We're in serious trouble

We’ve only been able to treat bacterial infections for the past 70 years or so. Other than our natural defences, which will be the subject of my next blog, we had no means to fight off these infections. None of our medicines were effective against bacteria. Then came the discovery and use of penicillin, first widely used by Allied troops during WW2. This discovery led to a class of drugs we refer to as antibiotics and these have revolutionised how we treat disease. Before this, what we see as minor, easily treated infections could often be fatal.

Penicillin and antibiotics were seen as a panacea. Until chinks began to appear in our medical armour. Let me start this with the story of syphilis. That is syphilis the sexually transmitted infection, not Sisyphus, the man from Greek mythology. Apart from sounding similar these two have a lot in common as we shall soon see. Bear with me. Soon after the use of penicillin to treat syphilis in hospitals, doctors noticed a strain of syphilis had emerged that was resistant to treatment by penicillin. The new uber-medicine was not as effective as thought. Now, not all bacteria were as susceptible as when treatment with penicillin was first used. Why? Bacteria reproduce rapidly via binary fission. One becomes two, then four, then eight. Like this. You get the picture. And due to binary fission they are all clones. Except for the occasional, rare, genetic mutant. As we will discover in Unit 4, which is just around the corner, often these mutations lead to death or suboptimal functioning but sometimes the mutation causes the organism to have an advantage. The competitive edge in the case of this bacterium was resistance to penicillin. When hit with a dose that killed all its non-mutant siblings, this bacterium survived. And reproduced passing that trait for resistance on to its daughter cells. And soon a strain had evolved that was resistant to treatment. But here comes the interesting part. While bacteria reproduce asexually, they also perform an incredible evolutionary act, they swap genes in an act called conjunction. Two bacterium can come together and exchange genetic information. It’s like a brunette going up to a red-head and taking a copy of the red-head’s gene for hair colour, while the donating a gene for lactose tolerance. The brunette now expresses the red-hair phenotype and the red head can now tolerate lactose. A resistant bacterium could, did and still does come in contact with non-resistant bacteria and swap genetic information, passing on this gene for resistance. New mutations can rapidly spread throughout populations. The drugs we use became less effective, so we would use a different antibiotic. Successfully at first, then, over time, less so. Hmmmm, a strain now resistant to two treatments. That’s OK, we have another drug...

Then humans come along and start over using and misusing antibiotics. Prescribing antibiotics for viral infections, using them at the wrong dosage level, or not for long enough. Placing antibiotics into the food we give farm animals. How many of you have started a course of antibiotics and not finished them? Every time you do this you are establishing the perfect evolutionary pressures for drug resistance to evolve. And it has. Rapidly. Each year nearly 500,000 cases of multi-drug resistant tuberculosis are diagnosed. Half a million cases that are resistant to all known treatments. 150,000 fatalities occur as a result. According to WHO extensively drug-resistant tuberculosis has been reported in 64 countries to date.
Many articles in the mainstream media refer to the 'superbug NDM-1'. A bacteria that is resistant to all of our medicines. This is pretty scary but it is also wrong. NDM-1 isn't a bacterium, it's a gene. And this gene is readily passed from one species of bacteria to another, through bacterial conjunction termed horizontal gene transfer (the passing of genetic information to an organism that is not a decendant). The media do have it right about one thing though. Bacteria that have the NDM-1 gene are resistant to all treatments we have available.

But it is not just bacteria. Plasmodium, the protozoan that causes malaria, is also developing resistance to many forms of treatment. Areas of Thailand, Burma, Laos and Cambodia now have malaria with resistance to some of the most effective treatments and preventatives. As do other regions in the world.

Anti-viral treatments for disease such as HIV/AIDS have been shown to be losing their efficacy as these viral strains evolve into new types as a direct response to the drug treatment. In a recent article I read, which I have attached, the idea of a world in the not-too-distant future where disease is resistant to our treatments is suggested by WHO. We will potentially be in a situation where ‘minor’ disease become fatal again. Scary shit.

