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A blog on microbiology , and various subjects attached to it.
Last February, an international controversy descended over the landlocked country of Malawi. The cause of this was a new bill about to be put forward that centred on the maintenance of clear air in public places.
Any person who vitiates the atmosphere in any place so as to make it noxious to the public to the health of persons in general dwelling or carrying on business in the neighbourhood or passing along a public way shall be guilty of a misdemeanourThis would prohibit smoking in public, the use of stinkbombs and outdoor barbecues. And more importantly, it could be interpreted as prohibiting public flatulence. That's right ! Citizens would be advised to clench hard or be prosecuted.
Surely this was a mistake ! No government would try to ban an involuntary physiological process. When pressed on this piece of legislation, the justice minister George Chaponda responded "Government has a responsibility to ensure decency, Would you be happy to see people farting anyhow?"He confirmed that the intent of this law was ban outbreaks of public flatulence. When news of this spread, Malawi became a worldwide laughing stock, and the bill was silently killed off. The then Justice Minister clearly disliked flatulence enough to support a draconian law against it. To be fair, is there anyone out there who actually likes the smell of flatulence?
Farts are unpleasant as a rule. I have yet to meet someone who, upon smelling a fart, inhales deeply and declares "mmm....Spicy ! "
But no matter how oleaginous, no matter how putrid, a fart has never killed anyone. Right?
The year is 1968. An outbreak of wound infections at Vanderbilt University Hospital was causing concern. The culprit, a bacterium known as Streptococcus pyogenes. This bacterium causes sore throats, skin problems and in the worst case scenario necrotizing fasciitis. A surgical wound infected with Streptococcus pyogenes can become life threatening.
So when nine patients contracted Streptococcus pyogenes infections during the month of august, there was a serious cause for concern. These patients had very little in common. They were operated on in different theatres. they were housed in different wards. In fact the only thing linking these patients was the anaesthetist attending them. He hadn't been ill with any of the disease associated with Streptococcus pyogenes. But it is possible for people to be asymptomatically colonised on their throats. So naturally they took throat swabs from him. They found nothing. There was no trace of Streptococcus pyogenes. So he couldn't possibly be the source of the infection.
The week after, another patient attended to by him developed a wound infection. This time they swabbed him again, in the throat and the nose. And again, all of these tests turned up negative. But taking no chances, he was prescribed a five day course of oral antibiotics anyway.
Despite this, during October, three more patients attended by this individual contracted the outbreak bacterium. The air in two operating theatres where this anaesthetist had attended tested positive for Streptococcus pyogenes.
An infection was found to have "took place in a room just vacated by the carrier". Yet this individual still tested negative for the outbreak bacterium. The staff at Vanderbilt were stymied. Where could the outbreak be coming from?
A similar case that had occurred at Washington University hospital two years previously held the answer. A similar outbreak had occurred, affecting eleven people. In this case, they had identified a carrier, who also mysteriously tested negative for Streptococcus pyogenes. In a desperate attempt to find out where he was harbouring this bacterium, they swabbed the following areas: Nose, Throat, Armpit, Groin, Teeth, ears, scalp, left foot, eyes, hands, anus and the right foot. They really did look everywhere, and they found the Streptococcus in an unexpected place. His rectum was teeming with Streptococcus pyogenes.
Upon finding about this case, the doctors at Vanderbilt decided to take a rectal swab from their suspected carrier. And they too found that the rectum contained the outbreak bacteria.
With this evidence in mind, it doesn't take a genius to figure out how the infection was spreading.
Whenever the anaesthetist expelled gas, Streptococus pyogenes was expelled along with it. The usually clean and sterile operating theatres became peppered with this dangerous bacterium. The course of oral antibiotics they gave the anaesthetist initially to clear the infection didn't work because they were targeted to his throat. Now they knew the exact source, they could give a more appropriate antibiotic treatment to completely clear the individual of this bacterium. He was relieved of his duties, and put on this course, after which he was completely clear of bacteria.
Luckily, thanks to the miracle of antibiotics, none of his patients actually died from these flatulence acquired infections. However we now live in times where more and more species of bacteria are becoming resistant to antibiotics, and perhaps we should reconsider reigning in our collective flatulence. If bacterial infections become untreatable, we may all need to "bung up" to prevent the spread of infectious diseases.
On a side note, Streptococcus pyogenes is also known as Group A streptococcus. Or GAS for short. Try reading through this article again with all instances of Streptococcus pyogenes replaced with GAS. It's confusing.
