Genetic tests use a variety of laboratory techniques to determine if a person has a genetic condition. Individuals may get tested if there is a family history of one specific disease or if they are concerned about passing on a genetic problem to their children (1). Infact, in a study published recently, doctors revealed that they can determine if a child is born of incest without testing the DNA of parents. This breakthrough was made while analyzing the DNA of disabled children to figure out which genes trigger various disabilities.

Genetic tests include techniques to examine genes or markers near the genes (1). Direct testing for diseases such as cystic fibrosis and sickle cell anemia come from an analysis of an individual's specific genes. A technique called linkage analysis, or indirect testing, is used when the gene cannot be directly identified but can be located within a specific region of a chromosome. This testing requires additional DNA from an affected family member for comparison. Genetic tests can be used for individual identification ("DNA fingerprinting"), because each person’s gene is unique, with the exception of identical twins.

Genetic testing is a complex process, and the results depend both on reliable laboratory procedures and accurate interpretation of results (1). Tests vary in sensitivity and their ability to detect mutations. Interpretation of test results is often complex even for trained physicians and other health care specialists. When interpreting the results of any genetic test, one must take into account the probability of false positive or false negative test results (1). Special training is required to analyze and convey information about genetic testing to affected individuals and their families.

Types of Genetic inheritances

Every cell within the human body contains DNA, made up of four chemicals including adenine, guanine, thymine and cytosine. Every human being inherits DNA from both his parents. Abnormalities within the inherited DNA results in genetic inheritance disorders, of which there are four types.

Monogenetic Inheritance

A single gene triggers the genetic disorder, which causes proteins within cellular structures to function improperly (2). Examples of monogenetic inheritance disorders are Huntington's disease and Marfan syndrome. Cystic fibrosis, a chronic genetic disorder that produces life-threatening lung infections also has links to monogenetic inheritance.

Complex Inheritance

Environmental influences in combination with multiple genetic mutations define disorders that result from complex genetic inheritance. High blood pressure is one example of a disorder linked to complex inheritance (2). Obesity is another prime example according to the University of Texas. While obesity does have genetic links, overeating, an environmental influence, also plays a large role, making the genetic disorder more complex.

Merits of Genetic testing

Genetic testing has potential benefits whether the results are positive or negative for a gene mutation. Test results can provide a sense of relief from uncertainty and help people make informed decisions about managing their health care (1,3). For example, a negative result can eliminate the need for unnecessary checkups and screening tests in some cases. A positive result can direct a person toward available prevention, monitoring, and treatment options (1). Some test results can also help people make decisions about having children.

Ethical Issues in Genetic Testing, Legal, and Social

Information from genetic testing can affect the lives of individuals and their families. In addition to personal and family issues, genetic disease or susceptibility may have implications for employment and insurance (1). Critical issues include privacy, informed consent, and confidentiality.

 Individuals have the right to maintain privacy. Some genetic tests are required or strongly encouraged for developing fetuses and newborn babies (1). If an infant is found to be a carrier or likely to develop or be affected by an inherited disease, these findings may affect the future employability or insurability of the individual.

To perform genetic testing, one must give consent. One must have knowledge of the risks, benefits, effectiveness, and alternatives to testing in order to understand the implications of genetic testing.

Genetic information is sensitive and access should be limited to those authorized to receive it. Future access to a person's genetic information also should be limited.

With respect to genetic testing, legislation in the U.S called the Genetic Information Nondiscrimination Act prohibits group health plans and health insurers from denying coverage to a healthy individual or charging higher premiums because of a genetic predisposition to developing a disease in the future. The legislation also prevents employers from using genetic information while making important decisions.

Shortcomings of Genetic testing

Current gene tests do not provide a convincing answer for people at risk for inherited breast or colon cancer. Shared environmental exposures could play a big role rather than inherited susceptibility. Identifying mutations remains a great challenge (3). Many of the genes contain many thousands of bases. Searching through long stretches of DNA is difficult. A positive test does not guarantee that disease is imminent and a negative test only evaluates the more common mutations and cannot completely rule it out. One person with a given gene may develop a disease, while another person remains healthy. Predictive tests deal in probabilities, not certainties. Last but not least, test information is not always supported by diagnostics and therapies.