I mentioned a Greek guy at the start with a name similar to a sexually transmitted disease, Sisyphus. Sisyphus was cursed to spend his life pushing a bolder up a hill and just when he would near the top the bolder would roll to the bottom and he would be back where he started. As we look at drug resistant syphilis taking us back to where we were 70 years ago I think syphilis and Sisyphus have more in common than similar sounding names.

http://www.abc.net.au/news/stories/2011/04/07/3185138.htm

UPDATE 15/5:
Todays's RadioTherapy program on 3RRR had an interesting discussion on NDM-1 and other bacterial infections. Listen to it here while studying

Agents of disease - stuff that makes you sick

I hate feeling sick. I’m one of those whingy blokes that always feels worse than symptoms may suggest. Yes, I’m a firm believer in the man-flu.

Disease is a condition an organism has or contracts that causes it to function at a less than optimal level. This disease causes a negative change in an organism’s state of health. Disease can be placed into two broad categories; infectious and non-infectious. An infectious disease is something that can be caught or transmitted, while, by definition a non-infectious disease cannot be transmitted. Non-infectious disease includes things like some cancers and genetic disorders. I will discuss non-infectious genetic disease or disorders during Unit 4. Remember that some cancers can be transmitted and are infectious, such as the Human Papillomavirus (HPV) that can lead to cervical cancer, and this is why it is important for everyone, guys and girls, to have the HPV vaccine. Why guys? What is the point of immunising everyone for this disease except for the carriers?

This rant will focus on agents of disease – the things that make you sick. The term for something that causes an infectious disease is pathogen. These are usually living, such as bacteria, but can be non-living, such as prions. I’m not going to get into the ‘are viruses living or non-living debate’ here.  I believe they are living but that is for another day and another blog. I’m going to divide pathogens up in this blog into micro-organisms, including bacteria, protists and fungi, macro-organisms, such as arthropods, annelids and nematodes, and non-cellular agents that will include viruses, viroids and prions.

Micro-organisms
Bacteria

Bacteria are an amazing group of organisms. The majority of life on this planet is bacterial. It was here before all other life and I believe it will be the last form of life to finally die off on this planet, many billions of years into the future. Bacteria inhabit just about every conceivable niche this planet provides, from kilometres under the surface within rock, to near-boiling hotsprings, in hyper-saline solutions and environments without oxygen, from the Antarctic to inside your gut. Yes, your gut. We are just another habitat for some bacteria, and most of the time we get along in a happy symbiosis. Bacteria is so good at surviving that some astrobiologists have suggested that life on Earth originated from Martian bacteria getting to Earth in a meteor ejected by some Martian supervolcano. While there is no evidence for this - there is no evidence that life once occurred on Mars in the first place - it’s still a cool little theory. The trouble with talking about bacteria as a group is that they’re not a homogenous group. There is more diversity in what we call bacteria than is all other forms of life. In general terms they are divided by shape: spherical cocci, rod-like bacillus, and spiral-shaped spirochaetes. But this is like saying a tall people are in one group, fat people in another and a third group made up by short red-heads. These gross morphological similarities do not necessarily mean they are related. Another way they are categorised is in the composition of the cell wall and how these respond to different types of dyes and stains. Those that can be stained are called Gram Positive, those that can’t Gram Negative. The final way bacteria can be grouped is by gaseous requirements: those that require oxygen (aerobic), those that thrive in the absence of oxygen (anaerobic) and those that don’t really care either way (facultative). It is a huge group that is all clumped together. The one thing that separates them from everything else is they are all prokaryotic. Despite our near pathological fear of bacteria, most bacteria leaves us alone or is beneficial and there are relatively few bacteria that make us ill. I mean there is so much of this stuff everywhere, it’s all over our bodies, the pillows we place our heads on, the utensils we eat with, if bacteria was ‘bad’ we would be in deep, deep trouble. As a rule, bacteria becomes a problem from a human point of view when in colonises a new habitat where it normally does not occur. An example of this may be bacteria entering a cut and forming a colony within the wound, or bacteria that is normally found in the lower intestine getting into the gut, usually by drinking water contaminated by faecal matter. Or not cooking food properly. There is a bacterium called Campylobacter sp that normal occurs in the intestines of chickens and causes them no problems at all. In fact, it is beneficial for chickens. The problem for us occurs in the processing of chooks for meat. Sometimes the meat becomes contaminated and, if you don’t cook your food properly, this bacterium is introduced into your gut. Where it will make you very sick.  So how do these microscopic organisms actually make us sick? One of the key factors is the virulence of the pathogen and how quickly they reproduce. In lay terms virulence refers to how good bacteria is at spreading and making you sick. The more virulent a pathogen is the better it is at making you sick. You need to remember here that bacteria aren’t trying to make you sick, that is not their purpose. They aren’t aware of you as anything other than habitat. Some bacteria make you sick by actively invading and destroying cells. Salmonella typhimurium will do this. We get Salmonella sp from contaminated food, and refer to its effects as food poisoning. It survives the acid of our gut and enters our colon where it destroys the epithelial cells of the intestine causing diarrhoea and vomiting. Another way that bacteria can make us sick is via their waste products. Like all life, bacteria eat and produce wastes. Some of the wastes from some bacteria are toxins and these make us sick and trigger responses in our bodies such as fever. As the bacteria colony grows and multiplies, the amount of toxin produced increases exponentially causing the host to become sick.

