Written by Dr. Keith Verner, Founder of LabLearner

On May 16, 1980 I was working as a young biologist for the National Marine Fisheries Service at a field station in the small town of Hammond, Oregon. Jimmy Carter was president and gas was nearly $1.00 per gallon. The field station, an old converted Coast Guard outpost, was located at the mouth of the Columbia River estuary. And for good reason, the Columbia River bar is one of the most deadly bodies of water anywhere.

Field Station in Hammond, Oregon in 1980

Our group studied the Coho and Chinook salmon population that ran annually up the Columbia River. We crisscrossed the massive four-mile wide (6.2km) estuary on a daily basis in our forty-foot fishing boat, the Egret.

One of the things I loved about the estuary was the feeling of its great size and a sense of its permanence. Tides were predictable each day. Juvenile salmon ran downstream after growing to fingerlings in the tributaries where they hatched, and adult salmon ran upstream after growing to enormous size feeding a few years in the Pacific Ocean. Commercial fishermen waited for them and they arrived each year like clockwork. These things were constant. In fact, except for the number of fish, Lewis and Clark saw the same thing we did when they reached the estuary in the first decade of the nineteenth century.

Mt. St. Helens Before Eruption

Perhaps offering even more of a sense of permanence than the estuary itself, was one of the large peaks of the Cascade mountain range, Mt. Saint Helens. On clear days, we saw its 9,677 ft (2,950 m) snow capped profile from the Egret. Even from our distance, we could see the snow cap increase and recede with the change of the seasons. Mt. Saint Helens has stood there for some 50 million years.

One of the most distinctive characteristics of Mt. Saint Helens was its smooth, conical peak – considerably different from the more jagged peaks of Mt. Hood and Mt. Rainer, for example. If one can have a “favorite” mountain, then I would say Mt. Saint Helen was mine for this reason – For its almost perfect, graceful, smooth symmetry from our vantage point. That was Friday.

Two days later, on Sunday, May 18, at 8:32 in the morning, Mt. Saint Helens erupted. With an enormous blast that hurled pulverized rock down the side of the mountain at speeds approaching 670 mph (1080 km/h), Mt. Saint Helens dropped from 9,677 ft (2,950 m) to 8,365 ft (2,550 m) in elevation. It changed from a perfectly smooth cone to a jagged peak. A crater approximately 2 to 3 miles wide (3.2 to 4.8 km) and 2,100 ft (640 m) deep replaced the symmetrical cone within a period of 10 seconds.

Mt. St. Helens After Eruption

After hearing about the eruption, several of us NMFS biologists rushed from home to the field station and scrambled up the three stories of stairs to the lookout tower on the roof. From there, we could clearly see the plume of volcanic ash billowing straight up into the atmosphere, reaching a vertical height of about 80,000 ft (24,400 m), where it then abruptly turned at a ninety-degree angle and headed east, presumably, we thought, because it must have reached the stratosphere. This cloud of ash would eventually come to settle on 11 U.S. states.

Gas, mud, rock, and debris, collectively known as pyroclastic flow, rushed down the side of the mountain at speeds up to 155 mph (250 km/h), destroying trees out to 19 miles (30 km) away, covering highways, and filling in lakes and river valleys with up to 600 ft (180 m) of mud. The flow of material down river valleys eventually reached the Columbia River, dumping enormous amounts of mud and felled trees that would then head downstream to the estuary, where we were, about 70 miles (113 km) from the blast.

Next morning, the field station chief, Terry Durkin, organized a biological and sediment study of fish and benthic (bottom) samples in the river and estuary and we boarded the Egret soon after for a 36-hour, non-stop collection trip. We all knew this was likely a once in a lifetime chance to directly observe the immediate impact of a volcanic eruption on a commercial fishery.

It is difficult to forget the sound of the many Mt. Saint Helens tree logs banging the side of the Egret all night as we worked aboard in the dark. I recall looking over the gunnel into the dark water and seeing bright, baseball-sized objects floating by. We reached down and grabbed one. It was a floating rock from the volcano, a pumice stone. We saw them on the river for several weeks afterward.

The Egret

Mt. Saint Helen is one of the many volcanoes in the Cascade mountain range that extends from Canada to Northern California. During the blast and the mudslides that followed, 57 people were killed. Most of them died on the day of the blast by asphyxiation, being buried alive, or burns. When the pyroclastic flow reached the first humans it was still as hot as 660 oF (349 oC).

The thermo energy released from the blasts was 1,600 times that of the atomic bomb dropped on Hiroshima. In a few seconds, Mt. Saint Helens lost 1,313 ft (400 m) in elevation of solid rock, roughly the height of the Empire State Building. Approximately 13% of the mountain’s volume was gone.

We learned many scientific lessons from our Columbia River estuary studies in May of 1980. Over the years, however, the one thing that “sticks” more than any single detail is the absolute certainty of enormous and awesome change on Earth. With time, forests can evolve into desserts. Lakes can fill in and become grasslands. Given enough time, continents can even drift over the surface of our planet like pumice stones over water. If an entire mountain could be so radically transformed before our very eyes, then nothing is permanent. Things change.

