A Ruthless Killer of its Own Kind

Inhabiting a wide variety of places on Earth; including but not limited to the soil, water, plants, animals, and even humans, Pseudomonas aeruginosa is known to many as the culprit which causes physical aliments such as pneumonia, urinary tract infections, and bacteremia (an invasion of the bloodstream by bacteria- http://medical-dictionary.thefreedictionary.com/bacteremia). Even though it’s usually not dangerous to individuals with healthy immune systems this bacterium strikes those who aren’t as healthy. Even more interesting, this bacterium is “the most common pathogen isolated from patients who have been hospitalized longer than one week” - http://emedicine.medscape.com/article/226748-overview. However, could this less than favorable bacterium be used for the good of all men, and if so, how could it?

In a recent study conducted at the University of Washington by Alistair Russell, Mr. Russell has found that these bacteria do something truly marvelous, they “inject toxins into rival bacteria with a needle-like puncturing device…[which] degrade competitors’ protective barricades—their cell wall” “By killing off its competitors, P. aeruginosa widens its territory, leading to its overall success,” say Russell. As Mr. Russell goes on to explain, these bacteria inhabit places where other types of bacteria take residence. They, like all living organisms, must find a way to survive in the environments they live in, which just happens to be by piercing other bacteria’s defense mechanisms, their cell wall. How exactly do they do this; break down the cell wall of an opposing bacterium to eradicate them? Russell has pinpointed down the exact mechanism that does this, the type VI secretion system, or the T6SS. This device, “transports toxins so that they never enter P. aeruginosa’s cell wall space… [this then] delivers toxic proteins that degrade the cell wall. After the cell wall is compromised, the cell bursts like an overfilled water balloon.” It’s interesting to have found that this type of bacterium does this. As Russell mentions, its actions of injecting and killing other bacteria are similar to those of viruses, or bacteriophages. To answer my question above, this bacterium, rather, this bacterium’s system, the T6SS, could prove to be useful to the common man. Russell did not overlook this possibility either, "We might be able to take helpful bacteria, give them this system genetically, and increase their ability to clear out professional pathogens -- those bacteria that make their living causing disease." However, this does draw another point, how would we do this? Again, Mr. Russell has thought about this question as well. “One limitation is that bacteriophages are relatively unstable and require a host bacterium to increase their numbers.” Even though there are limitations such as this one, this could ultimately mean that in the near future scientist and drug companies could collaborate together and create a new type of antibiotic drug in which could act like P. aeruginosa and attack invading bacteria. Until then, Mr. Russell, his colleagues, and others who wish to probe the potential positive effects of engineering new drugs with this capability will without a doubt have to go through more research and testing to become even closer to finding a way.

Sources:

http://www.sciencedaily.com/releases/2011/07/110720142129.htm

http://emedicine.medscape.com/article/226748-overview

http://medical-dictionary.thefreedictionary.com/bacteremia

They're Bad, But Can They Be Good?

Prions are known as infectious agents, but is it possible that they are an evolutionary adaptation in mammals that sometimes goes awry? First studied for their part in neurodegenerative diseases called transmissible spongiform encephalopathies (TSE) (mad cow disease in bovines, scrapie in ovines and Creutzfeldt-Jakob disease in humans) the role and function of normal prions has taken longer to determine.

Prions are proteins in misfolded form. They are different from other known infectious agents – viruses, bacteria, fungi, and parasites – all of which contain nucleic acids (either DNA, RNA, or both). A prion contains no nucleic acids. Misfolded prions are infectious by their effect on normal versions of the prion protein. A prion replicates by inducing other properly-folded proteins to convert into the disease-associated, prion form; the prion acts as a template to guide the misfolding of more protein into prion form. These newly misfolded prions then go on to convert more proteins themselves, triggering a chain reaction that produces large amounts of the misfolded prion form. All known prions induce the formation of an amyloid fold. Amyloid aggregates are fibrils, growing at their ends, and replicating when breakage causes two growing ends to become four growing ends. The incubation period of prion diseases is determined by the exponential growth rate associated with prion replication. The propagation of the prion depends on the presence of normally-folded protein in which the prion can induce misfolding; animals which do not express the normal form of the prion protein cannot develop or transmit the disease.

In a study done by Gerald Zamponi and colleagues it has been discovered that prions actually may have a good side. When not abnormally folded, the presence of prions has been shown to inhibit the activity of certain neurons; acting as a check or balance on the overexcitation of certain neural transmissions - protecting the longevity of the neuron by keeping it from running itself to an early death.

