In her mother’s shadow: Irène Joliot-Curie

This post is a bit of a departure from previous posts on this blog. It’s the first of a series of posts in which I will be exploring the lives, and contributions to science, of a variety of different people. In particular, I will be writing about scientists who are perhaps not as well recognised as they should be; who are controversial; whose demise occurred before they could realise their potential; or who were just downright quirky. As today is International Women’s Day, I will talk about a woman whose contribution to science was immense, but has been eclipsed by that of her mother.

Think of radioactivity and one name will almost certainly spring to mind: that of Marie Skłodowska Curie. Marie Curie is famous as the discoverer of radium and polonium. She was not only the first woman to win a Nobel Prize, she remains the only person of any gender to have won two for different disciplines: physics and chemistry. This post will explore the life of another female scientist who is less well known, but just as deserving of recognition: Marie’s older daughter, Irène Joliot-Curie. Not only did Irène make some very significant scientific discoveries, she was politically active, being both a pacifist and feminist.

Marie Curie with Irène and Ève in 1905

Irène was born in Paris in 1897 and her earliest years were not always easy. Her parents Marie and Pierre were absorbed in their work, putting in long hours on the research that would win them the 1903 Nobel Prize for Physics alongside Henri Becquerel. In these early years, Irène, and later her sister Ève, were largely raised by their paternal grandfather, retired doctor Eugene Curie. He taught Irène to love nature and the arts, particularly poetry, and also got her interested in radical politics. Marie herself acknowledged the difficulty of balancing work and family, writing that,

“I have frequently been questioned, especially by women, of how I could reconcile family life with a scientific career. Well, it has not been easy.”

By the time Irène was born, the health of her father, Pierre Curie, was declining rapidly, almost certainly due to his exposure to large doses of radiation. He was killed in 1906 when he was hit by a horse-drawn vehicle in a Paris street. This has been attributed to his having been distracted by thinking about his work, but it is highly probable that radiation exposure contributed. Cognitive impairment and fatigue are common in conditions associated with high radiation exposure, such as leukaemia and aplastic anaemia.

Marie was devastated by Pierre’s death, and struggled more than ever to balance her scientific work with the demands of bringing up two young children (Ève was only 16 months old when Pierre died). However, after Pierre’s death, Marie made the decision to spend more time with her children. She withdrew Irène from public school to educate her in a ‘co-operative’ organised by a group of 6 professors, including Marie, who taught each other’s children in their areas of expertise. In this way, Marie was able to nurture Irène’s love of, and obvious talent for, mathematics and science, and the two grew increasingly close. Marie was a demanding teacher though; even on holiday, Irène was expected to study for a certain amount of time each day.

The education that Irène received at the co-operative was not restricted to mathematics and science. On the contrary, it was wide ranging and included arts and languages; there was also considerable emphasis on self-expression and play. It is tempting to believe that Irène was forced into a life of science by her mother, but this was not the case, as is shown by her sister Ève. Ève did not have a scientific bent but preferred the humanities, and Marie supported her wholeheartedly. Ève would go on to have a distinguished career as a journalist and political activist, eventually living to the age of 102. Ève was just as close to her mother as Irène, and both sisters together nursed Marie through her final illness.

For the final two years of high school, Irène returned to a more conventional education, studying at the College Sevigne in Paris. In 1914, she took up a place at the Sorbonne to study mathematics and physics. However, like many young people at the time, her education was to be interrupted by the outbreak of World War 1 in August 1914.

Irène and Marie Curie in an X-ray unit at a hospital in Belgium, 1915

From the very outset of the war, Marie Curie recognised a need for radiography services to be provided as close to the Front as possible, to aid surgeons in operating quickly on wounded soldiers. Her first mobile radiography unit was operational in 1914, and she was appointed director of radiology services for the Red Cross. Irène assisted her mother when she could, taking a nursing course alongside her other studies. In 1916, Irène left the Sorbonne in order to work alongside Marie as a full time nurse-radiographer.

Within a few months, 19-year-old Irène was in sole charge of a battlefield radiography centre in Belgium. She taught herself how to maintain and repair the equipment, and she taught doctors how to locate bullets and shrapnel using X-rays. Irène worked in a number of locations, including Ypres and Amiens. Marie and Irène’s work in developing the use of medical X-rays saved the lives of many soldiers, and also helped to significantly advance the uses of medical radiography.

Irène descending from a mobile X-ray car. These were known to French troops as ‘Petits Curies’

Following the end of the war, Irène returned to the Sorbonne and completed her degree in maths and physics, before moving to the Radium Institute to work once again as her mother’s assistant. In 1925 she completed her doctoral thesis on the radioactive properties of the element polonium.

Irène was an expert in the highly specialised and precise techniques required to study radiation. So much so that in 1924 she was asked by Marie to train a newly appointed researcher at the Institute: chemical engineer Frederic Joliot. Irène and Frederic were married in 1926 and took the surname Joliot-Curie. Irène and Frederic combined their research efforts, just as Marie and Pierre Curie had before them, specialising in the study of atomic structure. Their early work identified the existence of both the neutron and the positron; however, they did not recognise the significance of their results, so the discoveries of both are credited to other scientists.

Irène at the Radium Institute in 1922

Irène and Frederic struggled to get some of their early work accepted by the scientific community. They carried out experiments involving bombarding aluminium with alpha radiation, and their results showed that a proton can change into a neutron by emitting a positron (similar to an electron, but with a positive instead of a negative electrical charge). However, when they tried to present their findings to the wider scientific community, they came in for extensive criticism.

Irène and Frederic at work

It was this early work that led to the discovery that would gain them recognition, and a Nobel Prize. Continuing their experiments with aluminium and alpha particles, they found that if a non-radioactive element is irradiated alpha particles, it is possible to turn it into a different, radioactive one.

How does this work? An alpha particle consists of two protons and two neutrons – it’s basically a helium nucleus without the electrons. If an alpha particle collides with an atomic nucleus with the right amount of energy, it will combine with the nucleus. Aluminium has 13 protons and 14 neutrons. When an alpha particle collides with an aluminium nucleus, two protons and one neutron combine with the nucleus, giving 15 protons and 15 neutrons. If you change the number of protons in a nucleus, you get a different element – in this case, phosphorous. Irène and Frederic had finally achieved what the medieval alchemists never could: changing one element into another.

More importantly, the phosphorous they made by this method was radioactive. The reason for this is that phosphorous normally has 16 neutrons, and the phosphorous made by Irène and Frederic only had 15. Atoms with the same number of protons but different numbers of neutrons are called isotopes, and the only stable isotope of phosphorous has 16 neutrons. The isotope made by Irène and Frederic quickly decayed into a more stable form, changing into the element silicon and emitting radiation in the form of beta particles. Using the same method, Irène and Frederic were able to create several other artificial radioactive isotopes.

The importance of the discovery of artificial radioactivity cannot be over-emphasised. The use of radioactive isotopes in medicine was growing rapidly, and Irène and Frederic’s discovery meant that radioactive materials could be created cheaply and in large quantities. Many of the radioactive isotopes used in modern medicine are manufactured using their method, although usually a beam of neutrons is used rather than alpha particles. For example, cobalt-60, which is used in radiotherapy to treat cancer, is made by bombarding stable cobalt-59 with neutrons.

Irène and Frederic in 1935, shortly before being awarded the Nobel Prize for Chemistry

In 1935, Irène and Frederic were awarded the Nobel Prize for Chemistry, and finally gained the recognition of the scientific community. Irène was also given a professorship in the faculty of science at the Sorbonne. Over the next few years, she and Frederic led research into the element radium which led in 1938 to the discovery of nuclear fission by a group of German scientists.

Throughout the 1930s, Irène and Frederic were aware of, and concerned by, the growth of fascism; during the Spanish Civil War they were strong supporters of the Republican faction. In the late 1930s they stopped publishing their work due to concerns about its possible military uses. In October 1938, they placed all documents relating to their work in a secure vault at the French Academy of Sciences, where it remained until 1948.

In 1941, Irène contracted tuberculosis and was forced to leave France and go to a sanatorium in Switzerland. Her husband and children remained in France, where Frederic became an active member of the resistance. Despite the danger, Irène made several trips back to France to visit her family, and on several occasions was detained by German guards at the Swiss border. In 1943 Irène returned to France, but it was becoming more and more dangerous. In early 1944, Irène returned to Switzerland, this time taking their two children, Helene and Pierre. They remained there for several months, not knowing whether Frederic, who had stayed behind to continue his work with the resistance, was alive or dead. Eventually, the family were reunited in September 1944 when the liberation of Paris made it safe for Irène and the children to return.

After the war, Irène followed in her mother’s footsteps by being appointed director of the Radium Institute. Irène and Frederic both turned their attention to the use of nuclear fission to generate electricity, becoming respectively the commissioner and director of the newly formed French Atomic Agency Commission. Under their direction, the first French nuclear reactor was created in 1948, and was able to generate five kilowatts of power. A long-lasting legacy of the Joliot-Curies is France’s extensive use of nuclear power, which generates approximately 80% of the country’s electricity.

Irène at the controls of the first French nuclear reactor

Irène was a passionate and active member of the feminist movement, who campaigned throughout her life for women in science to get the recognition they deserve. The French Academy of Sciences would not admit women, and she confronted this chauvinism head-on, writing letter after letter of application. She knew that she would be turned down, but felt it her duty to draw attention to their refusal to admit her because she was a woman. Irène used her position and influence to promote education for women, and she served on the National Committee of the Union of French Women. In 1936, she was appointed to a powerful political position as Undersecretary of State for Scientific Research by the French government – ironic, considering that at the time, women could not vote.

Irène with close family friend and fellow pacifist Albert Einstein on the steps of his home in Princeton, NJ, 1948

Irène was also a devoted pacifist. She knew that the discoveries she and Frederic had made could be put to military use, hence their decision to hide their research at the start of WW2. Her bout of TB in 1941 may have been a blessing in disguise; neither side could try to recruit her for their nuclear weapons programs because she was simply too ill. By contrast, her mother’s close friend Albert Einstein was coerced into signing a letter endorsing the Manhattan Project, which he would regret for the rest of his life. In 1948, Irène was an active member of the French delegation to the World Congress of Intellectuals for Peace, and she continued to campaign for peace throughout her life.

