White Nose Syndrome in Bats Spreading Rapidly

            I have been on one cave exploration; however reading this article has made me think twice about stepping into another cave. The idea that caves carry the fungus psedogymnoascus destructans that can infect bats, has made me think twice. The results displayed in the research article by Raudabaugh and Miller determined pseudogymnoascus destructans (P. destructans) could grow on a range of surfaces. P. destructans can live on carbon sources such as, undigested insect particles, dead fungi and wood. P. destructans can grow at different pH levels, however extremely acidic conditions inhibit the growth. The only limitations of the fungus are the increased temperature and taking up water. Temperatures above 20° C inhibit growth and the fungus has decreased ability to absorb water from surfaces. The results indicated a majority of the infections occur in caves where bats hibernate. The P. destructans can live for extended periods of time in caves even after bats have evacuated the cave after hibernation.   

            P. destructans is a fungus that causes white nose syndrome in bats, the fungus causes skin lesions. P. destructans can break down keratin in skin, it can also break down protein and urea that produces an alkaline environment. The alkaline environment can burn holes in the bats skin, and leave the bats susceptible to secondary infections. During hibernation bats have decreased body temperatures and suppressed immune systems. Therefore, hibernation makes bats more susceptible to infection. Once bats come out of hibernation the fungus is expelled, because body temperature increases and the immune system resume normal functioning. 

            The fungus, P. destructans can spread readily easily between bat especially during hibernation in infected caves. The fungus could be endangering the bat species if the fungus continues to spread rapidly. Research needs to be conducted on reducing the spread of the fungus and treatments to kill the fungus in caves.  

           

By Al Hicks brown bat with white nose syndrome 

References: 

University of Illinois at Urbana-Champaign (2103, October 25). Fungus that causes white-nose syndrome in bats proves hardy survivor. ScienceDaily. Retrieved November 4, 2013, from http://www.sciencedaily.com/releases/2013/10/131025091942.htm

Daniel B. Raudabaugh, Andrew N. Miller. Nutritional Capability of and Substrate Suitability for Pseudogymnoascus destructans, the Causal Agent of Bat White-Nose Syndrome. PLoS ONE, 2013; 8(10). DOI: 10.1371/journal.pone.0078300

PPMO as an antibacterial agent to fight antibiotic resistance

            Antibiotic resistance has become more prevalent in the recent years, resulting in reduced effectiveness of antibiotics in the treatment of microorganisms.  A common cause of antibiotic resistance is the misuse or overuse of antibiotics by patients and/or physicians. I, as a patient have misused antibiotics; a few years ago I had a sinus infection. I was prescribed an antibiotic, cephalexin that was to be taken for one week. However, after four days of the antibiotic making me feel sick I decided to discontinue the antibiotic. I felt the antibiotic had served its purpose, because my constant headache was gone. Therefore, the sinus infection was cured, right? I couldn’t of been more wrong, the sinus infection came back a few weeks later. Fortunately, I had refills on my antibiotic and continued to take the antibiotic for the full one week. As a biology student and pharmacy technician, I should of known better and accidentally contributed to antibiotic resistance.  However, a new potential antibacterial agent is on the rise that could eliminate antibiotic resistance. In the future this may reduce the overuse and misuse of antibiotics as seen in healthcare settings.

           According to the study by Geller et al published in the Journal of Infectious Diseases. The results of the study displayed A. lwoffii and A. baumannii are vulnerable to peptide-conjugated phosphorodiamidate morpholino oligomers (PPMO). The PPMO targeted specific genes in A. lwoffi and A. baumannii, resulting in the death of the bacteria. PPMO displayed to be a more efficient antibacterial agent and may be used in the treatment of bacterial infections combating the antibiotic resistance.

           In the study, Acinetobacter was investigated and consist of over 30 species. Acinetobacter can cause respiratory infections, sepsis and infections in battle wounds of military personnel.  Acinetobacter is difficult to treat with the increased resistance to antibiotics. This can result in morbidity and mortality in patients if the infection is left untreated. A. lowoffi and A. baumanni are strains of Acinetobacter that have several genes for antibiotic and toxin resistance. PPMO are unique and can fight antibiotic resistance in A. lowoffi and A. baumanni strains. PPMO are synthesized compared to traditional antibiotics that are found in nature. The design for PPMO are to complementary bind messenger RNAs to specific genes associated with viability. PPMO can be designed to target any gene of interest reducing the development of antibiotic resistance.