In this study the brain activity of knockout mice (PrP-null) which lacked the prion protein was examined and compared with the brain activity of wild-type mice in which the prion protein was present. It was found that the neurons of the knockout mice responded longer and more vigorously to electrical or drug-induced stimulation than did neurons of the wild-type mice that had normal prion protein. Both brains showed similar waveform patterns, with waveforms exhibiting a robust presynaptic volley, a sharp downward deflecting population spike, and upward deflecting field excitatory postsynaptic potential as well as robust paired-pulse facilitation. However the PrP-null mice showed an increase in the number of overriding polyspikes. This suggested to the researchers that neurons in PrP-null mice fired multiple action potentials in response to a single stimulus and indicated a basal increase in excitability. Further testing indicated that the enhanced excitability seen in the PrP-null mice was in large part caused by the activity of N-methyl-d-aspartate receptor (NMDAR). These receptors are known to play a part in neuronal excitability and excitotoxic neuronal cell death. Without the normal prion protein present to regulate or modulate these receptors, the neurons in the brains of these overreacted again and again eventually leading to early degeneration of the neuron.

The trick for scientists now is to determine just how to balance the good and the bad of prion proteins in the search for treatments and cures for the many forms of TSE’s. Prions may have a bad name right now, but unlocking the secrets to their proper workings may one day advance the cures for the diseases they cause.

sources:

http://www.sciencedaily.com/releases/2008/05/080507105649.htm

http://jcb.rupress.org/content/181/3/551.full

Enterococcus faecalis; Drug-Resistant "Super bug"

For humans, Enterococcus faecalis exists naturally in the gastrointestinal track and is among the first lactic acid bacteria to colonize an infant's intestines. However, despite occurring naturally in the human body, this microorganism has become one of the leading causes of nosocomial or hospital acquired infections. An Enterococcus faecalis infection is difficult to eradicate due to its multi-drug resistance. Enterococcus faecalis "is found to be frequently resistant to tetracycline, erythromycin, streptomycin, and kanamycin--common antibiotics used to treat human infections."

Enterococcus faecalis is known to have the ability to transfer its resistance to antibiotics to other pathogens. Its capacity for virulence is of great importance to the stability of public health. The acquisition of such antibiotic resistant infections is not limited to hospitals alone. Recent research has revealed that insects may be responsible for helping to spread Enterococcus faecalis infections from livestock, mainly pigs, to humans.

Enterococcus faecalis also exists in the gastrointestinal tracks of pigs. When farmers use antibiotics as "growth promoters" to cause pigs to gain weight faster, antibiotic resistant "super bugs" develop. The bacteria in the digestive track of the pig are exposed to the selective pressure of the antibiotics and new, drug resistant Enterococcus faecalis microbes develop. Humans are not exposed to the "super bug" from eating properly cooked pork meat, but from insects that exist on the pig farms. Insects such as flies and cockroaches have been studied and found to carry the antibiotic resistant Enterococcus faecalis in their digestive tracks. The insects travel from the farms where they acquired the bacteria and into the surrounding environment increasing potential exposure to humans. In order to decrease the possibility of infectious transfer from insects to humans, "effective management strategies aimed at reducing insect pest populations should be an important component of pre-harvest food safety efforts on animal farms."

It is important to prevent the spread of antibiotic resistant Enterococcus faecalis infections to humans both nosocomial and environmentally (through insects) because, outside of the gastrointestinal track, such infections pose critical health risks to humans. One such health risk is endocarditis and Enterococcus faecalis is the leading species that causes it. Endocarditis most commonly occurs as an abnormality of a heart valve. The treatment for endocarditis is given as intravenous antibiotics to remove the bacterial infestation from the heart. In an ideal treatment patients are first hospitalized to receive an initial intravenous antibiotic treatment which is then continued outside of the hospital by long-term antibiotic therapy to remove all of the bacteria from the heart chambers and valves. An Enterococcus faecalis infection existing in the heart can ultimately result in death. If the infection is from a "super bug" it will be harder to find an antibiotic to treat the infection. Enterococcus faecalis has also been reported as a cause of Meningitis infections, another potentially deadly infection. Meningitis has been found to occur through bacteremia or the presence of a viable bacteria circulating through the blood. Bacteremia is usually self-resolving but in the case of "super bugs" risk of bacterial infection increases and may become deadly.