Irène would follow in her mother’s footsteps in one last, tragic way. In the early 1950s her health began to decline and she was diagnosed with leukemia. It is highly likely that this was a result of years of exposure to radiation, just as Marie’s death from aplastic anemia had been. Much of Irène’s work had been with one of the most dangerous radioactive isotopes to human health: polonium-210. Polonium-210 is approximately 250,000 times more toxic than hydrogen cyanide, and was famously used in 2006 to kill Russian dissident Alexander Litvinenko. In 1948, Irène was exposed to polonium-210 when a container of it exploded on her laboratory bench; there is speculation that this caused her eventual death.

Irène underwent surgery and treatment with antibiotics to alleviate her condition, and continued to work as much as she could; in 1955, just months before her death, she was working on plans for new physics labs at the University d’Orsay. Her condition continued to deteriorate and on March 17, 1956, she died in hospital in Paris. Frederic did not outlive her by much; he died in 1958 from liver disease, also linked to radiation exposure. After her death, Irène’s family made sure that her principals of atheism and pacifism were upheld. When the French government asked to hold a national funeral in her honour, they insisted that the religious and military portions be omitted. Perhaps a bigger tribute to them both is that they made the use of radioactive isotopes in medical imaging and radiotherapy both practical and affordable. Who knows how many lives their discoveries have saved?


Ten pathogens which really scare me

The saddest aspect of life right now is that science gathers knowledge faster than society gathers wisdom – Isaac Asimov

In February 2020, when I originally wrote this post, I stated that:

“there’s a bit of a health panic going on (understatement!).  Masks are selling out, and I’ve just seen a post on social media from someone who had to visit five different stores in order to find hand-gel.  But how scared should we really be of coronavirus COVID-19?  As far as I’m concerned, there are plenty of candidates more deserving of our fear and respect.  Here, in no particular order, are nine of the worst.”

It’s now nearly 2 years since I originally wrote this blog post, and a year since I last revisited it. a lot has happened in that time.  When I initially wrote this post, COVID didn’t come close to making the list, because at the time, we still thought that quarantine and contact tracing would contain it.  The SARS outbreak of 2002, and the 2009 H1N1 swine flu pandemic had lulled us into a false sense of security. Now it’s February 2022 and there are encouraging signs that we are finally coming out of the pandemic. I’ll post on that later. Meanwhile, in no particular order, here are my scariest pathogens.

Helper T-cell infected with HIV


The human immunodeficiency virus (HIV) attacks the very cells that are meant to defend the body against it.  It attacks cells which have the CD4 protein on their surface; these include helper T-cells which play a vital role in the immune system.  Over time, the number of circulating helper T-cells decreases; when it drops below a certain level, the immune system effectively fails to function and the patient develops Acquired Immune Deficiency System (AIDS).  AIDS has a high mortality rate since patients are unable to fight off serious infections.

But HIV has been conquered, right?  Better awareness of the risks of unprotected sex; availability of condoms; provision of clean needles for IV drug users; all of these have helped to slow the spread of the infection.  Effective anti-retroviral drugs (ARVs) mean that the disease can now be regarded as chronic; it rarely, if ever, progresses to AIDS.

Well, all of the above apply in developed, Western countries.  In the developing world it’s a different story.  Condoms are not always widely available, and in certain cultures or religions, their use is forbidden.  ARVs are also not necessarily available.  In some countries there is denial that HIV is what causes AIDS, meaning that governments refuse to provide access to treatment – this was the case for many years in South Africa.

But in the West we are OK, right?  Wrong.  HIV is a retrovirus, which means it writes its own DNA into that of infected cells.  This means that it can never actually be eliminated from the body, and those infected must take ARVs throughout their lifetime.  HIV also mutates rapidly, meaning that it develops resistance; new ARVs must be constantly developed to keep ahead of it.  The fact that HIV continues to spread rapidly and go untreated helps it to keep mutating.  How long can the drug developers keep ahead of it?


Climate change means that currently malaria-free countries may develop conditions that allow the mosquito to breed

Malaria is caused by a plasmodium, a single-celled parasite spread through mosquito bites.  According to the World Health Organisation (WHO), in 2018 there were approximately 228 million cases of malaria, with around 405,000 deaths.  Malaria has a significant economic impact on countries where it is prevalent due to the cost of healthcare, loss of working days due to illness, and loss of worker productivity due to long-term effects.

The comparatively low death rate is due to the availability of effective anti-malarial drugs.  However, malaria is becoming increasingly resistant to anti-malarial drugs, particularly in south-east Asia (Laos, Cambodia and Vietnam) where strains are emerging that are resistant to all currently available treatments.  The development of resistant strains is partly due to the fact that organised criminal gangs in some countries are selling sub-standard or counterfeit drugs; these can only be detected using complex laboratory analysis.

A big problem with malaria is that there is no profit to be made from it.  Developing new drugs is expensive, and the countries where malaria is prevalent cannot afford to pay the kind of prices big pharmaceutical companies want to charge in order to make a profit.  Big pharma are not going to spend millions on developing a new anti-malarial just to make a loss on it, especially if the development of resistance means that after a few years, the drug will be ineffective.  So, most of the research into new malaria treatments relies on subsidies from governments, NGOs and charitable donations.  For example, one of the newest and most effective anti-malarials made it into clinical use because a partnership with the WHO meant that the manufacturing company could sell it at an affordable price and still make a profit.  Fair play to the company concerned though, they did front up a significant amount of money in developing the drug.  For the most part though, big pharma are putting their money into those diseases where there is most money to be made, such as cancer, diabetes and cardiovascular disease. 

Lack of investment has also impeded development of an effective vaccine against malaria.  A vaccine is currently undergoing pilot trials, but as yet there is no data as to how effective it is.  Another problem with malaria is that unlike viral or bacterial infections, a patient who has had the disease and recovered does not develop immunity straight away.  In fact, it takes multiple attacks of the disease for immunity to build up.

So, why does malaria worry me?  Two words: climate change.  The reason we don’t have malaria in the UK is that the conditions here are not suitable for the mosquitos which carry the parasite.  Historically, malaria was actually very common in Europe and North America.  In ancient Roman times, it was so prevalent in the city of Rome that it was known as ‘Roman Fever’.  Climate change means that climates are warming up.  Increasing incidents of flooding leave behind pools of standing water which may take a long time to drain away, providing a potential breeding ground for the malaria mosquito.  As westerners, our neglect of malaria in favour of diseases which are more profitable or more likely to affect us may be about to turn around and bite us (pun intended).


Weaponisation is always a good indicator that a pathogen is scary.  Plague is a highly infectious disease caused by the bacterium Yersinia pestis.  Without treatment it has a high fatality rate.  What makes plague particularly scary is the wide range of transmission routes.  It is transmitted through airborne droplets; direct contact; indirect contact (e.g. with a contaminated surface); droplets from coughs or sneezes; contaminated food or water; faeces; and it is also transmitted by infected animals such as rats or fleas.  Just about the only one missing from the list is sex, but I think that is because we can safely assume that if you get close enough to someone with plague to have sex with them, you are going to catch it.

Plague has a long history as a biological weapon.  In ancient China, there are accounts of infected horse and cow carcasses being used to contaminate enemy water supplies.  In medieval siege warfare, infected animal carcasses and even human corpses would be catapulted into enemy cities to infect the inhabitants.  Some researchers speculate that this is how the Black Death first began to spread through Europe.

More recently, the Japanese used plague as a bioweapon in World War 2.  The notorious Unit 731 developed bombs containing infected mice and fleas and used them against the Chinese in the city of Changde, contaminating the city and a wide area around it.  They also carried out hideous experiments on prisoners to test the effectiveness of these weapons.

After WW2, both the US and USSR developed biological weapons based on plague, including strains which had been genetically engineered to create antibiotic resistance, and strains which had been combined with other bacteria such as diphtheria.  Following the break-up of the USSR, it is possible that there are stocks of bio-weapons that are unaccounted for, and that could potentially fall into the wrong hands.

Still, shouldn’t be a problem because there’s a vaccine, and plague can be treated with antibiotics, right?  Wrong.  People are not routinely immunised against plague, and if it were used in, for example, bio-terrorism or a biological warfare attack on a civilian population, it would be too late for vaccination.  Antibiotics may prove useless against genetically engineered strains.  And, resistant strains have occurred naturally; for example, there have been outbreaks of a resistant strain in Madagascar as recently as 2017.


Anthrax spores can survive for decades in contaminated soil

Anthrax is another bacterial infection, caused by Bacillus anthracis.  It can affect the skin, respiratory system or gastro-intestinal (GI) tract.  Cutaneous (skin) anthrax is rarely fatal if treated, but is unpleasant and debilitating.  Untreated, it causes death from septicaemia in about 20% of cases.  Respiratory anthrax has a mortality rate of about 45% with treatment; untreated it is almost invariably fatal.  GI anthrax is rare but has a mortality rate of 20-65%, depending on how quickly it is diagnosed and treated.

Anthrax can also affect cattle and sheep and is generally fatal because once symptoms appear, death is very quick, typically 2-3 hours.  This means that both treatment and quarantine may be difficult.  Infection can spread to other animals and humans through contact with infected animals or their remains.

The really scary thing about anthrax is that the bacteria can form spores, going into a sort of dormant state.  These spores can survive for very long periods outside a host, for example in soil.  In 1942, Gruinard Island off the coast of Scotland was used in a biological warfare trial involving anthrax bombs.  Access to the island was forbidden until 1990, when it was re-opened to the public after a decontamination operation that had taken 4 years.

Anthrax was used as a biological weapon by Germany in WW1 and Japan in WW2 (Unit 731 again).  In 1944 the British manufactured about five million animal feed pellets contaminated with anthrax; the plan was to drop them over Germany, infecting millions of cattle which would then infect humans.  During the Cold War, the US and USSR continued to develop anthrax weapons.

