Signs of Summer 13: Our W.E.I.R.D. World

Klebsiella pneumoniae. Photomicrograph by NIAD, Wikimedia Commons

Two of the greatest accomplishments in human history were the formulation of germ theory (the recognition that many diseases were caused by microscopic entities (primarily bacteria and viruses)) and the development of sanitation technologies (which controlled our exposure to the potentially pathogenic bacteria and viruses around us). Stephen J. Gould, discussing the history of medicine, asserted that sanitation has saved more human lives and prevented more disease and human suffering than any other single medical invention or advance. No antibiotic or other drug, no medical therapy or surgical procedure comes close to the profound impact on human survival as sanitation.

Germ theory was first outlined in the Sixteenth Century, but it did not achieve widespread acceptance in science or medicine until Louis Pasteur and Robert Koch described and defined the science of microbiology in the mid Nineteenth Century. Even after Pasteur and Koch’s incredibly compelling experiments and papers many doctors and scientists clung to the old ideas of “bad air” (“miasma”) as the cause of disease and rejected the ideas of microscopic pathogens as delusional fantasies. The ongoing revolution in thought in the Nineteenth Century in which germ theory supplants these old ideas of disease is a fascinating story that highlights the inherent conservatism of human thought and the destructive influence of blind, collective belief in the control of our concepts of truth and reality. Two books about this time period that I highly recommend are Steven Johnson’s “The Ghost Map” and J. G. Farrell’s “The Siege of Krishnapur.”  Both focus on the causes and treatments of one of the great killers of humanity (cholera), and in both the “old guard” of medicine belittle and dismiss the forces of science and innovation until the reality of the new ideas is too overwhelming to ignore.

So, germ theory (and its technological outgrowth, sanitation) are concepts that have been solidly with us for less than two hundred years. The successes of these ideas and technologies in saving lives are undeniable, but we are starting to see some points of conflict between our new “sanitary” way of living with the bacteria and viruses (and also potential protist and invertebrate parasites) around and within us and the way we have co-evolved with these organisms over the past hundreds of thousands or even millions of years.

Public Domain

For example, modern industrialized societies have taken the idea of sanitation to its logical extreme especially when it comes to infants and children. If exposure to potential pathogens may cause disease, then, logically, you should do anything you can to eliminate the chance of any exposure or contact with any microbe at all. Extremely clean nurseries and homes (and all of the cleaning and sanitizing products that have made this possible) were the goals of the modern, industrialized household. Isolating children from portions of the human population that might carry pathogens and restricting the exposure of children to dirt and contaminants of the surrounding world were considered to be obligations of the modern parent.

These acts, though, had profound impacts on the immune systems of the “sanitized” children. The human immune system has evolved to “expect” a series of pathogen exposures especially in early life. These pathogens allow the immune system to learn to synthesize the correct types of proteins and immune cells to form an efficient, disease fighting system for life. Research indicates that when these early life microbial exposures do not occur, the immune system develops some odd, and potentially destructive pathways that include the generation of allergies, eczema, asthma and, possibly a number of “autoimmune” disease syndromes. This is the essence of the “hygiene hypothesis.” The stunting of the immune system’s evolutionarily derived education/maturation period may at least partially explain the epidemic of allergy and asthma cases that are seen in our industrialized societies.

Hookworm larvae, CDC, Wikimedia Commons

An intellectual continuation of the hygiene hypothesis involves the influence of parasites on the human homeostasis. A number of scientifically credible papers have been published over the past decade in which the influence of hookworm infections on the potential of an individual to resist immune disruptions were examined. For example, in the AAAS (“American Association for the Advancement of Science”) Newsletter of Feb. 20, 2011 a gene was described in a population of Brazilian school children that conveyed resistance to hookworm infections. The children that carried this gene, though, had a higher incidence of asthma than children who did not have a genetic protection against hookworm. Papers in the journal Inflammatory Bowel Diseases indicate that the presence (or introduction) of hookworms into patients with ulcerative colitis or Crohn’s disease lessens the severity of these autoimmune conditions. Further, other studies (some anecdotal and some scientific) point toward the efficacy of hookworm infections as protections against or treatments for a range of immune system disruptions including multiple sclerosis and many allergy syndromes.

Photo by RNW, Flickr

An article in a recent (July 14, 2017) New York Times describes Dr. Ben Trumble’s research on the Tsimané people of Bolivia. Dr. Trumble (of Arizona State University) studies evolutionary medicine and became interested in the incidence of late-onset Alzheimer’s disease in the Tsimané. Many of the Tsimané, once they survive a very high infant mortality period, live well into their ninth decade, so Dr. Trumble was able to test a substantially large cohort for mental acuity. He also did DNA analysis to look for the ApoE4 gene (the gene referred to as the “Alzheimer’s gene” in many industrialized nation studies). He was very interested to see if there were any differences in the incidence of dementia and correlations of ApoE4 in these pre-industrial people compared to the “Western Educated Industrial Rich and Democratic” people (which he refers to as the “WEIRD’s”).

The results were very interesting. In a WEIRD population, an individual with two ApoE4 genes (about 2% of the population) develops late onset Alzheimer’s ten times more frequently than someone who lacks this gene (about 75% of the WEIRD population, by the way, lacks ApoE4). In the Tsimané, though, individuals with two or even with just one ApoE4 genes actually had higher mental acuity test scores than those individuals who lacked the gene. The “Alzheimer’s gene” of western medicine seemed to be working in different ways in the pre-industrial Tsimané. The difference, Trumble hypothesized, was parasites. The Tsimané have very high levels of parasites in their bodies (70% of Tsimané are infected with parasites at any one time!). Trumble suggests that the presence of the parasites allowed the ApoE4 gene to take on a protective role in brain homeostasis, while the absence of the parasites led to the unregulated, and potentially destructive activity of ApoE4 which possibly caused or at least accelerated the mental declines of Alzheimer’s.

Last week, I had the pleasure of talking to Dan Cummings (a PhD student from the University of New Mexico) who is a member of the Tsimane Health and Life History Project.  Dan talked about not only the Alzheimer’s research mentioned above but also about some findings concerning the remarkable cardiovascular health of older Tsimané individuals. The working hypothesis in these studies is that the robust, late life health of these people is related to their life-long exposure to parasites!

Our immune systems are designed to identify and destroy foreign cells inside our body. When it works, our bodies stay free of disease and are able to maintain homeostasis. When our immune system does not work properly, though, cancers can grow out of control, powerful cells and chemicals can destroy our own tissues, and greatly exaggerated (and potentially destructive) reactions to non-dangerous substances can occur. We are just beginning to see how our immune system gets and stays “educated” and focused! Our microbiome, our surrounding microflora, and even our parasites may be important evolutionary and physiological players that enable us to keep the system functioning!

 

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Signs of Summer 12: A Spruce by Any Other Name

Photo by D. Sillman

Up and down my street Colorado blue spruces are dying from the bottom up. At first, I thought that the branch deaths were just normal self-pruning, but now I am afraid that it is more serious than that. Blue spruces are native trees of the arid, short-summer zones of the Rocky Mountains. Planting these trees in the moist soils of Pennsylvania and exposing them to our long, humid summers (summers that are getting longer and more humid with each passing decade) stresses the trees and sets them up for invasions by a wide variety of fungi and arthropod pests.