Sources Cited:

BioMed Central (2011, January 27). Household bugs: A risk to human health?. Science Daily. Retrieved July 20, 2011, from http://www.sciencedaily.com/releases/2011/01/110126081706.htm

Nallapareddy, S.R., Wenxiang, H., Weinstock, G.M., & Murray, B.E. (2005). Molecular Characterization of a Widespread, Pathogenic, and Antibiotic Resistance-Receptive Enterococcus faecalis Lineage and Dissemination of its Putative Pathogenicity Island. Journal of Bacteriology, 187 (16), Retrieved from http://jb.asm.org/cgi/conetnt/full/187/16/5709

Solheim, M., Aakra, A., Snipen, L.G., Brede, D.A., & Nes, I.F. (2009). Comparative Genomics of Enterococcus faecalis from Healthy Norwegian Infants. BMC Genomics, 194 (10), Retrieved from http://www.biomedcentral.com/1471-2164/10/194

Levy, D. (2010, April 27). Endocarditis. Retrieved from http://www.ncbi.nlm.gov/pubmedhealth/PMG0002088

Is it Possible that Brain Cells Abandon Mitochondria in Parkinson’s?

Parkinson's disease affects nearly five million individuals today by degenerating brain cells and by damaging nerve cells that control their muscles. In PD, there are neurons in an area of the brainstem called substantia nigra which means “large black area.” It is named for the dark pigment that neurons release as a by-product from synthesizing dopamine. When neurons degenerate, less dopamine reaches neurons’ synapses. The decrease in dopamine causes the poor motor symptoms of Parkinson’s disease. No treatments can cure or slow the course of PD, but replacing or enhancing use of dopamine can temporarily alleviate symptoms.

Recently researchers are reporting that the causes of Parkinson’s are because brain cells are abandoning mitochondria. First, it is important to know that mitochondria uses it’s DNA and ribosome’s to synthesize some of its own proteins. Mitochondria make usable energy for the cell and are often called the “powerhouses”. All cells require energy to grow and move. All cells can access energy for cellular processes by breaking down organic molecules and transferring that energy to a molecule called ATP. Mitochondria produce ATP by extracting energy from substrates. ATP is used by enzymes to perform a wide range of cellular functions. For example, our respiratory and circulatory systems deliver oxygen to the tissues to be used by mitochrondri and to eliminate carbon dioxide. Enzymes within the mitochondria’s membranes are designed to oxidize the substrates. Mitochondria are surrounded by two membranes: an outer and an inner membrane. This creates several different locations that can be used for different functions during the breakdown of organic molecules. Ultimately, in the matrix of the mitochondria the Kreb’s cycle takes place and the electron transport chain happens in the inner membrane.

Researcher, Clemens Scherzer, believes that neurons “divorce” their mitochondria which may cause Parkinson’s. Studies show that by targeting a specific gene set during the beginning stages of PD could slow or halt further damage. PGC-1alpha gene is found to be the most effective master regulator. “PGC-1alpha is a master switch that activates hundreds of mitochondrial genes, including many of those needed to maintain and repair the power plants in the mitochondria,” said Scherzer. Medications for diabetes also activate PGC-1alpha making it easier for future Parkinson fighting drugs to be developed. Drugs capable of targeting PGC-1alpha in the brain would be a huge benefit to PD patients if given early on, before too many dopamine neurons die.

Scherzer examined gene activity and identified gene sets from substantia nigra samples of deceased Parkinson’s patients. Ten gene sets were identified to be linked to Parkinson’s and had PGC-1alpha in common, making it clear that it’s the master regulator gene. All ten gene sets should have had proteins responsible for mitochondri to carry out correct cellular functions. However, the genes showed that they were suppressed which caused damage to brain energy metabolism, leading to Parkinson’s. Past studies have said that only one of the five gene complexes had to malfunction in order to cause Parkinson’s. However, Scherzer’s findings showed otherwise, all complexes used to build up the mitochondria’s electron transport chain were deficient. Scherzer believes mitochondrial activity may be affected by a combination of environmental chemicals, risk genes, and aging. “The combination may lead to the pervasive electron transport chain deficit we found in common Parkinson’s disease and to which dopamine neurons might be intrinsically more susceptible.”

Works Cited:

American Association for the Advancement of Science. “In Parkinson’s diseases, brain cells abandon mitochondria.” ScienceDaily. 8 Oct. 2010. Web. 20 July 2011.

