OREGON STATE UNIVERSITY

scientific research and advances

Collaborative project between researchers, fishermen aims to reduce West Coast seabird bycatch

ASTORIA, Ore. – A collaborative project between researchers and the West Coast sablefish fishing industry is showing promise for reducing the number of seabirds caught in longline fishing gear, in particular several albatross species including one threatened with extinction.

The combination of using streamer lines (also called bird-scaring lines) to protect longline fishing gear from seabird attacks on baits, and setting hooks at night when the birds are less active can significantly reduce seabird mortality, the researchers say.

Results of the study were just published in the journal Fisheries Research.

“The project was a great example of collaboration between researchers and industry,” said Amanda Gladics, a coastal fisheries specialist with the Oregon Sea Grant program based at Oregon State University and lead author on the study. “The fishermen invited us out onto their boats and provided us with a lot of insights.

“It was their idea for us to explore whether fishing at night could prevent albatross bycatch on the U.S. West Coast – and it turned out, that was the case. We were thrilled to find that albatross bycatch could be reduced without increasing bycatch of other non-target species or reducing target catch, as can sometimes occur.”

Incidental mortality of seabirds in longline fisheries has been an international conservation concern for decades, with estimates of 160,000 seabirds killed in longline fisheries annually. With 15 of 22 species threatened with extinction, albatrosses are especially vulnerable to bycatch mortality. They don’t begin breeding until they are five to 10 years of age and produce only one egg every year or every other year, Gladics said.

“Most of the mortality takes place when the birds attempt to forage on the baited hooks when fishermen deploy longlines,” she said. “In addition to the environmental impacts, there can be an economic cost as well. Losing baits to birds can be costly, and serious economic harm can occur if excessive seabird bycatch triggers a fishery closure.”

The sablefish industry in Alaska addressed the problem in part through the use of streamer lines, which are the most commonly used seabird bycatch mitigation measure worldwide. The technique runs a 300-foot line from the vessel’s mast or another high part of the vessel to a towed object like a float. A series of rubber tubes hanging down every 15 feet or so creates a visual barrier that prevents birds from attacking the bait.

However, there is a catch, the researchers discovered.

Some fishing boats use floats to keep their baits off the seafloor to conserve baits and protect their catch from damage caused by scavengers. For those that did use floats, streamer lines were less effective at preventing seabird attacks. In fact, albatross attack rates were 10 times higher on longlines with floats compared to those without.

“Using floats puts the longline more than twice as far behind the boat before it sinks beyond the diving range of albatrosses – to the point where bird-scaring lines just don’t reach,” Gladics said. “With the hooks at the surface for longer, the birds have more time to hone in on the bait.”

Gladics said some of the West Coast sablefish boats reported that they already fished at night to prevent bird attacks and fishermen suggested that night fishing should be explored as a seabird bycatch mitigation option for the fleet.

In response the authors examined over a decade of data collected by NOAA Fisheries at-sea observers, and found that when hooks were set at night, after civil dusk, albatross bycatch was 30 times lower and target catch was almost 50 percent higher compared with daytime fishing – a classic win-win, the researchers said.

“The combination of night fishing for vessels that use floats or going without floats on the longlines and using bird-scaring lines provide two options for helping fishermen reduce bycatch,” she said. “However, a single ‘one size fits all’ solution won’t work for all fishermen and all boats, so developing multiple seabird avoidance options that are specific to the region is crucial – and that requires collaboration between researchers and fishermen.”

The research was funded by The National Fish and Wildlife Foundation, David and Lucile Packard Foundation, NOAA Fisheries, Washington Sea Grant and Oregon Sea Grant.

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Amanda Gladics, 503-325-8573, Amanda.Gladics@oregonstate.edu

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Amanda Gladics

Communication among health care facilities key to preventing spread of drug-resistant bacteria

PORTLAND, Ore. – Communication breakdowns between care facilities can pave the way for outbreaks of infection, according to research on the spread of an extensively drug-resistant bacterium.

The OSU/OHSU College of Pharmacy teamed with the Oregon Health Authority and other collaborators on a two-year study of Acinetobacter baumannii, an opportunistic pathogen associated primarily with infections among patients who have compromised immune systems and are in health care facilities.

Looking at multiple sites in the Pacific Northwest, the scientists identified 21 cases, including 16 isolates of A. baumannii that contained a rare gene responsible for resistance to the carbapenem class of antibiotics.