Schaffner W, Lefkowitz LB Jr, Goodman JS, & Koenig MG (1969). Hospital outbreak of infections with group a streptococci traced to an asymptomatic anal carrier. The New England journal of medicine, 280 (22), 1224-5 PMID: 4889553
McKee WM, Di Caprio JM, Roberts CE Jr, & Sherris JC (1966). Anal carriage as the probable source of a streptococcal epidemic. Lancet, 2 (7471), 1007-9 PMID: 4162660
Edit- At the time of writing this post, I was unaware of the anti-governme... Read more »
Schaffner W, Lefkowitz LB Jr, Goodman JS, & Koenig MG. (1969) Hospital outbreak of infections with group a streptococci traced to an asymptomatic anal carrier. The New England journal of medicine, 280(22), 1224-5. PMID: 4889553
McKee WM, Di Caprio JM, Roberts CE Jr, & Sherris JC. (1966) Anal carriage as the probable source of a streptococcal epidemic. Lancet, 2(7471), 1007-9. PMID: 4162660
Last year, the UK was in the midst of an outbreak of anthrax, in which resulted in 47 infections, and 13 deaths. Bigger than the 2001 letter bomb attacks. Hospitals up and down the country were put on alert. The news media were notified, and the public were told of the dangers. But there was no panic amongst the general public. A case of the famous British stiff upper lip?
Not so much. This was not a terrorist attack. This was just another occupational hazard for heroin addicts.
These people were the victims of this outbreak. The drugs that they were injecting in their veins were contaminated with spores of anthrax.
To get to the source of this problem, we need to look at where the heroin itself is coming from. The main supplier of heroin to Europe for the past ten years is Afghanistan. Yes, that Afghanistan.
(I was inspired by Mitchell and Webb. see here )
It would be easy to jump to the conclusion that this was in some way related to terrorism. However, I personally don't believe this to be the case.
Nobody stepped up and admitted to causing this attack. And why would they? To out and out admit a connection to the sale of drugs would ultimately damage their support. If they were indeed targeting addicts, then they were vastly overestimating the compassion that the public has for these individuals. The panic and terror caused by this event was conspicuous by its absence.
So if this was not a terrorist attack, then what is the more likely way in which the anthrax got into the heroin supply?
The answer lies in the bug that causes Anthrax. We know anthrax as a terrifying biological weapon, but it is also a living micro-organism. It's been around longer than war itself. it has it's own life cycle, its own intentions that are separate from those who would use it as a weapon.
Bacillus anthracis is the bacterium that causes anthrax. It is a pernicious little bug, which can survive in soil for long periods of time. It can get stuck to grass, where it is eaten by a cow, sheep or other such creatures. It then multiplies, secreting virulence factors which ultimately lead to the death of the host, which can take weeks. over this time, the host can spread the bacteria over a wide area through faeces.Ultimately, the bacteria kill the host, and as it decomposes, they re-enter the soil, ready to re-start their lethal life cycle.
These bacteria can then form highly tenacious spores that lie in wait for their next victim to accidentally graze them. Humans who come into contact with these animals or their leavings can become infected by this bacterium.
It has been found worldwide in various places. There is an area that researchers refer to as the "Anthrax Belt" which stretches from the Middle east into Central Asia. And bang in the middle of it are the poppy fields of Afghanistan. These poppy field, which may be fertilized with the manure from infected livestock. Or carried from these fields in leather sacks made from the skins of animals with anthrax.The spores can tough it out through the various processes that turn the poppy plants into heroin.And the desperate user injects this bacteria into their blood stream.
This is a terrible problem, but it is just one of the many terrifying bacterial infections which a heroin user will expose themselves to. Contaminated needles are known to spread MRSA, Streptococcus pyogenes, Pseudomonas, and this doesn't even count various terrifying viral infections like HIV. It's yet another hazard to which I.V. heroin users expose themselves.
Knox D, Murray G, Millar M, Hamilton D, Connor M, Ferdinand RD, & Jones GA (2011). Subcutaneous anthrax in three intravenous drug users: a new clinical diagnosis. The Journal of bone and joint surgery. British volume, 93 (3), 414-7 PMID: 21357967
Schmid, G., & Kaufmann, A. (2002). Anthrax in Europe: its epidemiology, clinical characteristics, and role in bioterrorism Clinical Microbiology and Infection, 8 (8), 479-488 DOI: 10.1046/j.1469-0691.2002.00500.x
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Knox D, Murray G, Millar M, Hamilton D, Connor M, Ferdinand RD, & Jones GA. (2011) Subcutaneous anthrax in three intravenous drug users: a new clinical diagnosis. The Journal of bone and joint surgery. British volume, 93(3), 414-7. PMID: 21357967
Schmid, G., & Kaufmann, A. (2002) Anthrax in Europe: its epidemiology, clinical characteristics, and role in bioterrorism. Clinical Microbiology and Infection, 8(8), 479-488. DOI: 10.1046/j.1469-0691.2002.00500.x
Whilst combing the old literature, I found this gem of a paper from 1859. Aa normal blog post would not do the job for this paper, so I made a mad decision. I decided to tell the story through the use of comic.