           The results are significant in displaying the effectiveness of PPMO as a potential antibacterial agent. PPMO can be used to treat bacterial infections that have become resistant. This could improve quality of life for patients not responding to traditional antibiotics. Having antibacterial agents that can combat antibiotic resistance will reducing morbidity and mortality rates in patients with resistant infections.

By J. Carr, T. Gianoulis, and D. Massa
Electronic microscope image of A.baumanni and its genome

References 

Bruce L. Geller, Kimberly Marshall-Batty, Frederick J. Schnell, Mattie M. McKnight, Patrick L. Iversen, and David E. Greenberg. Gene-Silencing Antisense Oligomers Inhibit Acinetobacter Growth in Vitro and In Vivo. Journal of Infectious Diseases, October 2013

Oregon State University (2013, October 15). Beyond antibiotics: 'PPMOs' offer new approach to bacterial infection, other disease. ScienceDaily. Retrieved November 4, 2013, from http://www.sciencedaily.com/releases/2013/10/131015134922.htm

Sunscreen is Needed For Healthy Glowing Skin

About two months ago, my father was diagnosed with skin cancer. Fortunately, it was not a diagnosis of melanoma. However, the diagnoses was still devastating and mortifying. He underwent treatment shortly after and is now cancer free. The physician indicated the skin cancer was a possible result of not applying sunscreen. Unlike my father, I liberally apply sunscreen multiple times if I’m out in the sun for extended periods of time. Unfortunately, I’m cursed with pale skin and burn easily. The recent diagnoses of my father sparked my interest to read this scientific study. The scientific study examined the molecular changes of the skin cells associated with skin cancer with and without sunscreen.

According to the article, melanoma is a form of skin cancer that results from melanocytes, the pigment producing cells of the skin. It is hypothesized that the increased production of melanocytes may be associated with melanoma. The link between ultraviolet radiation and melanoma are undetermined and farther investigation needs to be conducted.  The p53 gene plays an important role in preventing skin cancer by repairing UV damaged skin. The p53 gene can be mutated overtime with increased exposure to ultraviolet radiation and repeated burning of the skin. The mutated p53 gene displays a loss in the capabilities to repair UV damaged skin resulting in the increased risk of skin cancer.

According to the study, 24 hours after solar-simulated ultraviolet radiation (SSUVR) keratinocytes and melanocytes both skin cells displayed UV induced DNA damage. The unexposed skin and skin protected with sunscreen displayed no UV induced DNA damage. The UV induced DNA damage can increase the risk of melanoma. The application of sunscreen can diminish DNA damage associated with ultraviolet radiation and reduce the risk of melanoma and other skin cancers.

The expression of the p53 gene was present in keratinocytes and melanocytes. The gene expression in both cells increased 24 hours after being exposed to SSUVR, the expression of the gene decreased at 14 days. The application of sunscreen displayed no p53 expression in keratinocytes and melanocytes after exposure to SSUVR. The expression of the p53 gene is to prevent cell death by repairing cells with UV damage. The application of sunscreen diminishes the expression of p53; the cells are not exposed to damaging ultraviolet radiation. Therefore, the expression of the gene is not needed to prevent cell death of normal healthy skin cells.

The study also displayed at day 14 there was an increased amount of melanocytes after SSUVR exposure when compared with sunscreen. According to the article the increased melanocytes increased the pigmentation of the skin and helps prevent against induced DNA damage. The results are significant and display the effectiveness of sunscreen. The application of sunscreen is imperative to prevent molecular changes in skin cells associated with skin cancer.

 Don't forget to apply sunscreen to prevent skin cancer! Don't forget your sunglasses and other sun protective gear to help protect against ultraviolet radiation!

References

Queensland University of Technology (2013, October 8). Sunscreen saves superhero gene. Sciencedaily. Retrieved October 13, 2013, from http://www.sciencedaily.com/releases/2013/10/131008102551.htm

Hacker, E., Boyce, Z., Kimlin, G.M., Wockner, L., Pollak, T., Vaartjes, A.S., Hayward, K.N., Whiteman, C.D. (2013). The effect of MC1R variants and sunscreen on the response of human melanocytes in vivo to ultraviolet radiation and implications for melanoma. Pigm. Cell Melanoma Res. 1-11.

Yamaguchi, Y., Coelho, S.G., Zmudzka, B.Z., Takahashi, K., Beer, J.Z., Hearing, V.J., and Miller, S.A. (2008). Cyclobutane pyrimidine dimer formation and p53 production in human skin after repeated UV irradiation. Exp. Dermatol. 17, 916–924.