Evolutionary pressure

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Any cause that reduces reproductive success in a proportion of a population potentially exerts evolutionary pressure or selection pressure.[1] With sufficient pressure, inherited traits that mitigate its effects - even if they would be deleterious in other circumstances - can become widely spread through a population. It is a quantitative description of the amount of change occurring in processes investigated by evolutionary biology, but the formal concept is often extended to other areas of research.

In population genetics, selection pressure is usually expressed as a selection coefficient.

Antibiotic Resistance[edit]

Drug resistance in bacteria is an example of the outcome of natural selection. When a drug is used on a species of bacteria, those that cannot resist die and do not produce offspring, while those that survive potentially pass on the resistance gene to the next generation. Because of this, the drug resistance increases over generations. For example, in hospitals, environments are created where pathogens such as C. difficile have developed a resistance to antibiotics.[2]Antibiotic resistance is made worse by the misuse of antibiotics. Antibiotic resistance is encouraged when antibiotics are used to treat non-bacterial diseases, and when antibiotics are not used for the prescribed amount of time or in the prescribed dose.[3]

Nosocomial Infections[edit]

Clostridium difficile, gram-positive bacteria that inhabit the gut of mammals, is a model example of one type of bacteria that a major cause of death by nosocomial infections.[2] When the normal gut flora is altered, for instance by taking an antibiotic, an environment suitable for foreign pathogens to proliferate is created and infection rates flourish. The rapid evolution of antibiotic resistance places an enormous selective pressure on the advantageous alleles of resistance passed down to future generations. The Red Queen Hypothesis shows that the evolutionary arms race of pathogenic bacteria and humans is a constant battle for evolutionary advantages to outcompete each other. The evolutionary arms race between the rapidly evolving virulence factors of the bacteria and treatment practice of modern medicine, requires evolutionary biologists to understand the mechanisms of resistance in these pathogenic bacteria, especially, considering the growing number of infected hospitalized patients. The evolved virulence factors pose a threat to patients in hospitals, who are immunocompromised from illness or antibiotic treatment. Virulence factors are the characteristics that the evolved bacteria have developed to increase pathogenicity. One of the virulence factors of C. difficile that largely constituents its resistant to antibiotics is its toxins: enterotoxin TcdA and cytotoxin TcdB.[4] Toxins produce spores that are difficult to inactivate and remove from the environment. This is especially true in hospitals where an infected patient’s room may contain spores for up to 20 weeks.[5] The threat of rapid spread of CDIs is therefore dependent on hospital sanitation practices to remove spores from the environment. A study published in the American Journal of Gastroenterology found that to control the spread of CDIs glove use, hand hygiene, disposable thermometers and disinfection of the environment are necessary practices in health facilities.[6] The virulence of this pathogen is remarkable and may take a radical change at sanitation approaches used in hospitals to control CDI outbreaks.

Natural selection in humans[edit]

The Malaria parasite can exert a selective pressure on populations. This pressure has led to natural selection for erythrocytes carrying the sickle cell hemoglobin gene mutation (Hb S)—causing sickle cell anaemia—in areas where malaria is a major health concern, because the condition grants some resistance to this infectious disease.[7]

Herbicide/Pesticide Resistance[edit]

Just as with the development of antibiotic resistance in bacteria, resistance to pesticides and herbicides has begun to appear with commonly used agricultural chemicals. For example:

  • In the US, studies have shown that fruit flies that infest orange groves were becoming resistant to malathion, a pesticide used to kill them.
  • In Hawaii and Japan, the diamondback moth developed a resistance to Bacillus thuringiensis, which is used in several commercial crops including Bt corn, about three years after it began to be used heavily.
  • In England, rats in certain areas have developed such a strong resistance to rat poison that they can consume up to five times as much of it as normal rats without dying.
  • DDT is no longer effective in controlling mosquitoes that transmit malaria in some places, a fact that contributed to a resurgence of the disease.
  • In the southern United States, the weed Amaranthus palmeri, which interferes with production of cotton, has developed widespread resistance to the herbicide glyphosate.
  • In the Baltic Sea, decreases in salinity has encouraged the emergence of a new species of brown seaweed, Fucus radicans.[8]

For more information see Pesticide resistance.

See also[edit]

Notes[edit]

  1. ^ "Selection Pressure". Iscid.org. Retrieved 2011-11-15. 
  2. ^ a b Dawson, L.F., E. Valiente, and B.W. Wren. 2009. Clostridium difficile—A continually evolving and problematic pathogen. Infections,
         Genetics and Evolution. 9:1410-1417.
  3. ^ "CDC - Healthcare-associated infections - HAI". Cdc.gov. Retrieved 2011-11-15. 
  4. ^ Terrier, M. C. Z., M. L. Simonet, P. Bichard, and J. L. Frossard. 2014. Recurrent Clostridium
         difficile infections: The importance of the intestinal microbiota. World Journal of Gastroenterology 20:7416-7423.
  5. ^ Kim, K. H., R. Fekety, D. H. Batts, D. Brown, M. Cudmore, J. Silva Jr., and D. Waters. 1981. Isolation
         of Clostridium difficile from the Environment and Contacts of Patients with Antibiotic-Associated Colitis. The Journal of Infectious
         Diseases 143: 42–50.
  6. ^ Hsu, J., C. Abad, M. Dinh, and N. Sadfar. 2010. Prevention of endemic healthcare-associated Clostridium
         difficile infection: reviewing the evidence. American Journal of Gastroenterology 105:2327–39 quiz 2340.
  7. ^ Kenneth R. Bridges, M.D. (2002-04-02). "Malaria and the Sickle Hemoglobin Gene". Sickle.bwh.harvard.edu. Retrieved 2011-11-15. 
  8. ^ Pereyra1, R.T.; L. Bergströ;, L. Kautsky and K. Johannesson (2009). "Rapid speciation in a newly opened postglacial marine environment, the Baltic Sea". BMC Evolutionary Biology 9 (70). doi:10.1186/1471-2148-9-70.