Most of the spruces on my street have lasted fifty or sixty years, but they are starting to fade. Typically, a tree sheds its older (lower) needles first and hangs on to the upper, younger, more efficiently photosynthesizing needles for as long as possible. Sometimes the trees keep an outer shell of living needles while the central core turns brown and dies, and sometimes entire branches turn brown and wither. Each of these patterns fit specific fungal diseases: the fungi are opportunistically invading the trees because the tree’s energy is diverted elsewhere fighting the environmental stresses that are challenging their homeostasis.  These spruces are a long way from home, and everything is changing rapidly all around them. Urban foresters at Michigan State University indicate that an increasing number of formerly harmless fungal species are now causing needle and branch loss and death in blue spruces that are planted outside of their native zones.

Photo by D. Sillman

Spruces are trees of genus Picea. You can recognize a spruce tree by its whorled branches (branches that radiate out like spokes of a wheel from a single level on the trunk) and by its singularly arising needles that spiral around on its branches. These needles are anchored to their branches by peg-like structures that remain on the branch even after the needle is shed. This makes the branches of a spruce rough to the touch.

I am sitting on my deck looking at a huge Norway spruce (Picea abies) and its bordering set of still healthy but not quite as large Colorado blue spruces (Picea pungens). These trees were planted seventy years ago on the west side of my house in the fresh, rocky spoil from the foundation’s excavation. They grew into a fine wind break and a great afternoon shade wall. They were planted not quite far enough apart, though, to prevent competitive shading and branch pruning. They had grown into a continuous mass of trees with intertwined branches and a dense, ground mulch of shed needles. The walls of drooping, skirting branches enclosed the “forts” in which my children played. Every once and a while acorns dropped by passing crows or blue jays germinated in these fort rooms, too, and their seedlings slowly grew in the deep shade.

Photo by D. Sillman

Nine years ago a wind storm took out two-thirds of my blue spruces. Maybe the insidious effects of stress and infection had weakened them and made them vulnerable to wind breakage. The “fort” of spruce rooms was broken up, and the now sun-drenched oak saplings grew up into the opened spaces. The single Norway spruce and a handful of unconnected Colorado blues remain. The Norway spruce leans disturbingly toward the house, and the blues have strange shapes from their competitive shading interactions with their now departed neighbors, but these trees, thank goodness, still seem sound and healthy.

In any list of common trees of Pennsylvania these two, alien spruces, Colorado blue and Norway, show up prominently. Drive any neighborhood, hike any trail, walk through any city park and there they are! All of these spruces were intentionally carried by humans to their spots and planted. Ninety-five percent of all of Pennsylvania’s primal forests have been cut down, and these adopted spruces are two of the common replacements. “Colorado’s” from the Rocky Mountains are growing throughout the Alleghenies, and “Norway’s” from the western Urals down to the Carpathians are covering Laurel Hill and Chestnut Ridge.

There is a town named Spruce just north and east of here. There is a Blue Spruce Park nearby, too. There is a Spruce Hill near Juniata and a great trout stream called Spruce Creek (notably fished by past presidents and famous football players). There are Spruce Streets in Philadelphia and Pittsburgh (and in many towns in between). There are law offices, schools, bakeries and churches with “spruce” in their names. There is even a Spruce Lake over in the Poconos. My guess is that all of these were named either for the alien spruce trees planted here by people, or for the memory of some faraway spruces, or by mistake due to a failure to identify and name trees that actually were not spruces.

There are only two native spruces in Pennsylvania: bog spruce (Picea mariana) and red spruce (P. rubens). The bog spruce grows in sphagnum bogs and the red spruce grows around the edges of those same bogs. Sphagnum bogs are not common parts of our landscape, and they are not places one usually finds people or streets let alone a bakery or a church. These native spruces are seldom seen: they never make the lists of the ten (or twenty or even thirty) most common trees in the state. They won’t grow on command in nice straight lines alongside streets or next to houses. They won’t survive if they are surrounded by concrete or if they are planted in loose, rocky fill. They need to have their roots kept very wet, and in the spring and summer they are often covered with black flies and mosquitoes. Most people keep their distance.

Photo by W. Hamilton

The eastern hemlock (Tsunga canadensis) is the state tree of Pennsylvania. It grew in dense stands in the primal Pennsylvania forest and covered vast areas of the state. It was, though, much to its ecological distress, a tree of great utility. Its coarse wood was used first to build cabins and then as mine props and railroad ties. Its bark was a rich source of tannins and other useful chemicals needed by the early industries in the state.

As important as the hemlock was, though, it was often called something else! Mason and Dixon (the famous line makers) called hemlocks “spruces.”  It is not recorded what they called pine trees or if they ever saw one of our true spruce species. Many of our more distantly named Spruce towns and streams might be due to this surprising and terribly common (and maybe contagious) error.

Photo by D. Sillman

I had to cut down one of my blue spruces this summer. It quite suddenly dropped all of its remaining needles and stood dead and increasingly brittle right next to the electric lines running into both my house and my neighbor’s. This tree had a very odd shape. It had lost limbs and apical branches in storms and had a twisted, cartoon-ish shape. We called it “Uggo the Tree.” The birds waiting for their turns at my front yard feeders often lined up on Uggo’s limbs, and one cold, fall night coming home late from teaching I saw a great horned owl sitting on Uggo’s upper branches waiting for a rabbit or skunk to come into the feeder area for a snack. Goshawks and sharp-shins used Uggo for their hunting perches, too. Uggo, though, succumbed to the fungi around him and had to be taken down before he fell down. Uggo will be missed by by birds and humans alike!

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Signs of Summer 11: More on Bees!

Photo by I.Tsukuba, Flickr

There have been a number of interesting research papers about bees that have been published over the past few months. Scientific teams around the world have been exploring the bacteria that live in bees’ digestive systems, the chemicals that bee feet secrete, and the detailed impacts of neonicotinoid pesticides on both honey bees and bumblebees. Let’s first sketch out some general features and functions of bees and then fill in our outline with some of the interesting new observations.

Photo Public Domain, Pixabay

There are 20,000 known species of bees around the world. Most of these bee species live solitary lives, but a small number of them form large, highly complex societies. These social behaviors have arisen several times during the evolutionary history of bees and can result in colonies of several dozen to many thousands of individuals. True social bees (the “eusocial” bees) have cooperative reproduction, specialized divisions of labor (“castes”), and a single reproductive individual (the Queen). Bees consume the sugary secretions made by flowering plants (“nectar”). Flowers produce nectar to attract bees (and other organisms) so that pollen (which contains the flowers’ sperm) can be distributed to other flowers to fertilize their ova. Some bees also collect the protein-rich pollen and use it to feed their larvae. One group of bees (called the “corbiculate” bees) have specialized sacks on their back legs called “pollen baskets” that help to make the gathering and transport of pollen more efficient.   Honey bees, bumblebees, and stingless bees are all eusocial, corbiculate bees.