The patients’ transfer history among the studied facilities and the isolates’ genetic profiles illustrated how the organism spread from place to place, aided by a lack of interfacility communication that patients who were infected or colonized by A. baummanii were being transferred.

Jon Furuno, co-author on the study and an associate professor in the College of Pharmacy, noted that the findings support a recent Oregon law requiring written notification from the discharging facility to the receiving facility anytime a patient carrying a multridrug-resistant organism, or other infection requiring transmission precautions, is transferred.

Extensively drug-resistant A. baumannii can contain many antibiotic resistance genes that can be transmitted to other organisms, he added.

“It just makes sense that you would want to alert a receiving facility if patients have a specific drug-resistant organism,” Furuno said. “The discharging facility needs to include that information with the discharge summary or somewhere on the chart, and the receiving facility needs to know where to look for it.”

The lead author is Genevieve Buser, a pediatric infectious disease specialist who worked as a Centers for Disease Control and Prevention Epidemic Intelligence Service officer based at the Oregon Health Authority when the study was done. Buser said communication can ensure appropriate contact precautions are taken.

“An entire chain of transmission can be prevented if staff at a receiving facility know about a patient’s multidrug-resistant organism status,” Buser said. “This outbreak might not have been identified if not for a new, limited, voluntary surveillance system in Oregon and an astute infection preventionist.”

Reporting of extensively drug-resistant A. baumannii infection is not required by most public health jurisdictions in the United States, and clinical laboratories generally do not test for an organism’s underlying genetic resistance mechanisms.

Other organizations collaborating on this research included the VA Portland Health Care System; the Division of Infectious Diseases at Oregon Health & Science University; the Oregon State Public Health Laboratory; the Louis Stokes Cleveland VA Medical Center; and Case Western Reserve University.

The CDC and the National Institutes of Health supported the study. Findings were recently published in Infection Control & Hospital Epidemiology.

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Steve Lundeberg, 541-737-4039

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Groundbreaking investigative effort identifies gonorrhea vaccine candidates

CORVALLIS, Ore. – Researchers at Oregon State University have identified a pair of proteins that show promise as the basis for a gonorrhea vaccine.

The findings are an important step toward a potential new weapon in the fight against a sexually transmitted disease that affects millions of people around the globe, with nearly 80 million new cases estimated each year.

The pathogen that causes the disease, Neisseria gonorrhoeae, is considered a “superbug” because of its resistance to all classes of antibiotics available for treating infections. 

Gonorrhea is highly damaging to reproductive and neonatal health if untreated or improperly treated. It can lead to endometritis, pelvic inflammatory disease, ectopic pregnancy, epididymitis and infertility. Also, babies born to infected mothers are at increased risk of blindness.

More than half of infected women don’t have symptoms, but those asymptomatic cases can still lead to severe consequences for the patient’s reproductive health, including miscarriage or premature delivery, said OSU College of Pharmacy researcher Aleksandra Sikora.

Subjecting N. gonorrhoeae to the phenotypic microarray screening method for the first time, Sikora’s team focused on seven proteins from the bacteria’s cell envelope, which consists of the outer membrane, the cell wall and the inner membrane. 

Phenotypic microarrays are a high-throughput system featuring plates with 96 wells per plate, each well representing a different condition under which to research the phenotypes – the observable characteristics – of the examined mutants.

The goal was to see which if any of the seven proteins would show strong potential as a vaccine antigen – a molecule that sends the immune system into action. Vaccines prevent disease because the antigens they contain trigger an immune response that allows antibodies to recognize and attack pathogens to prevent future infection.

“Proteins in the cell envelope play key roles in cell function and bacterial physiology,” Sikora said. “That and their location make them attractive candidates for developing vaccines. But a lot of them are hypothetical proteins – we know bacteria have them but we don’t know for sure how they function. Learning what they contribute to cell structure, permeability, membrane biogenesis and so on is important in vaccine research because antibodies against protein antigens can disable the protein’s function.”

In all, more than 1,000 conditions were used to study the effects of knocking out each of the seven proteins.

“It’s like a football coach trying to choose the top quarterback among seven candidates by looking at their performance on many different teams during many different games,” Sikora said. “Imagine being able to look at those seven quarterbacks in over a thousand different games simultaneously. Of course, that’s not possible with football, but this is what we are doing here to identify the most promising vaccine candidates.”