I fully recommend reading the original paper, as I have left out a lot of Gairdners more choice insults against Homeopathy.
Full size images can be found here:
Gairdner, W. (1859). Was Hahnemann a Nostrum-Vendor? A Question of Fact BMJ, s4-1 (110), 101-102 DOI: 10.1136/bmj.s4-1.110.101
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Gairdner, W. (1859) Was Hahnemann a Nostrum-Vendor? A Question of Fact. BMJ, s4-1(110), 101-102. DOI: 10.1136/bmj.s4-1.110.101
The history of science is peppered with great moments where people have gone above and beyond the call of duty in order to present their work in an accessible way. Think Florence Nightingale, and how she drew attention to the abominable conditions in hospitals through the use of a simple chart. Or perhaps Vesalius, and his intricate and detailed diagrams of the human anatomy. The following paper deserves it's place among the greats, as it too has taken the graphical representation of science to a whole new level.So what is this paper about?
The paper itself is about a bacterium known as Escherischia Coli, or E.coli for short. This species of bacterium lives in the digestive system of many animal species. Not all E.coli are the same, and there is a diverse set of different strains of this bacteria, including ones that can cause disease. The focus of this paper is on Enterohaemorraghic E.coli serotype O157, or EHEC for short. EHEC causes bloody diarrhoea in humans, and hemolytic uremic syndrome. This is best known for regularly causing food outbreaks due to improperly cleaned meat.It causes these diseases due to the way it attaches to cells in the large intestine. It has a set of genes, known as the LEE (Locus of Enterocyte Effacement), which causes the expression of proteins that force an attachment to the microvilli of the intestine. This attachment causes the microvilli to be severely damaged, and leads to diarrhoea.Like many bacteria that cause disease in humans, EHEC does it because it doesn't necessarily belong in the human digestive tract. The LEE, which make it cause this disease in humans, are actually essential to its survival in it's natural host: the humble cow.The cow's digestive system is far more complex than the human one, containing a stomach with four compartments, and a variety of different commensal bacteria to aid with digestion. Here, the EHEC's specific niche within the cow is at the reticulo-anal junction. When it gets there, it can express it's attachment genes in this area without causing the cow the slightest bit of discomfort.In order to get there though, it has to run through the acidic compartments of the stomach. But this bacteria doesn't have any idea of when it's going to have to cope with stomach acids. Nor does it have any idea of when it reaches the recto-anal-junction. What it does to work these out is quite clever. The first compartment of the stomach the EHEC encounters is the rumen. This is home to lots of other bacteria, which help the cow break down the tough cellulose in grass.These bacteria are in constant communication with eachother, using bacterial pheromones. These compounds are called Acyl-Homoserine Lactones, or AHL's for short. The rumen is choc full of them. Whilst the EHEC doesn't produce any of these chemicals itself, it can sense their presence using a regulatory gene called sdiA.This regulatory gene tells the bacteria when it can express it's attachment proteins. If AHL's are present, they will filter into the EHEC, and when they bind the SdiA protein, it undergoes a transformation that allows it to do two things:1. It will sit on the DNA encoding the LEE, preventing it being read. This stops the attachment proteins being made.2. It force other proteins to activate a gene called gad, which encodes acid resistance genes, and it will ensure that it is transcribed more. This will make the cell more resistant to acid.
So what do these two things mean? Well, the diagram of a cow pictured below will explain:
In the rumen, where there is lots of AHL's present, the genes encoding the LEE are repressed, whilst the genes encoding gad are upregulated. This prevents the bacteria sticking to the wrong place of the stomach, where there is high competition, and also prepares it for the environments within the acidic stomachs,
However, as it travels though the digestive system of the cow, the amount of AHLs decrease, until you get to the recto-anal junction. Here there are no AHL's, and so the LEE genes can be expressed, allowing for the bacteria to attach to this area.
So why do I think this diagram has a place in history?