About the Author

Born in Redwood City, California, Varun Mohan is raised in Sunnyvale, CA. He is currently a sophomore at The Harker School, who enjoys problem solving in math and science. While he is not solving problems, he reads fiction and listens to western classical music. Besides, he loves to play water polo and viola, and is part of Harker's water polo team and orchestra.

Citations

1.Human Genome Project Information[homepage on the Internet]. Washington D.C:  Human Genome Program; 2010 [Updated Sep 2010; cited 2011 Oct 29]. Available from: http://www.ornl.gov/sci/techresources/Human_Genome/medicine/genetest.shtml

2.Inheritance Patterns[homepage on the Internet]. Burlington, VT: Gene Primer; 2010[Updated Apr 2010; cited 2011 Oct 20]. Available from

http://www.uvm.edu/~cgep/Education/Inheritance2.html

3.Health and Wellness[homepage on the Internet]. Charlotte, NC. Potential Benefits; 2008[Updates Sep 2008; cited 2011 Oct 29]. Available from

http://impact-study.co.uk/public/geneticsandcancer/genetictesting/positiveandnegativeaspects

Alzheimer’s Disease, the sixth largest killer of Americans annually, has shown no signs of slowing down and the number of people it kills yearly is on pace to quadruple by the year 2050. Unlike the other top killers of Americans, such as heart disease, cancer, and stroke, Alzheimer’s is nowhere near having a cure or a reduction in cases; the number of people it affects currently is rising over 66% every year. The severity of Alzheimer’s patients’ plight can easily be seen in newly diagnosed patients,’ mentally shackled by the disease, inability to function in society, especially in a social setting, as well as the growing lack of funding for government subsidized treatment of the disease because of burgeoning costs of treatment. In fact, the most effective method of treating patients relies upon how early the disease is diagnosed; fear and stigma counteract this, often making patients reluctant to be checked for the disease, severely decreasing the chances of early diagnosis. Although the future for a cure may be bleak, by raising awareness about the importance of early diagnosis and simply providing more information to the public, Alzheimer’s does not need to be as major an issue for the American people as it is now, on the financial, medical, and even social fronts.

            Alzheimer’s disease was initially described by Dr. Alois Alzheimer after he saw a patient die from a unique mental disease, whose symptoms he noted to be memory loss, language problems, and unpredictable behavior. These three symptoms define the disease fairly comprehensively, although they do not account for the fact that the disease “is an irreversible, progressive brain disease that slowly destroys memory and thinking skills, and eventually even the ability to carry out the simplest tasks,” as noted by the National Institutes for Health. From a scientific perspective, the disease seems to be caused by tangles and the growth of plaques on the brain’s entorhinal cortex well before the symptoms begin to appear in victims. Despite the term “irreversible,” research has shown that the disease progresses in three main stages, and as the disease proceeds through each stage, it becomes progressively harder to treat effectively. In the first stage, patients experience short-term memory loss in regard to daily tasks, taking longer to complete them. As it moves to the second stage, patients start to forget more deeply ingrained pieces of information in their mind such as family and friends. In the final stage, people lose any sense of what is occurring around them and remain bed-ridden until their passing. The whole process is extremely fearful not only for the patient, but particularly for the family and friends of the patients who watch the mental deterioration of their loved ones over the course of sometimes more than 20 years.

            This poses major issues to our society from financial, medical, and social standpoints.  In 2010 alone, the United States federal government has spent $183 billion dollars on Alzheimer’s caregiving, and is projected to spend upwards of $20 trillion over the next 40 years as costs will rise – a drain on the already unstable economy. From a purely medical standpoint, it takes a major toll on both the patients who are facing an incurable disease, families who need to provide care for these patients, and caregivers who just this past year have given over 17 billion hours of free care. Socially, these individuals are literally about to lose their minds and the ability to function autonomously, losses that are both frightening for the individual and place a collective burden on their support networks. A survey by the Alzheimer’s Foundation of America notes that, “nearly half (45 percent) of those surveyed said the emotional toll of seeing someone they loved lose their ability to function was the hardest part of the disease.” The magnitude of the impact of not treating Alzheimer’s properly is immense on multiple levels, demonstrating the imminent need to find a solution.       