Researchers found 91 conditions that had uniquely positive or negative effects on one of the mutants, and a cluster analysis of 37 commonly beneficial compounds and 57 commonly detrimental compounds revealed three separate phenotype groups.

Two of the proteins, NGO1985 and NGO2121, showed extensive sensitivity to antimicrobial compounds and thus emerged as the most promising vaccine candidates. This study serves as a jumping-off point for further characterization of proteins in the cell envelope. 

“Neisseria gonorrhoeae is a difficult bacteria to work with, and it’s very diverse,” Sikora said. “It has great genome plasticity – there are huge variations between strains. Phenotypic screening allows us to see how similar and how different they are.”

The National Institutes of Health supported this research. Findings were recently published in the Journal of Bacteriology.

The study was designed by Sikora and performed by Ph.D. candidate Benjamin Baarda in collaboration with Philip Proteau, a colleague of Sikora in the Department of Pharmaceutical Sciences, and Sarah Emerson in the Statistics Department of the OSU College of Science.

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Steve Lundeberg, 541-737-4039

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New assay leads to step toward gene therapy for deaf patients

CORVALLIS, Ore. – Scientists at Oregon State University have taken an important step toward gene therapy for deaf patients by developing a way to better study a large protein essential for hearing and finding a truncated version of it.

Mutations in the protein, otoferlin, are linked to severe congenital hearing loss, a common type of deafness in which patients can hear almost nothing.

The research suggests otoferlin, which is in the cochlea of the inner ear, acts as a calcium-sensitive linker protein. The study also shows that a mutation in otoferlin weakens the binding between the protein and a calcium synapse in the ear, and deficiencies in that interaction might be at the root of hearing loss related to otoferlin.

The size of the otoferlin molecule and its low solubility have made it difficult to study, including how otoferlin works differently than another neuronal calcium sensor in the brain, synaptotagmin.

To combat those challenges, researchers in OSU’s College of Science developed a single-molecule colocalization binding titration assay – smCoBRA – for quantitatively probing otoferlin.

“It’s a one-trick pony of a protein,” said corresponding author Colin Johnson, associate professor of biochemistry and biophysics. “A lot of genes will find various things to do, but otoferlin seems only to have one purpose and that is to encode sound in the sensory hair cells in the inner ear. And small mutations in otoferlin render people profoundly deaf.”

The work by Johnson and collaborators in the Department of Physics and Department of Biochemistry and Biophysics provides a molecular-level explanation for the observation that otoferlin and synaptotagmin don’t have the same functional role.

The research, performed using recombinant protein from cell lysate isolated in vitro, also validates a methodology for characterizing large, multivalent membrane proteins in general.

“The otoferlin gene is really big, and it makes a huge protein,” Johnson said. “The traditional method for making a recombinant protein is using E. coli, but they loathe big proteins. This paper came up with a way of getting around that challenge.

“We were trying to shorten the gene, to find a truncated form that can be used for gene therapy. There is a size limit in terms of what you can package into the gene delivery vehicle, and otoferlin is too large. That’s the holy grail, trying to find a miniature version of otoferlin that that can be packaged into the delivery vehicle and then hopefully the patient can start hearing.”

Otoferlin’s size has precluded rescue experiments in which a modified mRNA for otoferlin is transfected into an animal model to replace a suppressed or knocked-down otoferlin gene causing deafness.

The study by Johnson, doctoral biochemistry student Nicole Hams, former biochemistry doctoral student Murugesh Padmanaryana and biophysicist Weihong Qiu identified a truncated form of otoferlin that can function in the encoding of sound.

The National Institutes of Health supported this study. Results were recently published in the Proceedings of the National Academy of Sciences.

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Steve Lundeberg, 541-737-4039

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Colin Johnson

Expensive drug driving up Medicare expenditures without evidence of greater efficacy

PORTLAND, Ore. – Medicare spent more than $1 billion over a five-year period on a high-priced drug that has not been proven more effective for a collection of inflammatory conditions than much less expensive corticosteroids, research by the OSU/OHSU College of Pharmacy shows.

The analysis also indicates that a comparatively small group of “frequent prescribers” combine to write prescriptions that lead to the bulk of Medicare’s expenditures on the drug, repository adrenocorticotropin, or ACTH.

In 2015 alone, Medicare spending topped $500 million on the drug, the cost of which has soared to $36,000 per course of therapy. 