The other really scary thing about anthrax is that the spores are relatively easy to cultivate; in theory, anyone with a moderate amount of microbiology and some fairly basic equipment can do it.  This makes it attractive to bioterrorists as well as the military. 


Smallpox causes pustules which leave patients disfigured for life

Smallpox is a highly infectious disease that is spread through airborne droplets, direct contact with an infected person or contact with a contaminated object.  Before Edward Jenner’s discovery of vaccination, it was one of the leading killers in Europe.  Those who survive smallpox are often left disfigured by scars or in some cases are blinded.  It’s been used as a biological weapon since the 18th century; most recently, the USSR stockpiled tonnes of weaponised smallpox during the Cold War.  And, of course, during WW2, our Japanese friends Unit 731 experimented with it extensively.

In 1980, the World Health Assembly officially declared that smallpox had been globally eradicated, thanks to a comprehensive world-wide vaccination program.  Only two known samples remain, stored under the strictest security at the CDC in America and a high security bio-research facility in Russia.  So, what’s the problem?

The problem is that word ‘known’.  Actually, since 1980, other samples have turned up.  For example, in 2014, six vials of smallpox dated 1954 were found in a cold storage facility in a Federal Drug Administration laboratory in the USA.  They were transferred to the CDC and destroyed, but not before tests showed that the virus was still viable.  Other samples may be hidden away in countries that would be less scrupulous.  For example, can we really be certain that all virus stocks held in the former USSR have been accounted for?

Another problem is that even if all remaining samples are eradicated, smallpox could still be recreated.  This was demonstrated in 2017 when Canadian researchers recreated the extinct horse pox virus, which is closely related to smallpox.  Worryingly, they also demonstrated that this could be done by scientists without specialised knowledge, using basic lab equipment and at a relatively low cost; meaning that in theory at least, it could be done by bioterrorists or rogue nations.


Mycobacterium tuberculosis infection (Pulmonary Tuberculosis)

Tuberculosis (TB) is an infectious disease caused by the bacterium Mycobacterium tuberculosis.  It most commonly affects the lungs, attacking and destroying lung tissue.  Scarring may occur where damaged lung tissue has healed.  In some cases, other organs such as the brain or bones are affected.

It is thought that approximately 25% of the world’s population are infected with the TB bacterium.  In 90% of cases, the infection is latent; the remaining 10% have active TB and are able to spread the infection through airborne droplets.  Latent TB may become active due to immunosuppression, aging, malnutrition and certain diseases such as diabetes.  At the present time, the biggest cause of latent TB becoming active is HIV.

M. tuberculosis is particularly dangerous because of its ability to evade the immune system.  It is enclosed in a thick, waxy capsule which protects it from the chemicals that are used to destroy bacteria during phagocytosis.  A M. tuberculosis bacterium that is engulfed by a macrophage will not be destroyed; in fact, it will reproduce inside the macrophage.  This also prevents antigen presentation, so that the adaptive immune system is not activated.

The same waxy capsule makes M. tuberculosis very difficult to kill with antibiotics.  Many antibiotics work by destroying bacterial cell walls; the waxy coating of M. tuberculosis is highly resistant to this.  TB must be treated using specialised antibiotics; for example, ones which inhibit the synthesis of the waxy coating.

The rate at which M. tuberculosis develops antibiotic resistance is increasing, with a growing number of strains that are resistant to multiple drugs.  Depending on the drugs used, treatment of TB with antibiotics takes 3-9 months, during which time the patient will usually be taking a combination of two or more antibiotics.  Some patients stop taking medication before the infection has been eliminated, meaning that their treatable TB is at risk of becoming resistant.  In poorer countries, the sale of sub-standard or counterfeit antibiotics also contributes to resistance.

Prior to 2005, all secondary school pupils in the UK were offered the BCG vaccine, which protects against TB.  In 2005 this practice was discontinued due to the very low rates of TB in the UK.  It was replaced with a targeted vaccination program in which the vaccine was offered only to those considered to be at risk of coming into contact with active TB.  The effectiveness of the vaccine is variable.  Studies have found that in the UK, the vaccine prevents TB infection in 60-80% of people.  The duration of protection from the vaccine is also highly variable, meaning that some people who were vaccinated in childhood may no longer be protected.  Outbreaks of TB in the UK are on the increase.  This is due partly to immigration from countries where there are high rates of TB, and also due to the fact that more people with latent TB are developing active TB as a result of HIV.

So why does TB make the list?  It’s difficult for the immune system to fight, and the vaccine may not offer effective protection.  TB is developing antibiotic resistance at a worrying rate.  There is a real risk that the rate of development of resistance will increase to a point where drug development cannot keep up, and strains emerge which are untreatable. 


While most people can fight off a bout of the flu, it should never be underestimated

They say familiarity breeds contempt, and nowhere is this truer than the humble flu virus.  Typically, seasonal flu will cause an illness which, in healthy adults, is unpleasant but rarely fatal.  However, even ‘normal’ seasonal flu can cause life-threatening complications in vulnerable people such as young children, the elderly, the immunosuppressed and those with pre-existing medical conditions.

Flu viruses mutate rapidly.  However, simple mutation leads to relatively minor antigenic variation, so that individuals immune to the old strain may still have some immunity to the new one, which limits the spread of normal seasonal flu.  A bigger problem is that influenza viruses can also undergo re-assortment; this occurs when different strains of the virus mix their genetic material and recombine it, resulting in a completely new virus.  It happens when two different strains of virus infect the same host and leads to major genetic shifts and completely new antigens.  When this happens, there is zero immunity in the population and available vaccines will not be effective; there is no herd immunity and this leads to a pandemic.  Examples of this are the Spanish Flu pandemic of 1918-19 and the H1N1 Swine Flu pandemic in 2009.

The new viruses that result from re-assortment are not necessarily any more virulent than existing strains; the higher death rate from pandemic flu is because there is no vaccine or herd immunity, so vulnerable members of the population are unprotected.  The Spanish Flu of 1918-19, which killed more people than WW1, was unusual because the mortality rate was highest among young, healthy adults.  Recent research suggests that the virus triggered a cytokine storm.  This is an abnormal immune response which caused activated immune cells to flood the lungs, leading to inflammation and build-up of fluid.  Medical professionals at the time called this ‘dripping lung’.  Patients either drowned in their own secretions or fell victim to secondary pneumonia.  Ironically, the better your immune system, the more likely you were to suffer a cytokine storm, which is why the pandemic killed so many healthy adults. 

More recent flu pandemics have not had the same mortality rate, partly because those viruses did not trigger a cytokine storm, and also because modern antibiotics were available to treat secondary bacterial infections.  New anti-inflammatory drugs to treat cytokine storms are being researched; let’s hope they come into clinical use before a Spanish Flu type virus occurs.

Foot and mouth disease

The 2001 UK outbreak of FMD led to the culling of over 600 million sheep and cattle

You may be surprised to see that two of the pathogens that make this list are ones which do not even infect humans.  Foot and mouth disease (FMD) is a highly infectious virus that affects cloven-hoofed animals such as cattle, sheep, pigs and goats.  Although it is rarely fatal, it is extremely debilitating to infected animals and causes significant suffering.  They suffer lameness due to blisters on the feet, and are unable to eat due to blisters in the mouth.  This leads to severe weight loss, and animals take several months to recover.  Milk production in females and fertility in males is also severely affected.  Humans cannot catch FMD; when people claim to have had FMD, what they have actually had is hand, foot and mouth disease.  This is a mild viral illness that typically lasts about a week.

FMD is highly infectious and can spread through direct contact between infected animals, or by indirect contact with contaminated items; for example, farm machinery or farmworkers’ boots and clothing.  Meat products from infected animals can also carry the virus and it can even survive pasteurisation of milk.  FMD has an incubation period of 1-12 days, during which the infected animal can pass the virus on to others.  Because of the potential for rapid spread of infection, once it has been detected on a farm, all susceptible livestock must be culled and the carcasses burned or buried at an approved site.

FMD cannot infect humans, so why include it in my top ten?  Quite simply because it has the potential to literally cripple a country, its infrastructure and its economy.  The last major outbreak of FMD in the UK was in 2001 and lasted 9 months.  Over 6 million cows and sheep were culled to try and halt the spread of the disease.  Severe restrictions on the movement of animals meant that even farmers whose farms were not infected suffered significant financial losses.  The tourism industry was also badly affected, with the number of overseas visitors to the UK dropping by 10%.  All public rights of way were closed, and some major events were cancelled.  It is estimated that the economic loss to agriculture was about £3.1 billion, with a loss of between £2.7 – 3.2 billion to other sectors of the economy such as tourism.  The potential of FMD to damage economies and divert resources into combatting it could make it a potentially attractive agent for biological warfare or bioterrorism.

Canine distemper

Rhesus monkeys are the latest species, and the first primates, to become susceptible to CD

Canine distemper (CD) is an infectious disease that can infect a range of carnivores including canines (e.g. dogs, wolves, and foxes), mustelids (e.g. ferrets, mink and otters), big cats, seals, and skunks.  Recently it has begun to cross into non-carnivores including Asian elephants, pandas and some species of primate.  CD affects the respiratory and central nervous systems, and has a very high fatality rate.  It is transmitted by droplets in the air or contaminated objects.  The virus can survive for a fairly long time outside a host, for example on fur that has been shed by infected animals.

The CD vaccine is highly effective.  CD does not affect humans, and does not have the potential to affect the economy the way FMD does.  So why does CD scare me?  Basically because of its remarkable ability to cross between different species.  Within a relatively short time, CD has jumped from canines and mustelids into other carnivores, and then into non-carnivores.  Most worrying of all is its recent jump into primates.  Laboratory experiments have demonstrated that the strain which affects monkeys has the potential to interact with proteins on the cell membranes of human cells, meaning that in theory at least, CD could at some point cross into humans.  The human population is mostly unprotected (immunity to measles does give some crossover protection against CD) and it would take time to develop an effective human vaccine.  Most of the UK’s domestic dog population is vaccinated, but vaccination is not compulsory.  Uptake of the vaccine among ferret owners is variable, and some vulnerable domestic pets such as skunks cannot currently be vaccinated.  There is a huge reservoir of disease in the wild animal population, meaning that if the virus did become capable of infecting humans, the risk of a major outbreak would be significant, potentially resulting in a large number of deaths.