Picture the economy of a honeybee hive: worker (“forager”) bees find flowers and gather nectar and pollen. They use their mouthparts to lap up the nectar (a watery solution of mostly sucrose) and store it in their “nectar stomach” (or “nectar pouch”). Laden down with up to half of their body weight in nectar, the foragers then fly back to the hive, brush off their pollen load, and transfer their nectar into the mouths of other worker bees (“hive bees”). The hive bees then continue to transfer (mouth to mouth) the nectar through a sequence of hive bees. With each transfer the nectar become less and less watery, and it is chemically altered via series of enzymes that are produced by the salivary glands of the bees and also by the bees’ microbiome bacteria. The warm temperatures of the hive and the collective wing flutterings of the hive bees further accelerates the water evaporation from the transforming nectar. This new substance, which is more concentrated than the original nectar and also more stable and resistant to bacterial decay, is honey. Honey is the stored food for the hive to help it survive through the winter. Honey is also mixed with pollen to make “bee bread” which is used to feed the bee larvae.

Photo by P. Vivero, Wikimedia Commons

A research paper published in Science Advances (March 29, 2017) by a team of scientists from the University of Texas at Austin looked at the bacterial components of social, corbiculate bee species’ gut microbiomes. They found that evolutionary lines of these bees maintained a similar core of bacteria in their microbiomes even if they had been separated from each other for many millions of years. They also found that these evolutionary microbiome similarities were unchanged in populations even if they lived great geographical distances apart! The social nature of these bee species and the intra-hive overlapping of many generations insures a continuity of microbiome inheritance. Possibly the conservative influence of the social environment on the bees’ microbiome flora is another significant evolutionary benefit of social behavior! It will be interesting to look at the specific microorganisms that make up this common core of the bee microbiome to determine their roles in bee metabolism, behavior or in the synthesis of honey.

Photo by Trounce, Wikimedia Commons

In another study, a research group at the University of Bristol looked at the chemicals synthesized by glands in the feet of bumblebees. Their paper (published in Scientific Reports on March 7, 2017) observed that bumblebees visiting a flower to collect pollen and nectar leave a unique chemical footprint behind. These footprints can be interpreted by other bumblebees to recognize flowers that have been visited by their hive mates and also to recognize flowers that have been visited by bumblebees from other hives. This information helps the bumblebees to avoid competition with each other and also to avoid flowers that have been drained of nectar. The bumblebees can also use the rate of chemical changes that occur in these footprints as clocks to time when the last flower visit occurred (and calculate if there has been sufficient time for the flower to regenerate a harvestable volume of new nectar!).

Photo by Buhl, Wikimedia Commons

There were three important papers about the effects of neonicotinoid pesticides on bees. The first, by a research team from the Royal Holloway University in London and the University of Guelf in Canada (published in Proceedings of the Royal Society B, May 3, 2017), showed that exposure to thiamethoxan (a neonicotinoid pesticide) inhibited ovary development in Queen bumblebees.   The second, by a group from the University of California, San Diego, showed that thiamethoxan interfered with the ability of honey bees to fly (thus reducing their ability to gather nectar and pollen and inhibiting their ability to make overwintering food stores).  These two, relatively small studies corroborated an extremely ambitious, multinational study conducted in Europe that looked into the field impacts of neonicotinoid pesticides on honey bees and bumblebees (published in Science, June 29, 2017). This field study showed that honey bees exposed to neonicotinoids have lower survival rates in the winter and that bumblebees similarly exposed have greatly reduced reproductive rates. These data match the observations of the two previous studies perfectly. This study also measured levels of neonicotinoids in a wide range of bee species and bee environments and determined that previous laboratory studies were using very appropriate levels of pesticides in their experimental designs. This study further observed that the water-soluble neonicotinoids were found well outside of their active spray areas suggesting that the chemicals were moving in soil and surface water.

So, our wonderful bees with their established microbiomes have distinctively smelly feet! We now very precisely know the harmful connection of neonicotinoid pesticides on these vital pollinators. Europe has banned the use of neonicotinoid pesticides and hopefully the United States will do the same.

And finally, a paper published two weeks ago (July 17, 2017) in the Proceedings of the Royal Society B indicated that 30% of bumblebee species worldwide are showing significant decreases in numbers. Climate change and parasitic infections are the two likely forces triggering these declines. Bumblebee species with small geographic ranges, narrow climatological tolerances and no evolutionary history of or defenses against parasites are the populations that have decline the most.

Bees need our help, everyone, or at least our consideration!

More next week!

 

 

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Signs of Summer 10: Cats as Canaries in Our Coal Mines

Photo by D. Sillman

Every time I write about cats my email responses go up. Many people love cats and also love to think about their evolution, behaviors, and ecology. I came across a very interesting article in the New York Times a few months ago (May 16, 2017) that talked about the hyperthyroid epidemic that is being seen in “senior” cats (cats over ten years old). The ideas and inferences from this article are really worth considering.

The facts: prior to the 1970’s feline hyperthyroidism was a very rare condition. Today, though, 10% of all senior cats are hyperthyroid. Symptoms of hyperthyroidism include weight loss (a wasting syndrome) with no apparent change in eating habits (often, in fact, appetite and food consumption increases). The cat is restless, has a rapid heart rate, and has poor coat quality. It is not a set of symptoms that a cat owner could ignore!

The question is, why has this change occurred in cats? What is causing this epidemic of hyperthyroidism? Many factors were explored as possible causes: there seemed to be a correlation between types of cat foods and the incidence of hyperthyroidism, and there were suggestions that chemicals in cat litters or in flea control medications might be having a stimulatory effect on the cats’ thyroid glands.  The strongest correlation, though, the most consistent factor regularly seen in hyperthyroid cases was the amount of time the cat spent indoors. Feral cats and barn cats, for example, did not show this trend toward hyperthyroidism. What was inside of houses and apartments that might be causing this endocrine reaction, and what might this feline hyperthyroid trigger be doing to the rest of us?

Figure by Leyo and Rhododenrdon Busch, Public Domain

The answer turned out to be the presence of a chemical called polybrominated diphenyl ether (or PBDE, for short). PBDE’s were developed in the 1970’s as fire retardants, and they were quickly incorporated into many household items (rug pads, furniture cushion fabrics, electronic devices (like television sets, etc.) and many types of plastics). The addition of these PBDE’s made homes and apartments safer and less likely to flash into flames during a fire. Widespread use of these chemicals, though, soon led to some serious problems.