            Currently, no significant progress is being made on an outright cure for Alzheimer’s; however, moderate success in prolonging the lives of victims has been made through physical and mental therapy. As identified by several researchers in the field, the only feasible way to combat the spread of the Alzheimer’s epidemic is to identify the disease’s symptoms early on in order to start treatment as early as possible. Success in treating the disease has been extremely sporadic when brought to doctors in its late stages, and patients’ lives have been able to be prolonged much longer when brought to their attention early. Unfortunately, a major obstacle prevents this very thing from occurring on a regular basis – the social stigma surrounding Alzheimer’s, as well as the fear it inspires in its victims. A 2005 study conducted by the University of New Brunswick found that fear of Alzheimer’s disease was increasing in younger generations. This led to, as per an Alzheimer’s Foundation of America study, “57 percent of caregivers [saying] an Alzheimer's diagnosis was delayed because either they were, or the person with the illness was, in denial about having the disease or feared the social stigma associated with it.” Accordingly, success rates in post-diagnosis treatment to dropped considerably. This denial experienced by many Alzheimer’s victims is a major cause for Dispelling the stigma surrounding the disease itself is crucial to ultimately being able to treat Alzheimer’s effectively.

With the deleterious financial, medical, and social impacts that stem from Alzheimer’s, it is clear that progress needs to be made on this front. Despite the lack of a definitive cure for the disease itself, given enough time doctors are able to significantly increase the lifespan of their patients – demonstrating the need to evaporate this social stigma that serves as a shackle to any solutions.

Works Cited

“Alzheimer’s Disease Fact Sheet.” National Institute on Aging. US National Institutes of Health, 19 Feb. 2010. Web. 29 May 2011. <http://www.nia.nih.gov/​Alzheimers/​Publications/​adfact.htm>.

Billingsley, Janice. “Denial, Stigma Delaying Alzheimer’s Diagnoses.” Health Day News. Healing Well, 21 Mar. 2006. Web. 29 May 2011. <http://news.healingwell.com/​index.php?p=news1&id=531624>.

McLean, Sharon, and Robert Laforce, Jr. “Knowledge And Fear Of Developing Alzheimer’s Disease In A Sample Of Healthy Adults.” Psychological Reports 96 (Feb. 2005): 204-206. PubMed. Web. 29 May 2011.

Smith, Rebecca. “Alzheimer’s disease being tackled ‘too late’: Lancet.” The Telegraph. N.p., 27 Aug. 2010. Web. 29 May 2011. <http://www.telegraph.co.uk/​health/​healthnews/​7965818/​Alzheimers-disease-b...>.

Williams, Toni. “Alzheimer’s Disease To Cost United States $20 Trillion over Next 40 Years.” The Alzheimer’s Association. The Alzheimer’s Association, 19 May 2011. Web. 29 May 2011. <http://www.alz.org/​documents_custom/​FINAL_Trajectory_Report_Release-EMB_5-1...>.

 Rapist and serial killer Brian Dugan was a psychopath. At least that is what brain scans presented by his defense attorney seemed to show.

But these detailed fMRI images were not enough to sway the courtroom officials in his favor, although they bought him a few hours’ extra time while the jury deliberated overnight. At the time, Dugan was already serving life sentences for two other murder cases, and on the morning of November 11^th, 2009, he was issued with a death sentence for the rape and murder of 10-year-old Jeanine Nicarico [3].

Steve Greenberg, Dugan’s lead attorney, argued that the criminal’s mental illness should be a “mitigating factor because it impaired his ability to control his behavior” [3]. He stated that although the deviations illustrated through the fMRI images did not justify Dugan’s actions, they provided a potential reason for the crimes and might warrant some leniency from the jury in terms of his sentence.

Similar to the Dugan, many murder suspects in parts of India, Europe, and the United States have sought the aid of neuroscans to prove their possibly abnormal mental state [2]. Even prosecutors have presented such scans for purposes of lie-detection.

However, this rising field of neurolaw has its shortcomings. Ranging from fMRI scans to CT scans to other EEG-based scanning techniques, the use of neuroimages as evidence in courtroom trials has been both controversial and questionable when it comes to accuracy and ethical risks.