March 2021: Ironically, the COVID pandemic may actually result in a significant reduction in the risk of CD crossing into humans.  In 2020, COVID-19 was discovered in mink on intensive fur farms in Scandinavia, resulting in a large-scale cull.  The overcrowding in such farms provides ideal conditions for a pathogen to jump species: if COVID could jump from humans into mink, there’s a definite possibility of CD going the other way.  If COVID means the end of intensive mink farming, then a significant risk will have been removed, as well as a major animal welfare issue.


Did not make the original list!  I wrote the original in January 2020, when it still looked as though the virus might be containable.  A year later, we were in lockdown #3, the UK death toll had passed 100,000, and new strains were emerging which became ever more infections.  COVID-19 really is the gift that keeps on giving! 

Now it’s February 2022 and the dominant strain is the omicron variant, which is highly infectious but causes only mild illness in the majority of people. This is likely to be due to the successful rollout of vaccines; but also that COVID-19 is following a well known evolutionary pattern by becoming more infectious but causing less severe disease. I will post more on this soon.

The COVID-19 virus

There is one good thing that has come out of the pandemic, and that is that immunology, and particularly vaccine science, has taken a huge leap forward.  RNA vaccines have been in development for a number of years, but 12 months ago, not a single one had made it into clinical usage.  Now, we have two RNA vaccines (Pfizer and Oxford/ AstraZeneca) being rolled out on a large scale, with others expected to gain regulatory approval in the next few weeks. It is my belief that the pandemic has advanced vaccine science in the same way that WW1 advanced radiography and blood transfusions; and WW2 advanced the use of antibiotics.

Ebola – the one that didn’t make it.

When I wrote the original blog post, a few people asked me why Ebola didn’t make the list of my top 10.  It still doesn’t, and here’s why.

The distinctive ‘shepherd’s crook’ structure of the Ebola virus.

Ebola is one of a group of viruses called filoviruses.  These have filament-like structures which coil to form a characteristic ‘shepherd’s crook’ shape.  Like all viruses, Ebola invades cells and uses their organelles to reproduce.  Ebola reproduces rapidly and efficiently.  It triggers the release of chemicals that cause healthy cells to die; it also causes cell death by using up resources such as proteins at such a rapid rate that the cell is no longer able to maintain membranes and other structures.

Ebola causes damage and death to the endothelial cells that line blood vessels, leading to vascular instability – blood vessels literally disintegrate.  At the same time it damages liver cells, impairing the clotting process.  This results in massive and often fatal internal bleeding.  It is able to evade the innate immune system by blocking the production of interferons.  These are chemicals that are normally produced by cells which are infected with viruses; they signal natural killer cells (NKCs) to destroy the infected cell.  Blocking the release of interferons allows Ebola to reproduce unchecked.  The average death rate from Ebola is about 50%, but it can be as high as 90% depending on the strain.  Death usually occurs as a result of hypovolemic shock – low blood pressure due to blood and fluid loss.

Remember when I said earlier that weaponisation is a good indication of how scary a pathogen is.  Ebola is a devastating disease, highly infectious and with a high mortality rate.  It’s a particularly gruesome pathogen as well – sufferers can literally bleed to death internally.  This generates fear in the wider population; on the face of it, Ebola has all the makings of a weapon that would induce mass panic and terror as well as widespread death.  But, Ebola has never been weaponised.  And the reasons it has never been weaponised are the same as the reasons why it didn’t make my original ten.

Put simply, Ebola is too efficient for its own good.  It reproduces so rapidly that it quickly destroys the cells it infects, killing its host in the process.  The most deadly viruses are the ones that keep their hosts alive for long enough to infect as many others as possible. Even without intervention, Ebola outbreaks burn out relatively quickly.

Effective use of PPE and decontamination procedures mean that Ebola can be contained.

There are two other reasons Ebola still doesn’t make the top 10: transmission and survival outside a host.  Ebola can only be transmitted through direct contact with the bodily fluids of an infected person: blood, saliva, vomit, semen etc.  This means that use of PPE is highly effective in bringing an outbreak under control.  In recent years, the importance of safe burial practices has also been recognised.  This involves burying the dead as soon as possible; sealing the body inside leak-proof body bags; and ensuring that those handling the dead use PPE and hygiene measures effectively.

The other problem Ebola has is that it can only survive for very short periods outside a host, and is very easily destroyed by simple agents such as soap, bleach or detergent.  The failure to weaponise Ebola (and trust me, several nations have tried!) is also down to its poor survival.  You couldn’t put Ebola in a bomb, for example, because the detonation of the bomb would kill it off.  A spray would also be of limited effectiveness, because the virus would only be viable for a very short period of time.

Nuclear Power: What If?

Renewables such as wind power are at the centre of efforts to reduce carbon emmissions

I think nearly all of us are aware of the urgent need to reduce carbon emissions and ideally create a carbon-neutral society. There’s a major focus on renewable energy such as wind, tidal, hydroelectric, solar and geothermal. I’m making my own small contribution through solar panels on my house. However, when it comes to talking about reducing carbon emissions, there’s an elephant in the room. A source of electricity that is not renewable but can generate large amounts of electricity with negligible carbon emissions: nuclear power.

Disasters such as Fukushima mean that nuclear power is widely rejected as a low-carbon option

There are obvious and understandable reasons why discussions on reducing emissions tend to ignore the nuclear option. Windscale, Three Mile Island, Chernobyl and Fukushima are four of them. The management of nuclear waste which may remain radioactive for hundreds of thousands of years is another; as is the safe decommissioning of reactors at the end of their working life. But it didn’t have to be this way.

In the late 1940s, when research was going on into the potential use of nuclear energy for generating electricity, two possible fuels were investigated: thorium and uranium. When bombarded with neutrons, thorium is converted into uranium-232, which will then undergo nuclear fission, releasing heat. This can then be used to create high pressure steam to drive turbines. The other fuel, uranium-235, also undergoes nuclear fission to release heat.

Thorium is abundant in the Earth’s crust and is often a waste product of mining for other metals

It was clear from the beginning that thorium had some very significant advantages over uranium as a fuel. Firstly, thorium is much more abundant than uranium, and it is a lot easier and safer to mine and process. In fact, massive amounts of thorium are created as a waste product from mining other metals. In addition, nearly all thorium is ‘fertile’ – meaning it can be used as fuel. Uranium, by contrast, is mostly the non-fertile isotope uranium-238; only 0.7% is uranium-235, which can undergo nuclear fission. This means that thorium does not require expensive fuel enrichment processes.

Another benefit is that a thorium reactor produces much less radioactive waste than a uranium reactor; up to 1000 times less, in fact. In addition, those small amounts of waste products remain radioactive for between 1 and 100 years; by contrast, the waste products from uranium remain radioactive for tens or even hundreds of thousand years. The decommissioning of thorium plants is also safer and easier.

A meltdown, such as that which occurred at Chernobyl, is impossible with a thorium reactor

Thorium reactors are much, much safer than uranium reactors. In fact, they are literally melt-down proof. The reason for this is that they use a liquid fuel – molten thorium fluoride. In the bottom of a thorium reactor is a plug which will melt if the temperature of the fuel exceeds a set limit. The fuel will then be drained into a tank for safe storage. Since thorium must be bombarded with neutrons to undergo nuclear fission, once removed from the reactor, nuclear fission ceases and the fuel is safe.

By contrast, uranium reactors use a solid fuel and rely on control rods which can be lowered into the reactor to absorb neutrons and slow down or stop nuclear fission. In addition, any failure in the cooling system can lead to a meltdown. If the cooling system of a thorium reactor fails, the plug described in the previous paragraph will melt and the fuel will drain from the reactor.

Thorium reactors are also highly efficient. It is estimated that one ton of thorium can generate the same amount of electricity as 200 tons of uranium or 3,500,500 tons of coal.

Liquid thorium fluoride is highly corrosive

There are some disadvantages. One is the cost of processing thorium ore into thorium fluoride fuel; however, uranium also requires extensive processing and enrichment before it can be used in a reactor. another disadvantage is that the molten thorium fluoride fuel is highly corrosive. However, it would be perfectly feasible to develop corrosion-resistant materials that could be used to line the reactor. There are a few other potential problems which I won’t go into as the science is quite complex; all of these can be solved if there is sufficient investment into thorium technology.

Between 1965 and 1969, an experimental thorium reactor was successfully developed and tested at the Oak Ridge National Laboratory in the USA. Nevertheless, in 1973 the US government made the decision to abandon thorium technology in favour of uranium. Other governments such as the UK and France had already made the decision in favour of uranium.

The experimental thorium reactor at Oak Ridge
The need to manufacture plutonium for nuclear weapons was a major factor in the decision to opt for uranium.

So, why did governments abandon a cheap, clean and safe fuel in favour of one that is more dangerous and generates more waste? The official reason was that uranium reactors are supposedly more efficient. The true answer lies in what is either thorium’s biggest advantage or its biggest disadvantage, depending on your point of view. Quite simply, a thorium reactor does not produce plutonium, which is needed to create nuclear weapons. In the climate of the Cold War, governments made the choice to go with the fuel that produced the plutonium they needed for their nuclear weapons programmes. In the late 1960s and early 70s, Alvin Weinberg, the director of Oak Ridge, argued passionately for the adoption of thorium as the fuel for nuclear power. His refusal to abandon what he considered to be a safer, cleaner option in favour of one with weapons applications eventually cost him his job.

Many countries continue to maintain a nuclear deterrent such as the UK’s Trident submarines

So, what is the future? Many countries, including the USA and UK, are reluctant to provide the funding that is needed to develop thorium technology into a viable method of generating electricity. A notable exception is India, which has abundant supplies of thorium and is aiming to generate 30% of its electricity from thorium by 2050. In addition, despite the ending of the Cold War, many countries including the UK continue to maintain a nuclear deterrent. This means that the demand for plutonium is unlikely to end any time soon.

