Sciencing The Sh*t Outta Things

Good morning blog reading community!

I’m back with an update on the sinister science, exciting experiments and monstrous methods those of us in phage-lab have been practicing in your name and with the aspiration of saving all of humanity from a microbiological apocalypse.

Since I last blogged a blog-post we’ve done plenty of terrible (and very exciting) things and so in the name of cutting to the chase I recommend reading my previous blog ‘A Killing Machine, a Chicken, a Group of Heartless Monsters & You’ as this newer and shinier post will build directly off of the information contained within the older (but not dingier or duller) one.

Welcome back.

Okay, so now that I’ve snared your attention what have I been doing? I ended my last blog having recently isolated and named Robyn phage and since then my classmates and I have been absolutely sceiencing the sh*t outta things, not in a Matt Damon, MacGyvering for survival on Mars type of way but in more of a playing with really expensive toys and making genuinely new discoveries type of way.

Details make the story huh? I agree, so read on!

In phage lab, affection for our microscopic killers runs high. As a proud parent the next step having successfully isolated a phage was to amplify the concentrations of said phage so as to extract DNA and send both phage and DNA samples off to the University of Pittsburgh for storage and archiving purposes. Our phage studies here at Massey are actually a part of the SEA-PHAGES (Science Education Alliance-Phage Hunters Advancing Genomics and Evolutionary Science) programme coordinated by the University of Pittsburgh. The programme has a purpose of fostering a passion for the biological sciences, in part through the sense of ownership participants develop with their discovered phages (“SEA-PHAGES,” 2013-2018).

Now the process of amplification involved a lot of agar plates and hours of work and incubation time but for me this resulted in a very concentrated solution of Robyn phage. How concentrated? Well, calculated roughly, I ended up with a conical-tube containing 1×1012Robyns per millilitre of solution, that’s 1000,000,000,000 Robyn particles per millilitre of solution! Plenty high enough to be archived, a special moment, as it is my opinion that sending a phage sample off to Pittsburgh is significant, not just a milestone in the course work, but also as a sort of graduation. A graduation from phage researcher to a fully fledged contributor to the global collection of knowledge and stuff that we so diligently build as humans.

Fortunately for my life as a nerd, the SEA-PHAGES programme offers further opportunities to contribute to said collection. In particular, having archived samples my classmates and I were authorised to conduct our own independent research, we devised our own protocols and implemented them with the objective of further characterising our phages. As any good parent does at some point I subjected my phage-baby Robyn to a range of different environmental experiences to investigate under which settings she thrives and under which settings she ceases to exist.

(Note, I’m using a female pronoun as a reflection of Robyn’s given name and not as a reflection of Robyn’s gender, Robyn as a virus is genderless).

Working with two fellow classmates we trialled our phages with exposure to different temperatures twice and the results are graphed as follows:

Screen Shot 2018-07-01 at 7.54.41 PM

Screen Shot 2018-07-01 at 7.54.20 PM

The vertical axis in both graphs represents the concentration of our phages whereas the horizontal axis (again in both graphs) represents the temperatures to which they were exposed. To move right along the graph is to move up in temperature and to move down the graph is to decrease in phage concentration.

So, what do the graphs tell us?

They seem to indicate that Robyn is not particularly well suited for temperatures approaching 80 degrees Celsius and yet more research is needed to draw anything conclusive.

Moving on!

I think I’ve saved the best for last as I proudly present Robyn (quantity x3).

Screen Shot 2018-07-01 at 8.03.31 PMNow she don’t look like much of a ruthless killing machine now does she?

Those of you with a keen eye may have noticed the scale in the lower left corner of the image and those of you with an even keener eye may have noticed said scale is measured in nano-meters, well what does this tell us? That Robyn is very very small, measurable in increments of 10-9meters small to be more scientific.

Okay, but if Robyn is so small, how’d I get the photos?

As much as the photographer in me would love to say I used a DSLR paired with a massive zoom lens the answer is in fact much snazzier. You see to get a picture of something this small requires the use of an electron microscope, equipment that Massey conveniently stores at their Palmerston North campus (a long drive for us Auckland based students) resulting in a van-ride visit to our friends at Auckland University so as to commandeer one of theirs.

Why an electron microscope?

Electron microscopes stand apart from their non-electron harnessing microscope brethren as they use electrons in place of photons (visible light) when producing an image. The machines themselves are large and bulky and contain components that range from lenses of different kinds to an electron detector and an electron gun (Khursheed, 2011). The advantage to such systems is that as electrons have a much shorter wavelength than photons they are vastly more capable for viewing structures and objects that are otherwise simply too small to see.

If you think all this sounds exciting (as I do) just you wait, the next step is to analyse the genetic material that makes Robyn tick. With luck I will soon be able to report on some of the individual genes Robyn carries, their function and their phenotype.

‘Til then, smile and be happy.

The research continues!



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Imagine a world 200 years from now where we have destroyed over 80% of living species on Earth, the human population has skyrocketed to 20 billion, antibiotics are no longer effective and bacteria are the top of the food chain. 200 years may seem too distant to concern anyone living today, but we have the power to control the quality of life that will be had by people living during this era. Time is the enemy, but for myself there is no better time to act than the present with the hunt for phage’s being the start of my journey. Phage hunting may not solve the world’s problems, but it could certainly help steer us in the right direction for reducing them.


Bacteriophages are the single most abundant organisms in the biosphere (the name given to an area which includes all living organisms on Earth) with an estimated number greater then 10^31. To put this number in perspective, at the moment the world population is roughly 7.6 billion. If every single person found a phage every second of their lives (assuming the population size remained constant) it would take 41.7 trillion years to find them all. Although more than 5000 individual phage’s have been successfully isolated, a mere 750 of them have had their genomes sequenced as of 2011 (Hatfull and Hendrix, 2011).  There are so many more to be sequenced and an uncountable number more to be discovered. For me this is the exciting thing, knowing that there is so much more knowledge to be gained from these fascinating viruses. Not only could they hold key information that could accelerate research in health but they could be one of our last opportunities to save our planet. What more reason could we need to find out more?


