Everyone knows just how bad an evolved bacteria or virus can be; I even wrote about Malaria, a commonly known virus-caused disease. However, a lesser known killer has been destroying animal, plant, and probably humans as well: fungus.
As those who have been following know, I have been reading Elizabeth Kolbert’s , “The Sixth Extinction: An Unnatural History”. As it comes to a close, I can’t help but be shocked how history can continually repeat itself. Kolbert gave two instances in detail in her book where an advanced fungal blight has spread throughout different species and quickly began killing.
The first is the golden tree frog of Panama also known as the Panamanian golden frog. These frogs were everywhere around Panama, and not just the wild either. These frogs have a cultural value there and are a symbol of luck, which is probably why they are printed on lottery tickets among other merchandise. It’s honestly surprising how long it took for people to realize the population was declining, and fast. By the time people began to set up little refugee sites for these frogs, thousands had died. A fungus was the cause of not only the huge decline of this frog, but lots of other amphibians around the world. Only two frog species were found to be resistant to the fungus: African Clawed Frogs and North American Bullfrogs. This suggested that the fungus co-evolved within these species, attempting to get the upper-hand. These two frogs are also well known to move around the world either to be consumed, used for medicinal purposes, or as pets. Odds are an infected individual spread the evolved fungus to another amphibian who had no natural resistance to it, quickly killing and spreading.
There are, unfortunately, other occasions of such an event happening in other species, bats to be precise. White-nose-syndrome is also a fungal infection, but found in bat species. It was also a very quick killer, partly because of how social bats are. It spread rapidly from one cave to another, it was safe to say that once it arrived in one cave, by the next day every bat in that cave had it. Again, certain species of bat, found in Europe, are resistant to the disease, but still carry it. European spelunkers wishing to go into and explore caves visited New York one day, and the fungus on their clothes managed to spread to a bat, and the rest is history.
In the past week, I have managed to conduct an interview with Dr. Ralston, who was kind enough to recount some of her previous research. Dr. Ralston conducted a study on osteochondritis dissecans (OCD), which is Developmental Orthopedic Disease that causes horses’ bones to be weak. Her team gathered a large sample size of very similar horses (both in genetics and how they were brought up). The only difference was that of the mothers, one mother would have OCD and the other would not. They took blood samples of the horses, and found interesting results.
To obtain this data, Dr. Ralston and her team used a process called Nuclear Magnetic Resonance (NMR). NMR is an analytical process that used different cells
magnetic fields. When introduced to NMR’s own magnetic fields, it creates a spectrum that can be measured.
The first result is that the data differed in a month period, which gave evidence that glucose levels were affected by the season/monthly period. The second of which was even more interesting; horses with OCD tended to have higher amounts of essential amino acids than nonessential amino acids. Normally, the horses would turn their essential amino acids into nonessential amino acids via a metabolic pathway. Since the levels of essential amino acids were so high, Dr. Ralston deduced that pathway that caused essential amino acids to turn into nonessential amino acids was probably malfunctioning in horses with OCD, which may be a reason why OCD exists.
Another interesting bit of research that Dr. Ralston has worked on deals with Diabetes. Insulin abnormalities are common in young horses, so it has been proposed that horses could make an apt model for the benefit of humans suffering from type 2 diabetes. Although more research needs to be done, the possibility is still there.
Evolution is one of life’s most powerful tools. Fueled by natural selection, it allows life to improve over generations. It makes people wonder why certain hereditary diseases are so common. However, sometime we have to take a closer look.
One classic example is Sickle Cell Anemia, or sickle cell disease (SCD), which is a hereditary disease that causes blood cells to have an irregular, sickle-like shape instead of their normal round shape. This causes complications in carrying oxygen and a risk of blood cells getting stuck and clogging blood vessels. It is common in certain parts of Africa and Asia. It would seem odd that a deadly hereditary disease would be common, but there is a secret this diseases possesses.
SCD is recessive (having 2 recessive alleles). However, if a person is heterozygous for this disease (one recessive and one dominant allele), they are actually resistant to malaria. The parasite that causes malaria has a hard time getting into sickle-shaped cells. Heterozygous individuals have some of their cells sickle shaped, but not enough to exhibit symptoms. Therefore, it is advantageous for a person to be heterozygous for SCD. Apparently, the resistance to malaria is worth the risk of having SCD.
SCD isn’t the only disease that is resistant to malaria. Hemoglobin E disease, common in Southeast Asia, is similar to sickle cell anemia, except that its symptoms are much milder. For some people, it’s a benign disease, but its effect on malaria is still the same.
However, despite being a much better alternative, it isn’t very common in Africa. This is mostly due to the fact that, even if it’s imperfect, sickle cell anemia is already there (The Power of Random). Despite being a better alternative because of its milder symptoms, the niche of malaria-prevention has already been filled and prospered for many generations. It will take a lot of time for Hemoglobin E disease to be more common in Africa, if it ever becomes more common.