The Science Behind Neuroimaging

Neuroimaging is the use of various instrumental techniques to generate images that represent the structure and function of the brain.  The most common method brought to the courtroom is the technique of functional magnetic resonance imaging (fMRI).  As a scanning technique that has been deemed reasonably accurate over the years, the fMRI is a noninvasive procedure that uses a magnet to generate images of changes in blood flow in the brain [1].

On the other hand, the CT scan is an invasive digital processing technique that displays a three-dimensional image from several two-dimensional X-ray images rotated about a central axis. While the fMRI has been proven to be the more sensitive of the two processes, it fails to correctly analyze age and gender of the subject, similar to the CT scan [1].

Assuming impartial and accurate analysis, both processes may provide proof that there is an abnormality in the brain, but the underlying causation that leads to the subject’s actions is absent. In other words, there is no linkage between the cognitive processes and actual behavior of the accused person.  For instance, the case United States vs. Hinckley (1982) tried a man for an attempted assassination of President Ronald Reagan, and the defense presented CT scan evidence. A psychiatrist witness was brought in to testify, who deftly said there was an atrophy in the accused person’s brain that could be linked to schizophrenia [1]. When a radiologist was brought in to validate the interpretation of the images, the abnormality was indeed identified but did not have any direct implications in terms of the sanity of Hinckley. Although there are missing links between interpretation of the data and the actions which they aim to explain, the process in which conclusions are drawn from the scans is inherently subjective.

Speculative in Nature: Real Evidence or Not? 

A certain amount of prejudice is an inherent constituent of any judicial system. However, the range of conclusions that may be drawn based on differing interpretations of these scans may lead to further bias; the question remains to be whether this potential for additional bias is enough to ban the use of such evidence from courtrooms.  

Many experts argue that judging based on apparently structural abnormalities in the brain “oversimplifies the complexity of the crime” (2). Any serious offense cannot be attributed to or explained solely by a series of images that simply show that the accused individual’s mind works differently than others.

Although these distinct scanning methods are theoretically psychological profiling tools, the collected data can often be analyzed in varying ways, leading to clashing conclusions and potentially drastically different verdicts. When it comes to lie-detection by tracking the subject’s memories, experts say that scans can “accurately decode whether people think they remember something, but not whether they actually remember something” (3). Therefore, the scans are only as strong as the person’s memories, and death sentences cannot be issued based on what the suspect believes to have seen or done.  So, can evidence that is based on human recollection ever be free of bias to the extent necessary to be considered trustworthy? If not, then perhaps such scanning technologies may not truly qualify as evidence fit for a courtroom trial.

An Appearance of Reliability

If brain scans are enough to hint that the defendant may be incompetent or insane in any way, the judge and jury may alleviate the nature of the punishment due to feelings of sympathy or pity for the accused.  Studies have shown that when dealing with cases of insanity, or in this case, potential insanity, the jury is more likely to return a verdict of not guilty (1).

The danger with any sort of scientific evidence is that it gives off an air of reliability, so any expert witness who is qualified to present conclusions drawn from the scan will appear  dependable, since no one else is the courtroom is likely to even understand the science behind his or her logic. 

As a result, the jury is often confused and may easily believe the seemingly credible images generated with cutting-edge technology and the latest breakthroughs in neuroscience.

Whether it is feelings of sympathy for a potentially mentally unstable defendant or easily-earned belief in the neuroimages due to their scientific nature, the response of other individuals in the courtroom is vital to the final judgment. In court systems where the jury has a great deal of power over the final verdict, these kinds of subtle psychological effects may lead to drastically diverse decisions. And when it comes to serious cases, there is a significant difference between sentencing someone to death and setting them free as “not guilty,” to the accused, to the victim, and to the rest of society.

A Change Brought About Too Early

Scientific evidence such as neuroscans could possibly be a considerable asset to any judicial system, but the ethical and psychological complications suggest that perhaps the technology is still too young and speculative in nature.

There is still great room for inaccuracy in the scanning methodologies themselves, and the risks involved in terms of potentially creating bias in the minds of the jury deem it to be a questionable change that must be deliberated carefully. 

But although forensic investigative science, specifically the relatively new branch of neurolaw, has its gray areas, it is a field to keep an eye out for. In an era inundated with scientific advancement, the inefficiencies and technical inaccuracies of brain scanning techniques will be overcome soon. But it is the ethical implications, the room for prejudice, the psychological effects, that provide the greatest hindrance to the permanent allowance of neuroscans into courtrooms.