With there already being an estimated 124 million people across 51 countries in food crisis, the continuously rising population poses a risk to the spread of further food shortages worldwide (, 2018). For first world countries, much of this suffering goes unnoticed as food is so abundant. Last night’s left over stir fry may find itself in the bin rather than the fridge due to the preference of a freshly cooked meal. Fruit is frequently left to rot on the ground due to the trees producing more than we know how to utilise. With such a contrast in the way food is appreciated around the globe, there is no better time for bacteriophages to step up and enhance food. It has been recently discovered that phages are suitable to decontaminate carcasses, act as a natural preservatives to extend shelf lives and to disinfect surfaces (García et al., 2008). What this could mean is a reduction in the amount of wasted food as well as a reduction in the potentially harmful substances used for food related decontamination. With overall less waste, food will be utilised more effectively allowing us to compensate for the ever rising population.


Say you get a spider bite on your leg. You leave it for a few days because you think nothing of it. On the fourth day, you notice that the area around the bite has started to go rather red. On the fifth day, this red patch has increased in size so you play it safe and go to the doctor to sort the problem. They give you some form of antibiotics which you take until you have finished what has been prescribed. The redness goes away and the infection is removed. Problem solved, right? Sadly, this solution may not always be one that we can rely on due to the rise of antibiotic resistance. Antibiotic resistance is where bacteria that cause certain infections become resistant to the antibiotics overtime. This makes the infection increasingly difficult to treat. With almost all introduced antibiotics now having a form of antibiotic resistance against them, there is no doubt a serious issue is arising (Ventola, 2015). For me I feel as though it’s not all doom and gloom. As bacteria change, our methods of fighting them change too. Bacteriophages could hold the solution for being the next form of antibiotics with the millions of phages that are still undiscovered. The future is both an ominous and exciting prospect. We have the power to determine which one of these two emotions dominates the way future generations live their lives.


It wasn’t until a couple of years ago that I realised how much every day activities affect not only the environment but the people around me and the generations to come. For many, thinking about the implications of their actions long term is hard to do which is understandable. Why should we go out of our way to buy a reusable bag to carry our groceries when plastic bags are often provided for us? Why should we bike half an hour to work in the morning when we can drive in the comfort of our own vehicles whatever the weather? Most importantly, why should we care about the environment when many do not? This is the issue we face as a society. We cannot sacrifice our quality of life for the benefit of the environment when so many other people aren’t doing the same. I hope that bacteriophages can give us some insight into not only improving our awareness of health but also of the way we treat the world around us.


  • Hatfull, G. and Hendrix, R. (2011). Bacteriophages and their genomes. Current Opinion in Virology, 1(4), pp.298-303.
  • Lee Ventola, C. (2015). The Antibiotic Resistance Crisis. Pharmacy and Therapeutics, 40(4), pp.277-283.
  • García, P., Martínez, B., Obeso, J. and Rodríguez, A. (2008). Bacteriophages and their application in food safety. Letters in Applied Microbiology, 47(6), pp.479-485.
  • (2018). 2018 Global Report on Food Crises | WFP | United Nations World Food Programme – Fighting Hunger Worldwide. Retrieved from



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People like us

At this very moment, over 30 million people are living with HIV. In December of 2014, I had the privilege of visiting a handful of these survivors. The Kathmandu HIV/AIDS Orphanage is located in Nepal and aims to provide much-needed support to children with AIDS. In the poorest country worldwide, Nepalese society ostracise those living with HIV. The government has little money to offer treatment, and hospitals often refuse to provide care. To be HIV positive in Nepal is to face abandonment and social neglect. The orphanage provides refuge for infected mothers and their children, and relies solely on donations and volunteers to manage their HIV.

Upon meeting these children, I was overcome with emotion. The orphanage had provided nutritionists and doctors- every child leaves the home with no presence of AIDS. We were asked to turn off our phones and refrain from taking pictures. If pictures of HIV positive families are found online, they can be neglected from their communities. The severity of this problem hit us volunteers instantly. The rate of HIV in Nepal is defined as “generalised and severe” by the World Health Organisation, largely due to the taboo nature of the subject. There is no education on HIV/AIDS and children with the disease are turned away from schools across the country.

HIV has been following human evolution for centuries. The disease passed from chimpanzees to humans in the 1920’s, and rapidly spread through migrants and sex trading. Within four decades it was labelled the ‘gay plague’, and homosexual men were barred from donating blood. The disease became an embarrassment, a taboo. As a virus, HIV cannot self-replicate. It attaches itself to T-cells, cells that function in the immune system to eradicate germs. Once attached, HIV injects its viral genome into the host. This genetic information is inserted into the host’s genome and the cell continues to reproduce. The result is an unstoppable virus that causes deadly acquired immunodeficiency, or AIDS.

There is no cure for HIV, and current treatment can only slow the progression of the disease. Antiretroviral therapy occurs when multiple drugs are used to reduce the virus count in bodily fluids. These drugs have been in use since 1990, yet have not proven to completely eradicate the HIV virus. The disease is able to mutate and evolve against antiretroviral therapy, making it nearly impossible to remain on the same medication for a lifetime. Changes in these strong medications have serious side effects, leaving scientists desperate for a new treatment plan.

Phage therapy is a technique new to the scientific community, wherein bacteriophages are used to treat bacterial infections and diseases. Bacteriophages are a virus that specifically targets bacteria, and often attributed as the best way of targeting bacterial resistance. Although phage therapy has proved incredibly successful, HIV does not attack bacteria and so cannot be cured with bacteriophages. Many of the practices within phage therapy, however, are still utilized. Phage display is an incredible technology that allows scientists to map the specific binding of HIV to T-cells. As a result of this process, billions of distinct genome sequences can be produced and used to distinguish drugs, binding, and analyse the success of specific antibodies.

Phage display technology is a complicated process that requires an immobilised DNA sequence on a dish. The outer coat of the protein displays characteristics that can be visualised on the surface of the HIV particle. Proteins that react with the T-cells will remain attached to the walls of the dish, the others washed away. These phage replicate within the T-cells, a process repeated multiple times until a sufficiently ‘enriched’ solution is obtained. In the final step, the DNA within the HIV virus is sequenced. Hence, this process provides incredibly accurate information on protein interaction between HIV and T-cells.

The use of phage display technologies in the treatment of HIV was outlined in the International Journal of Molecular Sciences. Scientists were able to analyse the antibodies in HIV/AIDS patients, and successfully map binding regions of HIV and T-cells. The result of this study allows for the engineering of specific antibodies with increased binding affinity, with the possibility of leading to an HIV vaccine. A vaccine would enable entire communities to be protected and immune to the deadly disease. If successful, this approach could be applied to many diseases worldwide. Millions of lives could be bettered because of bacteriophage technologies.