Photo by D. Sillman

One problem is that PBDE’s are incredibly resistant to degradation. They tend persist in any environment to which they are introduced or in any subsequent environment into which they travel. A second problem with PBDE’s is that they are fat soluble and, thus, will bio-accumulate in any organism exposed to low levels of the chemicals either through ingestion or inhalation. Certain fatty foods (like salmon, cheese, ground beef and butter) can have high levels of PBDE’s as can breast milk (leading to great concerns over PBDE exposure in infants)!  The third problem with PBDE’s is that they act as endocrine stimulators which can disrupt control of body’s homeostasis. These disruptions can involve the reproductive system (reduced fertility), the adrenal glands (one of my old students, Kirk Dineley, in fact, is working on PBDE impacts on adrenals!), and the thyroid! Thyroid disruption, in particular, is of great concern in infants and children because of the role that thyroid hormone plays in the development of brain tissue. Experiments in mice have shown that early exposure to PBDE’s can permanently alter brain activity and behaviors and can even cause hyperactivity. Studies in humans have suggested that IQ scores may be reduced from 5 to 8 points after early life exposure to PBDE’s.

Photo by M. Hamilton

But how do the PBDE’s that are intermixed with the polymers and other complex chemicals in the household items get into the people (and cats) that inhabit those homes? It turns out that PBDE’s don’t stay attached to their surrounding molecules. They tend to break loose and because they are so resistant to degradation float out into the household ecosystem in which they reside and accumulate in the dust. Contact with the dust of a household in which PBDE infused products reside, then, leads to inhalation or ingestion of PBDE’s (the Times article estimated that children ingest 200 mg of household dust each day!).

Cats and small children seem to be particularly pre-adapted to dust exposure and PBDE bioaccumulation. They both crawl about on the floor, rub and lounge on cushions and furniture, and both put potentially dust laden objects and body parts into their mouths.

Testing hyperthyroid cats has shown that they tend to have 20 to 100 times higher levels of blood PBDE’s than controls. Certain cat foods (especially seafood flavored canned foods) have very high levels of the fat soluble PBDE’s. Also, examination of thyroid samples taken from 7000 autopsies of cats conducted over the past decades showed that prior to the late 1970’s thyroid tumors were exceedingly rare in cats, but since 1979 they have become increasingly common.

Photo by M. Hamilton

Almost every person that has been tested has had detectable levels of PBDE’s in their blood, and children, very disturbingly, regularly have higher PBDE levels that adults! These chemicals may be causing a variety of fairly subtle brain changes and also endocrine changes in our population. High levels of PBDE’s have also been correlated with increased incidence of thyroid cancer, and thyroid cancer cases in the United States have been rising at a rate of 3.8% per year over the past ten years according to the National Cancer Institute. The good news is that blood levels of PBDE’s in humans seems to have peaked back in the early 2000’s and have been declining after these chemicals were effectively banned from use. The persistence of PCBE’s in the environment, though, means that older products will continue to be a PBDE source until they are removed from our ecosystems!

Now, the changes in human IQ levels and behavioral syndromes (not to mention the later in life occurrence of thyroid cancer) may be hard on their own to obviously link to PBDE’s in the home. These human impacts, though, when linked to the very clear cause and effect observations of hyperthyroid cats, describe a very frightening (and preventable) story of self-pollution and self-poisoning! Our cats are acting as sentinels, as canaries in our metaphorical coal mine warning us of the impact of these persistent chemicals on our health and well being.

Photo by D. Sillman

Let’s take care of our cats (veterinarians are developing treatments for our senior hyperthyroid felines), and immediately dispose of all of those PBDE laden products in an environmentally responsible way. Remember, PBDE’s will persist and travel out through our environment! They will bio-accumulate in any species unlucky enough to encounter them (everything from peregrine falcons to beluga whales!) and cause extensive endocrine disruption and disease! We can’t just pitch them into a landfill and be done with them! We have to be smarter than that!   Let’s also remember that there are hundreds of other biological active, human created molecules floating around in our homes (and blood streams!). We had better take a good look at them, too! We owe it to our cats!

 

 

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Signs of Summer 9: When the Kiski River looks like Mountain Dew

Photo by D. Sillman

Every summer sections of the nearby Kiski (more properly called the “Kiskiminetas”) River turn the chartreuse green of Mountain Dew. This year the color transformation has occurred a month or so earlier than usual. The color reflects some interesting aspects of the ecology of both the river and its watershed.

The hillsides all along the Kiski River have been extensively mined for coal. There are deep mines that tunnel into the heart of the underlying rock and strip mines that have scraped away their surfaces. Both of these types of mines have disturbed the covering and encasing rocks of the coal seam, and these overburden rocks are rich in a mineral called pyrite. Pyrite is a gold-colored mineral that is commonly called “fool’s gold.” Pyrite is most properly iron sulfide (FeS2).

When pyrite is exposed to oxygen and water it vigorously oxidizes into an array of molecules of iron and sulfur. Ferrous iron oxides (Fe2O3 (“rusts”)) make the red smears in the waters running out of exposed pyrite-rich sites. Ferrous hydroxides (Fe (OH)3 (“yellow boy”) makes the orange silts that collect on the rocks over which the waters from an exposed pyrite layer are running. Much less visible that these iron compounds, though, but much more dangerous, is the sulfuric acid (H2SO4) that forms from sulfur oxidation. The sulfuric acid quickly overwhelms the natural buffering capacity of stream water’s dissolved bicarbonate and plunges the pH of the stream to toxic levels. This sulfuric acid generation and dispersal is called Acid Mine Drainage (AMD).

Photo by D. Sillman

The picture to the left shows a hillside section along the Kiski River where uncontrolled acid mine drainage has erased the site’s vegetation and left a flowing, orange and red stream in its place. This particular site was too close to the Kiski River to be effectively cleaned up or sealed away from draining into the stream. It stands as an on-going reminder of the horror of AMD! To me, it looks like the surface of Mars!

The water from this pyrite-rich spot and probably from hundreds of other, less obvious locations throughout the Kiski watershed drips and dribbles iron and sulfur into the waters of the Kiski River. These molecules, then, begin to react both chemically and biologically as they flow along on their way to the Allegheny River.

Photo by D. Sillman

Usually the water in the Kiski is brown and foamy. The transformation of this silty, frothy stream into Mountain Dew green occurs in the quiet, still sections of the river. Many of these still areas are often located just upstream from the old stone-piled, slack-water dams that were built back in the early Nineteen Century to make sections of this shallow river navigable for barges. The dams have tumbled into decay and at high water are difficult to see, but when water levels fall sufficiently (usually in mid to late summer) the remains of these dams back up broad pools that begin to warm and stagnate. Oxygen levels fall in the stilled water and relic microorganisms, released from the competition from more robust aerobic species and the directly toxic effects of dissolved oxygen begin to process the dissolved irons and sulfates in new ways.

One group, the sulfate reducing bacteria, are true anaerobes. They use sulfates as their final electron acceptors in energy metabolism and slowly crank out usable metabolic energy from the oxidation of dissolved organic molecules in the water.  When they stick the spent electrons from their organic food sources onto the sulfates they generate sulfides (especially hydrogen sulfide) which radically changes the chemical environment of the river water.

Another group of bacteria, the photosynthetic, “purple” bacteria, respond to the build-up of the hydrogen sulfides. These bacteria need hydrogen sulfide as the hydrogen source for their unique form of non-green plant photosynthesis. As they use the hydrogen atoms (and the absorbed energy from photons of sunlight) to make sugars out of carbon dioxide they oxidize the sulfides back into elemental sulfur which can then further oxidize back into sulfates (and new sulfuric acids).