Image credit: Zhou, et al. ©2010 American Chemical Society.

Warmer weather and the summer season will soon be upon us.  For many extended time outdoors has the potential to produce more cuts and bruises and ultimately the need for more band-aids.  Although not ready yet, the band-aids of the future may be smarter and more effective at stopping infection if research by a group in England is successful.

Dr. Toby Jenkins and his colleagues at the University of Bath in England have pioneered a new type of dressing for wounds.  His engineered fabric contains small capsule-like vesicles containing antibiotics.  While this may not seem remarkable or different from some of the products on the market, what is different is the way in which bacteria “see” these vesicles.  The vesicles appear to bacteria like human cells that are prime targets for infection.  As a result, bacteria attack the vesicles, bursting them.  The burst releases the antibiotic, which then kills the infecting bacteria and any similar bacteria nearby.  What’s even more amazing is that his preliminary research has shown that the vesicles are only burst by pathogenic but not by non-pathogenic bacteria.  This means that the fabric can be selective in its targets, a major plus when treating wounds on the human body, an area that is covered and filled with many non-pathogenic and even beneficial bacteria.

So how exactly does this fabric work and how can it be selective?  One of the keys to this fabric lies in its ability to select pathogenic bacteria.  Pathogenic bacteria are generally defined as those bacteria that cause disease.  Examples of pathogenic bacteria include Staphylococcus aureas (pneumonia, toxic shock syndrome), Clostridium botulinum (botulism), and Streptococcus pyogenes (strep throat). Examples of non-pathogenic bacteria include certain strains of E.coli which are found in human intestines, Staphylococcus epidermis found as a normal part of human skin, and Lactobacillus acidophilus, a normal part of our intestines.

Structurally and chemically there are differences between pathogenic and non-pathogenic bacteria.  Many of these differences account for why pathogenic bacteria can invade the body and destroy human cells and tissues.  Two of the differences between pathogenic and non-pathogenic bacteria are invasiveness and toxigenesis.  In other words, pathogenic bacteria can invade and overcome host defenses (invasiveness) and can produce toxins (toxigenesis).  Toxins are lipids and proteins that can cause damage to cells and tissues through a variety of mechanisms.  Some toxins are specific such as botulinum neurotoxin, which attacks nerve cells and stops them from firing.  Other toxins are more broad in their actions and simply lyse (break apart) cells or travel through the blood stream and cause effects such as inflammation or inhibition the synthesis of proteins in cells.  Non-pathogenic bacteria are generally defined as those that do not invade tissue or produce toxins.

The idea behind the vesicles on the wound fabric is that they burst as a result of the toxins produced by pathogenic bacteria but remain intact around non-pathogenic bacteria since these bacteria do not produce toxins.  Jenkins and colleagues tested their design by using two types of pathogenic bacteria: Staphylococcus aureas and Pseudomonas aeruginosa and one type of non-pathogenic bacteria: a certain strain of E.coli.  They placed the wound fabric in petri dishes along with each type of bacteria and took samples of the bacteria populations every 20 minutes for 4 hours.  Over that period they found steady decreases in the concentration of the two pathogenic bacteria, Staphylococcus aureas and Pseudomonas aeruginosa, to the point of almost complete inhibition of growth.  In contrast they found almost no reduction in the growth of the E.coli. The very minimal reduction in E.coli growth was attributed to some leaking from the vesicles themselves.  They suggest that these results show the ability of the vesicle-coated fabric to select pathogenic versus non-pathogenic bacteria.  Jenkins and his group are quick to point out that this was a preliminary test and that more research and work needs to be done in order for this type of product to find its ways to hospitals.   One of the next steps is to expand the testing to include many, many more types of bacteria.  Others in the field agree, suggesting that for use in hospitals, a discrimination based only on the ability to produce toxins may not be as effective as other specific criteria.

However, most scientists in the field see this preliminary work as a step in the right direction, particularly since the medical field is facing a new era of antibiotic resistance.  Many theorize that this type of “smart” wound fabric would help to curb the rapid pace of antibiotic resistance since the antibiotic would only be released if pathogenic bacteria are “on site.”   This mechanism would reduce what scientists term “the selection pressure” on bacteria that helps drive the evolution of resistance to antibiotics.

For LabLearner students the research in this article emphasizes some of the major concepts they encounter in CELLs and GAP Units such as Cellular Organization, Genes and Proteins, Properties of Matter, Chemical Reactions, Adaptation, Classification. These concepts include an understanding of cellular membranes, organism and cellular reproduction, specificity of chemical reactions and selection, evolution and adaptation.   In addition it highlights the combination of problem solving and experimental design that students experience in LabLearner Labs and Performance Assessments.  And who knows where this research and research by LabLearner students will take us.  The next time you’re looking for band-aids, you might find the answer.

If you’re interested in learning more about bacterial pathogenesis or the evolution of antibiotic resistance check out these links:

The Microbial World: Bacterial Resistance to Antibiotics

The Microbial World: The Mechanisms of Bacterial Pathogenicity