Hello, all my lovely readers!

My apologies for not posting last week but it was my birthday on the 2nd February and so in true London style, I stretched it out to a week of celebration! 

Amazing news also I am officially a ZSL Seasonal Presenter at London Zoo so come and visit me this summer and watch out for my twitter!

Now let's get our weekly dose of Science in the City!

Lurking in the very depths of wastewater is a predator that has bacterial infections running for the hills - Micavibrio aeruginosavorus. This predator is ‘the vampire’ bacteria. Micavibrio aeruginosavorus attaches to its prey externally and then leeches of the victim's nutrients. This parasitic predator could be our greatest biological weapon in the fight against antibiotic-resistant bacteria.  Could this predatory species be our saving grace?

Micavibrio aeruginosavorus is a gram-negative obligate bacterial predator that feeds by being an ectoparasite (see image above: predator in yellow and bacteria in pink). Normally bacteria gain all their nutrients essential for survival and growth directly from their environment, however, this bacteria is unable to gain several proteins through either imports or their environment. Very similar to us in this manner, the only way to get the essential nutrients needed would be to consume others and gain it from them. M. aeruginosavorus kills its prey differently to other predatory bacteria such as Bdellovibrio bacterivorous. Bacteria from the Bdellovibrio genus bind to the surface of their victims and enter the periplasm of the bacteria, once inside Bdellovibrio consumes its prey’s nutrients and multiplies. When the preys nutrients have been exhausted, Bdellovibrio causes the bacteria to burst and moves onto its next victim. Micavibrio, on the other hand, kills its victims in a way that mirrors the sci-fi horrors of vampires. This predator attaches onto the surface of its victim and then ‘bleeds’ it dry!  This results in the ectoparasite growing in size.

Predatory bacteria have been shown to attack a wide range of bacteria, however, Micavibrio aeruginosavorus shows a strong preference to Pseudomonas aeruginosa. Bacteria from the Pseudomonas genus are known to cause infections of the blood as well as trigger pneumonia, as such infection can prove to be fatal. With the rise in antibiotic resistant bacteria, novel treatments must be explored.

A group of researchers evaluated the ability of M. aeruginosavorus to locate and destroy different strains of pathogenic bacteria. In order to test the effectiveness for this bacteria, they planted the M. aeruginosavorus on a ‘lawn’ of prey cells and then measured the ‘lytic halo’, this is the area where pathogenic bacteria is absent. Results looked promising when carried out on Petri dishes, however, when this treatment was carried out in animal models with the bacteria injected either intravenously or delivered via the respiratory system the results were not as promising.

A predators potential for avoiding a medical armageddon:

Using a natural predator as a way of dealing with prey populations is not new, in fact, it is being carried out on a regular basis - just on a larger scale. Predatory bacteria such as M.aeruginosavorus comes with some potential advantages if we could get it to work with us:

They are fussy eaters. Initially, this came as a problem as scientists preferred a predator that would ‘eat’ a wide range of bacteria as opposed to a specific species of bacteria.  However, this proves beneficial if these bacteria become a part of clinical practice. M. aeruginosavorus eats ‘pathogenic’ bacteria - bacteria that cause infections.  Not all bacteria is bad, in fact, without our healthy gut bacteria, things would go very, very wrong. Being a fussy eater means that our healthy gut bacteria are safe from being eaten.

A low and concentrated dose of a bacterial killer. Because species belonging to Micavibrio go straight for their selected prey species, a low initial dose would be all that is needed to rid the body of its bacterial infection.

Resistance, not such a problem. The relationship displayed by  M. aeruginosavorus and Pseudomonas aerguinosa, for instance, is a classic predatory-prey relationship. As a cause of this relationship resistance to being eaten is a lot trickier to evolve for the prey species because it is also in the predators best interest to evolve ways to get around it and eat them anyway!

Predators are determined to get to their food. In the case of Pseudomonas aeruginosa, this bacteria secretes a thick mucus that normally proves too great a barrier for antibiotics to penetrate, a barrier that is penetrated by M. aeruginosavorus.

In preparation for this post, I gathered sources of information from a range of sources and enjoyed reading through the comments left by other readers. One gentleman left a comment highlighting the similarities between using predatory bacteria and bacteriophages (image above). I remember my dad talking to me about this once before and decided to investigate further.