A third group of bacteria are sulfate oxidizers. They directly use electrons from the sulfates to run their energy metabolism. They also regenerate sulfides and may use oxygen or some other molecule (like nitrate, for example) as their final electron acceptors.

Backing up the river, then, and letting the waters settle and stagnate changes the environment significantly and generates new pathways for the sulfur molecule. Elemental sulfur (from the photosynthetic bacteria) is yellow. Sulfates (from the photosynthetic, “purple” bacteria) are green in solution, and the purple bacteria add their own array of blue and purple, light-capturing pigments to the mix until some shade approaching chartreuse is formed.

When the green water behind the rock dams flows over the old stone-dam piles it generates a vigorous line of choppy rapids that infuses oxygen into it. The green color is instantly lost and the brown returns. The fragile balance of the oxygen sensitive bacteria is disrupted and the colorful cycling of the irons and sulfurs is lost. This year’s early “greening” of the Kiski was re-set by a couple of big rainstorms, but a few weeks later the river water had warmed up and turned green again.

Photo by D. Sillman

A great deal of work up and down the Kiski Watershed has gone into controlling AMD. The photo to the left is Roaring Run (an important Kiski River tributary). The results of these efforts are impressive. The Kiski  and its tributaries now have a rich base of invertebrates and fish (the Roaring Run Watershed Association actually has a fishing contest on the Kiski each year!). I have seen hellgrammites (Dobsonfly larvae) in the Kiski and along the trails that follow it. Dobsonflies are a significant sign of environmental quality! I have also seen bald eagles regularly hunting up and down the Kiski. The green, river pools of summer, though, tell us that there is still a great deal of iron and sulfur in the waters of the Kiski. We still have a lot of work to do to get it back to health.

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Signs of Summer 8: Wild Pigs!

Photo by D. Sillman

An old friend from Texas was visiting me last week. As we sat on the deck of a Gateway Clipper riverboat and toured the bridges and riversides of Pittsburgh, we talked about old times and old friends and also about similarities and differences between Pennsylvania and Texas. One question he asked me was if Pennsylvania has any wild pigs running around in its forests? I told him about the pig Deborah and I met on our Baker Trail hike in 2010 (pictured to the left!). He was a domesticated pig (someone’s pet, I assumed from his demeanor), but he was a three-hundred pounds (estimated) representative of the Suidae and could have been the starting stock for a local population of wild pigs!

You can say it so many different ways: feral pigs, wild boars, feral hogs, wild swine! They are all one in the same animal: an incredibly destructive, rapidly reproducing hybrid pig that is a mix of domesticated pigs that have escaped from their farm-life captivities and an array of exotic, wild pig subspecies of Sus scrofa, including the Russian wild boar, the European wild boar, and the Asian wild boar, that have escaped primarily from private hunting preserves in which they had been kept and bred. Thirty-five states have feral pig populations and with the pigs’ steady territorial expansion and growth in numbers, it is expected that all fifty states will have wild swine in the next thirty to fifty years!

Photo by NASA, Wikimedia Commons

It is estimated that there are six million wild/feral pigs running loose in the United States and that nearly half of them live in Texas! Hence the appropriateness of my friend’s question. Texas is a big place (as Texans love to point out!) but two and a half million pigs (the estimated state population) are A LOT of pigs! These Texas pigs (sometimes called “razorbacks” just to add another noun to the mix!) are thought to date back to swine released by the original Spanish explorers of Texas (back in the mid 1500’s). Over the years, though, many escaped domesticated pigs and exotic boars have added to the vigor and genetic diversity of the Texas swine population.

In Pennsylvania, the feral hog numbers are much more modest: about three thousand pigs. There are three counties in Pennsylvania where feral pigs are known to be reproducing: Bedford and Fulton in the southcentral part of the state (right on the Maryland border) and Bradford up in the northeast (on the New York border), but wild pigs have been sighted throughout the state.

Photo by C. O’Neal, Flickr

So, what do these feral pigs do that is so bad for the environment? First, by their almost continuous rooting and digging behaviors they destabilize soil and increase soil erosion. They also eat many wild plants and destroy the roots of even more plant species. They eat ground nesting birds, they kill livestock (especially lambs, calves, and kid goats) and they even kill pets that happen to wander into pig-infested woods. They also eat huge quantities of “mast” (acorns, hickory nuts, etc.) upon which a wide variety of native, wild animal species rely for food. Feral pigs also carry a number of viral and bacterial pathogens that can afflict both wild and domestic animals and also humans. They also carry a diverse load of parasites that can be spread to both other animals and also to people. Feral pigs have no natural predators in our ecosystems and are capable of reproducing even before they are a year old. They can have up to two litters of usually five to six (but sometimes up to twelve) piglets every year! Mature males can weigh up to four hundred pounds, and females with litters are savagely aggressive against anything they perceive as possibly harmful to their offspring.

R. Bartz, Wikimedia Commons

Pennsylvania recently transferred jurisdiction of the state’s feral pig populations from the State Department of Agriculture to the Pennsylvania Game Commission. The Game Commission promptly established an open hunting season for these animals. A hunter may shoot as many pigs as they can, 365 days a year. Many guidelines concerning the safety of the hunters’ handling of the pig carcasses have also been established to try to limit the spread of the swine pathogens and parasites to humans.

Photo by USFWS, Public Domain

In Texas, wild pigs are a much bigger and much more complex problem. On one hand, the destruction they reek in the state’s natural and agricultural ecosystems is prodigious. Cost impacts of feral pigs in Texas alone has been estimated to be fifty-two million dollars a year (nationwide the estimated cost of feral pigs (both for their impacts and also for the costs to finance their removal) is 1.5 billion dollars a year!). On the other hand, though, in spite of these staggering impact costs, feral pigs are a very popular species for Texas hunters! Earlier this year the Texas State Agriculture Commissioner issued an emergency declaration to allow the use of bait laced with a coumadin-based poison to kill the feral hogs of Texas. Lawsuits against this declaration have been filed by the unlikely alliance of the Environmental Defense Fund (who are worried about the environmental impacts of loosing this poison out in the ecosystem) and the Texas Hog Hunters Association (who don’t want poisoned pigs!). It turns out that feral hogs are a big business in Texas! Slaughterhouses pay between $30 and $180 for a wild pig carcass. Less desirable parts of the pigs are sold to pet food companies while choicer parts of the hogs are sold to high-end restaurants as organic, range fed pork! An article about this plan to poison the wild boars of Texas (New York Times, April 29, 2017) mentioned a company near Waco, Texas called “Wild Boar Meats” that purchased from hunters and processed 5000 feral pigs a month! A wild pig poisoning program would, of course, destroy this wild pork industry.

So, floating down the Monongahela River with an old friend turned to a discussion about wild pigs and range-fed pork. It all seems normal, to me.