If Irene and Frederic Joliot-Curie had lived longer, they might well have been advocates for thorium power

A final note. Two of the most influential scientists in the development of nuclear power were Irene and Frederic Joliot-Curie, subjects of one of my previous posts. They oversaw the development of France’s first nuclear power station. Both died prematurely from radiation-related illnesses; Irene in 1956 and Frederic in 1958, when the nuclear program was in its infancy. As ardent pacifists, it is possible, even likely, that they would have championed the development of thorium as a nuclear fuel. Had they lived longer, would we now have a safe source of low-carbon nuclear energy?

Back again!

Hi all, it’s been a while but I am back in action. When I started this blog the intention was for it to be a science blog that looked at aspects of science that are overlooked, quirky, controversial etc. With the pandemic it rapidly morphed into more of a COVID-19 blog. Now that things have (hopefully) settled down a bit, I am going to try and return to the original intention. I will still post about COVID but it won’t dominate the way it has in the past.

Watch this space,


COVID Vaccine FAQs

Hi everyone. As you know, I had my first Astra Zeneca jab on March 23rd, appropriately enough the 1-year anniversary of lockdown #1.  I will be very relieved to get my second one on 8th June – I’m counting the days!  In this post I am hoping to answer some of the most common questions and debunk some common myths about the vaccine. 

How does the vaccine work?

All vaccines work on the same basic principle.  Something is introduced into the body that fools your immune system into thinking you have a disease, so it produces antibodies and other cells to fight that disease.  If you are then infected with the actual disease, your immune system ‘remembers’ how to produce those antibodies.  This means that your immune system will fight off the disease without you developing symptoms or becoming infectious.

The COVID vaccine contains a small segment of the virus’ RNA containing the instructions to make the spike protein, which is found on the surface of the virus.  When you are vaccinated, your cells will take up this RNA and use it to manufacture the spike protein; this provokes your immune system into producing antibodies and white blood cells to destroy it.  If you are then exposed to the actual virus, your body will be able to produce antibodies and destroy it very quickly.

What is the difference between the various vaccines?

All the vaccines contain the RNA for the spike protein, encased in a capsule.  When you receive the vaccine, the capsule breaks down inside the body and releases the RNA.  Different vaccines use different capsules.  The Pfizer and Moderna vaccines both use a lipid (fat) capsule; Astra Zeneca (AZ) uses a deactivated virus capsule.

Is the AZ vaccine less effective than the others?

No.  Apparent differences in the effectiveness of the vaccines are basically due to differences in the way the data has been processed and presented in the scientific literature; and the way the data has then been represented – or misrepresented – in the media. 

All three of the currently licensed vaccines in the UK have very similar effectiveness.  Data published by Public Health England at the end of March has shown that all three vaccines provide on average 60 % protection after the first dose and over 85% after the second.  To put that in context, the effectiveness of the seasonal flu vaccine is between 55 and 60 %.

It’s also worth noting that the higher the uptake of a vaccine, the more effective it is – this is because if the majority of the population is vaccinated, the probability that the virus mutates and becomes vaccine resistant is much lower.   

How have the vaccines been developed?

The various vaccines have been developed through collaborations between researchers who develop and test the vaccine, and pharmaceutical companies who develop and implement manufacturing processes. 

The big advantage of these collaborations is that by the time each vaccine had been developed and tested by researchers, the pharmaceutical companies had the manufacturing processes ready to go.  This dramatically reduced the time needed to get the vaccines into clinical use.

Is this untried technology that has been rushed into use too quickly?

Definitely not.  Research and development into RNA vaccines has been going on for over 30 years.  Several companies including Pfizer were already actively researching RNA vaccines for flu; however, without the pandemic, it would have been several more years before any RNA vaccines made it into clinical use.  The pandemic has accelerated the process because vast amounts of funding were made available. 

Is the vaccine safe?

The COVID vaccine is very safe indeed.   Traditional vaccines use either a dead or weakened version of the organism that causes the disease.  There is a small but significant segment of the population that cannot have these vaccines, including the elderly and people who are immunosuppressed.

Because the COVID vaccine uses RNA rather than dead or weakened virus, it can be given to the majority of the population including the very elderly and those who are immunosuppressed.

What side-effects might I get?

The most common side-effects are some soreness at the injection site, and mild flu-like symptoms.  Both resolve within a couple of days.  Many people, including myself, have experienced a metallic taste in the mouth for approximately 24 hours after the AZ vaccine. 

When you have the vaccine, you will be given a leaflet which includes a list of side-effects.  If you do get side effects, however mild, it is worth reporting them using the MHRA’s yellow card scheme: https://coronavirus-yellowcard.mhra.gov.uk/

Will I test positive after the vaccine?

The vaccine will not cause a positive test.  The vaccine causes your body to make the spike protein; both the lateral flow and PCR tests detect other parts of the virus structure.  If you have had the vaccine and get a positive result afterwards, you should follow the normal procedure for self-isolating.

What about blood clots?

The media has made much of the risk of a rare form of blood of blood clot associated with the Astra Zeneca vaccine.  However, the actual figures tell a different story.  As of March 31st, there have been 79 instances of this rare type of blood clot (14 fatalities) following the first dose of the AZ vaccine; this is out of 20.2 million doses.  Analysis has found that the risk is slightly higher among the under-30s; as a precaution, the AZ vaccine is no longer being offered to this age group.

To put these figures in context, according to Department of Transport statistics, in 2020 there were 24,470 people killed or seriously injured in road accidents – an average of 67 per day.  Personally, I was quite happy to have my first dose of AZ vaccine and will be even happier when I’ve had my second.

Will the virus’ RNA remain in my body forever?

One piece of disinformation that is doing the rounds on social media is that once you are vaccinated, the virus’ RNA will remain in your body forever; and that you will effectively have become genetically modified.  This is not the case.  RNA is a short-lived molecule which is broken down once it has served its purpose.  Once the RNA from the vaccine has been used to make the spike protein, it will be broken down and eliminated from your body.  The same thing will happen to the spike protein; your immune system will destroy it and it will be eliminated from your body. 

What if the virus mutates?

A big advantage of RNA vaccines is that if variants emerge that are resistant to the existing vaccines, a new vaccine can be created in a matter of a few weeks.  This is because all that needs to be done is to isolate the RNA for the new spike protein, then insert it into the existing capsule.  Manufacturing processes do not need to be altered, and much less safety testing is required.

Now that RNA vaccines are a reality, it possible that in the next few years they will replace traditional vaccines for other rapidly mutating viruses such as influenza.

Will I need a jab every year?

This is still being debated but it is likely that for the next few years at least, an annual COVID vaccine will be needed.  There are two reasons for this.  Firstly, we do not yet know how long the immunity provided by the vaccine lasts; a yearly booster is therefore a sensible precaution.  Secondly, it may be necessary to vaccinate annually due to changes to the virus that make previous vaccines ineffective.

Why is the vaccine not available to under-18s?

At present, clinical trials for vaccines have only been carried out in adults.  Children and adolescents are physiologically very different to adults.  Because of this, dedicated clinical trials must be carried out in children before any vaccine can be licensed for the under 18s. 

Now that the safety of the various vaccines in adults has been well established, small-scale clinical trials are underway in children and adolescents for both the Pfizer and Moderna vaccines. A trial of the AZ vaccine has been suspended as a precaution following the decision not to use it for those under 30.

Saviour of the World, or War criminal? The enigma of Fritz Haber

Haber’s life was the tragedy of the German Jew – the tragedy of unrequited love – Albert Einstein

Almost exactly 106 years ago, on the afternoon of April 22nd 1915, things were fairly quiet on the Northern edge of the Ypres Salient between Gravenstafel and Langemark.  Possibly too quiet, as subsequent events would demonstrate.  But for the French Territorial and Colonial troops in the trenches, there was nothing to indicate the horror that was about to be unleashed.

As the afternoon drew on, a slight breeze began to blow from the direction of the German lines.  At approximately 5pm, a strange greenish-grey mist was observed moving towards the Allied lines from the German trenches.  It was chlorine gas, and when it reached the French trenches, all hell broke loose.  Men died in agony as the chlorine reacted with moisture in the linings of their airways to form corrosive hydrochloric acid.  The French troops broke and ran, leaving 4 miles of the front line completely undefended.  The Germans could have broken through to Ypres and on to the Channel Ports; however, two things saved the day for the Allies. 

The first was that the effectiveness of the gas took even the Germans by surprise, and they simply did not have enough troops to exploit the breakthrough.  The second was the almost unbelievable courage of the Canadian troops on the Southern flank of the breakthrough. They moved into the trenches the French had abandoned and fought off multiple gas attacks. In two days, the Allies lost about 5000 killed and 15000 wounded.  It was the first large-scale use of a lethal, asphyxiating gas in warfare, and set the scene for 3 years of horror as both sides raced to develop ever more effective chemical weapons.

The man behind it all was a quiet, bespectacled, middle-aged German army lieutenant named Fritz Haber, who would become one of the most controversial scientists of the 20th century.

Before the War, Haber had been a Professor of chemistry at the University of Karlsruhe, and in 1911 had become the first director of the new Kaiser Wilhelm Institute in Berlin.  His most important work, however, was carried out while he was at Karlsruhe.

Look at a graph of world population, like the one shown below, and you will see that until about 1800 ACE, population growth was very slow.  From 1800 on, the world’s population began to grow with increasing rapidity, as improvements in food production, medical care and living conditions began to reduce mortality rates.  As the end of the 19th century approached, the world’s population was heading towards unsustainable levels.  Quite simply, the human population was about to exceed the Earth’s capacity to produce food.

The problem was a shortage of nitrogen.  This element is essential for plant growth, and without plants and their ability to photosynthesise, there is no food.  But nitrogen is one of the most abundant elements on Earth, so how could there be a shortage?  The answer is that the bulk of the Earth’s nitrogen is in the atmosphere, where it cannot directly be used by plants.  Plants require water-soluble nitrates, which can be taken up from the soil by their roots.  