But for now, the verdict of “not guilty” will not be determined by the machines, but by the human beings.

And only time will tell which is better.

About the Author

Paulomi Bhattacharya is a junior at The Harker School. Her hobbies include playing the piano, playing volleyball, and doing scientific research. Paulomi is interested in biochemistry and intends to pursue research in the field of bioengineering in her future years. She has written for the Harker School chapter of The Triple Helix for two years now. In 2010, she joined the staff as an Associate Editor and is now co-Editor-in-Chief.

References

1. Shafi N. Neuroscience and Law: The Evidentiary Value of Brain Imaging. Graduate Student Journal of Psychology, Columbia University [Internet]. 2009 [cited 2011 August 8]; Volume 11: 27-39. Available from http://noelshafi.com/uploads/V11_Article_4__Shafi.pdf

1. Palmer K. National Association of Science Writers [Internet]. [Place unknown]: 2010 February 24 [cited 2011 August 8]. Available from http://www.nasw.org/brain-imaging-courtroom-pretty-pictures-or-hard-evidence

1. Miller G. Huffington Post [Internet]. [Place unknown]: 2009 November 24 [updated 2010 March 28, cited 2011 August 9]. Available from http://www.huffingtonpost.com/2009/11/24/brian-dugan-brain-scan-us_n_369486.html

  Alba may seem like a generic carrot-munching, albino rabbit, but putting her under ultra violet rays would prove otherwise. Glowing bright green, Alba transforms from an average household pet to a creature more suited to the realms of science fiction. However, due to the rapid advancements in science and technology, the existence of a bright green rabbit is no longer otherworldly.

            Eduardo Kac, a pioneer in transgenic artwork and assistant professor of art and technology at the School of Art Institute of Chicago, had two goals: one was to “reveal the cultural implications of the [genetic] revolution underway and offer different ways of thinking about and with biotechnology” and the other was to demonstrate the integration of family life, biotechnology, and “social domain of public opinion” [1]. With those objectives in mind, Kac entreated scientists at the National Institute of Agronomic Research in France to create a glowing rabbit for one of his art exhibits featuring green fluorescent protein (GFP) technology. French geneticist Louis-Marie Houdebine headed the GFP bunny project. Houdebine and his fellow scientists produced Alba via zygote microinjection, which is a process that involves extracting the fluorescent protein from a species of fluorescent jellyfish called Aequorea victoria and enhancing the glowing properties of the protein before inserting it into a fertilized rabbit egg cell [2]. In February 2000, Alba entered the world as the “GFP Bunny” [1].

            Immediately, news of the creation of Alba sparked protests and debate regarding Kac’s project. Despite Kac’s initial intentions to take Alba home, Houdebine refrained from releasing Alba from the laboratory, fearing incitement of further protests among several reasons. Up until her inexplicable, nebulous death in 2002, Alba remained inside the laboratory [3]. Houdebine issued a statement claiming she died “without any reason” and then reassured the public that her death was commonplace by mentioning the fact that “rabbits die often” and she was “about four years old, which is a normal lifespan in [his] facilities” [4]. He denied any connection between the GFP gene and her death. However, Kac believed her death to be a hoax Houdebine used to reduce public attention and to avoid having Kac bring Alba home [4]. Kac also pointed out that Alba was two-and-a-half, not four, at the time of her supposed death, which would counter Houdebine’s assertion that she had a “normal lifespan,” raising questions about the details of the disappearance of this glowing rabbit [4].

            Alba was not the first animal to undergo zygote microinjection of GFP. In 1997, Japanese scientists created glowing mice [5]. So why was the creation of Alba especially controversial? Although scientists had already injected GFP into mammals such as mice prior to the creation of the GFP bunny, their experiments had been for scientific purposes to study biological processes and diseases rather than for artwork. Some believed Alba to be a victim of animal abuse since she had no say in her participation in Kac’s project, while others feared the impact of releasing Alba into natural ecosystems and allowing her to reproduce. To some, tampering with the genes of an animal as an artistic statement seems unnecessary. Woodland Hastings, a biologist at Harvard and the co-discoverer of the jellyfish’s glowing gene, called Kac’s project “frivolous,” reasoning that “there are many more important things” that can be done with the glowing gene [6]. Genetic engineering was formally a domain that consisted of only scientists with the intent of improving the quality of human life; however, galvanized by the advancements in science and technology, it may turn into a domain where anyone can carry out their whims.