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Sperandio, V. (2010) SdiA sensing of acyl-homoserine lactones by enterohemorrhagic (EHEC) serotype O157:H7 in the bovine rumen . Gut Microbes, 1(6), 432-435. DOI: 10.4161/gmic.1.6.14177
One of the reasons that I blog on Streptococcus pyogenes so often is because it is such a fascinating and adaptable pathogen. It causes so many different diseases. Diseases as different as a sore throat, and necrotizing fasciitis (The flesh eating disease !). It's even been implicated in tourettes syndrome. This is a hardy and adaptable pathogen, that primarily colonises the throat and the skin.
In a recent outbreak in japan, it was found S. pyogenes has apparently found a new niche to colonise. During the course of one month, researchers at Nagoya city hospital tracked the incidence of of a disease called balanoposthitis.
Now, whenever you see a disease that has "itis" at the end of it, it's usually caused by a bacterial infection. And another word for the "glans penis" is balanus. Still not clear on what balanoposthitis is? Why not Google Image it !
So these doctors looked at patients with an infection of the foreskin and penis. What they found was that it was caused by S. pyogenes. So how on earth did it get there ?
Remember how earlier I said that S. pyogenes likes to colonise the throat ? The Authors hypothesize that the causes of these balanoposthiteses (say that with a lisp, I dare you) are from penile to oral contact, likely from a sex worker.
The cluster of these individuals in one month would suggest something like an outbreak occurring. Perhaps a new strain of S. pyogenes that specifically causes this disease? Perhaps there was one really busy prostitute in serious need of a strepsil ?
What they found however was that these were all different strains of S .pyogenes. They looked at the surface proteins, and found that they were all different. So in fact, all of these guys had relations with different people with sore throats, each carrying a different strain of S. pyogenes.
This means that on each of these occasions, these bacteria, through no fault of their own, found themselves in a new environment. Instead of simply dying, they grew and multiplied and survived. This demonstrates the sheer tenacity of this bacterium. It's sort of inspiring.
In a really really gross way.
Minami M, Wakimoto Y, Matsumoto M, Matsui H, Kubota Y, Okada A, Isaka M, Tatsuno I, Tanaka Y, & Hasegawa T (2010). Characterization of Streptococcus pyogenes isolated from balanoposthitis patients presumably transmitted by penile-oral sexual intercourse. Current microbiology, 61 (2), 101-5 PMID: 20107992
[no cartoon today, snowed under with work]
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Minami M, Wakimoto Y, Matsumoto M, Matsui H, Kubota Y, Okada A, Isaka M, Tatsuno I, Tanaka Y, & Hasegawa T. (2010) Characterization of Streptococcus pyogenes isolated from balanoposthitis patients presumably transmitted by penile-oral sexual intercourse. Current microbiology, 61(2), 101-5. PMID: 20107992
The human body is a great niche for bacteria. Nutrients run through our blood vessels, and soak our cells. Within the gut, on the skin, and in the nasal tract, many bacteria make a home. And for the most part, we tolerate their presence. Some bacteria are even useful to us. However, there are some bacteria who are not friendly tenants. These bacteria try to invade the body. However, this in itself is no easy task. The body is defended by the immune system, a complex and organized collection of different cells dedicated to fighting off bodily intruders.
If bacteria are to successfully invade the body, they need to overcome this formidable defence. Many bacteria do this by producing virulence factors. These attack the cells of the immune system, and more importantly, they can interfere with their lines of communication. Antigen presentation is one form of communication that is important to immune defence, and is a ripe target for attack by bacteria.
What is Antigen Presentation ?
An antigen is sort of like a mugshot for the immune system to use to identify intruders. There are a variety of phagocytic cells which often patrol the body. Whenever the body is damaged, these cells eat up the damaged bits, and along with that, any infectious bacteria that have colonised the site of damage.
They then present them to T-cells. T-cells are basically in charge of the immune system, and they ultimately decide whether to go on the attack, and how that attack should proceed. After phagocytes have mopped up the debris, they chop it up into small manageable chunks which are bound to a molecule called MHC, and presented to T-cells. These small chunks are referred to as antigens.
Usually, they come from normal cells from the body. If however, there were bacteria present, then the phagocytes will have eaten a few whilst it was cleaning up. So some of the antigens it presents will come from these bacteria. If the T-cell correctly identifies the bacteria, it can then co-ordinate the immune response against them.
How do bacteria interfere with this process ?
The bacteria can interfere with this process by secreting compounds known as superantigens. These interfere by making all of the antigens presented to the T-Cells look suspicious. This causes the T-cells to marshal the local immune cells against completely harmless cells, and thus ignore the proliferation of a pathogen.