Fester, R. (2011). E-z microbiology. NY: Barrons Educational Series Inc.

Shier, David, Jackie Butler, and Ricki Lewis. Hole’s human anatomy & physiology. 12th ed. 2010. Pg. 406. Print.

"Substantia nigra and Parkinson's disease." Medline Plus. Web. 22 Jul 2011.

Human Immune System’s Defense Against Anthrax Infections

Recent studies have revealed that the human body’s immune system has its own self-defense mechanism against the anthrax bacterium, Bacillus anthracis. The findings suggest that the body sends out emergency signals when it is faced with a deadly infection.

Bacillus anthracis is a rod-shaped, Gram positive, aerobic bacterium that causes the anthrax disease. B. anthracis produces spores that can survive for years. Anthrax is a disease that mainly infects animals that ingest or inhale the spores while grazing on soils that are contaminated; however, in rare cases, anthrax can affect humans who come into contact with infected animals or animal products. Ingestion, inhalation, and skin contact are ways that anthrax can enter the human body. Once the bacterium is inside the body, it spreads from the tissues to the lymphatics. B. anthracis specifically targets immune cells, called macrophages, that protect the body from infection. The bacterium then produces two very powerful exo-toxins and lethal toxin that causes rapid cell death. If left untreated, the body’s immune defenses could collapse, which would allow the bacteria to reproduce and eventually cause septic shock and rapid person death.

The researchers at the University of California, San Diego School of Medicine and Skaggs School of Pharmacy and Pharmaceutical Sciences have discovered the macrophages that are initially infected by the anthrax bacterium, immediately send out signals to other immune cells as a defense-mechanism. Adenosine triphosphate (ATP) is the actual molecule that macrophages use in order to communicate with the other immune cells during this survival strategy. Michael Karin, PhD, distinguished professor of pharmacology and senior author of the study, said, “The warning alarm sounded during anthrax infection is elegant, complex and can be effective in slowing spread of the pathogen.” According to Karin, ATP that is released from the initial infected macrophage is sensed by a second macrophage. The second macrophage triggers the molecule inflammasome, and, in turn, inflammasome then releases a molecule called interleukin-1beta (IL-1beta) into the bloodstream. IL-1beta warns other macrophages to strengthen their resistance against cell death caused by anthrax.

The researchers performed a series of experiments, involving the use of genetically altered mice or inhibitor drugs, in order to confirm the significance of this molecular circuit. Several different results were discovered when the researchers interfered with the ATP channel, the ATP receptor, inflammasome or the IL-1beta molecule; the macrophages were not able to survive, there was unimpeded growth of the anthrax bacteria, or there was rapid death of the anthrax-infected mice. The researchers also concluded that only the most dangerous bacterial pathogens caused a response in the immune response pathway.

Victor Nizet, MD, professor of pediatrics and pharmacy said, “We hope these findings can be exploited for the design of new treatments to help the body combat serious bacterial pathogens. Supporting the survival of macrophages and preserving their immune function may buy patients precious time until antibiotic therapy is brought on board to clear the infection.”

References:

University of California - San Diego. "How the immune system fights back against anthrax infections." ScienceDaily, 17 Jun. 2011. Web. 18 Jul. 2011.

http://en.wikipedia.org/wiki/Anthrax

http://www.dhpe.org/infect/anthrax.html

http://scopeblog.stanford.edu/2011/06/human-immune-system-has-developed-elegant-self-defense-against-anthrax-infection/

Blood Type or Gut Type?

Big news in the world of bacteria! Scientists at European Molecular Biology Laboratory in Heidelberg, Germany have made some fascinating discoveries about the human gut. These studies are not nearly complete but have already shown that the microbes of the human gut ecosystem can be put into three distinct categories much like blood types.

What is so truly incredible about these studies is that these categories transcend all boundaries of age, sex, height, weight, health, and so far even ethnicity. The categories that have been developed are known as enterotypes. These enterotypes have shown to favor certain enzymes to synthesize vitamins and aid in digestion. Type 1 was seen to produce more enzymes for making the vitamin B7 while Type 2 favors for Vitamin B1. This discovery has the immense possibilities for the medical community in the form of tailored diets for patients and even a better understanding of what medications work better for certain people while they do not work as well for others.

