Emerging infectious disease

For the medical journal, see Emerging Infectious Diseases.


An emerging infectious disease (EID) is an infectious disease whose incidence has increased in the past 35 years and could increase in the near future. Emerging infections account for at least 12% of all human pathogens.[1] EIDs are caused by newly identified species or strains (e.g. SARS, AIDS)[2] that may have evolved from a known infection (e.g. influenza) or spread to a new population (e.g. West Nile virus) or area undergoing ecologic transformation (e.g. Lyme disease), or be reemerging infections, like drug resistant tuberculosis. Nosocomial infections, such as MRSA are emerging in hospitals, and extremely problematic in that they are resistant to many antibiotics.[3] Of growing concern are adverse synergistic interactions between emerging diseases and other infectious and non-infectious conditions leading to the development of novel syndemics.

Contributing factors

The U.S. Centers for Disease Control and Prevention (CDC) publishes a journal Emerging Infectious Diseases that identifies the following factors contributing to disease emergence:

Methicillin-resistant Staphylococcus aureus

An example of this is MRSA, a common nosocomial infection. MRSA, the pathogen that we know today, evolved from Methicillin-susceptible Staphylococcus aureus (MSSA) otherwise known as common S. Aureus. Many people are natural carriers of S. Aureus, without being affected in any way, shape, or form. MSSA was treatable with the antibiotic methicillin until it acquired the gene for antibiotic resistance.[4] Though genetic mapping of various strains of MRSA, scientists have found that MSSA acquired the mecA gene in the 1960s, which accounts for its pathogenicity, before this it had a predominantly commensal relationship with humans. It is theorized that when this S. Aureus strain that had acquired the mecA gene was introduced into hospitals, it came into contact with other hospital bacteria that had already been exposed to high levels of antibiotics. When exposed to such high levels of antibiotics, the hospital bacteria suddenly found themselves in an environment that had a high level of selection for antibiotic resistance, and thus resistance to multiple antibiotics formed with in these hospital populations. When S. Aureus came into contact with these populations, the multiple genes that code for antibiotic resistance to different drugs were then acquired by MRSA, making it nearly impossible to control.[5] It is thought that MSSA acquired the resistance gene through the horizontal gene transfer, a method in which genetic information can be passed within a generation, and spread rapidly through its own population as was illustrated in multiple studies.[6] Horizontal gene transfer speeds the process of genetic transfer since there is no need to wait an entire generation time for gene to be passed on.[7] Since most antibiotics do not work on MRSA, physicians have to turn to alternative methods based in Darwinian medicine. However prevention is the most preferred method of avoiding antibiotic resistance. By reducing unnecessary antibiotic use within society as a whole, antibiotics resistance can be slowed.

See also

References

  1. Taylor, L. et al. (2001). Risk factors for human disease emergence Philosophical Transactions of the Royal Society B, 356(1411):983-9.
  2. Fauci AS (2005). "Emerging and reemerging infectious diseases: the perpetual challenge". Academic Medicine 80 (12): 1079–85. doi:10.1097/00001888-200512000-00002. PMID 16306276.
  3. Witte, W (1997). "Increasing incidence and widespread dissemination of methicillin‐resistant Staphylococcus aureus (MRSA) in hospitals in central Europe, with special reference to German hospitals.". Clinical Microbiology and Infection 3 (4): 414–22. doi:10.1111/j.1469-0691.1997.tb00277.x.
  4. Witte, W., Kresken, M., Braulke, C., & Cuny, C. (1997). Increasing incidence and widespread dissemination of methicillin‐resistant Staphylococcus aureus (MRSA) in hospitals in central Europe, with special reference to German hospitals. Clinical Microbiology and Infection, 3(4), 414-422.
  5. Benson, M. A., Ohneck, E. A., Ryan, C., Alonzo, F., Smith, H., Narechania, A., & Torres, V. J. (2014). Evolution of hypervirulence by a MRSA clone through acquisition of a transposable element. Molecular microbiology, 93(4), 664-681.
  6. Krishnapillai, V. (1996). Horizontal gene transfer. Journal of Genetics, 75(2), 219-232.
  7. Krishnapillai, V. (1996). Horizontal gene transfer. Journal of Genetics, 75(2), 219-232.

External links