However, if there is too much superantigen present, the T-cells go into overdrive and cause the whole immune system to go into overkill. In an ordinary setting, chemical messages, known as cytokines, can control the behaviour of the cells of the immune system. In this situation, the activated T-cells are secreting a storm of cytokines.These cytokines causes the body's thermostat, the hypothalamus, to raise the core body temperature. This leads to a fever. These cytokines also cause an immune reaction to the skin, causing rashes and a condition where layers of skin can flake off. As the cytokines spread inflammation throughout the body the symptoms get more severe, leading to death.
Superantigens have been intensively studied in pathogens such as Staphylococcus aureus and Streptococcus pyogenes, and cause a terrible disease known as toxic shock syndrome. They have also been discovered in bacteria such as Mycoplasma arthritis and Yersinia pseudotuberculosis.
They are but one of the weapons bacteria use in their fight with the immune system, and an example of when that fight can get out of control, to the detriment of both bacteria and the host.
Fraser, J., & Proft, T. (2008). The bacterial superantigen and superantigen-like proteins Immunological Reviews, 225 (1), 226-243 DOI: 10.1111/j.1600-065X.2008.00681.x
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Fraser, J., & Proft, T. (2008) The bacterial superantigen and superantigen-like proteins. Immunological Reviews, 225(1), 226-243. DOI: 10.1111/j.1600-065X.2008.00681.x
The roles that bioluminescence plays in the lives of organisms today is fascinating. How did this trait evolve? This is a complex question, because bioluminescence is believed to have evolved around 50 different times in different species of animals.
So how do living creatures produce light? Well, the actual question that needs to be asked is how do living creatures produce visible light.
To fully work out the evolutionary roots of bioluminescence, we must look into the very earliest stages in the evolution of life as we know it.
Those roots begin, more than 2,500 million years ago. Back when bacteria and ancient life forms called archaea ruled the earth. Some of the bacteria had found a way to use the energy of sunlight to make food. Using this reaction, known as photosynthesis, these bacteria managed to spread and proliferate. However, as a waste product, they produced a molecule called oxygen.
Whilst we all know and love oxygen, it is actually a remarkably reactive compound. Back before there was oxygen, you would have a lot of difficulty , say striking a match , despite the fact that most of the atmosphere contains methane. The thing that makes oxygen reactive is that as a molecule is its stability, or lack thereof. To sum up, without delving two deeply into the chemistry, each of the oxygens in a molecule have an unpaired electron. Since electrons traditionally like to be in a pair, these extra electrons will often try to bond with electrons on other molecules, such as methane.
The methane atmosphere of early earth burned away as the oxygen built up, converting the methane to carbon dioxide. Vast deposits of iron began to rust as a result of reacting to oxygen. These reactions initially acted as "sinks" for the excess oxygen, and prevented its build up within the atmosphere. At around 2,500 million years ago, these sinks finally were exhausted. Oxygen began to build up in the atmosphere, and in the sea. This highly reactive compound corroded and changed almost everything it came into contact with. Organisms had to develop new ways to detoxify this compound or die out. This was probably the most destructive extinction that life has ever seen, and the closest it has come to being completely wiped from the earthThe organisms that survived did so because they managed to produce antioxidant compounds. One of the compounds that evolved was Flavin Mononucleotide. This molecule can shuttle excess hydrogen ions around a cell, which can neutralise the effects of oxygen by converting it to water.
Flavin mononucleotide can produce light when it is oxidised . Bioluminescence first occurred as a by-product of these antioxidant reactions.It is also believed that bioluminescence can also act as an intracellular signal to help prevent DNA damage.There are enzymes known as photolyases which act to repair DNA after damage by ultraviolet light. These can be activated by blue light, which coincidentally is generated by the bioluminescence reactions of Flavin mononucleotide.
As these bacteria proliferated, they eventually formed relationships with the multicellular organisms that were also evolving. It is unknown exactly what sort of relationships they started out with, although it is believed that they were initially parasitic. Eventually, these relationships became mutualistic, with organisms often developing specialist organs for housing bioluminescent bacteria.
Many bioluminescent organisms we see today are reliant on symbiotic bacteria.However, not all creatures that emit light use bacteria to produce it. One of the most famous organisms doesn't use bacteria at all, and had developed bioluminescence through a quite different route.The firefly is known for its dramatic sexual displays of luminescence. It did not start off like that. It is believed that its ancestor was a unassuming beetle that defended itself through being distasteful and poisonous.It did this by producing complex compounds and toxic compounds. One of the hazards of accumulating these compounds is that they have to be made safe for the organism producing them. And thus, this beetle needed to develop antioxidant reactions.
To do this, it produced a compound known as D-luciferin. This compound acts as an antioxidant, and can counteract the effects of excess free radicals building up within a cell. It also spontaneously produces photons of visible light when it decays.
