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

-----------------------------------------------------------------------------------------------------------------

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.

Image link: http://www.democraticunderground.com/discuss/duboard.php?az=show_mesg&forum=222&topic_id=90860

Bacterium Protects Against Asthma

            New studies from Germany suggest infection from the bacterium, Helicobacter pylori, offers protection against allergy-induced asthma. But in industrial societies this bacterium has disappeared from the human body because of the hygiene hypothesis. The hygiene hypothesis says “that modern hygiene measures have led to a lack of exposure to infectious agents, which is important for the normal maturation of the immune system.” Since the bacterium isn’t in the body, allergic diseases are increasing from the air pollution.

            Asthma is a chronic inflammatory disease of the airways, which can cause “wheezing, breathlessness, chest tightness and coughing.” It’s estimated that “ 6.8 million U.S. children have asthma.” People think asthma contributes to obesity; both are the two leading public health problems in the U.S. Allergy induced asthma occurs when then the body’s immune system falsely identifies a non-threatening substance, such as pollen or pollution, as a harmful intruder into the body. This causes a reaction from the human body in which the antibodies in your immune system attempt to attack the foreign substance. This is seen when the body produces

excessive amounts of mucus discharge, or what most people experience when battling allergies, but it can also lead to the lungs and airways being affected. When these are affected it can trigger asthmatic episodes and this causes allergy-induced asthma.

Helicobacter pylori infect half the world’s population and are resistant to gastric acid. It can cause different stomach problems or diseases but most have no symptoms and therefore killed off with antibiotics as a precaution.  The researchers at the University of Zurich and University Medical Center of the Johannes Gutenberg believe that early infection with the H. pylori bacterium will protect against asthma and other allergic diseases. They have tested their theory on mice and the mice that didn’t have the bacteria had weaker defenses in adulthood. In industrial areas asthma is linked to “the widespread use of antibiotics and the subsequent disappearance of microorganisms” in the human body.

But Helicobacter pylori can be a dangerous bacterium, even though the majority is harmless to the human body. Bacterial, host and environmental factors determines each individual disease risk. Helicobacter pylori usually colonize the body during childhood and can persist lifelong if left untreated and the various stomach diseases will occur during adulthood.  The most important H. pylori associated illnesses are duodenal and gastric ulceration, as well as inflammation of different parts of the stomach or intestines. Picture shown of H. pylori is shown below.

Since in industrial societies we kill the bacterium with antibiotics and then expose ourselves to pollution and smoke we need “to develop preventative and therapeutic strategies” to help combat asthma now that we understand a little bit more about it. 



Gastric Bacterium Helicobacter Pylori Protects Against Asthma
The inflammatory and immune response to Helicobacter pylori infection
Obesity and Asthma: A Dangerous Link in Children: An Integrative Review of the Literature

Universal Flu Vaccine A Step Closer

Annually changing flu vaccines may soon lead to a single, universal flu vaccine according to a new report from scientists at The Scripps research Institute and the Dutch biopharmaceutical company Crucell. They explain an antibody tested on animals, that can prevent and possibly cure infections within a broad spectrum of influenza viruses, including some seasonal and potentially pandemic strains.

The finding shows the influenza subtypes neutralized with the new antibody include H3N2, which killed an estimated 1 million people in Asia in the late 1960s. This antibody, and the one reported in 2009 have the potential to protect people against most influenza viruses.

Ian Wilson, the Hansen Professor of Structural Biology and a member of the Skaggs Institute for Chemical Biology at Scripps Research, has been working with Crucell scientists to help overcome the problem with current influenza vaccines, which is that they work only against the fe strains that the vaccine makers predict will dominate in a given year, making their effectiveness temporary. In addition, current influenza vaccines provide little or no protection against unforeseen strains.

These problems reflect a basic flu-virus defense mechanism. The viruses come packaged in spherical or filamentous envelopes that are studded with mushroom-shaped hemagglutinin (HA) proteins. These outer structures effectively serve as decoys for a normal antibody response. The outer loops on the HA head seem to attract most of the antibodies, but in a certain strain these loops can mutate to evade an antibody response within months. Antiviral drugs aimed at these and other viral targets also lose effectiveness as flu virus populations evolve. The goal of the research is to find and attack relatively consistent and functionally important structures on flu viruses.

