All organisms affect the evolution of the other organisms in their biological co
ID: 282694 • Letter: A
Question
All organisms affect the evolution of the other organisms in their biological community. Flowering plants probably are the reason insects developed wings, and insects almost certainly are responsible for the development of showy flowers and sweet nectar because they would pollinate only those plants having these attributes.
Human beings can also be considered "agents of selection" in the evolution of other species.
For this week’s discussion, choose a particular species that humans have “caused” to evolve. Name the species and explain how humans have caused the evolution of the species.
WORD COUNT 250 MINIMUM
Explanation / Answer
Evolution of microorganisms to resistance-
Bacteria have been evolving in response to threats from other species, including fungi, for hundreds of millions of years. Bacteria and fungi compete for food and often do so using chemical warfare. A fungus evolves an antibiotic and bacteria evolve resistance, so fungi evolve a new antibiotic. Recently, though, things changed. We invented (or rather stole from fungi) antibiotics, which allowed us to kill bacteria—and, importantly, treat bacterial infections. However, by using them too much, too incompletely or too indiscriminately we cause bacterial strains resistant to our drugs to evolve. Unlike fungi, we cannot retaliate by simply evolving new antibiotics. Hundreds of bacterial lineages have evolved resistance to more than a dozen of our antibiotics. In response, we are forced to discover new antibiotics, an endeavor that has proved ever more difficult. Viruses generally evolve even more quickly than bacteria. For example, multiple drugs for HIV infection are taken together as a cocktail for one reason: the HIV virus evolves quickly. The cocktail slows the evolution of full resistance. Even if HIV evolves resistance to one drug, the odds it will evolve complete resistance to all three are far lower. Similarly, the flu that usually starts each year in Asia is different by the time it reaches North America. The flu virus evolves to get by not only as a function of how we respond to it but also in response to our population size and patterns of movement. It, and other viruses, even evolve within our bodies. The virus that makes you sick is almost inevitably different than the one you give someone else.
It is a specific type of drug resistance.
Antibiotic resistance evolves naturally via natural selection through random mutation, but it could also be engineered by applying an evolutionary stress on a population.
Once such a gene is generated, bacteria can then transfer the genetic information in a horizontal fashion (between individuals) by plasmid exchange.
If a bacterium carries several resistance genes, it is called multiresistant or, informally, a superbug.
Causes Antibiotic resistance can also be introduced artificially into a microorganism through transformation protocols.
This can be a useful way of implanting artificial genes into the microorganism.
Antibiotic resistance is a consequence of evolution via natural selection.
The antibiotic action is an environmental pressure; those bacteria which have a mutation allowing them to survive will live on to reproduce.
They will then pass this trait to their offspring, which will be a fully resistant generation.
Several studies have demonstrated that patterns of antibiotic usage greatly affect the number of resistant organisms which develop.
Overuse of broad-spectrum antibiotics, such as second- and third-generation cephalosporins, greatly hastens the development of methicillin resistance.
Other factors contributing towards resistance include incorrect diagnosis, unnecessary prescriptions, improper use of antibiotics by patients, and the use of antibiotics as livestock food additives for growth promotion.
Researchers have recently demonstrated the bacterial protein LexA may play a key role in the acquisition of bacterial mutations.
Resistant pathogens Staphylococcus aureus (colloquially known as "Staph aureus" or a Staph infection) is one of the major resistant pathogens.
Found on the mucous membranes and the skin of around a third of the population, it is extremely adaptable to antibiotic pressure.
It was the first bacterium in which penicillin resistance was found—in 1947, just four years after the drug started being mass-produced.
Methicillin was then the antibiotic of choice, but has since been replaced by oxacillin due to significant kidney toxicity.
MRSA (methicillin-resistant Staphylococcus aureus) was first detected in Britain in 1961 and is now "quite common" in hospitals.
MRSA was responsible for 37% of fatal cases of blood poisoning in the UK in 1999, up from 4% in 1991.