Finding a cure for HIV/AIDS does not, however, begin with science. The taboo of the disease must be eradicated with conversation and education. In countries such as Nepal, thousands are dying because they are afraid to speak up. Schools need to offer education on practicing safe-sex and consent, and communities need to provide support. In my volunteer work I was overwhelmed by the animosity between society and the orphanages patients. These children were like no other, blissfully unaware of the isolation they may face in adulthood. HIV is no longer a ‘gay plague’ spread only by homosexuals and IV drug users. It is an epidemic washing through developing countries. Cultural differences must be put aside and the well-being of humanity placed at the forefront. An HIV-free world is not possible until we accept the survivors as people.

People like us.

To donate or volunteer with the HIV/AIDS Orphanage in Kathmandu, Nepal please visit

Delhalle, S., Schmit, J., & Chevigné, A. (2012). Phages and HIV-1: From Display to Interplay. International Journal of Molecular Sciences, 13(4). 4727–4794. Retrieved from

Humbert, M., Antoni, S., Brill, B., Landersz, M., Rodes, B., Soriano, V., Wintergerst, U., Knechten, H., Staszeqski, S., Laer, D., Dittmar, M., Dietrich, U. (2007). Mimotopes selected with antibodies from HIV‐1‐neutralizing long‐term non‐progressor plasma. European Journal of Immunology, 37(2). 501-515. Retrieved from

Jha, R. (2009, April 7). Bacteria Therapy: Cure for HIV? [Web log message]. Retrieved from

Nall, R. (n.d.). How HIV Affects the Body. Retrieved from

U.S. Department of Health and Human Services. (2017). The HIV Life Cycle. Retrieved from

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The Mount Rushmore of Bacteriophages

Mount Rushmore. A mountain in the black hills, of Keystone, South Dakota USA. Depicting the faces, of four of the most influential men in America’s early history. Now I know what you are thinking. Why are you talking about this…?

Well….As I was writing my second blog post on the history of bacteriophage discovery, and in the process becoming more familiar with its important figures. I began to draw comparisons between them and the leaders on Mount Rushmore, and started to think. Who would be on a bacteriophage Mount Rushmore?


The first person on the mountain, would have to be the first person recorded with discovering bacteriophages (although at this point they were not named).Ernest Hanbury Hankin. Born 4th February 1965, in Ware, Hertfordshire, England, (“Obituary Ernest Hanbury Hankin”, as cited in wikipedia) (1). He went on to study medicine at St Batholew’s hospital and medical school, and became enrolled at Cambridge University’s, St John’s College from 1886 to the 1900’s. Eventually becoming a bacteriologist, aeronautical theorist and naturalist, in his own right.
Image result for ernest hanbury Hankin

Hankin went on to research in India. Particularly of importance was his research on cholera, a bacterial disease of infection in the small intestine by strains of the bacterium Vibrio cholerae, (R.A.Finkelstein, 1996)(2). While researching cholera in the Ganges and Jumna rivers in India, Hankin observed the presence of “marked antibacterial activity against Vibrio cholerae,” (Hankin 1896)(3). From this observation Hankin “suggested” that an unidentified substance, managed to pass through his filtering equipment and was destroyed or altered by heat (“heat-labile”). And was responsible for this ‘marked antibacterial activity’, and for limiting the spread of the bacterium Vibrio cholerae.

With the evidence we now have on bacteriophages, we can say that the ‘marked antibacterial activity’, was most likely indeed a bacteriophage. One in fact, that specifically attacked the bacterium Vibrio cholerae. This remark by Hankin, is widely considered to be the first discovery of bacteriophages. However Hankin’s review was merely an observation, and nothing more. There is no evidence to propose that any further study was conducted on the rivers, concluding Hankins observations as meager throw away facts (at the time of course). Now whether this was just dependant on the experiment apparatuses of the time, or whether this mystery did not intrigue Hankin enough to further his studies of it, we do not know. Nevertheless this was still an important discovery and is deserving of Hankin’s position on the Mountain.


The second figure is Frederick William Twort. Born 22nd of October 1877, in Camberley, Surrey, England. He was the first man to truly delve further into the simple observations that he (like Hankin before him had made), advancing his hypothesis further. Twort studied medicine at St. Thomas’s Hospital in London, and eventually went on to become a professor of Bacteriology at the University of London, (Paul Fildes, 1951)(4).

Image result for frederick twort

Twort’s groundbreaking research of bacteriophages came in 1915. Before this however, Twort had  proposed other innovative research that was important at the time. Twort’s research on Leprosy (Hansen’s Disease), lead to a breakthrough in the knowledge of ‘growth factors’. Twort recognised that the bacillus (gram-positive rod-shaped bacteria) of Leprosy, was very closely related with the bacillus of tubercle (outgrowth on exterior of plants). Leprosy was unculturable, but tubercle was, so Twort incorporated dead tubercle bacillus into the growth medium of leprosy, successfully culturing leprosy. This experiment became important as it showed an example of an organism only being able to grow when supplied with a substance produced another organism. Which became the essential feature of all growth factor investigations, (Twort, 1910)(5).

This previous knowledge and intuition ultimately helped Twort discover the basics of bacteriophages in 1915. Twort had now been researching bacteriophages for a while, and had been trying to grow viruses (bacteriophages), on artificial media. However he could not figure out the ‘substance’ needed, for the viruses to grow. At the time smallpox vaccines, were being made in the skin of calves, but because of this were always contaminated with bacteria. Twort had the epiphany that bacteria may be the ‘essential substance’ needed on the media, for viruses to grow in vitro. Twort plated countless of phages on media, and although not all worked. On closer inspection, he discovered tiny, glassy areas that exhibited no growth, (later would become called ‘plaques’). Twort came to the conclusion that these plaques, are areas that the bacteria cells have been destroyed (by the bacteriophages), (Twort, 1915)(6).

Tworts findings, ultimately set the basics of bacteriophages. That they are viruses, and they infect bacterium’s, killing the bacterial cells, resulting in the formation of ‘glassy’ areas, called plaques. Sadly Twort could not continue his research as World War 1 broke out, and when he came back Felix d’Herelle had begun research that overshadowed his. Ultimately Twort is an incredibly important figure in bacteriophages history, and progression, earning him a spot on the Mount.