So this highly poisonous beetle began to glow in the dark. And because of this, predators would associate luminescence with this little poisonous beetle. So the beetles evolved to be brighter, to spread the message of their toxicity further. More predaotrs got the message, and the bugs survived. The progeny of these beetles evolved into a diversity of bioluminescent organisms, including fireflies.
Great though fireflies and bacteria are at producing luminescence, it did take them a long time to evolve it.
Some organisms hijack bacterial bioluminescence through forming direct sympbiotic relationships with bacteria.
However, there is another way that organisms can become bioluminescent without having to evolve it themselves, or form relationships with bacteria.
There are marine copepods that have evolved to produce a compound called coelentarazine. This compound naturally decays to produce bioluminescence. Predators who consumed these creatures and found a way to metabolize coelentarizine so that they themselves can become bioluminescent. This way, they simply need to eat copepods in order to become luminescent.
In researching this post, I was surprised by the amazing variety of different mechanisms for bioluminescence that there are out there. Considering that bioluminescence is believed to have evolved independently around 40 times, I've barely scratched the surface with this post.
I've attempted to give a few examples that illustrate some of the underlying trends in the development of bioluminescence. Many creatures that are bioluminescent can become so through partnerships with micro-organisms, through feeding on bioluminescent organisms, or through co-opting antioxidant reactions to produce bioluminescence.
Whilst there is a massive diversity I haven't talked about, they all seem to have evolved along the same lines. But scientists still haven't pieced the whole picture together, and we are still in the dark about much of the evolutionary history of bioluminescence.
What is interesting is how the roots of bioluminescence are so intimately tied into our evolution. The same antioxidant reactions which enabled bioluminescence were the same ones which also gave single celled organisms the ability to become multicellular, and in turn the ability to form into more complex life forms. Life forms like us.
At the beginning of this article, I made a note that what makes bioluminescent organisms special is that they can emit visible light. This distinction is important, because those antioxidant reactions are present in all life forms. These reactions are weakly bioluminescent, and as a result, we all emit small numbers of photons. We just can't see them. You could say that to some extent, we are all luminous beings.
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Branham, M. (2003) The origin of photic behavior and the evolution of sexual communication in fireflies (Coleoptera: Lampyridae). Cladistics, 19(1), 1-22. DOI: 10.1016/S0748-3007(02)00131-7
Dubuisson M, Marchand C, & Rees JF. (2004) Fire fly luciferin as antioxidant and light emitter: the evolution of insect bioluminescence. Luminescence : the journal of biological and chemical luminescence, 19(6), 339-44. PMID: 15558801
Timmins GS, Jackson SK, & Swartz HM. (2001) The evolution of bioluminescent oxygen consumption as an ancient oxygen detoxification mechanism. Journal of molecular evolution, 52(4), 321-32. PMID: 11343128
Kozakiewicz J, Gajewska M, Lyzeń R, Czyz A, & Wegrzyn G. (2005) Bioluminescence-mediated stimulation of photoreactivation in bacteria. FEMS microbiology letters, 250(1), 105-10. PMID: 16040205
Kobayashi M, Kikuchi D, & Okamura H. (2009) Imaging of ultraweak spontaneous photon emission from human body displaying diurnal rhythm. PloS one, 4(7). PMID: 19606225
As near exclusive surface dwellers, we only see the sun-kissed top layers of the vast oceans of our planet. As we descend into the depths, the light from the sun dies away. And as we reach the bottom, we should be plunged into absolute blackness.
But we aren't. There are lights at the bottom of the ocean, and they don't come from nuclear reactions in stars far in the sky. This illumination comes from living creatures. The great deeps of our planet are populated with creatures who have only ever known light coming from other living things. Species as diverse as Sharks, Squids, Shrimp can exhibit this trait known as Bioluminescence. This is what happens when organisms really shine.This is the first of a number of posts I will produce on bioluminescence.In this first post I will explore the many ways organisms use bioluminescence to survive.
The hatchet fish is not the most pretty of creatures. Rarely do humans find it in it's natural habitat, the deep ocean. There it hunts what ever prey is unfortunate to cross its path. But fierce though they are, there are always bigger fish waiting to hunt them.When swimming through the deep blue, it is actually difficult to camouflage oneself. Many predators spot prey based, not on their colouration, but on the shadow they cast. That's why sharks often swim below their prey before attacking, and why they confuse surfers for seals.So to truly camouflage oneself in the sea, one needs to get rid of that shadow. The hatchet fish has worked out a clever way of doing this, through the use of a technique called counter illumination.On it's underside there are organs on which bioluminescent bacteria grow. These organs emit light which cancels out their shadow, so that when predators look at the fish from below, they can't make out a silhouette. And the Hatchet fish is camouflaged, by light.