Protozoans - amoebas and their friends

In general terms, protozoans such as amoeba make us sick in a similar way to the bacteria previously mentioned. This Kingdom, again extremely diverse, is comprised mainly of single celled eukaryotes. The two examples I will give of disease caused by these protozoans is amoebic dysentery and ciguatera poisoning. Amoebic dysentery is caused by the amoeba Entamoeba histolytica. Humans are the host of this amoeba and it is spread by drinking water or eating food contaminated by the cysts of this protozoan. It is much more common in developing nations. It is nasty, I’ve had it. Many years ago when travelling through Nepal I made the mistake of drinking from a mountain stream high in the Himalaya. The problem was this stream was contaminated by this amoeba. Nepal is a developing country and no matter where you go you will find people up to, and beyond, the snow line. There were no roads where I was, I had walked for days to get there. Needless to say there were no flushing toilets either. Human waste is transported by rain or snow melt into the streams and carry the amoeba cysts with it. And that’s how the cysts got into me. I was luckily back in Kathmandu when the cysts hatched and the amoeba multiplied. It affected me in a similar way to the Salmonella sp mentioned before, eating away at the cells lining my intestine and has the same impact on your body. I lost many kilograms over several days before I was able to crawl into a rickshaw and get to a doctor. Holidays...
To go off on a wee tangent, my favourite species name of all time belongs to an amoebia. It is called Chaos chaos.

Another protozoan that can make you sick is the dinoflagellate Gambierdiscus toxicus, which is responsible for ciguatera poisoning. Dinoflagellates are single celled marine plankton. These are ingested by small fish at the base of the food chain and here, it is not the plankton that causes illness it is the toxins produced by it. These toxins are bioaccumulative and are magnified as they are passed up the food chain; small fish is eaten by big fish which is eaten by bigger fish until you catch yourself a large snapper or coral trout for dinner. You then ingest the toxins – which are heat resistant and not destroyed by cooking and you become sick yourself.

Apicomplexans are another protozoan that causes the disease malaria. I’ll discuss this later when I talk about vectors. Maybe, time and space dependent.

Fungi

I’ve spent too long talking about stuff I wasn’t going to mention so I will keep the last of the micropathogens, fungi, to a short paragraph.  Ringworm, athlete’s foot and thrush are fungal infections they colonise the external surface and digest your dead skin cells. External environment? Thrush? Thrush often occurs in the vagina and the mouth. Technically these are external environments. Vagina, etymologically speaking, means a fold and that’s what a vagina is. It is an envagination of the skins surface. These infections occur when a colonising cell reproduces successfully and produces many thousands of daughter cells. Enough said.

I’ve just looked at the word count and hit 1,500 so I’m going to skip over macro-organisms briefly. I’ll write another short blog about multiple-host life cycles of things like tapeworms tomorrow. Pathogenic macro-organisms are things like pubic lice, ticks, tapeworms... they are varied as are the effects and the impacts. They can be internal or external parasites. I’ll leave the details to your teacher. An interesting note though is that while rates of sexually transmitted bacterial infections such as Chlamydia are rising rapidly in the community, rate of pubic lice infections have decreased. The reason suggested? The popularity of Brazilians.