The last man to talk about is Felix d’Herelle. The so called ‘founder’ of phage therapy, and arguably the most important discoverer of bacteriophages. Of French-Canadian descent, d’Herelle was born 25th of April 1873, in Paris France. Astoundingly d’Herelle never formally attended University, only attending the University of Bonn for several months. Meaning he was a self-taught scientist. Due to his arrogance and pride however, he became quite a disliked figure in the science community. And undertook many failed business ventures, including a chocolate factory.

Image result for felix d'Herelle

d’Herelles ultimate calling in life however was not chocolate factory’s, but instead bacteriophages. As he officially discovered bacteriophages, 2 years after Twort’s discoveries in 1917. It was during the 1st world war that d’Herelle had his revelation, when he was charged with seven sick French soldiers exhibiting hemorrhagic (bacterial) dysentery. He made bacterium’s from the patient’s feces, and isolated Shigella (gram-negative rod-shaped bacteria) strains of the patients. This mixture was both tested on animals, and exposed to agar medium. The mixture that was plated on an agar medium, formed glassy areas of dead bacteria, and it is d’Herelle who officially named the plaques, (although he initially called them ‘taches’), (Summers, 2000)(7).

Unlike Hankin or Twort, d’Herelle continued with his studies, being sure of what he discovered. Proposing that bacteriophages where viruses that parasitize bacteria. He even named them bacteriophages, (‘phage’ is Greek from to eat or devour). d’Herelle did not stop there however and delved deeper into bacteriophages utility, performing the first recorded example of phage therapy. Administering his ‘anti dysentery’ phage to a young boy of 12 years of age. The patients symptoms vanished after a single dose, and a full recovery occurred a couple of days after the phages administration. (Sulakvelidze, Alavidze, Morris Jnr, 2001)(8). d’Herelle went on to continue his research, and spread the word of bacteriophages around the world. And that is why d’Herelle is the final member on the Mount.


Now obviously there are other figures that are also deserving of a position on the Mount, but to keep this post (relatively) short I cannot talk about them. But Hankin, Twort and d’Herelle are who I think are the most important and influential in bacteriophages history, as they show the progression of bacteriophage discovery. From observation to hypothesis through to conclusions. Which is why they have they have the most claim/right to sit atop this mount.



  1. (H.H.B.) (1939). “Obituary. Ernest Hanbury Hankin”. The Eagle. 51 (223): 181–183. Cited from
  2. Finkelstein, R. A. (1996). Cholera, Vibrio cholerae O1 and O139, and Other Pathogenic Vibrios. Baron S, editor. Medical Microbiology. 4th edition. (Chapter 24). Galveston, Texas: University of Texas Medical Branch at Galveston.
  3. Hankin E. H. (1896) L’action bactericide des eaux de la Jumna et du Gange sur le vibrion du cholera. Ann. Inst. Pasteur 10:511. Cited from
  4. Fildes, P. (1951, November 1). Frederick William Twort, 1877-1950. The Royal Society.
  5. Twort, F. W. (1910). “A Method for Isolating and Growing the Lepra bacillus of Man. (Preliminary Note.)”. Proceedings of the Royal Society B: Biological Sciences. 83 (562): 156.
  6. Twort, F. W. (1915). The Lancet. An investigation on the nature of ultra-microscopic viruses, 186(4814), 1241-1243.
  7. Summers, W. C. (2000). Félix d’Herelle and the Origins of Molecular Biology. Journal of the history of biology, 33(1), 191-194.
  8. Sulakvelidze, A. Alavidze, Z. Morris Jr, J. G. (2001). Bacteriophage therapy. Retrieved from:


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Phage hunt so far…

As if I were mining for gold, I had been digging and scraping soil samples from different locations within Auckland. With each sample I had collected, I sensed hope; that I would perhaps find gold. Bacteriophages (phages) are like specs of gold found in dirt, they hold potential powers that could be the answer to many bacterial diseases.


Image 1. Both gold and bacteriophages show similarities in its origins in the soil and value.

Who knew that phages could be found almost everywhere on Earth? They are found ranging from soil, sewage, the depths of oceans to the food we eat (3). Phages are viruses that are abundant in the biosphere with an estimation of 10^32 phages (7). It is often the case that when something becomes abundant, the value drops. But that is not the case here. Several university education programs such as the ‘Science Education Alliance-Phage Hunters Advancing Genomics and Evolutionary Science’ (SEA-PHAGES) are located across the globe. Students participating in these programs such as myself cannot get enough phages. There is a lot we do not know about phages. Currently, 13,074 phages have been found worldwide and counting according to (5), which is comparable to a grain of sand within a desert. The more phages found, the better as we can add to the existing databases of sequenced phage DNA and increase our understanding.

Phages are in fact an old discovery. They were first found in 1915 by Edward Twort and later 1917 by Felix d’Herelle (10). Phages, a strange looking organism as pictured in (Image 2) that resembles a spider. They are specific in that they only target specific strains of bacteria, whilst being ineffective towards mammalian cells (7). Phages infect bacteria by inserting DNA or RNA that incorporates into the bacterium and undergoes either lysogenic cycle or lytic cycle (3). The lysogenic cycle is when genetic material is integrated within the bacterial DNA, and remains dormant, allowing bacteria to replicate normally until it is triggered by an environmental factor, switching it to a lytic cycle. The lytic cycle is when the phage genetic material is replicated by mechanism in bacteria, synthesizing new phages, that build up inside the cell walls of a bacteria until it bursts open (lyses), killing the bacteria (3). 


Image 2. A bacteriophage resembling the shape of a spider.

By the 1940s, phages were outshone by chemical antibiotics which emerged. Antibiotics have same superpowers as phages by destructing bacteria, however, they work differently. Instead of lysing bacteria, they can destroy the cell wall or inhibit bacteria to synthesize proteins for growth (6).

Antibiotics, like an ageing old man, grew weaker and weaker. Even a walking stick cannot aid this old man. He could not handle the younger and more active bacteria that adapted faster and increased their resistance. Antibiotic resistance rose rapidly, especially with misuse and over-prescription of antibiotics (1). 

We have come to a point where modern medicine is no longer effective. This problem worsened as fewer pharmaceutical companies are manufacturing new antibiotics. Luckily, an alternative exists called phage therapy, one of the strategies implemented the Department of Health (2). Once again, phages were rediscovered.