Bacteriophages are another type of bacterial predator but are not bacteria themselves they are actually viruses. These viruses invade a bacterial cell and disrupt the bacteria’s machinery eventually leading to cell death. These remarkable naturally occurring bacteria killers are able to penetrate much deeper to where the infection has spread and they stop replicating once they are no longer needed. Bacteriophages have been used in certain countries as a form of treatment since the Iron Curtain! As to why it is not available in the West could be due to things such as public reluctance to believe that a virus could be helpful, and there is actually no money to be made in pushing this forward.

Overall naturally occurring bacterial predators as a way of managing future bacterial infections is most definitely exciting. However, there is still a way to go before human trials could even be considered.

I hope you have all learned something today guys. Just to let you know keep an eye out for my post this Valentine's day! Next week's post will be published on Valentine's day and not Friday and I have a real treat for you romantics and bachelors!

Until next week you wonderful lot

Science in the City

xoxo Resources used: Predation of human pathogens by the predatory bacteria Micavibrio aeruginosavorus and Bdellovibrio bacteriovorus.
Genomic insights into an obligate epibiotic bacterial predator: Micavibrio aeruginosavorus ARL-13
Vulnerability of Pathogenic Biofilms to Micavibrio aeruginosavorus
Examining the safety of respiratory and intravenous inoculation of Bdellovibrio bacteriovorus and Micavibrio aeruginosavorus in a mouse model

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Topaz

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Greetings everybody

Hope you have all had an amazing week. It is time for that lovely fix of science you get from me on Friday! This week is all about looking into the world's antibiotic resistance crisis; What is it? Why should we care? And how we have reached a crisis point?. Let's launch into it then.

What is antimicrobial resistance and why should we care about it? 

WHO (World Health Organisation) defines antimicrobial resistance as the change seen in bacteria, fungi, viruses and parasites once exposed to antimicrobial drugs. Antimicrobial resistance carries the potential of plunging the world back into the dark ages of the pre-antibiotic era. What does this mean for me, you, your family and friends? Bad news. If we are unable to keep up with constantly changing microorganisms as they continue to accumulate resistance to antibiotics, deaths from the common cold and flu would rise and once simple and curable bacterial infections will lead to hospitalisation.

Let's talk money for a moment:

An independent report was published releasing the results of the impact Antimicrobial resistance would have on our future economy. I have extracted the main results from the report to read the full report click here.

They calculated the costs based on two inevitabilities in a world where antimicrobial resistance is common:

Increased mortality - deaths directly caused by the resistance of microorganisms would greatly reduce the size of the working-age population.

Increased morbidity -  these were characterised as being prolonged periods of time taken off work due to sickness. In the short-term, this would cause a temporary reduction in the workforce and in severe cases lead to a long term loss in team productivity.

It was estimated that by the year 2050 the world economy would have lost a whopping $2.1 trillion if the levels of resistance remain low. However, if this problem is not handled and resistance increases globally, the loss could peak at $124.5 trillion. If those numbers were not enough to highlight the effect this biological crisis has on the world, it is important to note that they are an underestimate. The report only considered two aspects of the economies challenges, the cost of healthcare (longer stays and an increased demand for intensive care) as well as funding to manufacture new antibiotics were not factored into the analysis.  A number not yet totalled but based on the underestimate... it's a cost best to keep as minimal as possible.

How did we get to this crisis point? 

Antimicrobial resistance is a story that stretches all the way back to the very first microorganisms. Chemical warfare has been a strategy used against rivalling microorganisms in competition for resources for centuries. Ever since the first weapon was used against another, microorganisms had to learn how to evade or neutralise those threats. Those chemicals used by one microorganism to disadvantage another or completely destroy it gave us the inspiration for many antibiotics, antivirals and antifungals on the market today. This widespread exposure of microorganisms to antimicrobials has led to accelerated development of resistance because we have placed the pressure on them to do so. In simple terms, the microbes must 'adapt' or 'perish'. Survival of the fittest. 

Since then, it has been an arms race between humanity's innovation of antimicrobials and the microorganisms ability to acquire resistance to it. If you are a betting person you would not like the 'odds' take a look at the image below showing the number of antibiotics released over the years. 