This research was done with stool samples from 25 Europeans from Denmark, France, Spain, and Italy which were then compared to 13 Japanese samples. All of these samples as well as 154 American and 85 Dane samples could all be put neatly into the three enterotypes. This is an astounding discovery seeing as the last distinct categories that were found was the blood typing system that is used today.

In all research there is going to be some limitations and this research is no different. More research is definitely necessary especially in non-industrialized nations with much different diets than the industrialized countries that were studied.

Scientists hope that this discovery will help the medical field in finding alternatives for antibiotics, which are not nearly as effective as they once were because of continued resistance. This could also help with assessment and diagnosis of patients because not only can they search the patient’s body but this not gives them the ability to investigate the bacteria within the person as well. Treatment could also be aided with more personalized care from knowing better how the individual’s body works.

The expectations for this research are high with the whole medical community looking forward to the finished results and the vast effects in can have in their field as well. Much more research with more varied samples is definitely necessary but this is an astounding discovery the world should be very excited for the possibilities.

Sources:

Zimmer, Carl. "Bacterial Ecosystems Divide People Into 3 Groups, Scientists Say." The New York Times. 20 Apr. 2011. Web. 17 July 2011. http://www.nytimes.com/2011/04/21/science/21gut.html?_r=2&ref=microbiology

Bork, Peer. "Enterotypes of the Human Gut Microbiome." Nature. Nature Publishing Group, 08 June 2011. Web. 17 July 2011. .

Arumugam, M., Raes, J. et al. Enterotypes of the human gut microbiome. Nature Advance Online Publication 20 April 2011. DOI:10.1038/nature09944.

Human Gut Microbiota Linked to Obesity

Obesity has recently become a hot topic in the United States as the number of cases of it rise in both adults and children. Because it can lead to many serious problems such as heart disease, cancer, musculoskeletal disorders and type 2 diabetes mellitus, and pulmonary hypertension, many scientists are searching for potential causes and preventive measures to combat it (Dibaise, 460). Recently, a connection has been discovered between obesity and certain forms of bacteria found in the human gut.

According to the article "Gut Microbiota and Its Possible Relationship with Obesity," gut microbiota is formed during the first year of development, and can be very different from person to person (462). However, the type of gut microbiota that is formed seems to have little to do with the lifestyle and age of the host, but is based mostly on its genetic information. This microbiota plays an important role in immune functions, food digestion and gastrointestinal tasks.

Some believe that gut microbiota have a specific metabolic rate and some of its traits may cause susceptibility to obesity. Though there are trillions of microbes living in the human gut, according to "Human Gut Microbes Associated with Obesity," two seem to be highly influential to adiposity- Bacteroidetes and Firmicutes. People who are obese have less Bacteroidetes than lean people and more Firmicutes.

To support this hypothesis, a study was done of 12 obese people who were put on a carbohydrate or fat restricted eating plan. Stools samples were collected over the course of one year and tested to determine the characteristic changes of their gut microbiota. The study found that, "Before diet therapy, obese people had fewer Bacteroidetes (P<0.001) and more Firmicutes (P=0.002) than did lean controls. Over time, the relative abundance of Bacteroidetes increased (P<0.001) and the abundance of Firmicutes decreased (P=0.002), irrespective of diet type" (Ley, 1023). Furthermore, increases in the amount of Bacteroidetes corresponded with the percentage of weight loss. As said by the conductors of the experiment, "Obesity is, to our knowledge, the only condition in which a pronounced, division-wide change in microbial ecology is associated with host pathology" (Ley, 1023).

This study supports their hypothesis that gut microbiota is connected to obesity and will hopefully aid in the development of preventive measures to fight obesity. As said in "Gut Microbiota and Its Possible Relationship with Obesity," "Although clearly no substitute for proper diet and exercise, manipulation of the gut microbiota may represent a novel approach for treating obesity, one that has few adverse affects" (466).

References

Dibaise, J.K., Husen, Z., Crowell, M.D., Krajmalnik-Brown, R., Decker, A.G., & Rittman, B.E. (2008). Gut Microbiota and Its Possible Relationship with Obesity. Mayo Clinic Proceedings, 83(4), 460-469. Retrieved from Ebscohost.