 

 

 

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Signs of Summer 7: The American Chestnut: Trans-genetics and Hybrids

Forest History Society

The America chestnut (Castanea dentate), as I have written before, was once one of the most abundant trees in the forests of the eastern United States.  They were not the tallest tree in these forests, but they did have huge, ten or twelve feet diameter, trunks and thick, extending branches that spread out over remarkably large areas (Photo of virgin American chestnut trees used with permission from the Forest History Society).

The American chestnut also produced large numbers of extremely nutritious nuts that were eaten by squirrels, birds, deer, and bears and also humans. The American chestnut produced these nuts in abundance every year (unlike oak trees, say, that make their acorns over multi-year, boom and bust cycles). Many animals relied on the yearly production of chestnuts to sustain their populations.

In 1904, though, the American chestnuts lining the roads and walkways of the Bronx Zoo began to sicken. Their leaves withered and great lesions appeared in their bark. The trees then died one by one. They were the first recorded casualties of Chestnut Blight epidemic that swept through the eastern United States. There is evidence that the fungus responsible for this disease (Cryphonectria parasitica) had been present in the southern U.S. since the 1820’s, but the death of the chestnuts in New York set off alarms that reverberated through the country. By 1950, the American chestnut was for all intents and purposes “gone.” It was no longer a reliable source of nuts or timber. It was no longer a tree of size and majesty.

Photo by D. Sillman

The species, though, persisted even in the face of this awful disease.  The fungus is transported either via insects or on the wind and infects a tree through cracks in its bark. The fungal mycelia then grow into the cambium layer of the tree (the part of the tree’s vascular system that transports sugars and nutrients). The tree responds to the infection by sealing off the infected cambium with a dense callus tissue. But the fungus grows faster than the callus and eventually the tree loses its ability to transport nutrients and dies. The fungus, though, does not affect the tree’s roots, and new chestnut trees are then able to sprout from the still living roots and stumps.  Depending upon the site density of the chestnut trees and the abundance of the fungal spores, these new sprouts may grow for ten to fifteen years before the fungal infection kills them. They can reach heights of fifteen to twenty feet and can even produce nuts for several years before they die back. This growth and die-back cycle has caused the American chestnut to become more of a shrub than a tree!

Photo by B. Marlin, Wikimedia Commons

In February 2016 I wrote about two scientists (Bill Powell and Chuck Maynard) at Deborah’s and my alma mater (State University of New York, College of Environmental Science and Forestry (“ESF” for short)) who have developed a transgenic American chestnut tree that is resistant to the chestnut blight fungus. Powel and Maynard isolated a gene from wheat plants that codes for an enzyme (oxalate oxidase) that breaks down oxalic acid and inserted it into the genome of the American chestnut tree. It turns out that wheat and many other grass species use this oxalate oxidase as a generalized protection against their own fungal infections, and it further turns out that this enzyme is equally as effective as a fungal control agent in the transgenic chestnut tree! The chestnut blight fungus makes large amounts of oxalic acid at the margins of those calluses (or “cankers”) that the chestnut trees make to try to seal the fungal infection off from the tree’s healthy tissues. The acid eats away the wall of the protective callus and allows the fungus to then run riot through the tree’s tissues. Breaking down the oxalic acid at this margin not only neutralizes the erosive tool of the fungus but also, via the impact of the hydrogen peroxide that is generated as a consequence of the oxalic acid oxidation, strengthens the lignins in the wood of the callus! The callus, then, very effectively seals off the blight fungus and the tree remains healthy!

Photo by D. Sillman

The Chinese chestnut tree and other Asian varieties are resistant to the chestnut blight fungus through other genetic mechanisms, but it turns out that the transgenic American chestnut with its oxalic oxidase enzyme and lignin enhanced calluses  is even more resistant to the fungus than those Asian chestnut species to this disease.

Researchers at Penn State (see Penn State News, N0vember 10, 2016) have also been working on resurrecting the American chestnut tree using traditional breeding techniques and also gene transferring biotechnologies.

At the Chestnut Orchard at the Arboretum at Penn State a labor-intensive, controlled pollination program is attempting to interbreed blight resistant Chinese chestnut trees with blight susceptible American chestnut trees. The hoped for outcome is an American chestnut hybrid with a natural, blight resistance. The time involved, though, in the painstakingly controlled pollination, chestnut germination and seedling to sapling growth of the hybrid trees (followed by testing for relative susceptibility to the blight fungus) will run to many decades. Also, in a given cross-year, only 1% of the subsequent trees are at all resistant to the blight fungus. Small numbers for such a herculean effort!

Photo by J. Grandmont, Wikimedia Commons

To augment these traditional breeding efforts, molecular biologists are painstakingly going through the genomes of the American chestnut and the Chinese chestnut to try to determine the precise genes involved in the Chinese chestnut’s blight resistance. If these genes can be found, it might be possible to insert the resistance genes into the American chestnut’s genome and directly generate resistance to the fungus. Other teams of molecular biologists are also looking at the blight fungus itself in the hopes that something in its genetic makeup may allow a genetic mechanism of biocontrol that could weaken or maybe even kill the fungal pathogen.

Maintenance of genetic diversity of the American chestnut is vital regardless of how the blight resistant American chestnut is generated. These trees must not be “horticultural clones” or they will not be able to ecologically and evolutionarily thrive in the complex ecosystems of the northeast United States. Deborah and I are participating in the ESF program by germinating and growing a set of genetically diverse, wild American chestnut trees that we were sent back in 2014. These trees, growing in our garden and out in our orchard, along with the thousands of similar trees that are being grown throughout the northeast, will serve as a broad genetic base for either the transgenic or traditionally bred American chestnut that develops blight resistance.

 

 

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Signs of Summer 6: A Good (Bad?”) Year For Ticks

Photo by D. Sillman

Ticks are a recurring topic on the pages of this blog. We are exploring the ecology of Western Pennsylvania, after all, and Pennsylvania has been experiencing a population explosion of black legged ticks and is also the epicenter of the national Lyme disease epidemic. So ticks and their symbionts have to be a part of our discussions!

A quick review of what we know about black legged ticks and the bacterium that causes Lyme disease:

The black-legged tick (Ixodes scapularis) (formerly called the “deer tick”) is a small, common tick found throughout the northeastern and north-central parts of the United States. It is the transmission vector for a number of bacterial and viral pathogens including the bacterium that causes Lyme disease, Borrelia burgdoferi. For the last five years, Pennsylvania has led the nation in the number of human cases of Lyme disease and the number of cases is growing each year (From the Center for Disease Control, human Lyme disease cases in Pennsylvania: preliminary 2016 (12,092 cases), 2015 (9000 cases), 2014 (7400 cases), 2013 (5900 cases)).