This comes back to the reason to why I and several other students in 246.202, a class in Massey University may have been out collecting soil. Be it at the crack of dawn or in the thick of the night. At random locations, such as the urban forests, parks, or sidewalk where other passersby would probably question if collecting soil was a weird hobby of mine. It has been a difficult journey so far, with many failed attempts to find a phage, totaling up to 20 soil samples and many other repetitive procedures in the laboratory. Currently, I am up to the stage of characterizing my phage, all derived from a singular pinprick plaque (a clearing on an agar plate due to bacterial lysis) I had found in my 19th soil sample. 

The future of phages looked promising to me. Phage therapy so far has been proven successful, having already treated a few diseases before antibiotics (3). They are natural and not chemically harmful such as antibiotics. They are safe towards humans as they specificity targeted bacterial cells. Due to the specificity, they also did not target the good bacteria in your body, unlike antibiotics (6).

Until I heard a question in class; could bacteria could become resistant to phages? I started to question all our efforts of phage hunting. What was the point of finding phages, if the same outcome of resistance were to occur? I wonder if these minuscule things found in soil really is the answer? I have primed myself into seeing phages as gold from the beginning, thinking that resistance would not be possible. However, phage resistance is a possibility. It arises differently from antibiotic resistance, from the incapability of detecting the bacterial antigen (a molecule found on the surface of the bacteria). A mutation on a bacterial antigen will mean that phages cannot attach onto and infect its host (4). Another way a phage becomes resistance is the bacteria’s natural mechanism to cut foreign DNA with enzymes (4). This causes a phage to be resistant to that bacteria it used to be able to infect. While converting to another phage that targets the same bacteria, or a cocktail of phages (use of multiple phages) could be hopeful. This could also fail yet again if no phages or if one phage in the phage cocktail is effective (4). If it were hopeful, new phages would need to be continuously found to make these cocktails, and additionally have ideal characteristics such as fast infection and lysis producing numerous phages (4). It seems like a cycle of needing more phages. It comes down to an ongoing search to isolate more phages that infect the same bacteria in case of phage resistance, which for now is at low risk in comparison to antibiotics.

For now, digging for more soil may be the way to go. Alchemy has not reversed its magic. Gold is still gold. However, not pure gold as it seems.



(1) Antibiotic resistance. (2015). Retrieved from

(2) Henein, A. (2013). What are the limitations on the wider therapeutic use of phage? Bacteriophage, 3(2), e24872.

(3) Kutter, E., Guram, G., Alavidze, Z., & Brewster, E. (2013). Chapter 8: Phage therapy.In Grassberger, M., Sherman, R.A., Gileva, O.S., Kim, C.M.H., & Mumcuoglu, K.Y (Eds.). Biotherapy – history, principles and practice: a practical guide to the diagnosis and treatment of disease using living organisms (pp. 191-231). Dordrecht, Netherlands: Springer Netherlands.

(4) Nilsson, A. S. (2014). Phage therapy-constraints and possibilities. Upsala Journal of Medical Sciences, 119(2), 192-198.

(5) The actinobacteriophage database. (n.d). Retrieved from

(6) Trimarchi, M. (n.d.). How do antibiotics work? Retrieved from

(7) Wittebole, X., Roock, S. D., & Opal, S. M. (2014). A historical overview of bacteriophage therapy as an alternative to antibiotics for the treatment of bacterial pathogens. Virulence, 5(1), 226-235.

(Images 1) Smarter hobby. (n.d.). Gold nuggests [Photograph]. Retrieved from

(Images 2) Usagi no Nedoko Kyoto. (n.d.). Enterobacteria phage T4 [Photograph].  Retrieved from

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A Killing Machine, a Chicken, a Group of Heartless Monsters & You

The concept of a lifeless machine made of DNA and protein hijacking the innards of a living being to then use these innards to replicate itself is frightening. For this machine to replicate in such numbers that the unfortunate host bursts at the seams as it fatally-births the offspring of its assailant is objectively terrifying.

For not just one but for a group of six individuals to intentionally subject countless beings of lesser complexity to this fate is cruelty of the highest degree. For these six individuals to willingly and knowingly cultivate, perpetuate and propagate this process, well that’s just what we do in phage-lab.

Perhaps we’re heartless monsters but if it’s of any consolation, I know that I, for one, have my reasons for being so and although I doubt I could sell M. smegmatis on them, I could sure get Robyn’s approval and I think I’ll get yours too.

To kick things off, let’s talk a little background.

What’s M. smegmatis? Put simply, M. smegmatis is a bacterium in the phylum Actinobacteria and the genus Mycobacterium. Along with this M. smegmatis is a genus relative of the deadly M. tuberculosis and is the host, the ‘being of lesser complexity’ mentioned above.

Okay, well what was the grizzly process described above and is it really that nasty?

Yeah it is, although the host isn’t sentient, and we are therefore unable to say much to how M. smegmatis feels about the whole ordeal the results are as described above. The ‘lifeless machine made of DNA and protein’ is a phage (a form of virus) and the description is a summary of the lytic cycle and the culmination of the lysogenic cycle, two of the ways that phages make baby phages.

More details – phages and making babies.

Viruses can replicate only via host cells. Unlike all living species on this earth, viruses lack the ability to reproduce, which in most circumstances would be seen as a factor that would limit their potential to exist. Phages though have found a way around this. A phage attaches to a specific host cell, infects it with their own genetic material and uses some of the organelles (the cellular-machinery that makes up the innards of a cell) to make clones of itself. In the lytic cycle, this leads directly to the whole seam-rupturing-death-thing where in the lysogenic cycle there are a few ‘dormant’ stages, during which the host cell makes more host cells that are also infected with the phage-DNA before all of the infected cells transition to the seam-rupturing-death-thing too.

Okay, so who’s Robyn?

Originally, Robyn was a chicken (pictured below and at her very sassy best).

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Unfortunately, after a long and truly happy life, this incarnation of Robyn passed away earlier this year, which poses the question, who’s Robyn now? Well, Robyn is the name I’ve lovingly given (in tribute to the chicken) to my phage. My very own virulent-phage, more specifically a bacteriophage (a phage that targets only bacterial cells). I isolated Robyn (the phage not the chicken) from a compost-based environmental sample and have since studied and kept ‘her’ happily fed and sustained with a steady supply of our bacterial friend M. smegmatis.In summary, Robyn is a genetically unique bacteriophage that predates M. smegmatis and whose discovery I’m hoping will be entirely new to science.

In the picture below Robyn-phage is far too tiny to see, but the apparent holes (called plaques) visible in the agar-gel are areas where Robyn and or/other phages have killed all the bacteria growing in the plate.


Time to wrap things up.