Known by the trade name H.P. Acthar Gel, often shortened to just Acthar, the drug’s primary use is to treat rare epileptic spasms in children under age 2.

“The drug has an interesting back story,” said Dan Hartung, lead author on a research letter that was published today in JAMA Internal Medicine. “It’s a fairly old drug, first approved in 1952, prior to many of the FDA rules about clinical efficacy. The bar for what constitutes approved indications was much different then, much lower; it has many indications that came before the current rules were set in stone in the 1960s.”

The drug, classified as a “biologic,” was initially approved for a broad range of corticosteroid-responsive inflammatory conditions.

“It’s a hormone produced in the human body that signals the release of steroids,” Hartung said. “It does the same job as low-cost corticosteroids. And it really wasn’t much on anyone’s radar until 2007.”

Questcor Pharmaceuticals purchased the rights to the largely forgotten Acthar in 2001 for $100,000 and began steadily raising Acthar’s price. In 2007 Questcor increased the price of the drug, which once sold for $40 for a vial, or course of therapy, from $1,650 to $23,000 overnight.

Questcor, acquired by Mallinckrodt Pharmaceuticals in 2017, markets the drug aggressively for relatively common conditions such as rheumatoid arthritis, multiple sclerosis and nephrotic syndrome, Hartung said. The Food and Drug Administration approved Acthar for those types of conditions decades ago when requirements were less strict; no clinical trials were required.

“There are a variety of FDA-approved indications that lack a lot of evidence that Acthar is even effective, let alone better than inexpensive corticosteroids,” Hartung said. “And what allows for this kind of pricing is that it’s a fairly complex molecule and no competitors can exactly duplicate it; they have a monopoly on this particular molecule.”

In 2015, Acthar generated gross revenue of about $1 billion – more than half of which came from Medicare, and much of the rest coming from Medicaid, Hartung said, meaning public expenditures likely accounted for almost all of the sales.

Hartung and the other collaborators found Medicare spending on the drug increased tenfold and totaled $1.3 billion from 2011 to 2015.

In 2014, a total of 1,621 prescribers were responsible for $391.2 million in Acthar spending; among those, 203 frequent prescribers – 94 rheumatologists, 55 neurologists and 54 nephrologists, each with more than 10 prescriptions – accounted for $165 million of the total.

“And in general these physicians are prescribing about the same number of other drugs compared to their peer specialty groups, so we suspect they are not treating more severely ill patients,” Hartung said. “Mallinckrodt is really aggressively marketing in ways that possibly subject prescribers to conflicts of interest. From the payer side, there’s really little that little justifies this drug and its exorbitant cost over much cheaper alternatives. If Medicare were to take a firm stand on reimbursements, this wouldn’t be happening.”

Joining Hartrung on the study were Kirbee Johnston, Shelby Van Leuven, Atul Deodhar, David Cohen and Dennis Bourdette.

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Steve Lundeberg, 541-737-4039

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Dan Hartung, 503-494-4720

Protein transport channel offers new target for thwarting pathogen

CORVALLIS, Ore. – A bacterium that attacks people suffering from chronic lung disease and compromised immune systems could be halted by disrupting the distribution channels the organism uses to access the nutrient-rich cytoplasm of its host cell.

The findings by researchers in Oregon State University’s colleges of science and veterinary medicine are important because they suggest a new therapeutic target for one of the leading causes of bacterial infection in patients with HIV/AIDS.

The bacterium is Mycobacterium avium, the most common pathogen among non-tuberculosis mycobacteria. Highly opportunistic, M. avium invades and proliferates within a variety of human cells; it resides in a cytoplasmic vacuole and survives by remodeling its vacuolar compartment and resisting its host’s antimicrobial mechanisms.

“Most bacteria that grow in phagocytic cells export their effector proteins that impair or redirect macrophage function by using a needle-like apparatus that perforates the vacuole membrane and delivers virulence-associated molecules to the cytoplasm,” said co-corresponding author Luiz Bermudez of OSU’s College of Veterinary Medicine. “But mycobacteria don’t have that, so the question has always been, how do all these proteins get exported, how do they cross the vacuole membrane?”

They likely do so because proteins of the pathogen dock to transport proteins of the phagosome in the host cell in a way that allows for the efficient secretion of effector proteins. Co-corresponding author Lia Danelishvili, also of the College of Veterinary Medicine, identified voltage-dependent anion channels as a possible means of exporting those proteins.