Non-cellular pathogens

Finally: non-cellular agents of disease. Viruses, viroids and prions. These pathogens are all non-cellular and technically non-living – remember that cells are the smallest independently functioning unit of life. I’m not going to argue that viruses are living here.

Viruses
Viruses are comprised of nucleic acid (DNA or RNA) surrounded by a protein coat. Some of these are further covered in a modified membrane. Smallpox, herpes and warts are examples of DNA viruses, hepatitis, influenza and HIV are examples of RNA viruses. Usually DNA viruses are double stranded but can be single and RNA viruses are single stranded but can be double. Viruses are obligate intracellular parasites. This means they must infect a host cell to reproduce. As they lack ribosomes and other organelles they hijack these in the host cell and force the cell to make viruses. How they do this is pretty cool. They insert their genetic information into the host cell and this interrupts the cells normal functioning. Two things can happen: the genetic information is spliced into the host’s cells genome where it lurks until later OR it forces the cell to make many, many virus particles until the cell eventually undergoes lysis (bursts) spreading these to infect new cells. I’ll use herpes as an example. The common cold sore is caused by the herpes virus. For example, if you kiss someone with a cold sore the virus passes to you where it inserts its information into your lip’s cell’s genome where it lurks. As your lip cells under mitosis and divide, the virus is also copied. This is called a lysogenic cycle. Then as a result of some trigger, your infected cells start producing virus particles, swell and burst. This is the lytic cycle and results in cold sores.

Viruses mutate and evolve regularly and rapidly, changing the markers on the outside of them to confuse your immune system. This is why it is hard to build immunity to some viruses such as influenza. Remember a few years ago we were worried about bird flu and SARS? Viruses can and do mutate and jump species. Fantastic evidence for evolution. It IS evolution.

Viroids are small virus-like pathogens that infect plants. That’s all I’m saying about them.

Prions

And to end this we have prions. Prions are abnormal proteins that change, denature, normal proteins by changing their shape. Eventually this leads to cell lysis which spreads the prions to infect other cells. Prions are usually found in neurons. The most well known prion disease is spongiform encephalitis. This disease causes huge holes in your brain (spongiform) and is commonly known as Mad Cow Disease, the only disease to be named after my ex-wife. This disease became a huge problem in England when infected sheep’s brains were mushed up and fed to cows, and then in turn fed to people. And you thought cows were vegetarians... Other prions disease include Kuru, a disease from PNG that came from eating the brains of dead relatives, and Creutzfeldt-Jakob disease.

Google these for more information. My pizza has arrived and I’m hungry. Hope this helps. Sorry it’s so long.
Watch a couple of these for giggles:
HIV life cycle. Pretty cool 
Bacteria 
Virus 

Pheromones

I remember hearing about a study where a group of women were asked to rank a series of photos of different men according to how attractive they found them. Once this was done, several of the photos around the median were treated with a pheromone from a boar. Not a person who talks in a monotone about the benefits of superannuation, rather, a male pig. The experiment was repeated several times with different groups of women and each time, the pheromone treated photos were ranked as more attractive than they were in the control group. Unfortunately, sitting here on a Saturday night with a beer in my hand, I have no way of checking if this study is true but for a minute let’s believe it is true and valid because I like the story. This study, if true and not an urban myth, seems to indicate that pheromones, an external signalling hormone, can affect the way we perceive another’s reproductive worth. What is even freakier is that pheromones from a pig are attractive to humans!

This shouldn’t be a shock. For years, human females have been applying pheromone extracted from the anal glands of various animals to themselves in an attempt to be found more attractive. This is where musk originated from. However, musk is a male scent originating in the male Musk Deer, and it seems that women apply this scent to themselves because they find it attractive. Why else would you consciously apply an odour to yourself?  Regardless to whether perfumes come from deer, civet or flower sources the idea behind a perfume is to make oneself more attractive by smelling nice.

