalized patients who have open wounds or invasive tubes. Methicillin-resistant aureus (MRSA), causing thousands of patients to die. MRSA infections are also beginning to appear in community settings, such as high school gyms or children's day-care centers. In many cases, vancomycin is the only drug that can prevent these infections. 

Obtaining a cluster of MRSA vancomycin showed that Maybe resistant, a gene resistant to another bacterium face, a common cause of hospital-based infections. So far, no known vancomycin-resistant MRSA has been able to gain a foothold in either a hospital or community setting, but it may only be a matter of time. Infectious disease specialists, for this reason, have isolated patients from hospitals to establish better hygiene programs and at the first sign of infection. These have been proven to reduce the occurrence of fatal infections where they are kept in place.

2. Components of the system by which bacteria transcribe, duplicate and Translate their genetic information 

Eukaryotic and bacterial cells have a system for storing and using genetic information, which are the many differences between the two types of cells that pharmacologists can take advantage of. Streptomycin and the Tetracycline’s, for example, bind to bacterial ribosomes, but not eukaryotic ribosomes. This is a rare example of fully synthetic antibiotics. Quinolones, such as ciprofloxacin brand name Cipro, inhibit the quinolone enzyme DNA gyrase, which is required for bacterial DNA replication.

Almost all of the new compounds present in antibiotics are derivatives that have been chemically modified in the laboratory. New compounds are tested in two ways. The compound is tested for its ability to kill bacterial cells that bind to and inhibit a laboratory-specific target protein that has been purified from bacterial cells. It was hoped that the genome sequencing of pathogenic bacteria starting in 1995 is the new drug target.

There are only two new classes of antibiotics specifically developed and developed since 1963. One of these classes includes the antibiotic linezolid introduced in 2000, which acts specifically on bacterial ribosomes and interferes with protein synthesis. The other new class of antibiotics, introduced in 2003 and represented by distamycin are cyclic lip peptides, which disrupt bacterial membrane function. Many researchers are hoping that Zibo and Cubic will be used sparingly so that resistance can be kept to a minimum.

3. Bacteria that specifically catalyze metabolic reactions in enzymes

Sulfa drugs are effective antibiotics, as they are similar to the compound p-aminobenzoic acid (PABA), एफ़
antibiotic resistance

for example, which bacteria necessarily convert to coenzyme folic acid. Since humans lack a folic acid-synthesizing enzyme, they must obtain this essential coenzyme in their diet and, consequently, sulpha drugs have no effect on human metabolism.

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