            Nevertheless, on the other hand, one can argue that Kac’s project and other works of transgenic art serve to prompt essential debates over animal rights and bring animal cruelty issues into the spotlight. The public’s awareness and attention was re-focused on questions regarding legal and moral boundaries of genetic engineering and animal experimentation when news of Alba’s creation went viral. While animal cruelty laws are in place in the United States, some nations do not rigidly reinforce or even have laws fighting for animal rights, allowing experiments like Alba to be performed.

            Moreover, Alba provides a marker in the development of science and technology. In 1973, the first genetically engineered organisms were produced; now, 38 years later, science and technology has advanced to the point where people are able to produce transgenic artwork [7].

 Kac opened the eyes of the general public and helped people realize that genetic engineering is not as otherworldly as people may have imagined it to be. Instead, it can be in the form of a bunny that behaves “like any other rabbit” and needs the same things [1]. However, Alba also highlights the more chilling aspects of the progress of science and technology. The age-old concern of tampering too much with nature resurfaces. Has Kac’s desire to manipulate genes crossed the line? Are scientists wielding too much influence with the power to alter nature for the ‘benefit’ of humanity?  As Mary Shelley so aptly concluded in Frankenstein, "How much happier that man is who believes his native town to be the world, than he who aspires to be greater than his nature will allow” [8].

About the Author

 Emily Chu is currently a junior at the Harker School located in San Jose, California. She contributes to the school’s newspaper and participates in research as well. Her specific area of interest is neurology, and she volunteers at clinics that aided people with autism and Parkinson’s disease. She is also a major animal lover and has a wide range of pets including a dog, two turtles, and fish. In her free time, she enjoys hanging out with friends, reading, jogging, playing basketball, drawing, and playing with her dog.

References

1. Eduardo K. GFP bunny [Internet]. 2000. Available from: http://www.ekac.org/gfpbunny.html.
2. Becker C. GFP bunny. Art Journal 2000; 59(3): 45.
3. Kac E. GFP bunny. Leonardo 2003; 36(2):97-102.

1. Philipkoski K. RIP: Alba, the glowing bunny, Wired. 2002 Aug 12.

1. Onion A. Artist’s glowing, live rabbit creation causes fuss, ABC News. 2000 Sept 19.

1. Phillips T. Genetically modified organisms (GMOs): Transgenic crops and recombinant

DNA technology. Nature Education 2008; 1(1).

1. Klein K. The transgenic mouse [Internet]. Washington: University of Washington; 1996

 Nov. Available from: http://www.washington.edu/research/pathbreakers/1982b.html 

1. Shelley M. Frankenstein. 3rd ed. Hunter R, editor. New York: W.W. Norton &

 Company; 1996. 

Sudden Oak Death (SOD) is a plant disease that has killed thousands of oak trees in California, Oregon, and parts of Europe. From its earliest infections, SOD has caused detrimental ecological and economic impacts. Since hundreds of plants, birds, and insects depend on oaks such as Douglas-firs and Coast Redwoods, a continued spread of SOD will devastate local ecosystems and the food chain. Additionally, SOD has disrupted natural forest fire patterns because dead fallen trees increase the risk of wildfires. Nurseries, lumber yards, tree harvesters, and other related industries have also lost millions of dollars because of this sudden decrease in oak population. [1]

About SOD

SOD first arose in the mid 1990’s, when several tanoaks in southern California died unexpectedly. Alarmed scientists throughout California congregated to research the perplexing phenomenon. They realized that Phytophthora ramorum, a water mold recently discovered in Europe, had fatally infected these oak trees. As SOD reports increased rapidly, the state introduced new nursery regulations and funded preventative efforts, such as the COMTF (California Oak Mortality Task Force), to combat the disease. However, it was soon discovered that P. ramorum was also infecting a variety of other trees and nursery plants. [2]