The nitrogen cycle

In the ordinary way of things, this is taken care of by Mother Nature.  Bacteria in the soil and in the root nodules of leguminous plants ‘fix’ nitrogen into ammonia, and a small amount of atmospheric nitrogen is also ‘fixed’ by lightning. Other bacteria and fungi convert nitrogen from dead plant and animal matter into ammonia; a third group of bacteria then convert the ammonia into nitrates.  This is known as the nitrogen cycle. By the late 19th century, these natural nitrogen-fixing processes could no longer produce enough nitrates to meet the increasing need for food crops.  A cull of the world’s population by means of a catastrophic world-wide famine was imminent, unless a way could be found of artificially fixing atmospheric nitrogen. 

Apparatus used by Haber and Le Rossignol

Enter Fritz Haber and his assistant, Robert Le Rossignol, who in the summer of 1909 succesfully produced ammonia by reacting hydrogen and nitrogen gases at high temperature and pressure, using an iron catalyst. Once you have ammonia, it is then relatively straightforward to convert it into nitrates for fertilisers.

The first operational ammonia plant at Oppau in Germany

Carl Bosch of the BASF company scaled-up the process to industrial level, with the first operational ammonia plant opening in 1913 at Oppau.  Now known as the Haber-Bosch process, this was one of the biggest breakthroughs industrial chemistry has ever seen, and paved the way for the large-scale manufacture of nitrate fertilisers, meaning that food production could continue to increase and meet the needs of the expanding population.

Guano from seabird colonies in Peru were a major source of nitrates. Bloomberg photo by Vera A. Lentz

By a (not so?) happy coincidence, Haber and Bosch’s work also meant that if war broke out, Germany would be able to manufacture nitrates to make explosives. Prior to the invention of the Haber-Bosch process, the main source of nitrates for both fertilisers and explosives was guano. Yes, you did read that right, guano as in bird poo. Guano is a rich source of nitrates, and the best sources of guano in terms of both quality and quantity could be found in South America, particularly the Chincha Islands in Peru, where millions of seabirds create mountains of guano up to 150 feet high. In the 19th century, the importation of guano by sea was big business. In the event of a war, it was possible, even likely, that a Royal Navy blockade would be able to prevent Germany from importing guano. The Haber-Bosch process meant that in this event, Germany’s munitions factories could continue to churn out shells and bullets. Despite this, the invention of ammonia synthesis was, overall, something that benefited humankind. So how did Haber go from that to chemical warfare?

Fritz Haber was intensely patriotic.  Part of this was due to his having been born into a Jewish family. In the early 20th century, antisemitism in Germany was nowhere near as prevalent as it would become in the Nazi era. However, it was significant enough for Haber to feel that despite his having converted to Christianity, he needed to prove his patriotism and devotion to the Fatherland. Haber was enthusiastic about the war, and was one of 93 German intellectuals to sign a proclamation which enthusiastically endorsed the declaration of war.

Haber (pointing) with gas troops and equipment

In addition to his patriotism, Haber had two areas of expertise that made him the ideal person to lead Germany’s efforts to develop poisonous gas as a weapon. The first was in electrochemistry, which is crucial in the manufacture of chlorine gas. The second was in working with gases under pressure, which enabled him to develop equipment with which to deliver the gas, and meant that throughout the war, German equipment was superior to anything used by the allies.

For the duration of the War, Haber led the German efforts to develop both chemical weapons and defences such as gas masks. The result was that Germany was always one step ahead of the allies in both. It is estimated that there were about 1.3 million casualties as a result of gas, with approximately 90,000 fatalities – relatively trivial in relation to the overall numbers of casualties. But gas was, first and foremost, a weapon of terror; its aim was to disrupt, damage morale and consume resources treating the wounded. During the first gas attack at Second Ypres, many of the troops who broke and ran did so out of sheer terror, having seen the effects of the gas on others. Mustard gas in particular was designed to maim and terrorise rather than kill.

Clara Haber committed suicide shortly after the gas attack at Ypres

Haber’s involvement in chemical warfare was to cost him dearly. On 2nd May 1915, his wife Clara committed suicide, shooting herself through the heart with Haber’s own army revolver while her husband was celebrating his promotion to captain. A dedicated pacifist and a talented chemist in her own right, her husband’s involvement in the war is thought to have been a major factor in Clara’s suicide.

After the war, Haber came in for a great deal of criticism from the scientific community. He was awarded the 1918 Nobel Prize for Chemistry for his work on ammonia synthesis, and this was controversial to put it mildly. Many eminent scientists boycotted the award ceremony in 1919, and it is said that Sir Ernest Rutherford refused to shake Haber’s hand.

In the post-war years, Haber continued as Director of the Kaiser Wilhelm Institute, where he led Germany’s secret efforts to develop new chemical weapons, in direct contravention of the Treaty of Versailles. But dark clouds were gathering on the horizon. When Hitler became Chancellor in 1933, he immediately began to target Jewish scientists. Haber was personally targeted, with Hitler claiming that his appointment as director of the Institute was a result of his being the nephew of a Jewish profiteer (which he wasn’t). This came as a shock to Haber, who had thought that his service in WW1 and his conversion to Christianity would be enough to protect him. Although Haber could not legally be dismissed, the Nazis made his position untenable and he resigned in October 1933. He left Germany and after a brief spell in England, in January 1934 he set out to take up a new job in Palestine. But he never reached his destination. Events had taken a severe toll on Haber’s health and on 29th January 1934 he died of heart failure while breaking his journey in Switzerland.

Zyklon B, used at Auschwitz-Birkenau and other death camps during the holocaust.

There is a final hideous twist to the story of Fritz Haber, the scientist hounded out of Nazi Germany because of his Jewish roots. Between the wars, the research Haber was overseeing at the Kaiser Wilhelm Institute included the development of new pesticides and fumigants. This included the development of a highly effective class of fumigants which consisted of hydrogen cyanide gas adsorbed onto diatomaceous earths. When exposed to air, the lethal gas was released. These agents were given the name ‘Zyklons’ and included Zyklon B, which would be used in the murder of 1.1 million people in the Holocaust. Among those who would perish in the gas chambers were several members of Fritz Haber’s own extended family.

The costliest death of WW1? The tragedy of Henry Moseley

In view of what he [Moseley] still have accomplished … his death might well have been the most costly single death of the War to mankind generally – Isaac Asimov

The First World War was one of the most deadly and wasteful conflicts in human history. An entire generation torn apart, and many brilliant minds lost. Who knows what Wilfred Owen might have gone on to achieve, had he not been killed in action almost exactly a week before the armistice? And he was just one among many. But while most people have heard of Wilfred Owen, many of you reading this may never have heard of Henry Gwyn Jeffreys Moseley.

Henry Moseley, known to his friends as Harry, was born in 1887. His father was a professor of anatomy and physiology at the University of Oxford, and his mother, herself the daughter of an eminent biologist, went on to become the British women’s chess champion in 1913. So it’s hardly surprising that Harry excelled at science, winning the physics and chemistry prizes at Eton where he had been awarded a King’s scholarship. What is perhaps more surprising is that Harry did not follow the family tradition and go into biology – his interests lay in chemistry and physics, and particularly in the structure of the atom.

After graduating from Trinity College, Oxford, Harry Moseley went to Manchester to work under Sir Ernest Rutherford, one of the most eminent scientists of the time, who was studying radioactivity. In 1913 Rutherford offered Harry a fellowship, which he declined, preferring to return to Oxford where he could work on his own independent research. In particular he wanted to work on solving the problem of how to measure atomic number.

The periodic table of the elements is one of the most powerful tools known to science, and one which we now take for granted. Russian chemist Dmitry Mendeleev created the first true periodic table by putting the elements in order of mass. He noticed that this resulted in certain pairs of elements (for example, iodine and tellurium) being ‘back-to-front’ based on their properties, and incorrectly assumed that this was due to errors in calculating their atomic masses.

Mendeleev assigned each element an atomic number based on its position in the periodic table; however, in cases such as iodine and tellurium, this was semi-arbitrary (science-speak for ‘educated guess’) and based on chemical properties. Moseley would be the one to prove that these elements were placed correctly, based on atomic structure. He would also be the first to find experimental evidence to support the existence of atomic numbers – a concept that until then had been theoretical only.

Moseley’s speciality was X-rays. Not medical X-rays, but the study of how X-rays relate to atomic structure. I won’t go into too much technical detail, but basically what he did was to shine a beam of high energy electrons onto different metals in a vacuum. As you can see on the left, this causes the metal to emit X-rays at an angle to the electron beam. This is called diffraction.

Moseley holding one of his X-=ray tubes

By using a detector, Moseley could measure the angles at which the X-rays were emitted. By applying Bragg’s Law (a mathematical formula relating angle and wavelength), he could then calculate the wavelengths of X-rays given off by each metal. So far, so what? The important breakthrough came when Moseley compared wavelengths to the position of each metal in the periodic table, and found that there was a direct mathematical relationship – now known as Moseley’s Law. Finally, atomic number could be proved experimentally. Amongst other things, Moseley was able to show that Mendeleev’s positioning of problematic elements such as iodine and tellurium was correct. He was also able to solve the problem of where to put the lanthanides – in the periodic table, that is – which had been occupying chemists for years (we don’t get out much…).

Royal Engineers manning a communication post where orders would be relayed by telephone or wireless

In August 1914, Harry Moseley’s work was rudely interrupted by the outbreak of the First World War. In the rush of patriotism following the declaration of war, young men flocked in their thousands to enlist. Despite the efforts of his family and friends to dissuade him, Moseley felt it his patriotic duty to join them, and enlisted in the Royal Engineers. In April 1915 he was sent to Gallipoli where he served as a communications officer. On 10th August 1915, at the age of 27, one of the most brilliant young scientists of his generation was killed in action – shot by a Turkish sniper whilst relaying an order over the telephone.

The consequences to science of the loss of Moseley were significant, and his death provoked an outcry within the scientific community. Robert Millikan, who would go on to win the Nobel Prize for Physics in 1923, wrote that,

“Had the European War had no other result than the snuffing out of this young life, that alone would make it one of the most hideous and most irreparable crimes in history.”