The life cycle of the black-legged can involve combinations of over one hundred different potential hosts (fifty-two different species of mammals, sixty species of birds, and eight species of reptiles) and can stretch out over a two or even a three year period with staggered emergences of different instar stages during different months of the year. Also, early instars of this tick are extremely small and difficult to see!  Below is an idealized version of the life cycle that I described in a blog a few years ago:

Photo by California department of Public Health (Flickr)

Eggs deposited in the fall in low, grassy or scrubby vegetation hatch the next summer into the very small, six-legged larva life forms. These tiny ticks typically seek out small hosts (white-footed mice (Peromyscus leucopus) seem to be the preferred host for this life stage) but are able opportunistically to attach to larger mammals, too, including humans. These larva, though, are not born with any of the pathogens associated with Ioxdes scapularis and are, thus, unable to transmit any of its diseases (a small piece of good news!). If these larvae feed on a host that is carrying one of I. scapularis’ bacterial or viral pathogens, though, that tick will become infected with that disease causing agent and will carry it and be able to transmit it throughout the rest of its life cycle.

After the larva has taken its blood meal it molts into the larger, eight-legged nymph life form. This molt often is delayed until the following spring. These nymphs, then, seek a host for their blood meal. These hosts are usually mammals ranging in size from white-footed mice to dogs to cats to deer to humans. Because of the timing of this nymph emergence the spring (May and June here in Western Pennsylvania) is a time of great risk for ticks bites (and disease transmission) for humans!

Photo by D. Sillman

After the nymphs have taken their blood meals they molt into adults. These adults are especially abundant in the fall. These much larger ticks (like the one in the picture to the left) typically attach to large mammals. The female adult ticks take a large blood meal from their hosts and then use the energy from this feeding to make eggs. The adult male ticks attach to the same hosts, but do not feed (and, therefore, do not transmit pathogens at this stage). They are there to find a female and to mate! The males die shortly after mating and the females die after dropping off of their hosts to lay their eggs in the grassy and scrubby vegetation. Those eggs then overwinter and hatch in the summer to start the life cycle all over again.

So why have the number of Lyme disease cases increased in recent years? Media reports stress the “common sense” inference that our increasingly warm winters (possibly due to climate change) are leading to increased survival of the ticks and increased spring and summer populations. Unfortunately, scientific research does not support this logical connection. A study published in 2012 in the Journal of Medical Entomology clearly showed that in spite of “common knowledge” to the contrary, cold winters (and they used Upstate New York as their cold winter site!) do not reduce the numbers of overwintering black-legged ticks. The ticks just have too many adaptations for cold tolerance and too many protected microhabitats available for even the brutal winter temperatures of New York State to have any effect on them at all.

Most researchers looking at these ticks attribute their increases to increases in the most critical host in the black-legged tick’s life cycle: the white-footed mouse. Fragmentation of forest habitats and the optimal conditions of suburban ecosystems for these mice along with significant declines in their natural predators have led to great increases in their numbers. Black legged ticks, then, in their larval and nymphal life stages are increasingly likely to find a white-footed mouse on which to feed and are, therefore, increasingly likely to survive to the next instar level. White-footed mice are also significant reservoirs for the Lyme disease bacterium, so the ticks have a higher probability of assimilating and then passing on these bacteria.

Weather and climate factors can have an impact on populations of white-footed mice, but it is not temperature that is the most important weather/climate feature but precipitation. Wet and humid conditions favor the growth of the plants upon which white-footed mice feed and thus can lead to increased population sizes. More white-footed mice means that nymphal black-legged ticks have an increased chance of finding its ideal “blood meal” host thus increasing the numbers of later instar stages.  Further, right after a black-legged tick has taken its blood meal its ability to control its body water concentration is greatly impaired. A tick, then, right after a blood meal is very likely to die if it encounters a dry environment. Increased precipitation and higher relative humidity, then, also favors survival of the tick!

Photo by Jamaine Wikimedia Commons

An article in the Wall Street Journal this past April (sent to me by my WSJ watcher, Larry in California!) warned of a “bad summer for ticks” because of the mild winter (probably not) and because of the 2015 “bumper crop” of acorns in the Northeast! These acorns fed more white-footed mice which in turn sustained (and infected) more black-legged ticks! The adults of the tick explosion are out there this year searching for their last blood meal!

Your best defense against Lyme disease is a “tick check” after any potential tick exposure. Remember, the ticks may be anywhere that white-footed mice might live (yards, fields, woods, etc.). The ticks have to be attached to you for 36 hours before they can begin to transfer the Lyme bacterium. Use a tick puller and dispose of the tick in a creative manner (drown them in alcohol or flush them down the toilet). Don’t let the threat of ticks keep you from the woods or hiking trails!

The story of the Lyme disease vaccines is very interesting, by the way! I will talk about that in a future blog!

 

 

 

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Signs of Summer 5: Leaf Shapes (and great questions!)

Photo by D. Sillman

A couple of weeks ago I got an email from a Seventh Grade student named Gordon. Gordon was doing a Life Science project that involved coming up with a question that could not be answered by simply doing a Google search. Gordon’s question was, “What determines each tree’s type of leaf and their structure?”  Gordon found my essay out on the Virtual Nature Trail about leaf shapes and strategies and thought that I would be a good person to possibly answer his question. Here is my answer! My compliments to Gordon for coming up with such an interesting question and also to Gordon’s science teacher for coming up with such a creative and meaningful project!

 

Gordon:

What a great question!

Leaves are incredibly important to any plant since they are the organs where photosynthesis occur. Since the shape of a leaf is controlled by a number of very specific genes most scientists feel that natural selection and evolution must have played a role in determining leaf shape. It is not clear, though, what exact factors in a tree species’ ecological and evolutionary environment were the determining, natural selection variables for leaf shape.

Looking at the extremes of leaf shapes (needle shaped leaves vs. broad, flat leaves) (and this is what I wrote about in the on-line essay that you found), it is pretty clear what evolutionary factors were in play: needles can withstand the very dry and very cold conditions of winter and, thus, persist for many years on a tree. Broad leaves cannot handle the dryness and freezing conditions of winter, but they are more efficient photosynthesizing organs! So a tree balancing its energy demands either makes a leaf (a needle) that lasts for several photosynthesizing seasons but generates, each season, less sugar from photosynthesis, or it makes a single season leaf (the broad leaf) which generates a lot of sugar in one season and then “throws the leaf away” in the Fall! You would expect in colder or drier environments the “needle leaf” solution would work best for a tree!

Looking at overall leaf size, it is also pretty clear which selection factors are at work: in any type of stressful environment (very cold, very hot, very dry, low nutrient, or high salt conditions) trees tend to make very small leaves. These leaves, while less efficient in photosynthesis than large leaves, match the energy balances required for the tree to survive under these very stressful conditions.

All of the more subtle differences in leaf shape, though, are much harder to explain! There are a few really interesting hypotheses, though.

First of all, when a leaf develops on a tree its tissues (where the cells are that contain the chlorophyll that accomplish photosynthesis) develop and grow around the leaf’s vascular tissues (its “veins”). These leaf veins bring water to the photosynthetic cells and take away the sugars that they make in photosynthesis. Overall leaf shape seems to be correlated to the energy efficiency of this water delivery/sugar transport system! Each photosynthetic cell has to be close to a leaf vein! Lots of different shapes can “solve” this energy requirement successfully!