To hunt in the dark depths of the ocean, predators often need very sensitive vision. Using this, they can spot prey in the low light conditions. However, some prey emit a bright flash of luminescence when approached by a predator. The effect of this on the predators eyesight can cause it to hesitate, and in that time, the prey can make good it's escape.
So imagine a predator, perhaps like the deep sea hatchet fish coming across a smooth nylon shrimp. This juicy looking customer would be tasty pickings. Just as the predator approaches, the shrimp sprays out a glowing slurry of bioluminescent bacteria directly in the face of the predator, encompassing it in a glowing cloud. The predator, startled and distracted by the cloud, loses the prey.
The enemy of my enemy is my friend
There is another reason why the smoke screen above is damaging to the predator is that in some cases when prey spray these bioluminescent slurries, they stick to the predator. So the predators camouflage is now compromised. It is now clearly visible to other predators, which will hunt it down. In this way, the prey forms an alliance with a predator further up the food chain to combat a common enemy.
Octopoteuthis is a small bioluminescent squid. It is presumed to be a creature of a nervous disposition, as it literally goes to pieces when its attacked. The bioluminescent tips of its tentacles drop off, and brightly emit light. The predator focuses its attack on these organs, and the squid can make it's getaway with it's remaining limbs.
This attraction some predators have to light in itself can make them vulnerable to attack. You may be familiar with a predator that uses this weakness. The deep sea angler fishes have a long filament on the end of which there is a bioluminescent lure. The angler fish uses this to attract its prey into its gargantuan maw.However, you don't necessarily even need to emit light to take advantage of it. Sperm whales and megamouth sharks are known to have whit colouring around their mouths, which has been speculated as having reflective properties, that make them slightly luminescent. Prey that investigate these sources of light will fall prey to these predators.
Some predators have bioluminescent organs situated near their eyes that act as headlamps. Dragonfishes have red luminescence emitters. The great thing about red emitting light is that it causes the shrimps to fluoresce. In the same way that UV lamps make the lint (and other stains) on your clothes glow, the red light emitted by the dragon fish highlights the shrimp, allowing for a precise attack.
CourtshipBioluminescence can be used by some creatures in elaborate displays to attract mates using elaborate displays.The most famous example of this is the firefly, which emits flashes of light, so that the males and females of the species can find eachother over long distances. The patterns of flashes allow the fireflies to distinguish between different species.
So in summary, bioluminescence has many functions in the natural world. Many of the creatures described above can use their bioluminescence for more than one of the functions described above. the female deep sea angler can use her bioluminescenct lure to attract males. Predators who consume the tips of the octopoteuthis tentacles will unintentionally emit a bioluminescent signal, attracting bigger fishes.And we don't even know the full diversity of interactions in which bioluminescence plays a role. But it is known that based on the diversity of chemical mechanisms for bioluminescence, it evolved on at least 40 separate occasions.
It is because of these complex interactions that even in the depths of the oceans, far from the sun, the light of life shines on.
Next week (work permitting) I hope to delve a little deeper into the evolutionary origins, and the basis for bioluminescence.
Haddock, S., Moline, M., & Case, J. (2010). Bioluminescence in the Sea Annual Review of Marine Science, 2 (1), 443-493 DOI: 10.1146/annurev-marine-120308-081028
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Streptococcus pyogenes (I'll call it strep for short) is one of many pathogenic bacteria which are known to colonise the respiratory tract. as a result it causes the disease known as strep throat, and another known as scarlet fever. If you are lucky, it gets confined to the respiratory tract. However, in some cases Strep can spread to other organs, where it can cause a disease known as necrotizing fasciitis.
How and why it suddenly causes this disease is not known, although there is some evidence that it follows from a bruise or contusion. Current hypotheses state that somehow the damage enables strep to colonise.However, in order for it to colonise these damaged sites, it has to be able to go systemic first without alerting the immune system.To do this, bacteria like strep secrete proteins and other compounds which attack immune cells, and the communication systems immune cells use in order to co-ordinate their response against the bacteria.I am going to talk about one specific protein secreted by strep called "Streptococcus pyogenes Cell Envelope Protease". For short, we'll call it SpyCEP. And I'll show how this one virulence factor can have an extraordinary effect on the immune system.It is known that this protein sits on the cell envelope, and that it can actually be sheared off through an as of yet unknown mechanism. It is also known that it has an active site which cleaves an interleukin. Interleukins are molecules through which immune cells (often referred to as leukocytes) interact with eachother. During the initial stages of infection, when normal cells undergo damage due to the presence of pathogen, they can secrete interleukins. These interleukins act as "help me" signals which recruit phagocytic cells which can engulf the bacteria.