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In the picture below, a scientist is holding up two Petrii dishes. If you observe them closely you will notice that on each petri dish there are small white circles. Each one of those is a small paper disc dipped in a different antibiotic, the aim is to grow a certain type of bacterium on the plate and see how effective each antibiotic is at killing the bacteria.  The first petri dish shows you that the anitbiotics are effective at killing the bacterium (observe the zone surrounding each circle that is completly clear of any bacteria). Compare this to the second petri dish, the antibiotics are largely ineffective in killing of the bacteria - sadly this is the situation we are heading towards. 

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The overuse and misuse of current antibiotics:

Lack of new innovative drugs is not the only factor playing into the accelerated growth of antimicrobial-resistant microorganisms. Some of the blame falls on individuals within the public. Every time a doctor has prescribed you a course of antibiotics to help you with some form of bacterial infection, you begin taking it religiously out of desperation to feel better. As the symptoms begin to subside you start missing a dosage or two or perhaps, you skip the last day completely. This could leave the last few remaining bacterium behind and these guys are placed under a selective pressure 'adapt resistance' or 'die in the next dosage'. If you were a bacterium which would you pick? Below is an image showing just a few ways become resistant to antibiotics. 

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Antibiotic misuse relates to the scenario where a doctor gives you antibiotics for some form of infection that is so mild, that the body should be left to fight it on its own. For resistance to happen microorganisms must be in contact with some form of an antibiotic. In the case of giving antibiotics for a mild bacterial infection, you  may think what is the real harm. If it becomes resistant then the body will overcome it anyway, right? You would be correct. There would be no worry if the mild infecting bacterium kept the code of resistance to itself. The nasty thing about bacteria is that they like to share these codes for resistance with each other. Suddenly a more severely infecting bacterium has the code to resistance to multiple different drugs that it itself has never come in contact with. 

These are reasons that many have heard before and you will hear more and more as this issue becomes more and more public. I went in search for the lesser known ways of how we got to where we are today. 

The real monster lurking in our sewers:

Antibacterial products discarded into the sewage from our own communities and even hospitals   all collect to form the perfect reservoir for antibiotic resistance to cultivate. This hotspot of antibiotics, pollutants, detergents, and disinfectants creates such a hostile living environment that it truly drives the incentive of each bacterium to develop resistance to multiple chemicals designed to kill them. 

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There are many ways that resistant microorganisms can be transferred onto us. Take a look at the image below to check out a few more. 

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21st Century Problem in need of a Solution... 

We could panic after this post. You would be well within your right but as I have been told by one of my students I am incredibly optimistic. It will be a tough battle to fight, one of the greatest in our history perhaps due to it global impact on both our health as well as our economies. Microorganisms have had to adapt under increased exposure to antimicrobials. I believe that 'Necessity is the mother of invention' as such in the face of an enemy we will overcome it. We are left with two choices 'Adapt' or 'Die'. Which do you choose? 

Biobunch

Over and Out 

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Unknown

Greetings everybody, 

It is the end of the week finally! Not sure if you guys saw my tweet a couple of days ago, but I have enrolled myself on to a free online course introducing Cancer Immunotherapy. Ever since the beginning of this course, my passion for immunology has been booted up again, I mean our immune system is crazy awesome! So, I decided to dedicate an entire Friday Facts post on Immunology, so enjoy it guys. 

Wasn't it awesome! have you learnt something new about your immune system, or therapeutic treatment? How about those DNA patents hey how do you feel about this? If you find this extremely interesting TEDx have an amazing video on DNA patenting and it is all about the BRCA1 gene. Totally recommended! 

Guys as always have an amazing weekend, whether you are going for an awesome let your hair down, put you heels on kind of night or are preparing for the ultimate relaxer weekend, have an amazing time! 

Biobunch, 
Over and out

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Unknown

Greetings everybody,

Happy Friday! Todays post will be on  ‘The Battle for the soul of Evolutionary Biology’. Evolutionary Biology is a hot topic in science of late due to an all out war on whether Evolutionary Theory is just fine the way it is (Standard Evolutionary Theory) or if it needs a total reboot in order to fit with modern phenomena (Extended Evolutionary Synthesis). For you guys to form your own opinion, I am going to give you a crash course on what both sides are saying. Enjoy. 