“A VDAC is very small, but it can become larger if several VDAC proteins get together through polymerization,” Bermudez said. “We found that yes, mycobacteria use surface proteins to bind to the VDAC. But although we tried to see if the proteins of the mycobacterium were exported by the VDAC, we couldn’t show that. However, we did show that another component of the cell wall of the mycobacterium, lipids, are exported by that mechanism.”

Next up is determining what specific physical and chemical interactions occur to make effector protein transport possible.

“The idea is to find out the mechanism bacteria use to secrete proteins produced in the cells that have important functions in controlling the phagocytic activity that’s supposed to kill them,” Bermudez said.

Findings were recently published in Scientific Reports. 

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Steve Lundeberg, 541-737-4039

Conference at OSU explores intravenous vitamin C as treatment for cancer, sepsis

CORVALLIS, Ore. – The Linus Pauling Institute will host its biennial “Diet and Optimum Health” conference Sept. 13-16 at Oregon State University, attracting an international audience of experts in nutrition, preventive medicine and oncology.

The conference will also honor recently retired Linus Pauling Institute director Balz Frei and welcome new director Richard van Breemen.

The ninth edition of the event takes place 100 years after Linus Pauling began his OSU studies as an undergraduate. It also coincides with the ramp-up of the university’s 150th anniversary celebration and the 20th anniversary of the Linus Pauling Institute’s move to Oregon State from Palo Alto, Calif.

The conference will include a day-long symposium on vitamin C with a focus on the micronutrient’s capabilities in treating cancer and sepsis, as well as sessions on dietary components and the microbiome; lipid metabolism; vitamin E; bioactives; and diet, neuropathy and dementia.

“Linus Pauling wanted to cure the common cold with vitamin C, and there’s some indication that by taking vitamin C you can shorten the duration of a cold – this is a natural progression of that idea to preventing bacteria from killing you,” said conference chair Maret Traber, principal investigator and Ava Helen Pauling Professor at the Linus Pauling Institute. “We really are changing people’s lives.”

In addition to the professional conference, the Linus Pauling Institute will host a free public session from 9 to 11 a.m. Saturday, Sept. 16, at the CH2M Hill Alumni Center on the OSU campus. It will feature Emily Ho of the Linus Pauling Institute, who will talk about diet and cancer prevention, and Jeanne Drisko of the University of Kansas Medical Center, who will discuss treating cancer with intravenous vitamin C.

“Linus Pauling and his colleagues tried to show people in the 1970s that intravenous vitamin C was beneficial in treating cancer, and they forced the National Institutes of Health to do several clinical trials,” said Drisko, director of KU Integrative Medicine and the Riordan Endowed Professor of Orthomolecular Medicine.

“The Mayo Clinic ran the trials and said vitamin C showed no benefit in double-blind, placebo-controlled testing. It wasn’t until years later that it was found out that Linus Pauling and his colleagues had been giving it intravenously and the Mayo Clinic used only oral vitamin C, and that’s a huge difference. When it’s given in a vein, it makes hydrogen peroxide around the cancer cells, and the hydrogen peroxide kills them.”

Anitra Carr of New Zealand’s University of Otago, chair of the professional sessions on the mechanisms of vitamin C in cancer, said “vitamin C administration appears to have a clear impact on patient quality of life, particularly in those receiving chemotherapy.”

It’s not yet clear, though, which types of cancer respond best to intravenous vitamin C.

“There is also considerable debate around the potential anti-cancer mechanisms by which vitamin C works,” she said. “Future preclinical and clinical studies will help to elucidate these questions through clarifying the mechanisms by which vitamin C works and also if these vary depending on the type of cancer. This will facilitate personalized medicine, whereby the right treatment can be targeted to the right patient.”

Carr is also one of the presenters during the session on intravenous vitamin C therapy for sepsis, as is Berry Fowler of Virginia Commonwealth University.

“Over the past 30 years, over $2 billion has been spent by the National Institutes of Health and the pharmaceutical industry on over 15,000 patients with sepsis. No treatment has proven effective that doesn’t have side effects,” said Fowler, professor of medicine in the Pulmonary Disease and Critical Care Medicine Division and director of the VCU Johnson Center for Critical Care and Pulmonary Research.

