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How can we solve the antibiotic resistance crisis? - Gerry Wright

Microbial resistance properties -

Therefore, it does not take long for the antibiotic-resistant bacteria to comprise a large proportion of a bacterial population. To date, all antibiotics have over time lost effectiveness against their targeted bacteria. The earliest antibiotics were developed in the s.

These "miracle drugs" held at bay such devastating diseases as pneumonia and tuberculosis, which had previously been untreatable. For example:. Nearly all strains of Staphylococcus aureus in the United States are resistant to penicillin, and many are resistant to newer methicillin-related drugs.

Since , strains of S. aureus have been reported to have a decreased susceptibility to vancomycin, which has been the last remaining uniformly effective treatment. Today, one out of six cases of Campylobacter infections, the most common cause of food borne illness, is resistant to fluoroquinolones the drug of choice for treating food-borne illness.

As recently as ten years ago, such resistance was negligible. Clearly, it is important to extend the useful lifetime of any drug that is effective against human disease. And today, this is even more important because few new antibiotics are being developed, and those that are developed tend to be extremely expensive.

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You can learn more about the issues surrounding MRSA and measures to control is by exploring iFrame below which links to the CDC web page on MRSA. As we noted above, novel genes arise from random mutations, and occasionally such a mutation may confer a bacterium with resistance to an antiobiotic.

Once a bacterium has acquired resistance to a particular antibiotic, it passes the resistant allele to subsequent daughter cells that result from binary fission. In addition, bacteria that have acquire a trait such as antibiotic resistance can transfer this allele to other bacteria throught any one of three mechanisms:.

When bacterial cells die, they frequently lyse burst releasing their intracellular contents, including fragments of DNA, to the environment. These fragments can be taken up and incorporated into the chromosome of a living bacterium to provide the recipient with new characteristics.

This process is called bacterial transformation, and if the incorporated DNA contains genes that encode for resistance to an antibiotic, a previously susceptible bacterium can be "transformed" to now be resistant.

The video below 23 sec. provides a quick overview of transformation. Many bacteria have plasmids, which are small circular pieces of DNA separate from the primary bacterial chromosome. These plasmids can carry genes that provide resistance to antibiotics, and bacteria that contain plasmids are able to conjugate with other bacteria and pass a replicate to recipient bacteria.

The electron micrograph below shows two bacteria that are joined by a temporary hollow tube-like connection called a pilus. Animation Illustrating Bacterial Conjugation. In a Shigella epidemic killed 12, people in Guatemala.

The Shigella bacteria that caused the outbreak had a plasmid carrying resistances to four antibiotics. Genetic information can also be carried from one bacterium to another by a virus. Bacteriophages or simply "phages" are small viruses that infect bacteria and use their cellular components to make bacteriophage replicates.

During the infection and replication, it is possible for bacterial genes to get incorporated into the viral genome. One of the viral replicates carrying the bacterial allele may then subsequently infect another bacterium and pass the new allele on.

In the 2nd and 3rd scenes the viral proteins and genetic material are replicated and then self-assemble into new viral particles. The development and spread of bacterial resistance to antiobiotics is inevitable, but it could be greatly curtailed through relatively simple measures.

As noted earlier HIV is a retrovirus consisting of a single strand of RNA inside a protein coat. When HIV enters a CD4 lymphocyte, it sheds its protein coat and uses a viral enzyme called reverse trancriptase to create a segment of DNA using the viral RNA as a template.

This double-stranded DNA version o HIV then gets incorporated into the DNA of the infected host cell, and this process is called "reverse transcription. Given the persistence of HIV with high rates of replication and high error rates during reverse transcription, mutations in HIV are inevitable, and some of these mutations lead to the eventual development of drug resistance.

HIV infects CD4 lymphocytes and hijacks the cell's machinery to create viral proteins and RNA. HIV's genetic material in RNA, and in order replicate reverse transcriptase results in results in very rapid production of new HIV particles.

Two concepts are important to an understanding of the development of drug resistance. First, HIV infection is characterized by high levels of virus production and turnover. In most untreated patients, the total number of productively infected cells in the lymphoid tissue has been estimated to be approximately to cells.

During the chronic phase of HIV infection, this number is relatively stable, reflecting the balance between the infection of new target cells and their clearance.

Because the half-life of infected cells is remarkably short one to two days , the maintenance of this steady state requires that HIV infect new target cells at a very high rate. Second, the viral population in an infected person is highly heterogeneous. The reverse transcription of viral RNA into DNA is notoriously prone to error,introducing on average one mutation for each viral genome transcribed.

Most of these errors are base substitutions, but duplications, insertions, and recombination can also occur. The high rate of HIV infection, combined with the high mutation rate that occurs during each cycle of infection, ensures that patients have a complex and diverse mixture of viral quasispecies, each differing by one or more mutations.

Under these circumstances, it is easy to understand why if any of these mutations can confer some selective advantage to the virus, such as a decrease in its susceptibility to an antiretroviral agent, the corresponding quasispecies will overtake the others, following a simple darwinian selection process.

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