Extended Evolutionary Synthesis (EES): 

IDEOLOGY: 

Extended Evolutionary Synthesis is built on one fundamental idea. Genes cannot take all the credit for evolution. Scientists in support of this idea claim that Standard Evolutionary Theory can cause scientists to have tunnel vision as such they can miss crucial parts of the picture. They argue that the original theory neglects the role processes involved in an organisms growth and development have on their evolution. At present, evolutionary theorists have maxed out on researching an organisms genes and  their phenotypes but have neglected the link between the two. Development.

According to Kevin Laland and his colleagues four phenomena should be integrated into Evolutionary Theory 2.0. Developmental Bias, Niche Construction, Phenotypic Plasticity and Extra Genetic Inheritance. For todays post I will focus on two!

PHENOTYPIC PLASTICITY: 

Now I am not going to go into too much detail about this process because it will be featured in its very own post on Biobunch in the not too distant future. This phenomena describes an organisms ability to reconstruct their developmental path by changing their phenotypic state or activity (e.g. rate of metabolism) in response to novel or varying environmental conditions. 

Below are two examples of this process in action check it out! 

EXTRA-GENETIC INHERITANCE: 

There is a lot more to inheritance than genes. Extra-Genetic Inheritance takes parent-offspring similarities one step beyond genetics, by explaining the maintenance of behavioural traditions, cultural inheritance and so on. Classic example is the passing of nut cracking knowledge in chimps. 

Closing points: 

Overall, the four phenomena above mentioned may have a far larger explanatory power of why and how evolution occurs than currently given credit for. Overall the synthesis provides an interesting and arguably novel view on evolution by providing more than one route for an organism to ‘fit’ into its environment. 

Scientists that are behind this synthesis, are not completely undermining current evolutionary biology, however, what they are calling for is a wider stance on topics by revamping Standard Evolutionary Theory. After all it has been shown countless times plurality is always the best policy. 

Standard Evolutionary Theory (SET):

IDEOLOGY: 

This is the evolutionary theory that everybody has come across at some stage in life whether it be through the national curriculum, or higher education the point is, it is widely taught to us. This theory was largely formed on the principles set out by ‘The Modern Synthesis’. What is this? Well the great Charles Darwin provided us with natural selection as a process by which evolution is likely to occur. But its missing something, genetics. Thus, ‘The Modern Synthesis’ was born with the union of natural selection with modern age genetics. 

I know that you know this story but take a quick look at the wonderful process Darwin proposed! 

COUNTERARGUMENT:

Scientists in favour of the EES called for a pluralistic approach to be adopted in terms of evolutionary theory. However, this call had been answered long before they asked. Those four phenomena up to this date have been the stars in many papers and many evolutionary biologists would agree that these phenomena are extremely interesting. Indeed, interesting, but not enough to warrant the rebranding of evolutionary theory. 

Never underestimate the power of genes. The discovery of these little hereditary units have allowed for precise predictions and the quantification for many components of evolution! In fact it is thanks to our understanding of genes  as to why we understand one of the biggest scare of the 21st Century- antibiotic resistance.

Now what do we know we need a lot of in the field of science? Evidence. According to those in support of SET, EES are bursting with enthusiasm and optimism but their evidence is not so optimistic. Several of the phenomena have not established a solid link with evolution, whereas the theories in SET (genetic drift, natural selection, mutation and recombination) have been linked as causes of evolution many times over. 

CLOSING POINTS:

Needless to say the concept of an Extended Evolutionary Theory is extremely exciting, and it is likely that the four phenomena listed above will play al large part in the rebranding of the theory in the future. For now, until more studies are done there is no need for such large scale modification. 

It is easy to get the idea that Standard Evolutionary Theory is like the worlds grandfather, set in its ways, unwilling to change and static whereas Extended Evolutionary Synthesis sounds like your bright eyed bushy tailed kid brimming with promise. This is not the case according to scientists Standard Evolutionary Theory has had a brilliant year thanks to many technological advances!

Lastly, ‘Gene-centric’ is not a bad thing! 

Charles Darwin, sorry for the mix up both yourself and your theory are rehired! That brings us to the end of this weeks post, hope you have learnt somethings along the way! Now it is down to you, SET or EES, either way you choose to go, this post has highlighted that this area is growing every day and needs innovative and passionate people! Personally I am interested in the future role phenotypic plasticity may play in an organisms ability to adapt to climate change (the looming threat). 

Until next time guys thats Biobunch

over and out

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Unknown