Pheromones can be extremely powerful. They can cause extreme behavioural responses in incredibly tiny concentrations. Many animals communicate sexual availability via pheromones and more than just availability, their worth as a prospective partner is also assessed by smell. In humans most of this happens on a subconscious level. First let me preface this by saying that visual stimulation is incredibly important. When you see someone across the room who you  find attractive, it is not their scent that is initially appealing. It is their appearance. The limbic brain including the hypothalamus is often referred to as the emotional brain and is the region that is responsible for your libido. Have you ever wondered why when you meet someone you find attractive you can’t seem to hold a conversation and become a giggling idiot? The visual arousal causes dopamine and many other neurohormones to be released from the limbic brain causing you to feel that rush that is hard to explain but all of us have experienced. Pupils dilate, you start getting sweaty armpits and clammy palms and your body language changes – up to 55% of flirtation according to psychologists, is all in the body language.

Now while your brain is causing this rush of hormones in you, your genetic health is being actively assessed by your prospective partner. They may not realise it but they are smelling your genotype. And you are doing this too in return. Human pheromones are also released at this time of attraction. These are found in your sweat. When you find someone attractive on a pheromonal level it is because their smell is different to yours. We want genetic variation in our offspring and we literally sniff this out. We are seeking a partner who has major histocompatibility complex (MHC) genes (these are important in immunity and I will talk about in the next rant when I start disease) that are different from yours. Studies indicate that couples with different MHC markers are more satisfied in their relationships and are more likely to be faithful. Further, they tend to have less fertility issues than couples who have similar MHC markers.

The type of sweat produced in the armpits and groin is different to that produced elsewhere in the body. As well as being rich in pheromones it is thick and oily. And this is why we have hair under our arms and in our groins; it traps this sweat creating a reservoir of pheromones. This is not body odour. Body odour is caused by not washing regularly and bacteria building up and feeding on this oil sweat. It is their waste products that cause the bad smells and have the exact opposite effect of pheromones!

The genetic compatibility, which is actually genetic difference, that we are seeking in a partner (actually we are seeking this difference in the other parent of our child and often a male partner did not contribute to the genetic make up of the child it helps raise as its own – serious shit. Will rave about this in Unit 4) can be masked causing us to be attracted to a partner we actually aren’t attracted to. Huh? Let me explain. Studies suggest that women who take the oral contraceptive pill have their pheromonal responses skewed. Instead of being attracted to someone with different MHC markers, they are attracted to someone who has a similar MHC odour to themselves. Things move along well until it comes time to have a child. The woman stops taking the pill and, after a bit of time, starts looking at her partner differently, hormonally speaking. And these couples, statistically, are more likely to be unhappy in their relationships, have affairs and have fertility issues.

Actually, an interesting aside, studies have indicated that woman are attracted to different ‘types’ of males depending on where they are in their menstrual cycle. Again, hormones, and again, something I need to look up.

Let’s leave humans for a few brief paragraphs but still stick with sex. In the animal kingdom, pheromones are also used for reproductive purposes. Most of this is common knowledge and is found in all textbooks so I’m only going to talk about finding a mate and I’m going to give to insect examples. A male moth can and does respond to the pheromones of a female from kilometres away. In fact the male silkworm moth can detect a female from 11 kilometres away. I don’t know if there are others who can detect pheromones from greater distances, there most likely is, this statistic just sticks in my head. When they detect a pheromome they fly into the wind and locate the female by small, ever increasing responses of pheromones hitting those receptors on their antenna . And eventually they find the female. Let’s just hope there wasn’t another male moth closer as their mating rituals aren’t quiet as intricate as human systems. Nor are they as fussy. But what I want you to consider is just how much pheromone a female moth can produce – they’re not that big – and how powerful these molecules must be. They have such a major impact in such small quantities.

Wasps also use pheromones to find a mate. Again it is the female releasing the pheromone and the male responding. It works really well over long distances as we saw in the moth example, however, other organisms have managed to use these pheromones against the wasp. These organisms are orchids. Yep, those beautiful flowering plants. Not all orchids but some also use pheromones to have sex, however, they use wasp pheromones. When these orchards are ready to be pollinated they release a pheromone that is remarkably similar to those produced in certain wasps. Male wasps are attracted to the flowers that smell like female wasps and superficially resemble a female wasp. The wasps then try unsuccessfully to mate with the flower. In the attempt the orchid’s pollen sacs are attached to the back of the wasp. Finally the wasp gives up and flies off to find another female. Often this female is another orchid and the pollen is transferred, the plant fertilised and the male wasp remains frustrated.