Why, oh why study bacteriophages?

For me the reasons are myriad, although primarily it falls to my love of science and my favourite aspect of science. Science is about discovery and exploration. To uncover something entirely new to science has been a goal of mine since childhood and studying bacteriophages gives me a chance to do just this. Unless you’re my biased mum, that doesn’t inherently benefit you though, and I said before I’d get your approval, so why should you care?

How’d you like to die of a papercut? It could be a real possibility for the human race in the near future. Antibiotic resistance amongst bacteria has been termed as a crisis (Neu, 1992). The issue here is that bacteria are not only capable of becoming resistant to antibiotics but via natural selection, research indicates the more that we use antibiotics the more likely it is that antibiotic-resistant strains of bacteria will emerge (Gregory, Saunders, & Saunders, 2010), potentially taking our biggest guns for keeping bacterial infections at bay out of commission. This is where the phages and their incredible bacteria-killing-powers come in.

I mentioned earlier that M. smegmatis (which is relatively benign) is related to M. tuberculosis (which is very much the opposite of benign) and fortunately for us, there are phages out there that are adapted to kill each. Phages are highly specialised to their host cells which means that, although it is extremely unlikely that Robyn as phage of M. smegmatisis also a phage of M. tuberculosis, to study Robyn and other bacteriophages is to better understand how bacteriophages operate. To better understand how bacteriophages operate could just be the silver bullet that humanity needs to prevent a bacterial driven apocalypse.

This field of research in its early stages, but we’re doing our bit, we’re being monsters for you and I hope that makes you smile.

I’ll keep you posted.


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Trust the Process

It’s fair to say that the phage journey so far has taken me by surprise. For someone who is more passionate about chemistry, physics and mathematics I did not expect to enjoy my time in the laboratory as much as I have. Although it has been far from smooth sailing, the hurdles have been positive stepping stones for becoming a better overall scientist.

A bacteriophage or in short, a phage is a virus which infects and kills bacteria. Phage’s can vary significantly in their genetic material with some of them being useful towards killing unwanted bacteria(1). In my phage hunt class this year we are specifically targeting phage’s which infect the bacteria mycobacterium smegmatis, which is closely related to Mycobacterium Tuberculosis. Mycobacterium Tuberculosis is a bacteria responsible for one of the oldest known human diseases(2). The research we are conducting will hopefully yield results which could be used to help combat this disease, improving our ability to control it.

My phage journey began with an unexpected positive start. Having minimal existing experience in biology labs, I was unfamiliar with certain techniques which were vital for carrying out successful experiments. However, to my surprise this didn’t seem to be an issue initially with the early discovery of plaques. These are small transparent clearings on the plates which are good indications that the host bacteria have been infected by phage(s). Below is an example of some of the positive results I received when I diluted my samples to attempt to isolate phage’s. The photos from left to right represent 10-3ul, 10-4ul, 10-5ul and 10-6ul (ul=10-6L) dilutions of the original neat sample. The small clearings are they plaques formed as a result of the presence of phage(s).

plate 1plate 2plate 3plate 4

Diluted plate 10-3ul  Diluted plate 10-4ul  Diluted plate 10-5ul  Diluted plate 10-6ul

I had spoken to students the year above me about their phage experience and had been given the impression that if it does go to plan, it doesn’t last for long. I was fortunate enough to have the first couple of weeks go reasonably well. However, things didn’t continue this way for very long.

It all started with the second round of serial dilutions. The first round went well, I recorded all my results and left the lab feeling positive. The next lab session I had to carry out serial dilutions once again but this time using a well isolated plaque from one of the diluted plates. This was successful to begin

plate 5

Above is an example of a contaminated plate.

with but when I returned the following week every single plate had been contaminated as shown to the right. This threw me a bit as it pushed me back and made me rethink my techniques. From here I had to use my neat samples from last time to carry out dilutions once again. Returning to the next lab after my previous contamination, I found no plaques on any of the plates which is when I realised I may have lost track of which tubes I was meant to be using. By this time, I realised I may have made a crucial mistake by not labelling my tubes properly. All the work leading up to this point could have been for nothing.journey

However, there was a silver lining. After my fourth round of serial dilutions my persistence was rewarded as I finally managed to regain some plaques. I had managed to find my original neat samples so was able to revive my phage, which I thought had been lost. This was very satisfying and helped me realise every day in phage is going to be different as well as a challenge, which will be both difficult and rewarding. I have now been able to gain more of an insight into what life in the scientific community will be like after my studies. In some ways it seems daunting, but in others I see it as a number of challenges which can only make me better.

What I’ve found interesting from the experience so far is that nothing will ever go according to plan no matter how well you think you’ve followed instructions. It is important to anticipate minor hiccups along the way so that when they do occur you aren’t confused as to where to go next. Although this was an inconvenience, I am thankful for this experience as it has made me focus more on the process rather than the end result. Too often it becomes easy to get caught up in striving to reach completion without actually understanding and trusting the process. I feel as though I am guilty of this and so it seems appropriate that this has acted as a wakeup call.




  1. Brussow, H., & Hendrix, R. W. (2002). Phage Genomics: Small is beautiful. Cell, 108(1), 13-16.
  2. Smith, I. (2003). Mycobacterium tuberculosisPathogenesis and Molecular Determinants of Virulence. Clinical Microbiology Reviews, 16(3), 463-496.
  3. Image retrieved from
  4. Image retrieved from

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My Phage Hunt Experience

After thinking about what to write for my blog post, I decided to write about my experience so far in 246.202. However rather than be proactive, and finish my blog post early. I was…unproductive and left it to sit. Now coming back to it later (and close to its due date), I looked at what I had written, and saw that I was talking about all my struggles at the time, and what I had done wrong. And now, still see what I did wrong. But now just see more where I wasn’t right, and what I should’ve done differently. The following are those thoughts:

I have finally found a phage, HOORAY! (imaginary confetti cannons explode). And am feeling great as I have not just found one morphology of phages but….two. Yes I have done it, I have officially completed one of my learning objectives, and am looking forward to the road ahead of nurturing and growing my phages as I study them more indepthly. But now as I hold my two phages in my hands and proceed forward with them I look back at my other 30 or so samples, and reflect on what I did differently, what I did wrong and where I was just unlucky.