Ley, R.E., Turnbaugh, P.J., Klein, S., & Gordon, J.I. (2006). Microbial Ecology: Human Gut Microbes Associated with Obesity. Nature, 444(7122), 1022-1023. doi: 10. 1038/4441022a. Retrieved from Ebscohost.
Image Link: http://www.gdayindia.com.au/healthy-bacteria-could-prevent-obesity

Chytrid Fungus Killing Frog Populations

Chytrid fungus is a zoosporic fungus, Batrachochytrium dendrobatidis. Once it infects a host, it will feed off the host for a few days. Then it will asexually reproduce, forming a zoospore. This zoospore is released into the surrounding moist environment. It will move through the water, but it is most often through direct contact that it is spread. It moves by use of a flagellum. It once again infects a host, and the cycle begins again. This process takes up to two weeks. Some of the zoospores will stay embedded in the skin, and re-infect the host. It prefers cool, moist environments, and it infects amphibians, mostly frogs. It can live in aqueous environments for months, but cannot live but a few hours in warm, dry conditions.

Once it has infected a frog, it feeds off the keratin in the frog's skin. It makes the skin thick, which affects the frog's ability to uptake water and electrolytes through its skin. This can cause complications in the frog's heart due to a lack of these important electrolytes. The frog also uses its skin for respiration, so an infection will make it difficult for the frog to "breathe." in come cases, it can also affect the nervous system. A frog that is infected with the chytrid fungus will most likely present with discolored skin, lethargy, not protecting itself from the environment, peeling of the skin, and its legs will be splayed away from its body instead of underneath. (Frog Chytrid Fungus, 2011) Some instances of seizures have also been noted.

As stated above, the chytrid fungus is spread through direct contact or through water that is infected. Scientists have realized that the zoospores can be relocated through transfer on wet clothing and footwear. Moving frogs and amphibians that are infected to new locations where the fungus is not present can also aid in its spread. Sometimes birds and insects that move between different environments can also transfer the fungus. This fungus was first discovered in amphibians in Australia in the early 1990's. It is now widespread around the world. (Briggs, Knapp, & Vrendenburg, 2010)

One thing that scientists are studying is the effect of climate on the chytrid fungus. It does not thrive in temperatures above 82 degrees F, or below 50 degrees, although it prefers temperatures between 63 degrees and 77 degrees F. This is one reason it is abundant in the tropical rain forests. Cool days and warm nights provide a perfect atmosphere for the fungus to thrive. And with global warming, it continues to flourish. As the earth's temperature increases, it causes more cloud formation in the rain forest. This cloud cover causes the cooler temperatures in the day and warmer ones at night, creating the perfect environment for the fungus to grow. (Altwood, 2009)

The problem with this fungus is that frog species are now becoming extinct. There are approximately 6,200 species of frogs worldwide, and one third of these are endangered or extinct. This fungus is playing a large role in this. (Borrell, 2009) The Amphibian Conservation Summit reports that this fungus is the "worst infectious disease ever recorded among vertebrates in terms of the number of species impacted, and its propensity to drive them to extinction." (Briggs, Knapp, & Vrendenburg, 2010)

There are studies being done to determine a fix for this problem. Some researchers see using the natural bacteria found of the skin of frogs, which may block the fungus. Another way is to catch and treat the infected frogs. But finding all the infected frogs and preventing them from becoming reinfected poses a problem. (University of Zurich, 2011) But finding a way to stop the spread of this fungus has not been found.

References:

Frog Chytrid Fungus. (2011, April 15). Retrieved July 17, 2011, from www.environment.nsw.gov.au/animals/frogchytridfungus.htm

Altwood, S. (2009). Say Goodbye to Kermit. The New Islander.

Borrell, B. (2009, August 11). Is the Frog-Killing Chytrid Fungus Fueled by Climate Fluctuations? Scientific American, p.12

Briggs, C., Knapp, R., & Vredenburg, V. (2010). Enzootic and epizootic dynamics of the chytrid fungal pathogen of amphibians. Proceedings of the National Academy of Sciences.