“Trials have been predominantly performed with proteins like antibodies and inflammatory protein inhibitors. These protein treatments don’t get transported into the cell where they are needed. Vitamin C is a micronutrient – it’s effectively transported into every cell in the body.”

When vitamin C is infused intravenously, Fowler said, it’s actively moved from the bloodstream into the cells where the injury and damage are happening.

“When it’s there it acts as an antioxidant and, importantly, it decreases the inflammatory process that leads to injury,” he said. “This micronutrient theory may be the secret as to how vitamin C works so effectively. There’s finally a therapy that can be transported into places where it needs to be to be effective as opposed to remaining free in the plasma. That’s what differentiates vitamin C – it’s effectiveness is because the body moves it across tissue planes.”

Carr said critically ill patients with sepsis and septic shock have very low levels of vitamin C and that several recent clinical studies have shown that administration of vitamin C to these patients can significantly decrease organ failure and also decrease death rates by up to 80 percent.

“Sepsis and septic shock are the leading causes of death in critically ill patients and the incidence of severe sepsis continues to rise around the world,” she said. “If these results can be reproduced in other studies, this will be the biggest breakthrough in care for these patients since antibiotics.”

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Steve Lundeberg, 541-737-4039

Country’s largest estuary facing increasing acidification risk

CORVALLIS, Ore. – Chesapeake Bay, the largest estuary in the United States and one of the largest in the world, is facing new risks from a layer of highly acidified water some 10 to 15 meters below the surface, a new study has found.

This “pH minimum zone” is 10 times more acidic than the bay’s surface waters and may pose a risk to a variety of economically and ecologically important marine species, including oysters, crabs and fish, the researchers say. A decline in the number of calcium carbonate-shelled organisms – particularly oysters – may be hampering the bay’s ability to deal with the increase in acidity, they add.

Results of the study are being reported this week in Nature Communications.

“Oysters and other bivalves provide a built-in Tums effect that naturally helps the bay deal with corrosive water,” said George Waldbusser, an Oregon State University marine ecologist and co-author on the study. “They generate large amounts of calcium carbonate structures, which may be able to buffer the increasing amounts of carbon dioxide entering the bay.

“Overharvesting and disease have reduced the number of oysters, however, and we’re seeing the results.”

Lead author Wei-Jun Cai from the University of Delaware led the study, which found pH levels in this stratified layer of water to be about 7.4, nearly a unit lower than surface waters where the average pH is about 8.2. A combination of factors likely caused this corrosive zone, including hypoxia and generation of toxic hydrogen sulfide in the bottom waters mixing with other layers of the bay.

“This study shows for the first time that the oxidation of hydrogen sulfide and ammonia from the bottom waters could be a major contributor to lower pH in coastal oceans and may lead to more rapid acidification in coastal waters compared to the open ocean,” Cai said.

Previous studies, including work by Waldbusser, have shown that agricultural nutrients entering Chesapeake Bay have progressively depleted oxygen levels in the bottom waters – a process known as hypoxia – as well as acidifying the bay more quickly than offshore ocean waters. Animals need oxygen to live and without it, they die. Bacteria, however, can “breathe” without oxygen, often producing hydrogen sulfide, which further increases oxygen demand and also enhances acidification, Waldbusser said.

“Hypoxia in this case leads to an amplification of acidification,” he pointed out. “If more oysters were there, they would help pull the food out of the water, reduce oxygen demand, and sequester carbon from the system. Now the acidification is such that we have to be concerned that it will make it harder for some marine organisms to produce their calcium carbonate shells. We don’t yet know what those thresholds are all around.”

Oysters have been shown to be sensitive to changes in acidifications, particularly on the West Coast where corrosive waters severely affected the industry several years ago. Waldbusser and OSU colleague Burke Hales helped growers mitigate the issue by identifying times of the day when local acidification levels were lower so hatcheries could draw in more favorable waters to use in raising their oysters.

East Coast oysters are a different variety, Waldbusser said, and may actually be somewhat more resilient than the West Coast’s Pacific oysters. But scientific understanding of how much acidity they can withstand is limited.

“We know that in some areas of Chesapeake Bay where there has been high acidity, oysters have survived, but we don’t know if there are sub-populations that have more resilience, or what the threshold is for their ability to create shells.”