Today, the pathogen’s known host list has expanded to over one hundred plant species [3]. These plants have been divided into two categories, called bark canker hosts and foliar hosts [1]. Bark canker hosts include various types of oak trees, notably tanoaks and coast live oaks. In these hosts, P. ramorum creates cankers (areas of diseased tissue), which fatally damage the trees’ immune systems. Meanwhile, foliar hosts encompass all types of plants, from bay laurels to camellias and rhododendrons. In foliar hosts, the pathogen only causes minor infections, such as leaf spots and twig dieback, which are rarely fatal. However, these plants are the primary spreading agents of the disease. [1]

The pathogen P. ramorum is an oomycete, commonly known as a water mold. It reproduces asexually by creating spores in the form of either sporangia or chlamydospores. Sporangia are miniscule sacs containing the new spores, whereas chlamydospores are thick-walled spores that can survive extreme conditions. P. ramorum’s disease cycle begins with infecting a foliar host, such as a rhododendron or bay laurel. There it produces spores, which spread to a bark canker host through water, air, or animal movement. On the oak tree, the sporangia germinate and infect the host, then restart the entire sequence. The pathogen’s infection cycle is polycyclic, meaning it repeats several times within a single growing season. Its ideal infection conditions include a temperature of 20 C and plenty of moisture; therefore, the oomycete is most active during the rainy season. [4]

Current Research

            Following the first detection of SOD, scientists have conducted a great deal of research to improve our efforts against the disease. Most notably, Dr. Matteo Garbelotto of UC Berkeley recently developed a treatment that immunizes bark canker hosts from P. ramorum. It involves injecting the tree’s trunk with a phosphite named Agri-Fos, then coating its bark with an organosilicate surfactant called Pentrabark [5]. This protective treatment is particularly effective because it both blocks the pathogen and boosts the tree's immune system to prevent future infection [5]. Meanwhile, researchers in Colorado are testing a different approach to the disease. They extracted heartwood oil from trees that naturally withstand SOD infection, then applied it on susceptible oaks [6]. In vivo, the oil successfully prevented P. ramorum from germinating, but the treatment is yet to be tested in planta [6].

            Additionally, limited research has been conducted in the scope of foliar hosts. Dr. Garbelotto discovered that applying copper hydroxide to infected bay laurels dramatically decreased the trees’ topical symptoms [7]. However, he was unable to determine the treatment’s effect on the actual pathogen [7]. Researchers from UC Santa Cruz, California, also tested the effectiveness of various fungicides on rhododendrons, camellias, and viburnums. They found that dimethomorph, fenamidone, and pyraclostrobin successfully prevented symptoms from appearing on all three plants [8].

Future Action Plan

            Although research has significantly advanced our ability to combat SOD, much work still lies ahead. Future action plans should focus on the following key topics: gaining a better understanding of P. ramorum’s biology, developing treatments to protect foliar hosts, and enforcing new regulations to gain community support.

Firstly, our limited knowledge of P. ramorum’s biological characteristics is a glaring weakness in our efforts against SOD. Field tests should be conducted to determine the ideal environmental conditions for infection, in terms of topography, climate, and season. This will allow communities to channel resources towards the most susceptible regions. In Addition, discovering the pathogen’s unfavorable conditions for infection will reveal P. ramorum’s weak spots. Furthermore, because the water mold has a variety of reproduction methods and can spread through diverse types of media, future research should attempt to understand these processes better. This experimentation should also investigate the likelihood of P. ramorum mutating and reproducing sexually. In laboratory simulations, scientists have already synthesized two different mating types of the pathogen, named A1 and A2 [4]. The two mates successfully reproduced sexually by forming a fertilized spore known as an oospore [4]. If similar forms of sexual reproduction occur in nature, P. ramorum could proliferate faster and perhaps mutate into stronger breeds.

Next, although there is already an immunizing treatment for bark canker hosts, it is equally important to develop one for foliar hosts. Because foliar hosts are SOD’s primary spreading agents, protecting these plants is crucial for stopping the overall disease movement. Though copper hydroxide and certain fungicides appear to be viable options, both Dr. Garbelotto and the UC Santa Cruz researchers are afraid that the treatments simply eradicated the symptoms but not the pathogen [8]. If so, infected hosts could be incorrectly identified as SOD-free, then may be transported and sold without regulation, helping spread the pathogen. Another concern raised by the UC Santa Cruz scientists was that P. ramorum could easily develop fungicide resistance [8]. Both these points emphasize the need for an alternative treatment to protect foliar hosts from SOD.