Many scientists, including Sir Ernest Rutherford, speculated that had he lived, Moseley would certainly have been awarded a Nobel Prize for his work on atomic structure. Moseley did leave one important legacy though. His death in the First World War was a significant factor in ensuring that in the Second World War, scientific research would be designated as a reserved occupation, ensuring that scientists who would otherwise be eligible for military service were unable to enlist. Just one of many scientists whose life may well have been saved by this was Alan Turing, who made crucial discoveries in the field of computer science and played a key role in cracking the Enigma code.

My Vaccine Experience

So, as planned, I had my first injection of the Astra-Zeneca COVID vaccine on March 23rd and it couldn’t have gone more smoothly. I thought I’d post about my experience to reassure people about the vaccine in general and AZ in particular. And to let people in the UK know what to expect when you attend a mass vaccination centre.

The first thing you should be aware of is that you won’t be allowed to enter the building until five minutes before your appointment. Not a problem if you are driving and can wait in the car, but worth bearing in mind if you are going on foot. When you go in you will be asked to sanitise your hands and wear a face mask; if you are exempt, you will be given a plastic visor to wear.

A receptionist will check your details and give you your NHS number if you don’t know it. You will then be directed where to go next. The mass vaccination centre I attended was very much a multi agency affair; as well as NHS staff there were personnel from the Fire Service, Army, RAF and St John Ambulance.

When it’s your turn you will be called forward to sit at a table where you will be asked a series of questions to determine your eligibility and suitability for the vaccine. This is a safety check where they will ask about things like allergies, underlying medical conditions and whether you are taking certain medications. When this is done, they will tell you which vaccine you are getting and ask for your verbal consent. They will also give you a detailed information sheet and will answer any questions you have.

Once that is done, the person processing you will call a medic over who will give you the actual injection. Don’t be surprised if this is a member of the Armed Forces. I was processed by a RAF medic and given the injection by an Army medic. You can be reassured that they will have had the same level of training as NHS staff.

After the injection you will be given a card which you need to bring to your next appointment. For me, getting through the next 12 weeks without losing it, or forgetting where I’ve stashed it so I won’t lose it, is possibly the most stressful part of the process! You also get a sticker but sadly no lollipop – that’s NHS cutbacks for you!

If you have driven to the vaccination centre, you will then be asked to wait in a waiting area for 15 minutes. The waiting area is socially distanced and is monitored by someone trained to spot any signs of anaphylaxis. Make sure you take a book or tablet or something – I didn’t and had to resort to reading the BBC news on my very small iPhone SE!

So, what about side-effects? There has been a lot of adverse publicity about the AZ vaccine and particularly its safety in younger age groups. Well, I am 48 and had absolutely no concerns about having the AZ vaccine. About 3 hours after the vaccine I started feeling very tired and generally a bit off-colour. I also developed a strong metallic taste in my mouth. Since this is a COVID symptom and is not yet on the official list of AZ side-effects I had to leave work, get a PCR and self-isolate until the result came in.

The PCR result was negative and the symptoms disappeared almost exactly 24-hours after they first appeared. I had a sore arm for a few days but no worse than the flu vaccine. And nothing compared with the pneumococcus vaccine – anyone reading this who’s had it will know exactly what I mean!

I mentioned that altered taste is not yet officially a side-effect of the AZ vaccine, although I know a number of other people who experienced it. This is why it’s really important that people use the Medicines and Healthcare products Regulatory Agency’s Yellow Card system to report any side effects. The Yellow Card system is used to collect data on all medications, but they have a dedicated site for COVID medications and vaccines. You can access it using the link at the end of this post. Note, this only applies to the UK but other agencies such as the FDA in the US and the EMA in Europe have similar reporting systems.

All in all, other than the lack of lollipops, my experience of getting the first jab was entirely positive. I look forward to getting my second one, not least because then I can stop worrying about where I put that darned card…

Link to yellow card:


What is mRNA, and how does it work?

I am very, very happy and excited today! The reason? I have a date booked for my COVID vaccine. 23rd of March is the day (coincidentally, the anniversary of the first UK lockdown), and it can’t come soon enough for me. The speed at which the various COVID vaccines have been developed, tested and approved for clinical use is impressive and means that we should, finally, have the end of this pandemic in sight. Unfortunately though, the anti-vaxxers are coming out of the woodwork in droves, and there are all sorts of myths and misinformation being pedalled on social media.

This is the first in a series of posts I am planning about the COVID vaccines. Many of the vaccines, including Pfizer and Astra Zeneca, are mRNA vaccines. So, I am going to start with the basics: what mRNA is and how it works.

mRNA is one of a group of biological molecules called the nucleic acids. These are DNA, and various types of RNA. Nucleic acids consist of molecules called nucleotides, joined together in long chains. Each nuclotide consists of a sugar, a phosphate group and a nitrogenous base. The sugar and phosphate make up the backbone of the chain, and the nitrogenous bases make up the genetic code.

A DNA molecule consists of two single strands, which combine to form the familiar double-helix.

DNA stands for deoxyribonucleic acid. It is a stable, information storage molecule that contains the ‘instructions’ for making proteins. In humans, all the instructions (genes) for every protein the body needs to make are stored on 46 molecules of DNA, called chromosomes. These make up the genome, and are found in the nucleus of every cell. DNA nucleotides consist of a phosphate group, the sugar deoxyribose, and one of four bases: adenine (A), thymine (T), guanine (G) and cytosine (C).

mRNA is single-stranded and much shorter than DNA.

DNA never leaves the nucleus of a cell. For one thing, it’s too big and cumbersome. For another, it needs to be protected against damages. So, when a cell needs to make a particular protein, the gene for that protein is copied in the form of messenger RNA or mRNA. Ribonucleic acid (RNA) differs from DNA because it is a short-term molecule used for the transfer and processing of genetic information. There are many types of RNA, of which mRNA is just one. RNA nucleotides consist of a phosphate group and the sugar ribose. Three of the nitrogenous bases are the same as those in DNA: A, G and C. However, thymine (T) is replaced with uracil (U).

When a cell needs to make a particular protein, an enzyme called RNA polymerase copies the gene in the form of a molecule of mRNA; this is called transcription. The mRNA leaves the nucleus of the cell and enters the cytoplasm, where it binds to a structure called a ribosome; the ribosome then assembles the protein. This is called translation.

A virus like COVID-19 cannot manufacture its own proteins. Instead, it must infect a cell and take over its organelles.

Viruses like COVID-19 cannot carry out transcription and translation, since they do not have ribosomes and various other things that are needed. Viruses carry their genetic material in the form of DNA or RNA – RNA in the case of COVID-19. When COVID-19 infects a cell, the virus capsule breaks open, releasing the RNA into the cell’s cytoplasm. Ribosomes in the cell will bind to the viral RNA in the same way they bind to mRNA, and will manufacture the necessary proteins for producing new viruses.

Lateral flow vs PCR: how do they work?

Lateral Flow Test

There has been some controversy in England this week surrounding the mass testing of pupils for COVID-19 as they return to school. The problem is that the government seems to be contradicting itself regarding the relative reliabilities of the lateral flow test (LFT) and the polymerase chain reaction test (PCR). If a student has a positive LFT from a test done at home, and they subsequently have a negative PCR test, they can return to school. If a student has a positive LFT from a test done at school, then they must self-isolate for ten days even if a subsequent PCR is negative. In this post I am going to explain how the two tests work, and why a positive LFT is always followed up by PCR.

When a new LFT for detecting small amounts of EPO was developed, Lance Armstrong decided to confess.

LFT or, to give it its full title, lateral flow immunoassay, is not new; in fact, it’s been around for years. LFT is a quick, cheap and simple method used to detect specific analytes or biomarkers. Prior to COVID, the most common use of LFT was in pregnancy testing. Lateral flow testing is also used in drug testing, for example in testing athletes for performance enhancing drugs such as EPO. In fact, it was the development of LFTs that could test for EPO that led Lance Armstrong to confess to having used it in his 7 Tour de France wins; he knew that when stored urine samples were tested using the new method, the game would be up.

LFTs are used to check for substances or biomarkers in bodily fluids or swabs. Urine is commonly used in drug testing, while swabs are used to test for pathogens. LFTs use two lines: one is a control line, which confirms that the test is working; the other is the test line. The lines are made up of labels; these are nanoparticles of substances which will bind to the substance being detected and cause a visible line to appear. Labels include nano-beads of coloured polystyrene or latex (a nano-bead is a bead that is around one millionth of a millimetre in diameter!).

This LFT is positive for COVID. You can clearly see the control and test lines.

So, how does it work for COVID? When you have done your throat and nasal swab, you or whoever is carrying out the test will swirl the swab tip in a small amount of extraction buffer. This is a solution which will break down any virus particles, releasing their RNA; it also maintains the pH (acidity) at a constant level, because changes would affect the result. When you do your test, the control line will appear within a couple of minutes to show that the test is working. If the test is positive, the test line will appear within about 30 minutes.

Polymerase Chain Reaction

The enzyme used in PCR was isolated from bacteria that live around underwater thermal vents. This means that it can withstand the high temperatures used in PCR.

PCR is basically a process which uses an enzyme called polymerase to make multiple copies of DNA or RNA; this is called amplification. This means that PCR can detect extremely small amounts of either substance. One of the most widespread uses of PCR is in forensic science where it is used to amplify minute amounts of DNA to a level where it can be analysed.

In forensics, PCR is particularly useful in solving cold cases. Famously, PCR was used to identify the remains of Tsar Nicholas II and his family from very small samples of mitochondrial DNA.

PCR was used to identify the remains of the Romanovs.

The major advantage of PCR in testing for COVID is that it can detect the virus at much lower levels than LFT. This means that it is particularly useful in testing close contacts, who may have the virus but whose viral load is too small to cause symptoms or a positive LFT. Analysis of the swab is also carried out entirely by professionals working in sterile laboratories, so the potential for human error or contamination is very low.

A PCR machine

PCR has several disadvantages. It requires specialist equipment so must be done in a lab, making it more expensive. It also takes much longer. Amplification of the virus’ RNA using PCR requires multiple cycles of heating and cooling, taking several hours. Some people argue that because PCR is a multi-stage process, there is actually more potential for human error than with LFT; personally, I do not agree with this. PCR has been used for many years in forensic and diagnostic applications, and has consistently been found to be reliable.