University of Zurich. (2011, June 21). Science Daily. Retrieved June 26, 2011, from www.sciencedaily.com/releases/2011/06/110620094856.htm

Arsenic and Life

Arsenic (As) can be found in many dangerous synthetic chemicals. Such chemicals consist of pesticides, wood treatment, and so on. So this may go without saying that arsenic can be very dangerous, especially for multi-cellular organisms like humans. When arsenic (a metalloid) is introduced into a human body it interferes with cellular longevity by isolating specific metabolic enzymes through allosteric inhibition (Oremland, 2005). Many undeveloped nations have had a long standing problem with arsenic contaminated water sources. Arsenic poisoning can cause many unpleasant symptoms as well as death. Scientists however, have now trained certain bacterium to live on a purely arsenic diet. This new ability may lead to an answer to the arsenic contamination problem for many people around the world. The bacterium strain GFAJ-1 usually likes to dine on phosphorus, but scientists over a period of time isolated the bacteria from anything but arsenic and the full scope of adaptation was then observed (Overbye, 2010). NASA and astrobiologists everywhere are also excited by this new discovery in the ability for life to thrive. If an organism can live solely on arsenic, then what else or where else could it live? Life, it seems, could be more easily facilitated than once assumed. Mono Lake in California is where this survivalist bacterium calls home. Geomicrobiologist Felisa Wolfe-Simon and her team sought out Mono Lake because of its already high concentration of arsenic (Overbye, 2010). After scooping the bacterium out of the lake with the mud Simon and her team continued feeding the bacterium more and more arsenic until it had replaced the environment with the element. Simon decided to use this bacterium as a starting point, since after many millions of years living in arsenic contaminated water the assumption was that the bacteria would have some evolutionary resistance or appeal to the element (Overbye, 2010). After also introducing radioactively stained arsenic to the bacteria; under a microscope the team could observe the arsenic already embedding itself with in the DNA of the organism (Overbye, 2010). This was a monumental finding as not only did it consume arsenic, but also used in replacement of other elements (phosphorus) in its basic biological processes. Carbon, Sulfur, Nitrogen, Hydrogen, Phosphate, and Phosphorus are the five known elements essential for life; though these elements are still vital, it now seems that they can however be replaced (Oremland, 2005). Arsenic is positioned just below phosphorus in the periodic table, and the two elements can play a similar role in chemical reactions. For example, the arsenate ion, AsO34-, has the same geometric structure and bonding sites as phosphate. It is so similar that it can actually get inside cells by hijacking phosphate's transport mechanism (Oremland, 2005). It is no doubt that this new discovery will lead to many more interesting searches for other life forms who defy our limited view of how and where life can survive. This is also a step in the right direction for the creation many new poison eating microbes that may be able to assist humanity in living long enough to maybe, one day finally find life elsewhere in the universe.

REFERENCES

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Oremland, R. (2005). Arsenic, microbes and contaminated aquifers. Trends in Microbiology,13(2), 45-49.

Overbye, D. (2010, December 2). Microbe finds arsenic tasty; redefines life. The New York Times.

Jelly Fish and Marine Bacteria

In the oceans, marine bacteria play a role in the carbon cycle. They help by absorbing the carbon, nitrogen, phosphorus and other organic byproducts produced when other organisms are decaying, and from waste products. This aids in the energy source and reproduction for the bacteria, and helps protect the ocean's pH. The ocean helps buffer the earth by absorbing carbon dioxide for the atmosphere. The bacteria are then able to provide the carbon for energy higher up the food chain as the bacteria themselves are consumed.

Jelly fish are in every ocean, and in some fresh water. Recently, it has been noted that there is an increase in jelly fish populations. This can be attributed to various reasons, including over fishing, climate changes (jelly fish prefer warmer climates), and increased nutrients in the water (from agricultural/industrial run-off). There has also been a decrease in the number of predators of the jelly fish, such as sharks and tuna. When these conditions happen, the jelly fish populations can sky rocket. This is causing numerous problems. One is the danger to humans from jelly fish stings. This ranges from mild stinging to rare fatalities. Another problem has arisen in Japan, where the jelly fish have entered into power plants, causing some destruction by clogging various pipelines. But most importantly, they are eating large amounts of plankton. Plankton is made up of phytoplankton (algae), zooplankton (protozoans and metazoans), and bacterioplankton (bacteria and archaea). This is the food source for many marine animals from tiny shrimp to large whales. As more plankton is consumed by the jelly fish, the less food for the other marine animals, which will cause a decrease in the numbers of marine life.