Also, when sunlight hits a leaf LOTS of heat is generated! So the leaf, when it photosynthesizes must dissipate this excess heat out to its environment. Some of the sculpting of the leaf edges (the serrations and deep invaginations into the leaf mass) may be related to solving the problem of efficient heat dissipation.

Here are a couple of types of oak leaves that illustrate these ideas: (the images are from Wikivisual and are listed under Creative Commons usage rights):

Chestnut oak leaf

You see the leaf veins in each type of leaf, and you can imagine the leaf forming by growing the leaf tissue around those veins. The close proximity of the leaf tissue to the veins sets up a very efficient water delivery/sugar exporting system! The deep invaginations of the pin oak leaf, though, means that although there is less leaf tissue for photosynthesis, there is more efficient heat dissipation from the leaf! The balance between overall photosynthesis rates and heat dissipation may be the factors determining the subtle differences in the shapes of a particular

Pin oak leaf

tree species’ leaves! Not surprisingly, chestnut oaks tend to grow in colder environments, and pin oaks tend to grow in warmer environments!

Thank you for your wonderful question! I plan to use some of my answer in my weekly ecology blog sometime this summer! I will be sure to give you credit for the question! You can find my blog at http://sites.psu.edu/ecologistsnotebook/

Keep enjoying science!

Dr. Hamilton

Department of Biology

Penn State New Kensington

There are a few other possible variables that might be important in some leaf shape natural selection systems. Plants growing in environments with low light levels might show evolutionary patterns for shapes that optimize light reception. Other plants under intense herbivore pressures might show selection patterns for shapes that resist that herbivory. Leaf shape might also be subject to the complex constraints of biomechanical factors and overall structural integrity of the leaf. There are also a number of hypotheses that consider leaf shape the consequence of selection for genes that code for completely different features of the tree (like flower shape, for example). The impact of these genes on the development and shape of the leaves, then, is just an inadvertent tie-in to the actual selection for that different factor!

I can imagine some experiments that should be conducted to explore this question. For example, do the leaves of a northern red oak (which have very subtle edge invaginations) photosynthesize better than the leaves of a scarlet oak (which have very pronounced edge invaginations) in cooler environments? Or, do those scarlet oak leaves photosynthesize better that northern red oak in warmer environments? Or, do these very different leaf shapes have no effect on their efficiency of photosynthesis? Experiments like these could help to focus the evolutionary discussion of leaf shape and help to define the significance of its possible natural selection variables.

 

 

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Signs of Summer 4: Fledglings in the Yard

Photo by D. Sillman

Watching the fledglings around my yard:

A robin with a juvenile speckled breast follows an adult around my concrete slab basketball court. You assume the adult is teaching the fledgling how to find food, but the fledgling seems to be staring off into space rather than watching what the adult is doing. The adult frequently finds worms and larvae and insects in the slab cracks of the court and instantly the fledgling pops out of its mental fog and rushes up to the adult. She flutters her wings and chirps and puts her open beak an inch away from the adult. The adult stuffs whatever she found into the fledgling’s mouth and then goes back to hunting. The fledgling does not seem aware of the process, only the end result.

Photo by I. Taylor. Wikimedia Commons

The front yard crows made their nest up in the red pines of my street-side woodlot. I watched them back in early April flying in and out of the pines with great beaks full of sticks and grass. A couple of weeks ago a fledgling (as large as the adult she was following but not quite as glossy black) showed up at the morning peanut and shelled corn feast out under my sunflower feeders. The fledgling watched the adult crow closely and raised her wings and shook her head when the adult picked up a peanut or a piece of corn. That went on for several days until finally all of the morning crows were independently gathering their breakfast bits. The fledgling still shows himself through the day by lingering in the yard even when I step off the porch, or by not immediately flying to the high, safe perches when cars or dogs or cats cruise by. Breakfast was an easy lesson, there are many harder things that a young crow needs more days (and weeks) to learn. Two adult crows frantically chased off a sharp-shinned hawk yesterday afternoon. The crow fledgling just sat out in the middle of the field agitated by all of noise but uncertain as what to do.

This morning when I went out to fill the bird feeders a house finch fledgling kept her spot on the perch of my hopper feeder even after I opened the top and began to pour in a scoop of sunflower seeds. She only flew when the noise (or vibration?) of the falling seeds rattled her perch.

Photo by K. Thomas, USFWS Public Domain

Also this morning a cardinal fledgling was standing on the sidewalk and let me walk right past her as I went in and out of the porch door. No fear. No flight. As I sit at my writing desk, I am watching an adult male cardinal jumping down into the leaf compost pile out in the backyard.  He grabs the odd wiggler or tidbit from the compost and then jumps back up on the surrounding wire fence to give the morsel to his fluttering fledgling. When he hops back into the compost the fledgling freezes in place. When he hops back up she flutters like mad and chirps. This goes on for fifteen minutes and then they both fly away.

A Carolina wren and her fledgling are chirping loudly in the lower branches of the arbor vitae. They are being incredibly conspicuous in a zone frequently prowled by the neighborhood cats! The fledgling, though, can’t seem to keep her volume down when the parental bird is in sight! I

Photo by D. Sillman

have watched the adult stick her beak into the open beak of the fledgling. I can only imagine the tasty mix of branch-gleaned insects and larvae that she is sharing! The adult immediately moves up to higher branches to keep hunting. The fledgling sits down low, in the danger zone, waiting for more. Later the wren and the fledgling join us on the deck. The fledgling sits on the surrounding fence like a Christmas ornament while the adult frets and fusses.

The mortality rate of these fledglings is incredible. Probably half of them won’t make it to their one or two month birthday. Predators can just walk up to them (or swoop down on them) and grab a quick snack, and the learning curves for self-sustained food gathering are incredibly steep. Many of them have only just figured out the basic physics of flying, but they are having difficulties avoiding obstacles like branches or buildings. Windows especially are something that takes a long time to understand. Some of the fledglings will be eaten, others will starve, some will break their necks or wings in collisions, and then their parents (the creme-de-la-crème from their own generations!) will start all over again.

Photo by Neonorange, Wikimedia Commons

I mentioned the geese down on Roaring Run a few weeks ago. I was on a bike ride and saw two adult Canada geese with six brand new, feather-fuzzy goslings. The parent’s both hissed at me as I biked past (bringing back some really vivid memories of being chased by goose when I was a kid (I climbed up into an apple tree to get away!)). Well, the next week there were only four goslings. Today, there were only three. The parents still hissed when I rode past, but they don’t seem to have the same energy they did when they had their full family.

The fledglings are born without fear and without any innate hunting behaviors. Both must be learned very quickly if they are to go to the head of their generation and have the chance to mate and pass along their DNA. The slaughter of the young, though, like Malthus inferred and Darwin described, sculpts the population (and the species) into its wild, functional form. If all of these baby birds survived, the population would be full of inept buffoons who had no idea of what it really meant to be a bird!

Good news! The robin fledgling is by herself on the basketball court. She is hopping from crack to crack and probing the weeds with her sharp beak. I haven’t seen her catch anything yet, but she is making all of the right moves! She will graduate from her juvinile spots soon, I am sure!

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