I want you to take a deep breath. Have you done it? Good. You just breathed in about half a litre of air. It is possible to capture the liquid in your breath by cooling it down – a bit like when you breathe on a cold mirror. If you do this, over one minute you can recover 100 microlitres of fluid (about the size of a lentil).
If you then grow what you recover from that fluid you get between 100 and 10,000 bacteria, 5,000 viruses and one or two fungi. Every time we breathe, we inhale a cocktail of potential pathogens. And we inhale about 20 times a minute, nearly 30,000 times a day, sucking in 15,000 litres of air.
The world through which we move is awash with potential pathogens. They are not just in the air we breathe; they are in the water we drink, on the lettuce we eat and in the soil on which we stand. And we don’t just find microorganisms in the external environment; they are on and in us.
Our skin plays host to thousands of bugs and our guts are packed full of bacteria – by some ways of counting there are more cells of bacteria in your body than there are cells of you (more of which later). We very much live in a microbial world. Most of them either ignore our existence or live side by side in perfect harmony. But all of the pathogenic micro- organisms – the infections – are just waiting for an in.
Most remarkably, it can take fewer than ten actual viruses to infect you. A virus is 100 nm in diameter, which means that in a sugar cube made of virus there would be about 1,000,000,000,000,000 viruses, enough to infect every single person on the planet one hundred thousand times. It was estimated that if you had collected all of the SARS viruses from all of the infected people at the peak of the pandemic, they would not even have filled a Coke can.
Which leads us to the big question: why don’t we get sick all the time?
It might seem obvious, but you can’t get infected with a pathogen if you never come across it. None of us will ever get smallpox, because of its complete eradication from the globe. There are regional variations in pathogen exposure and these can be determined by a range of factors. For example, you cannot catch a vector-borne pathogen if there are no vectors where you live, so you cannot catch malaria in the UK because the Anopheles mosquito is no longer native to the UK.
Other pathogens are limited to certain countries, either due to deliberate efforts to eradicate them or because of interventions to reduce their prevalence. Clean water removes the likelihood of exposure to a range of gut (also called enteric) pathogens such as cholera and typhoid.
The weather also has an impact: for reasons we don’t completely understand, some pathogens are much more common in the winter than in the summer. For example, influenza virus, which has a predictable seasonal pattern in the UK – between October and March. Peak influenza routinely falls between weeks 48 and 52 (ie December) each year because air temperature affects the seasonality of influenza.
In warmer temperatures the droplets evaporate quicker, increasing the concentration of chemicals in the drop, like spilled Coca-Cola getting stickier if left. This increase in concentration alters the acidity of the droplet, which in turn affects how the virus gets into our cells. In the cooler winter months, the droplets that spread the virus are more stable.
The amount of sunlight also contributes to seasonality. The sun can protect us directly, its UV rays killing viruses, and also indirectly, as more sunlight means more vitamin D, which plays an important role in our immune response. Changes in social behaviour also contribute to seasonality – in winter we are more likely to be inside; especially children, who are a key vector for viral spread. Parents of nursery age children will be painfully aware of this.
The winter flu season is only a feature of temperate climates – countries in the tropics don’t have a winter flu season, because they don’t have winter. There are two rather than four seasons in tropical countries: dry and wet. The patterns of influenza are not as well characterised in these countries, but where measured influenza tends to occur more in the wet season.
For many pathogens, social contacts are required for spread – plagues emerged only when humanity settled down into larger communities. The most likely place to get an infection is at home and the second most likely place is at work. Basically, anywhere you spend a lot of time in close proximity with someone else: in the UK, Covid-19 clusters in homes with larger multigenerational families.
Frequency of exposure is also important. If there is a set risk of getting a disease each time you encounter it, then the more times you are exposed to it the more likely you are to catch it. If you do something often enough, rare events will eventually happen. The risk of infection can be quantified as a function of the number of contacts between an infected person and a susceptible person, the length of time they spend together and the likelihood of transmission each time they make contact.
There is, however, an element of chance to who will get sick. But because we are scientists and it doesn’t sound great to say the reason you got infected is down to shitty luck, we dissemble and use the word stochastic. This causes some eyebrow raising but unfortunately biology is messy, even when we know a lot about the virus: in the case of newly emerged pandemics, we know even less.
Of course, exposure isn’t everything. Some people can be repeatedly exposed to a pathogen and never get infected; for example, a group of around 140 sex workers in Nairobi remained uninfected with HIV despite frequent exposure to the virus. Critically, there is a difference between infection and disease. The outcome of what happens once a pathogen gets into the body will depend upon the person infected and is determined by a combination of dose, genes, sex, age, behaviour and underlying conditions.
Much of whether exposure to a pathogen leads to infection and disease will come down to the dose. Going back to the root of the word virus, viruses do behave a bit like a poison: the more you get, the sicker you get. If you stand two metres away from someone infected with SARS-CoV-2 while wearing a mask, you will get a much lower dose than if you stand next to them and they cough in your face.
Fundamentally, the pathogen must enter the body to cause an infection. This most frequently happens at the interfaces between us and our environment: the lungs, the guts, the genito-urinary tract and the skin. Transmission can happen directly through contacts (eg kissing) and droplets (eg sneezing) or indirectly from a contaminated surface (beware the infected lettuce leaf) or via a vector (mosquitoes, again).
Luckily, we possess a whole arsenal of host defences that stop pathogens getting into our bodies. Understanding these defences and how we can augment them underpins our successes in controlling pathogens, particularly through vaccination.
As a card-carrying immunologist, I would like to claim that the sole reason we don’t get infections is because of our immune system. This would be entirely out of self-interest: the more important your subject sounds, the more money you can wring from the government! But the immune system is really the last resort – activating it comes with some risk of damage to your body.
Many non-communicable diseases are caused by your immune system going rogue – including allergy, arthritis, asthma, Crohn’s, diabetes, Lupus and multiple sclerosis. These are often described as autoimmune conditions, because the body attacks itself. There is a Yin and Yang balance: not enough immunity get infections; too much immunity get arthritis.
This is clearly a massive simplification, but the idea that you should boost your immune system with supplements, however much they smell like Gwyneth Paltrow’s vagina, is as unwise as it is impossible. Even if you could boost your immunity, you are just as likely to boost the damaging aspect as the protective one.
So, before we take the plunge and activate our immune system, we use other lines of defence. The first of these is behavioural. One of our most deep-seated behaviours is disgust. It is so deeply ingrained that you don’t even physically need to see a disgusting thing to be disgusted.
Let’s try, shall we?
What’s the most unpleasant thing you can think of? Now imagine eating it. Would you want to? Hopefully not. And in not eating whatever monstrosity the dark places of your mind came up with you have stopped yourself getting infected. We find spit, sick and snot disgusting because they are all associated with disease. Not going near them reduces our risk of infection. Some of this is learned behaviour; children get so many colds because they haven’t yet learned that eating boogers is wrong.
Our disgust instinct can only go so far to protect us. Sadly for us, not all pathogens have an obvious calling card and they may even pass between people before symptoms develop.
Excerpted with permission from Infectious: Pathogens And How We Fight Them, John S Tregoning, Simon & Schuster India.
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