So pheromones are hormones that work externally and communicate information between members of the same species. Often, the information communicated is about sex. It can also be used to communicate location of food, threats to the colony or territorial boundaries but these are relatively straight forward in concept and are easily understood by reading your textbook.

And to that woman who I am psychologically and genetically attracted to; sorry, I don’t mean to blabber, it’s my pheromones reacting to yours. Makes it sound so romantic doesn’t it?

A rave about hormones

Hormones don’t really do much themselves but the effects of hormones on an organism is huge. Hormones are signalling molecules. They tell a cell or group of cells it is time to do something. That’s it. They simply carry a message. Once that message is received though, the effects can be staggering. This is called signal transduction.
Homeostasis and negative feedback

Hormones are one of the mechanisms humans and other animals use to maintain homeostasis, the other being the nervous system. They are also used to initiate change such as growth and reproductive maturity. There is a narrow range that most variables within the body, such as pH of your blood and your body’s temperature, need to be kept within.  Think of enzymes. Remember them? Little worker proteins that catalyse the chemical reactions that occur inside you. What happens to them when they get too hot, or placed in a solution too acidic? They denature, change shape and stop working and you end up feeling pretty shitty at best, dying at worst. The primary mechanism that the body uses to keep things in this narrow range is called the negative feedback system. Positive feedback, while uncommon, is also used but I’m not going to go into that here. Negative feedback is often made to sound incredibly complex, and, while the body’s biochemical pathways can be very complicated, negative feedback is actually a very simple concept. Imaging you are driving, car is flying along the road and you decide to take your hands off the wheel and put them on your head. You continue driving with hands on your head and all of a sudden the car hits the gutter. This is the stimulus, if you don’t do something you’ll crash. You respond by quickly grabbing the wheel and steering the car back into your lane. And then you put your hands back on your head. And after a while the car swerves into the oncoming traffic. And you respond again to avoid crashing. This is how the body drives itself- with its hands on its head! It waits until something goes wrong and then responds. It waits until one of the many variables it is monitoring moves out of a given range, then responds to return it to within those narrow limits. Bad way to drive but seems to work in animals.
Hormones, receptors and signal transduction

You should know by now that, hormones are produced by the endocrine system and, generally, are released into the blood stream. It takes about a minute for your blood to do a lap of your body – pretty quick really when you consider the length of all those arteries, arterioles, capillaries, venuoles and veins. There are two main types of hormones: peptide (protein) and steroid (lipid). This is where you really need to recall hydrophilic and hydrophobic molecules and movements in and out of membranes. Peptide hormones are hydrophilic. Stop here and think: how will this hormone respond when secreted into blood and what will happen when it gets to the cell membrane? While you’re thinking about that, I want you to also recall how important shape is to all the biomolecules you’ve studied so far. Shape is extremely important for hormones and will continue to be important as you look at disease. You may release a hormone from one of your glands and want it to trigger a response in the testes or ovaries. How does the hormone make these cells/organs respond but leave others, say the pancreas, alone? Again it is shape. The cells that the hormone is trying to get a response from are called Target Cells, and these target cells have shape-specific receptors for these particular hormone. And they would most likely have other receptors for other hormones as well. When the right hormone connects with the receptor of the target cell a response is triggered.

Let’s get back to that question I posed a while back. A protein hormone is hydrophilic and is readily carried in the blood around the body until it reaches the target cell. As a hydrophilic molecule it is lipophobic and therefore has issues crossing the cell membrane. So the receptors for protein-based hormones are on the outside of the cell membrane. Steroid hormones, being lipid-based, are hydrophobic and need carrier proteins to help them get around, however, they easily pass through the cell membrane and the signal receptor for them is on the inside of the cell membrane. The triggering of a hormone receptor and the response it causes within a cell is referred to as signal transduction. A signal transduction pathway includes the activation of a receptor by a hormone and the series of responses it causes within the cell. This is often referred to as a cascade effect, like sneezing in the alps and triggering an avalanche. The response seems disproportionate to the stimulus. For the cell to do whatever it needs to do once stimulated by the hormone there are usually a series of steps that are amplified at each stage causing a tsunami of biochemical reactions, each one having a greater impact until the final produce molecule is synthesised or whatever was supposed to happen, happens.