Firstly I look back at all the other environmental samples I took. From the soil and dirt, to the pond, stream and puddle water, and finally, to the compost, compost and compost. Compost from the beginning of the paper had been identified as an ideal environment to acquire a sample from, with it being the most successful in years prior. However, I did not find initial success with compost, and ended up collecting 38 samples before  finding my phages. And guess what medium the sample was from….it was compost. Samples 22 and 23 both contained bacteriophages, and were both located in the compost bins from my Grandfather’s garden. Now I know what you are thinking ‘why am I complaining about finding a phage in compost, when I was told that compost was the best environment to obtain phages from’ or ‘why did it then take me so long to figure this out’ or ‘why was compost not even my first pick’ or ‘why did I not take all my samples from compost’ or ‘why’….Ok, ok, ok, I get it. Maybe I should have had more compost samples, but at the end of the day, that still did not ensure that I would find a bacteriophage.

A big part of finding a bacteriophage is just luck. Some people get lucky and find a phage on their first try, and others (me)…don’t. I mean there is countless bacteriophages in the biosphere, with them making up a large group of organisms in the global population. With estimates claiming up to 10^31 bacteriophage particles on earth (1). On top off this the global phage population is both old and dynamic, but yet the knowledge on bacteriophages is incredibly shallow, as a large proportion of bacteriophages are still undiscovered and unsequenced. So surely I would have been able to find a bacteriophage, I mean I can’t be that unlucky…can I?

So if it wasn’t that my samples were bad, and that I’m not that unlucky, then what could the reason be that it took me so long to find phages, hmmmm….(jaws theme starts playing)…dunnn…hmm what could it be….dunn….no surely not that….dunn dunn…no…dunn dunn…..CONTAMINATION! Yes maybe the reason that I could not find any phages was that I contaminated all my samples during my direct phage isolation protocol. Maybe the whole time it wasn’t bad luck, or choosing the wrong sites for my samples. It was just me, entirely…my…fault.

Now I don’t know whether I contaminated all my previous samples, or whether I even had bacteriophages in those samples. But now, after having archived my bacteriophage and waiting to look at it under an electron microscope I look back at what I have done to get to this point, and how different I see it all now.

I now look back at my choice of samples, and question some of them. Not because they weren’t all compost, but because I did not really think before choosing them. Bacteriophages inhabit environments that mirror the bacteria that it infects. We used the bacteria Mycobacterium smegmatis. If I had thought more carefully about my samples, by simply digging deeper for my soil and compost samples, I may very well have had more luck at finding phages.

Speaking of luck, whether I was lucky or not, and found or did not find phages is negligible. As finding a phage was not a race, and neither is scientific discovery…okay, okay. A race by definition is “a situation in which individuals or groups compete to be first to achieve a particular objective.” And scientific discovery is kind of a race, but not in a sense of the first one wins, and that is the end of it. There are many different paths that can lead to the same objective in science, and all can be ‘winners’.

‘Winning’ in science is not defined by being the first person to the end goal, but the person with the best and most sound theory. This can mean that you are not ‘lucky’ and discover something right away. It can also mean that you do contaminate your results, but as long as you gain information and knowledge from it that is fine. As doing well in scientific discovery is putting your best information forward, and that includes your mistakes.

So, in conclusion I have learnt a lot from 246.202, as it has been much more of practical paper that has really simulated what an actual laboratory would be like. It has taught me to think more scientifically about my investigatory choices. To accept that discovery and progression both take time in science, and that there is no time limit for either of them. And finally, that doing something wrong is not always bad, as you still gain information and experience from it.


  1. Hendrickson, H. (2018). 246.202 Bacteriophage Discovery and Genomics, Course and Assessment Guide. Auckland, New Zealand: Massey University
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Bacteria Wars Episode 5. The Bubonic Strikes Back!

Just a mere 150 years ago, a small cut could easily seal your fate. Just a small cut, enough to form what was one of the greatest killers in human history. Infection! An infection can be a multitude of things, being a broad term to cover many different ailments all deriving from a bacteria breeding and living inside your flesh. Potentially leading to life threatening septicaemia – poisoning of the blood – this leads to bacteria entering the heart, brain and other vital organs. Potentially leading to complete shutdown of vital systems. However, we have the greatest discovery of the 20th century to thank! ANTIBIOTICS!

Discovered by near accident in 1928 by Scottish scientist Alexander Flemming. When he noticed a small culture of Staphylococci had been left open, now contaminated with a blue-green mould. Upon closer inspection Flemming noticed that the bacterial growth had been inhibited or completely stopped by the presence of this fungus. Known as Penicillium. This would lead to the eventual creation of the worlds first true antibiotic. Penicillin. (1)

However, this was not a discovery without issue. Flemming himself, and other scientists knew that bacteria would develop resistance to these antibiotics through horizontal gene transfer and evolution through the selection pressure we were now applying. However, this warning was not heeded. In the decades since antibiotics have been overused, and abused by the medical industry, households, and most of all, the food industry. With saturation of antibiotics into animal feed we have advanced the rate at which bacteria are exposed to these antibiotics, increasing the speed at which they can develop resistance. (2)

Now then, how can we stop, prevent or mitigate these effects? well the answer is simple and may sound like your nutty aunt. WE USE NATURE! There are organisms called BACTERIOPHAGE which are a type of virus that targets and use bacteria to reproduce. How they do this is through injecting their own genetic material into the bacteria. This then integrates its self into the hosts DNA forcing it to produce more of the Bacteriophage. This stops the bacteria from reproducing.  In the same token, it further produces more of the Bacteria fighting Phage.

But, I hear you ask “aren’t viruses potentially dangerous to us too?” technically yes. BUT, in this case it is a Bacteriophage and these types of viruses target a specific strain of bacteria. This is of no danger to the human body and tests are already being done on human subjects as to its potential use and effects. However this poses other issues, with the high specificity of Bacteriophages a specific treatment will have to be developed for each individual off of a cocktail of different phages.

Bacteriophage were first reported in 1915 by Frederick Twort and in 1917 by Felix d’Hérelle. Both noticing when the phage was present in in stool samples of patients sick with dysentery they would soon begin to recover. This was an imediate recognition in the medical field as a new way forward for eliminating bacterialpathogens. However, the equipment necessary to isolate, locate and purify specific Phages had not yet been developed. Since 1923 the Eliava institute in Tbilisi, Georgia has carried on this research and is the first noted institute to use Phage therapy as a legitimate medicine and viable treatment option. (3)

Screen Shot 2018-05-02 at 7.33.36 PM.png

(F.1)          Frederick Twort

However, currently a major issue with Phage therapy is that it has not yet been legislated as safe in western hospitals. With the exception of “experimental” or “supplemental use” in some US states. However change is on the horizon, and it has to be with the rising cases of “super bugs” in hospitals across the world. In 2013 there was the 20th biennial evergreen international phage meeting. Showing promise for international cooperation in this new field of medical science.