These signals are essential, as the immune system comprises many different cells that perform different functions. Phagocytic cells can engulf and eat bacteria. They can then recruit other cells, such as T and B cells, and shows them the proteins from the offending bacteria, and so allowing these specialist cells to recognize them in the future. The communication between these cells is very important and quite subtle. So when strep enters a host, the best way for it to ensure its own survival is to disrupt this immune communication, especially the initial signals that summon phagocytic cells. This is where SpyCEP comes in.As described before, it acts to cleave interleukins. More specifically, it is known to cleave Interleukin 8, which is specifically known to affect the recruitment of some special phagocytic cells known as neutrophils. In essence, shutting down that initial help signal early on in infection.
Whilst these facts seem to indicate what SpyCEP does during an infection, demonstrating it's effectiveness during an actual infection has been challenging. One of the ways to demonstrate this is to knock out the gene that codes for SpyCEP. In a recent paper, a group has done this for a strain of strep which is known to produce lots of this protein.They then injected these bacteria into mice, and then observed how the infection progressed. it's important to note that mice themselves don't quite have a similar immune system to humans. They have two proteins which perform the same role as interleukin 8, known as KC and MIP-2. Fortunately, spyCEP is able to cleave both of these, and so it's role in mouse infection can be said to be similar to that of humans.What they found when they injected the streptococci that expressed spyCEP and streptococci that didn't express spyCEP, the numbers of phagocytic cells coming to the site of infection was reduced.They also measured the amounts of working KC in the mouse thigh tissue and serum, and found that it was reduced in the strain that expressed spyCEP compared with the the strain that had it knocked out. In short, the strain which produced spyCEP managed to spread to other tissues better than the strain without it, and also produce a more severe infection.However, strep produces a whole variety of different virulence factors. And it is possible that the expression of SpyCEP could help the expression of other virulence factors which are the actual effectors in infection.
To counteract this possible criticism, they took the gene encoding spyCEP, and incorporated it into a "friendly" bacterium. Lactococcus Lactis is a very different bacterium to strep. Lactococcus doesn't cause any human disease. It is used in industry to produce buttermilk and cheese. By all accounts, its quite helpful to humans, and completely harmless.So they placed this virulence gene into lactococcus lactis by adding DNA with the spyCEP gene on it. So this would show the effect of spyCEP without all the other interfering virulence factors expressed by strep. It ended up turning Lactococcus from a friendly bacterium, into a quite unfriendly bacterium.
It was found that when this virulent strain was infected into mice, it was no longer the benign bacterium it was before. Instead of being engulfed, consumed and cleared by neutrophils in quick sharp time, the bacteria not only persists, but causes damage to the surrounding tissues in the same way that strep does. In fact, the expression of this one protein allows the lactococcus to spread to other tissues such as the spleen and the liver. [It should be noted that Lactococcus never at any stage produced an infection as severe as Strep, and also the gene itself is unstable]This is a unique study, in that they demonstrated how the expression of just one protein is necessary to cause a non-pathogenic bacterium into a pathogenic one, and more importantly they were able to demonstrate the importance of this protein as a result.
This shows the importance of spyCEP in infection, and if it's action can be counterracted, it may provide a way of treating this disease.The incorporation of this protein in a vaccine will help alert the immune cells early on in infection, and will allow them to recognise bacteria better, and prevent it from using spyCEP to evade the immune system.
Kurupati, P., Turner, C., Tziona, I., Lawrenson, R., Alam, F., Nohadani, M., Stamp, G., Zinkernagel, A., Nizet, V., Edwards, R., & Sriskandan, S. (2010). Chemokine-cleaving Streptococcus pyogenes protease SpyCEP is necessary and sufficient for bacterial dissemination within soft tissues and the respiratory tract Molecular Microbiology, 76 (6), 1387-1397 DOI: 10.1111/j.1365-2958.2010.07065.x
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Kurupati, P., Turner, C., Tziona, I., Lawrenson, R., Alam, F., Nohadani, M., Stamp, G., Zinkernagel, A., Nizet, V., Edwards, R.... (2010) Chemokine-cleaving Streptococcus pyogenes protease SpyCEP is necessary and sufficient for bacterial dissemination within soft tissues and the respiratory tract. Molecular Microbiology, 76(6), 1387-1397. DOI: 10.1111/j.1365-2958.2010.07065.x
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