Avalanche? Tsunami?  Time to move on...

Ever wondered how these molecules are removed from the blood? In a nutshell they are broken down, filtered from the blood by the kidneys and peed away. Read your textbook.
Plant hormones and tropisms

Plants also use hormones to regulate themselves and to maintain homeostasis. As they lack a nervous system, they rely on their hormonal system. One would intuitively think that by relying on this system alone, plants would have developed an intricate and complex system of hormones. They have but they only use five of them. (Six if you want to include florigen, the hormone that no one has ever found but some botanists argue must be there). They work by combination and concentration: how much of them there is and what other hormones are with them. They are transported in the phloem and also diffuse through and around cells and are responsible for everything a plant does, from bending toward the light to flowering. I’m going to rant a little about tropisms in plants, then flowering and the importance of environment in the synthesis of hormones in plants. These five hormones and their general impact on a plant would be a good think for a Yr12 student to learn, they are in all textbooks and I’m not getting into them here.

Tropisms in plants are responses in plants to certain stimuli and auxin is a very important hormone in these responses. The three main tropisms that are covered in this course are phototropism (a response to light), gravitropism (a response to gravity) and thigmotropism (a response to touch) and they way they work is relatively simple in concept, the particulars though are quite complicated but unnecessary to discuss at Yr12. Phototropism is a plants response to light. It is usually positive in that a plant will bend and grown toward the light. This occurs by auxin in the growing stem diffusing away from cells in the light and building up in concentration in the cells that are more shaded. Once in these cells they cause them to elongate. These cells grow longer taking up more area and bending the plant toward the light. What actual causes the hormone to move though? The light triggers the response however, what actually causes the auxin to move... I can’t remember. I’ll get back to this later. Gravitropism is similar. If a shoot is on its side gravity causes auxin to move to the underside, causing these cells to elongate and the shoot growing up. Gravitropism also occurs in the roots but works in the opposite way, causing the roots to grow down. I won’t go into thigmotropism but will say that this is a response to touch. It’s what causes pea to wrap those spring-like shoot around branches to give the plant support, or causes a plant to move away when crowded. Don’t worry about this too much.
Environmental stimulation of hormone production

Hormones in plants are often stimulated into production by environmental factors such as light. The example I’m going to give comes from a conversation I had many years ago in Nepal with a Dutch guy. We were sitting in a cafe looking out at a vacant block of land that was covered in wild marijuana plants. This dude started telling me how he grew marijuana hydroponically in Holland. Apparently, the parts of marijuana that drug addicts and malcontents smoke are the flowers. He told me that light prevents these plants from producing flowers and they need at least 10 hours of darkness to allow the build up of the hormone that triggers flowering. If they are exposed to any light during this dark period, the flowering hormone isn’t produced. He was telling me that he had several plants growing in a cupboard and all but on were flowering successfully. He worked out that the one plant that wasn’t flowering was getting a little bit of light through a crack on a couple of leaves. As hormones are transported around the plants even the parts of this plant that were receiving uninterrupted darkness weren’t flowering as the hormones move throughout the plant. Drugs are bad. This is just an example.
Pheromones: external communication hormones

Finally, I’m going to return to animals and pheromones. These are an interesting group of hormones as they work externally and impact primarily behaviour. They are used to communicate and the information is usually species specific. They can communicate territory. This is why dogs pee on poles. They are marking their area with their pheromones. They can communicate a food source. This is why ants will follow a trail. They are following a trail of pheromones laid down by the ants that found the food. And most importantly they can communicate sexual availability. For example a female dog in heat will attract male dogs from all around as they smell her pheromones. Male moths can smell a female moth from kilometres away. That’s how sensitive they are. I’ve got heaps to say about pheromones but I’m going to stop here. That’s about all you need to know. It’s late and I’m tired. I'll type some more about pheromones tomorrow.