So, should students who have had a positive LFT in school but a subsequent negative PCR be allowed back to school? Having considered all the scientific evidence, my opinion both as a scientist and as a teacher is yes they should. The argument is that LFTs in school are administered by staff, so they are more reliable than those done at home. That may be the case, but it certainly does not mean that they are more reliable than PCR, which is widely regarded as the ‘gold standard’ within the scientific and medical communities. To me, this is yet another example of the lack of medical and scientific understanding at the highest levels of government, but don’t get me started on that one!

Spanish Flu, and what it teaches us about social distancing

First of all, hi there to all my readers! I’m sorry I haven’t written anything in a while. Things have been intense with the day job – any teachers reading this will know that working from home and delivering remote learning is actually a lot more labour intensive than face-to-face teaching. Like so many other people, I’ve also been finding social distancing tough. I’ve been asked how I cope with it, and the simple answer is, because I know that I have to. In this article I will be looking at the 1918-19 Spanish Influenza pandemic, and explaining the lessons we can learn from it about social distancing.

It’s inevitable that parallels will be drawn between the situation now, and the Spanish Flu pandemic. This time 100 years ago, the world was reeling from a devastating global pandemic that had killed more people than the preceding four years of war.

It has been suggested that Chinese labourers brought the disease to Europe

The origins of Spanish flu have been hotly debated. There is speculation that the virus originated in China, and was brought to Europe by Chinese labourers working for the British and French armies – a theory that has been seized upon by conspiracy theorists looking for evidence of sinister Chinese involvement in the current pandemic.

Those studying Spanish flu, particularly epidemiologists, have a wealth of data to work with. It was the first global pandemic to occur in an age where there was good record keeping in both military and civillian hospitals.

The initial outbreak was probably Fort Riley in Kansas

Detailed studies of records kept by the US Army have actually narrowed down the origin of the disease to the state of Kansas, and the US Army training camp at Fort Riley. The evidence strongly supports the theory that the disease jumped directly from birds into humans, with ‘patient zero’ being a farm worker from a poultry farm who caught the disease just before enlisting in the US Army.

Wartime conditions were almost ideal for spreading the virus. After the first cases were reported, the illness spread rapidly through Fort Riley; movement of troops ensured that it spread rapidly to other camps and into the civilian population. Troops with the illness were sent overseas to fight, meaning that the disease very quickly spread to England and to continental Europe. It is ironic that the entry of the USA into the war, which was instrumental in bringing it to an end, also ensured that the Spanish flu outbreak became a pandemic.

Nurses in a military hospital treating a patient with Spanish Flu

I won’t dwell here on the disease itself and its effects. If you want to know more, I thoroughly recommend Lyn McDonald’s book ‘The Roses of No Man’s Land’ which contains harrowing first-hand accounts from doctors, nurses and others, of the effects of the illness in crowded military hospitals, camps and troopships.

Spanish flu spread rapidly on troopships such as the RMS Olympic (sister ship to the Titanic)

What I find interesting, and highly relevant, about the Spanish flu pandemic, are the lessons we can learn about social distancing. Wartime conditions meant that social distancing simply wasn’t possible – in fact, the opposite was the case with people crammed together in hospitals, training camps, troopships and, of course, the trenches themselves.

King Alfonso XIII of Spain became seriously ill but survived

Another, more pernicious factor that contributed to the spread of the disease was lack of public information. Basically, the public were not told about the illness for fear that it would damage morale in the critical final months of the First World War. People who could have practiced social distancing didn’t, for the simple reason that they did not realise there was any need to. The pandemic got its name because in neutral Spain, there were no restrictions on the press; they were even free to report when King Alfonso XIII became seriously ill. This led to a misconception that Spain was particularly hard hit.

Not only was social distancing not practised, the British government actually discouraged authorities from putting measures in place to limit the spread of the infection. Medical officers in large cities were discouraged from closing schools, churches, cinemas, theatres, dance-halls etc.; again, out of fears that this would damage morale.

Dr James Niven, medical officer for Manchester during the pandemic

One man who went against this was Dr James Niven, medical officer for Manchester. Against direct advice from the government, he closed schools and entertainment venues, and distributed posters and leaflets giving information about the illness and advice on how to protect against infection (mainly, ‘wash your hands’ – sound familiar?). Niven insisted on quarantine for those who were sick, gave regular interviews to the Manchester Guardian to keep the public informed, and took measures to deal with delays in funerals.

As a result, the rate of infection in Manchester was lower than in other large cities with similar population densities. The death rate among those infected was also lower, because medical services were now overwhelmed as they were elsewhere. High tech devices such as ventilators were not available in those days, but high quality medical care, particularly intensive nursing, could make all the difference between surviving or dying from the illness.

One of Niven’s posters informing the people of Manchester about the Spanish Flu

I’ve no doubt that during the Spanish flu pandemic, there were those living in Manchester who resented the restrictions. Why were their cinemas closed when those in other cities remained open? No doubt, too, there were those who regarded Niven’s information campaign as exaggerated or scare-mongering. I also am in no doubt that if I went back in time to 1918 and had to live in a large city in the UK, I would choose Manchester with its social distancing.

In my next post I will be discussing the differences between oxygen therapy, continuous positive air pressure (CPAP) and ventilation; and the role they all have to play in helping people survive COVID-19. Stay well and safe, everyone.

Social distancing: Why it’s important, and why we find it so difficult

Social distancing has been in the news a lot in the last few days here in the UK, mainly because we Brits seem to be very bad at it! Friends in countries that are locked-down, like France and Spain, are telling me how shocked and horrified they are by scenes this weekend of crowds flocking to parks, beaches and beauty spots. The UK government is threatening lock-down unless we start to take things seriously. In this post, I will discuss why social distancing is important, and some possible reasons why we are finding it so difficult.

Exponential growth curve for hypothetical ‘Virus X’.

Why do we need social isolation? Let’s think about how disease spreads. A person gets infected with a disease, we’ll call it Virus X. That first person to be infected is called Patient Zero. On the first day, Patient Zero infects two other people. On the second day, they each infect two more, and so on. After a week, we have 256 patients.

If each patient infects 5 people a day, then after one week there will be 78125 people with the disease. If each infected person passes the virus on to 10 people, then after a week there will be 1 million with the disease. You get the picture. This process is called exponential growth and is shown on the right. If the shape of that curve is familiar, it’s because you have probably seen it on graphs showing the number of cases of COVID-19 in the UK, like the one below.

Cases of COVID-19 in the UK. In blue, you can see a classic exponential growth curve.
Comparing the spread of ‘Virus X’ with and without social distancing.

How does social distancing help? Basically, unless an infected person is in close contact with someone else, they can’t spread the virus. Exponential growth will still occur, because there will always be some in the population who cannot practice social distancing, i.e. key workers. But the rate of exponential growth will be much slower. This is known as ‘flattening the curve’ and is shown on the left.

An additional consideration is that although discoveries about COVID-19 are being made at an unprecedented rate, there is still a lot that we don’t understand. When you get an infection, it will be several days before you start to show symptoms; this is called the incubation period and varies between different pathogens. When the level of the pathogen in your body drops below a certain level, your symptoms will go away; but you are not yet fully clear of the infection.

A few people have asked me why this pandemic is so different from the 2009 Swine Flu pandemic. With Swine Flu, we were dealing with a new strain of a very well understood virus. In particular, it is known that influenza viruses can only be passed on to other people by patients who are symptomatic. During the incubation and recovery periods, patients cannot pass the virus on except under exceptional circumstances. This meant that only those who were actually ill needed to be isolated. In addition, it is known that patients who recover from influenza viruses will then be immune to the disease.

With COVID-19, the incubation period is up to 14 days, and we still don’t know at what point patients become infections. We also don’t know how long it takes for recovered patients to cease to be infectious, and whether people who have recovered have immunity. We need to know whether immunity develops; how strong it is; and how long it lasts.

Look at the two diagrams below, showing the spread of the hypothetical Virus X through a population. On the left is the situation on Day 1, on the right is the situation after one week. The top diagram shows a population that is not practising social distancing, the bottom diagram shows a population that is. Speaks for itself, doesn’t it?

So, why is social distancing so difficult? Especially for us Brits, who historically have a reputation for doing as we are told. One reason is that we are having to break habits that have become ingrained over many years. Take this scenario: you are in a queue at the supermarket. The person in front of you moves forward, what do you do? You move forward too, to close the gap. This is not neccessarily deliberate, it’s a habit, and changing habits requires conscious thought. The good news is that it doesn’t take long for new habits to develop. I went shopping today (because I needed to, I hasten to add), and everyone was keeping their distance in the queue without needing to be reminded.

Another reason is people are used to freedom of movement. It’s a sunny spring weekend, the kids have been stuck in the car, let’s go to the beach because social distancing means no one else will be there. Unfortunately, hundreds of other people have had the same idea, and when you get there, it’s heaving. Do you have the strength of mind to turn the car round and tell the kids we aren’t going to the beach after all?

Recent panic buying is not helping either. Those of us who have continued to shop sensibly and responsibly have found that due to panic buying, we have had to visit multiple shops to get the basics. I’m trying to practise sensible social distancing due to my asthma, but it’s difficult when you have to visit 3 different shops to find toothpaste! Thankfully things seem to be settling down a bit. This morning I went to a local supermarket and was able to pretty much get my normal weekly shop, much to my relief!

Possibly the biggest barrier to social distancing, though, is the fact that we are primates, and by and large, primates are social animals. Our brains are not wired for isolation and I know I am not alone in worrying about how this will affect my mental health. However, there is a lot we can do to combat this.

The good news is that we live in an age where technology has made it easier than ever to keep in contact with friends and loved ones. So take advantage of Facebook, Zoom, WhatsApp, Skype and everything else that’s out there. Reconnect with people you’ve lost touch with. Share memories of good times! And keep remembering, social distancing isn’t forever; and the better we are at it, the less time it’s likely to last.

In the next couple of days I will be posting some ideas about simple experiments you can do at home to engage children with science while they aren’t at school, so watch this space! As always, if you have specific questions or concerns you’d like me to address, let me know. Stay safe and well, everyone.