Half of all S. aureus infections in the US are resistant to penicillin, methicillin, tetracycline and erythromycin.
This left vancomycin as the only effective agent available at the time.
However, strains with intermediate (4-8 ug/ml) levels of resistence, termed GISA (glycopeptide intermediate Staphylococcus aureus) or VISA (vancomycin intermediate Staphylococcus aureus), began appearing the the late 1990s.
The first identified case was in Japan in 1996, and strains have since been found in hospitals in England, France and the US.
The first documented strain with complete (>16ug/ml) resistence to vancomycin, termed VRSA (Vancomycin-resistant Staphylococcus aureus) appeared in the United States in 2002.
A new class of antibiotics, oxazolidinones, became available in the 1990s, and the first commercially available oxazolidinone, linezolid, is comparable to vancomycin in effectiveness against MRSA.
Linezolid-resistance in Staphylococcus aureus was reported in 2003.
CA-MRSA (Community-acquired MRSA) has now emerged as an epidemic that is responsible for rapidly progressive, fatal diseases including necrotizing pneumonia, severe sepsis and necrotizing fasciitis.
Methicillin-resistant Staphylococcus aureus (MRSA) is the most frequently identified antimicrobial drug-resistant pathogen in US hospitals.
The epidemiology of infections caused by MRSA is rapidly changing.
In the past 10 years, infections caused by this organism have emerged in the community.
The 2 MRSA clones in the United States most closely associated with community outbreaks, USA400 (MW2 strain, ST1 lineage) and USA300, often contain Panton-Valentine leukocidin (PVL) genes and, more frequently, have been associated with skin and soft tissue infections.
Outbreaks of community-associated (CA)-MRSA infections have been reported in correctional facilities, among athletic teams, among military recruits, in newborn nurseries, and among active homosexual men.
CA-MRSA infections now appear to be endemic in many urban regions and cause most CA-S. aureus infections.
Enterococcus faecium is another superbug found in hospitals.
Penicillin-Resistant Enterococcus was seen in 1983, Vancomycin-Resistant Enterococcus (VRE) in 1987, and Linezolid-Resistant Enterococcus (LRE) in the late 1990s.
Streptococcus pyogenes (Group A Streptococcus: GAS) infections can usually be treated with many different antibiotics.
Early treatment may reduce the risk of death from invasive group A streptococcal disease.
However, even the best medical care does not prevent death in every case.
For those with very severe illness, supportive care in an intensive care unit may be needed.
For persons with necrotizing fasciitis, surgery often is needed to remove damaged tissue.
Strains of S. pyogenes resistant to macrolide antibiotics have emerged, however all strains remain uniformly sensitive to penicillin.
Resistance of Streptococcus pneumoniae to penicillin and other beta-lactams is increasing worldwide.
The major mechanism of resistance involves the introduction of mutations in genes encoding penicillin-binding proteins.
Selective pressure is thought to play an important role, and use of beta-lactam antibiotics has been implicated as a risk factor for infection and colonization.
Streptococcus pneumoniae is responsible for pneumonia, bacteremia, otitis media, meningitis, sinusitis, peritonitis and arthritis.
Microorganisms such as bacteria and viruses reproduce rapidly and can evolve in a relatively short time. One example is the bacterium E. coli. Its DNA can be damaged or changed during replication, and most of the time this causes the death of the cell. But occasionally the mutation is beneficial (to the bacteria). For example, it may allow resistance to certain antibiotics. When those antibiotics are present, the resistant bacteria have an advantage over the bacteria that are not resistant. Antibiotic-resistant strains of bacteria are an increasing problem in hospitals.
DNA
Scientists can now examine the DNA from different species of organism and use the data produced to see how closely related the two species are to each other. By collecting a lot of this data, scientists can compare the results with conventional ideas about how organisms have evolved. What they found was that DNA data supported the conventional theory of evolution.