Phage therapy is a proven form of treatment for terminal bacterial diseases. As in the Russian federation they report a 50% efficacy of their treatment. Meaning out of every 100 patients with a terminal illness 50 are healed and survive the condition that would normally kill them. Although this is not a desirable percentage. It must be remembered that this treatment is still in its infancy and it is at times very difficult to determine the cause of the infection to create a valid treatment.(4)

Now, the question lies in the hand of the next generation of scientists and the public. As more research needs to be done in the field. While public knowledge and opinion needs to change on the topic. This is potentially the medical discovery of the century. However, when you are at the cutting edge of science, it is very easy to slip.




Figure 1:Obituary Notices of Fellows of the Royal Society, Vol. 7, No. 20.

1  Haven, Kendall F. (1994). Marvels of Science : 50 Fascinating 5-Minute Reads. Littleton, CO: Libraries Unlimited

2  Bud, Robert (2009). Penicillin: Triumph and Tragedy. Oxford University Press. 

Twort, F. W. (1915). “An investigation on the nature of ultra-microscopic viruses”

4 В.Н.Крылов (5 April 2007) (translated)

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When life gives you mould, make penicillin.

You’re lying in a bath with water over 50 degrees. There isn’t much time; veins under your skin are pulsating in distress. In seconds heatstroke paralyses your body. Your vessels expand, dragging the blood to the surface. Sweat emanates, pooling in the crevices of your skin. Every cell in your body is beginning to die.

The most powerful of humans are incapable of surviving such extreme temperatures. No other organism could, right?


Where humans can only survive temperatures of 45 degrees, select bacteria thrive upwards of double this. Some are able to survive in extreme salt, others prefer uninhabitable cold. Extremophiles are organisms that can survive in historically unlivable environments. Discovered in a boiling hot spring in the 1970’s, these tiny remarkables could rid humanity of some of the most dangerous diseases.
In the same decade, the success of vaccinations had eradicated smallpox worldwide. The measles, mumps and rubella preventatives had massive success and were combined into one life-saving vaccine (MMR). While most of the world was waiting in hope and anticipation, some were impatient and suspicious. The Diphtheria, Tetanus and Pertussis vaccine had only been created twenty years prior, but the 1970’s saw the world’s first international controversy over its safety. 25 years later, this small rumble sparked an avalanche. The vaccine under scrutiny? MMR. The allegation?

The MMR vaccine may have direct links to autism.

In Britain, a doctor named Andrew Wakefield wrote a paper accusing medical professionals of unsafely releasing the vaccine. Fear seized the public instantly, taking hold even stronger than in the 1970’s. Through further investigation, it was found that this “successful” doctor had been bribed by a law firm. The firm wanted evidence in support of parents who alleged MMR had harmed their children. It was only in 2010 Wakefield’s initial paper was retracted and he was barred from practicing medicine. All further studies have found no link to autism, but some still support Wakefield’s work.

All the while, the increasing use of antibiotics was wreaking silent havoc on our world. Since Sir Alexander Fleming first discovered the antibiotic penicillin, resistance has been known and feared. In the acceptation of his Nobel Prize, Fleming stated, “It is not difficult to make microbes resistant” in a warning over the future of antibiotics. To this day, almost all antibiotics have undergone some form of resistance. According to ‘The Review on Antimicrobial Resistance’, these mutant bacteria will kill more people than cancer by 2050. Antibiotic resistance is deadly and holds immense dangers for the future of humanity.

You may be thinking that at this point it’s time to throw in the towel. How could we possibly get control of microscopic killers when our global culture can’t decide if pineapple goes on pizza? Simple: we find something else to take control of the bacteria. Bacteriophages are viruses that specifically attack bacteria. They inject their DNA into the bacteria and force reproduction of countless bacteriophages. These offspring go on to inject more bacteria, producing an army of viruses.
If we were to imagine a bacterial disease such as Tuberculosis, the manipulation of bacteriophages could be revolutionary. Our ability to engineer a bacteriophage to override the deadly Tuberculosis DNA may be far more successful than the mildly-successful vaccine that already exists. Instead of fighting bacteria with more bacteria, we can use a medium that has no detriment to the future of humanity.  It seems a fool-proof way to destroy bacterial diseases without the side-effects of current antibiotics.
It is not, however, that easy. Researchers are stuck in that most bacteriophages struggle to survive harsh environments. Our body undergoes extremes, especially when sick with a bacterial infection or cancer. To harness the power of bacteriophages, we must manipulate rare strains’ abilities to survive extremes. A perfect example is of geophiles, extremophiles that thrive in soil. It was recently discovered that these extremophiles prevent gastric cancer caused by bacterial infections. Overall, we have the process’ of bacteriophage reproduction and the survival success of extremophiles. Bacteriophage extremophiles may save humanity.

Fast forward to 2012 and Samuel Dubosie is awarded a grant that merges together these powerful elements of biology. The ‘Bill and Melinda Gates Foundation’ works to “combat infectious diseases that particularly affect the poorest”. They award the grant with developing countries in mind and create products that are easily available and cheap to source. In awarding Dubosie, there is vital funding for creating a new wave of vaccines. One that doesn’t overuse antibiotics or encourage their evolution into resistance.
In hideously scientific terms, this grant will aid in “developing a vaccine platform that uses bacteriophages that are structurally stable in one of Earth’s most extreme environments”. This extreme environment is the toxic soda lakes in Kenya, Africa. It’s a lake of extreme salt and high pH, deadly to almost all organisms on Earth. Certain bacteriophage extremophiles thrive in these lakes, injecting their DNA into other extremophiles and reproducing at immense rates. In harnessing these bacteriophages, Dubosie can engineer them to fight the diseases that kill millions worldwide. Extremes of disease within the body can be directly targeted, opening the world to a whole new form of medicine.

The work that Dubosie is attempting is representative of how science needs to evolve. Our current practices with antibiotics will lead us nowhere but to extinction. This is our future unless we harness new ways of thinking. Manipulating the successes of nature for our own survival is something only humanity can do. Instead of plaguing the future, we must protect the future.

P.S. Pineapple does go on pizza

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