By sifting through the blood of people who have been immunized with flu vaccines, researchers discovered an antibody that bound to one such exposed structure. In mice, an injection of the antibody could prevent or even cure a lethal infection by about half of flu viruses, including H1 viruses such as H1N1, which caused deadly global pandemics in 1918 and 2009.

Researchers determined the 3D molecular structure of CR6261 and its binding site on HA. The binding site turned out to be on HA’s lower, less-reachable stalk portion. The bind of CR6261 to that region interferes with flu viruses’ ability to deliver their genetic material into host cells and start a new infection.

Crucell researchers searched for an antibody that could neutralize some of the remaining flu viruses unaffected by CR6261, and recently found one called CR8020. CR8020 powerfully neutralizes a range of human-affected flu viruses in lab-dish tests and in mice. The affected viruses include H3 and H7, which have already caused pandemic or sporadic human infections.

Crucell is about to begin initial clinical trials of CR6261 in human volunteers, and the company expects to begin similar trials of CR8020. If those trials succeed, the two antibodies could be combined and used in a passive immunotherapy approach. This would mainly be useful as a fast acting therapy against epidemic or pandemic influenza viruses. The ultimate goal is an active vaccine.

Sources:

http://www.telegraph.co.uk/health/healthnews/8625929/Universal-flu-vaccine-a-step-closer.html

http://www.telegraph.co.uk/health/healthnews/8625929/Universal-flu-vaccine-a-step-closer.html

http://www.sciencemag.org/content/early/2011/07/06/science.1204839.abstract

Discoveries in Mitochondria Open New Field of Cancer Research

A whole new field of epigenetics research from Virginia Common Wealth University Massey Cancer Center has been discovered with the possibility of developing future gene therapies to treat cancer as well as other age-associated diseases. Epigenetics refers to the process that controls which genes get expressed in the nucleus of a cell, ultimately determining that cell's biological characteristics.

Shirley M. Taylor, Ph.D., researcher at VCU Massey Cancer Center and associate professor in the VCU Department of Microbiology and Immunology at VCU School of Medicine, was a graduate student when her research helped establish the field of epigenetics. Many years later Dr. Taylor and her colleagues have expanded their knowledge from understanding enzymes are in existence not only in the nuclei but also in the mitochondria.

All of an organism's hereditary information exists in two distinct genomes of all mammal's cells. Taylor's study found two DNA modifications in the mitochondrial genome. From the article, "In diseases such as cancer, epigenetic control is lost," says Taylor. "Genes that should be switched on are switched off and vice versa, leading to uncontrolled growth. Our research indicates that errors in gene expression could be unfolding in mitochondria, possibly contributing to loss of mitochondrial function typical of cancer and a host of other age-related diseases." One of the main areas of focus for Taylor and her team is trying to determine whether epigenetic control is a factor contributing to defects that lead to serious illnesses. Understanding the impact drugs have on gene expression in the nucleus and discovering beneficial ways of using it for the mitochondria would be huge.

It is always interesting to me when new studies and discoveries come out about steps taken towards cancer research. Cancer affects millions of people worldwide every year and is the world's leading cause of death. According to the World Health Organization, "Deaths from cancer worldwide are projected to continue rising, with an estimated 12 million deaths in 2030." Although the cure for cancer or other serious age related diseases may not be discovered shortly, it still gives hope that new research in the field of Microbiology is taking strides toward making that a reality one day!

References

Virginia Commonwealth University (2011, June 21). Discoveries in mitochondria open new field of cancer research. ScienceDaily. Retrieved July 3, 2011, from http://www.sciencedaily.com­ /releases/2011/06/110620161306.htm

L. S. Shock, P. V. Thakkar, E. J. Peterson, R. G. Moran, S. M. Taylor. DNA methyltransferase 1, cytosine methylation, and cytosine hydroxymethylation in mammalian mitochondria. Proceedings of the National Academy of Sciences, 2011; 108 (9): 3630

http://www.who.int/cancer/en/