Waldbusser said individual oysters can filter upwards of 50 gallons of water each day. Researchers have estimated that prior to European settlement, Chesapeake Bay had so many oysters that they could filter the entire bay in three days. Today, it would take roughly 300 days because of fewer oysters and more nutrients in the water, he said.

“Dredging of the bay in the 1950s and 1960s removed a lot of oyster shells that formed a base for creating oyster reefs,” said Waldbusser, who began his research on oysters and acidification at the University of Maryland more than 10 years ago before coming to Oregon State.

“Since the 1980s, many of the restaurants on the East Coast participated in a program to recycle oyster shells into the bay to create more habitat, but it hasn’t been enough to replace what has been take out.”

Waldbusser is on the faculty of OSU’s College of Earth, Ocean, and Atmospheric Sciences.

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George Waldbusser, 541-737-8964, waldbuss@coas.oregonstate.edu

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As Tolstoy noted (sort of), all unhappy microbiomes are unhappy in their own way

CORVALLIS, Ore. – The bacterial communities that live inside everyone are quite similar and stable when times are good, but when stress enters the equation, those communities can react very differently from person to person.

A microbiological version of the “Anna Karenina principle,” it’s a new paradigm suggested by scientists at Oregon State University – one that has key implications for a more personalized approach to antibiotic therapy, management of chronic diseases and other aspects of medical care.

The principle gets its name from the opening line of the novel “Anna Karenina” by 19th century Russian author Leo Tolstoy: “All happy families are alike; each unhappy family is unhappy in its own way.”

It turns out that this observation also applies to perturbed microbiotas of humans and animals.

“When microbiologists have looked at how microbiomes change when their hosts are stressed from any number of factors – temperature, smoking, diabetes, for example – they’ve tended to assume directional and predictive changes in the community,” said Rebecca Vega Thurber, corresponding author on the perspective study funded by the National Science Foundation. “After tracking many datasets of our own we never seemed to find this pattern but rather a distinct one where microbiomes actually change in a stochastic, or random, way.”

Findings were published today in Nature Microbiology.

Lead author Jesse Zaneveld of the University of Washington-Bothell collaborated with Vega Thurber and her student, Ryan McMinds, to survey the literature on microbial changes caused by perturbation. Together they found those stochastic changes to be a common occurrence, but one that researchers have tended to discard as “noise” rather than report.

“Thus we present the Anna Karenina principle for microbiomes,” Vega Thurber said. “When microbiomes are happy they are all similar in their composition but during stress or unhappiness they change in a multitude of distinct ways. This piece draws together diverse microbiome research. We think this is an important emerging paradigm for thinking about microbiome data. We present ways of identifying it and distinguishing it from other patterns.”

In addition to the literary reference, Vega Thurber offers a wintry metaphor to explain what she and her collaborators have discovered.

“When healthy our microbiomes look alike, but when stressed each one of us has our own microbial snowflake,” she said. “You or I could be put under the same stress, and our microbiomes will respond in different ways – that’s a very important facet to consider for managing approaches to personalized medicine. Stressors like antibiotics or diabetes can cause different people’s microbiomes to react in very different ways.”

Humans and animals are filled with symbiotic communities of microorganisms that often fill key roles in normal physiological function and also influence susceptibility to disease. Predicting how these communities of organisms respond to perturbations – anything that alters the systems’ function – is one of microbiologists’ essential challenges.

Studies of microbiome dynamics have typically looked for patterns that shift microbiomes from a healthy stable state to a dysbiotic stable state; dysbiosis refers to the microbial communities being out of their natural balance, which can result in the interruption of basic biological functions for the host person or animal.

“The Anna Karenina principle is a complementary alternative,” Vega Thurber said. “The changes induced by many perturbations lead to transitions from stable to unstable community states – dysbiotic individuals vary more in microbial community composition than healthy individuals.”

Scientists found patterns consistent with Anna Karenina effects in a range of systems, from corals exposed to above-average temperatures to the lungs of smokers to patients suffering from HIV/AIDS.

“Our message to researchers is, don’t throw out these observations as noise, but include this principle in the microbiome pipelines and software so that scientists can press a button that gives you the answer to, ‘Do I see the Anna Karenina principle in the dataset,’” Vega Thurber said.

OSU researchers have already given multiple presentations on the principle and it’s been well received in the microbiology community, Vega Thurber said. 