When jelly fish come together, due to searching our warm waters, ocean currents, and abundance of food, they form what is called a "bloom." As the populations are growing, some of these blooms can have as many as 100,000 jelly fish in each one. A study done by Ph.D. graduate Rob Condon in 2011 at the Virginia Institute of Marine Science (VIMS) shows how these blooms are affecting the ocean ecosystem. When the jelly fish die, they form a large biomass of gelatin-like substance. As the oceans' bacteria work to decompose this, they are unable to properly absorb the carbon in this biomass. The bacteria us the carbon from these masses in respiration instead of energy and reproduction. Then they release more carbon dioxide into the oceans from this respiration. This is raising the levels of carbon in the ocean, forming a more acidic environment. This is affecting the life forms in the ocean both directly and indirectly. According to Dr. Carol Turley at Plymouth University's Marine Laboratory, this is "happening at a rate that hasn't occurred in 600 million years." (McVeigh, 2011) Ocean life cannot sustain itself in high levels of carbon, and the oceans are more unlikely to be able to absorb carbon dioxide from the atmosphere.

Another change is the type of bacteria found. Bacteria more adept to consuming the biomass will begin to flourish. Condon states that his team's findings "suggest major shifts in microbial structure and function associated with jelly fish blooms, and a large detour of energy toward bacteria and higher trophic levels." (VIMS, 2001)

RESOURCES

McVeigh, T. (2011, June 12). Explosion in jelly fish numbers may lead to ecological disaster, warn scientists. The Observer.

VIMS. (2011, June 6). Jelly fish blooms shunt food energy from fish to bacteria. VIMS Press Release. Gloucester Point, Virginia: William & Mary University.

Condon, R. (2011, June 6). Jelly fish blooms result in microbial respiratory sink of carbon in marine systems. Proceedings of the National Academy of Sciences. Vol 108, no 25.

Power Paint Pummels MRSA

Scientists are continually looking for new methods by which to combat dangerous pathogens such as methicillin resistant staphylococcus aureus, commonly referred to as MRSA. A new way they have discovered that may prevent the spreading of MRSA is through an antimicrobial coating that can be added to paint that destroys those particular bacteria. According to an M2PressWIRE article, "In tests, 100 percent of MRSA in solution were killed within 20 minutes of contact with a surface painted with latex paint laced with the coating" (Rensselaer 1). This paint is safe to everything except for MRSA and can be used on a variety of surfaces. This paint potentially will be a great asset to hospitals and other health care facilities trying to prevent MRSA infections.

Methicillin resistant staphylococcus aureus affects approximately 53,000,000 people throughout the world and has caused a significant amount of hospitalizations and deaths. (Dordick 3). These bacteria operate by using endopeptidases, amidases, and muramidases to damage the cell walls of their victims, allowing them to infect the cell (Dordick 4).

The MRSA killing coating works by using an enzyme secreted by nonpathogenic types of Staphylococcus to defend against staphylococcus aureus. This enzyme, lysostaphin, joined with a carbon nanotube is embedded into a polymer allowing it to be more stable and flexible, increasing its ability to connect to MRSA (Rensselaer 2). After connecting to the MRSA bacteria, lysostaphin begins to break down the peptidoglycan portion of the cell wall by destroying its pentaglycine bridges (Rennsselaer 2). This lyses the cell wall and spills the cell contents, killing the bacteria. As said by Ravi Kane, this method is, "very effective. If you put a tiny amount of lysostaphin in a solution with Staphylococcus aureus, you'll see the bacteria die almost immediately" (Rensselaer 2).

This method of killing MRSA is better than other coatings and ways of fighting these bacteria. Some coatings use biocides to kill the bacteria. However,they also can be harmful to other organisms and lose potency when there biocides enter the surroundings (Rensselaer 2). Other paints may use amphipatic polycations or anitmicrobial peptides against MRSA, but they sometimes clog causing the coating to be less effective. Also, the lysostaphin coating does not use antibiotics, which helps to reduce anitbiotic resistance building.

The lysostaphin coating can be mixed with paint or used to coat a variety of objects such as door handles, medical masks, stethoscopes and other medical paraphernalia. It can be cleaned many times and still be successful in destroying MRSA. Due to its selective nature, the lysostaphin coating has no side effects to human cells that may come in contact with it. This coating could definitely become a great asset in creating a safe environment for hospital patients by helping prevent the spread of MRSA.

Works Cited

Dordick, Jonathan S. "Antistaphylococcal nanocompsite films based on enzyme-nanotube conjugates." ACS Nano 4.7 (2010): 39930 4000. Medline. Ebsco. Web. 10 July 2011.

"Rensselaer Polytechnic Institute Researchers Develop Coating That Safely Kills MRSA on Contact; scanning electron microscopy image of nanocomposite film." M2PressWIRE (2010): Newspaper Source Plus. Ebsco. Web. 10 July 2011.

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