Finally, it is critical to raise awareness of SOD and implement a community effort against it. Sudden Oak Death is currently unmanageable because it spreads rapidly and is difficult to control. Therefore, before even conducting research, our first step should be to contain the disease. If scientists can increase awareness about P. ramorum, then more people can make a determined effort to take precautionary measures in infected areas. This includes disinfecting outerwear and disposing of tools used in positively tested sites. After our community helps bring SOD to a manageable level, researchers can then focus on eradicating the disease. From there, we can gain offense on the disease and eventually overcome it.

About the Author 

Zareen Choudhury is currently a sophomore at The Harker School. Having a strong interest in various scientific issues, she independently conducts science research every year to address such concerns. In addition to presenting her work at numerous fairs and symposiums, she has achieved both state and national-level awards since sixth grade, including First Place at the California State Science Fair (2008), First Place from the Society for the Advancement of Material and Processing Engineering (2009), and Semifinalist Award in the national SSP Competition (2008). Last year in her research, she investigated the issue of Sudden Oak Death and sought a cost-effective treatment to protect plant hosts from this disease. Although she was unable to fully resolve this problem, she hopes to raise awareness of Sudden Oak Death through this article. 

References

1.      APHIS [Internet]. United States: United States Department of Agriculture Animal and Plant Heatlh Inspection Service; c2010. Biology of Phytophthora ramorum; 2011 Sep 9 [cited 2011 Oct 31]. Available from: http://www.aphis.usda.gov/plant_health/plant_pest_info/pram/downloads/surveyplan/appendixa.pdf

2.      Sudden Oak Death [Internet]. Berkeley (CA): California Oak Mortality Task Force; 2011. A chronology of Phytophthora ramorum, cause of sudden oak death and other foliar diseases; 2009 [cited 2011 Oct 31]. Available from: http://nature.berkeley.edu/comtf/pdf/PRamorumChronology.pdf

3.      APHIS [Internet]. United States: United States Department of Agriculture Animal and Plant Heatlh Inspection Service; c2010. APHIS list of regulated hosts and plants proven or associated with Phytophthora ramorum; 2011 Sep 9 [cited 2011 Oct 31]. Available from: http://www.aphis.usda.gov/plant_health/plant_pest_info/pram/downloads/pdf_files/usdaprlist.pdf

4.      Parke JL, Lucas S. Sudden oak death and ramorum blight. The Plant Health Instructor [Internet]. 2008 [cited 2011 Oct 31]:[about 17 screens]. Available from: http://www.ncbi.nlm.nih.gov/books/NBK7281/#A55912

5.      Garbelotto M. A report on a comprehensive series of experiments, both in vitro and in planta, to develop treatments for Phytophthora ramorum, the cause of Sudden Oak Death [Internet]. Berkeley (CA): Department of Environmental Science, Policy, and Management. c2004 [cited 2011 Oct 29]:[20 p.]. Available from: http://www.cnr.berkeley.edu/garbelotto/downloads/DPR_rep.pdf.

6.      Manter DK, Karchesy JJ, Kelsey RG. The sporicidal activity of yellow-cedar heartwood, essential oil, and wood constituents toward Phytophthora ramorum in culture. Forest Pathology [Internet]. 2006 Sep 15 [cited 2011 Oct 29];36:[297-308]. Available from: http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=181452.

7.      Garbelotto M, Harnik TY, Schmidt DJ. Efficacy of phosphonic acid, metalaxyl-M and copper hydroxide against Phytophthora ramorum in vitro and in planta. Plant Pathology [Internet]. 2008 [cited 2011 Oct 29]:[1-9]. Available from: http://nature.berkeley.edu/garbelotto/downloads/PPchemicals2008.pdf.

8.      Tjosvold SA, Koike ST, Chamberes DL. Evaluation of fungicides for the control of Phytophthora ramorum infecting rhododendron, camellia, pieris, and viburnum. Plant Management Network [Internet]. 2008 Feb 8 [cited 2011 Oct 29]:[13 p.]. Available from: http://cesantacruz.ucdavis.edu/files/51742.pdf.