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Steve Lundeberg, 541-737-4039

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Study: Methane from tundra, ocean floor didn’t spike during previous natural warming period

CORVALLIS, Ore. – Scientists concerned that global warming may release huge stores of methane from reservoirs beneath Arctic tundra and deposits of marine hydrates – a theory known as the “clathrate gun” hypothesis – have turned to geologic history to search for evidence of significant methane release during past warming events.

A new study published this week in the journal Nature suggests, however, that the last ice age transition to a warmer climate some 11,500 years ago did not include massive methane flux from marine sediments or the tundra. Instead, the likely source of rising levels of atmospheric methane was from tropical wetlands, authors of the new study say.

While this certainly is good news, the study also points at a larger role of humans in the recent methane rise, noted Edward Brook, an Oregon State University paleoclimatologist and co-author on the study

“Our findings show that natural geologic emissions of methane – for example, leakage from oil seeps or gas deposits in the ground – are much smaller than previously thought,” Brook said. “That means that a greater percentage of the methane in the atmosphere today is due to human activities, including oil drilling, and the extraction and transport of natural gas.”

The study suggests that human emissions of geologic methane may be as much as 25 percent higher than previous estimates. Although not as abundant as carbon dioxide, methane is a much more powerful greenhouse gas and therefore the rising levels are an important contributor to global warming.

“This means we have even more potential to fight global warming by curbing methane emissions from our fossil fuel use,” said Vasilii Petrenko, an associate professor of earth and environmental sciences at the University of Rochester, and lead author on the study.

Anthropogenic methane emissions are the second largest contributor to global warming after carbon dioxide, but there has been uncertainty as to the source of that methane and whether it has changed over time, Brook noted. The new study sheds light on the issue by analyzing levels of atmospheric methane from the last deglaciation in air bubbles that have been trapped in pristine ice cores from Antarctica’s Taylor Glacier.

The researchers were able to estimate the magnitude of methane emissions from roughly 11,500 years ago by measuring radioactive carbon isotopes in methane, (carbon-14, also known as 14C or radiocarbon), which decay fairly rapidly. Methane released from those marine hydrates and permafrost is old enough that any 14C originally present has now decayed away.

They found that amount of methane from ancient “14C-free sources” was very low – less than 10 percent of the total methane – during the entire range of sampling, from 11,800 to 11,300 years ago.

“A lot of people have painted the Arctic as a methane time bomb,” Brook said, “but this shows that it may be more stable than we thought. Past performance isn’t always a predictor of the future, but it is a good analog. We should be more concerned about anthropogenic sources of methane into the atmosphere, which continue to increase.”

The levels of 14C in the ice cores suggest that the increase in methane during the last deglaciation had another source – likely from tropical wetlands, said Christo Buizert, an Oregon State University researcher and co-author on the paper.

“Methane is not stored in the tropics for long periods of time, but produced every day by microbial activity in wetlands,” Buizert said. “We know from other studies that rainfall increased in the tropics during the last warming period, and that likely created more wetlands that produced the additional methane.”

Atmospheric methane has increased from 750 parts per billion in the year 1750 to more than 1,800 parts per billion today – mostly from anthropogenic sources, especially leakage from fossil fuel production, the creation of rice paddies, and cattle ranching, the researchers say.

“All of the natural gas that we mine is very old and leaking inevitably occurs during that process,” Brook said. “Natural gas is considered a cleaner energy source than coal, but it can be a significant problem depending on how much of the methane is leaking out.”

The key to documenting the source of atmospheric methane is the pristine ice cores of Taylor Glacier in Antarctica, where dry, windy conditions have allowed this ancient ice to be slowly brought to the surface. One reason scientists had yet to pin down the sources of methane during the last ice age is that the amount of 14C is so small, it takes enormous amounts of ice to get enough air to measure the isotope.

In fact, it takes some 2,000 pounds of ice, running a melting instrument over three days, to get enough air to produce one sample of measurable 14C. Drilling down in the center of the ice sheet to find that much ice from the end of the last ice age would be prohibitively costly and labor-intensive, but the unique conditions at Taylor Glacier – pushing that old ice toward the surface – made it possible.

Brook and Buizert are on the faculty of OSU’s College of Earth, Ocean, and Atmospheric Sciences

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Ed Brook, 541-737-8197, brooke@geo.oregonstate.edu;

Christo Buizert, 541-737-1572, buizertc.science.oregonstate.edu

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Taylor Glacier in Antarctica