I might never have met Rob if it hadn’t been for his disease. At university he could be a very hard man to find between lectures, orchestra rehearsals, choir, trampolining – his enthusiasm for life would rival that of three people. But Rob does a lot of what he does because it literally helps him survive.
“When he was born I thought, right, I’ll do everything and anything in my power to give him the best chance,” says his mother, Alison. Doctors told her exercise was crucial – and the earlier the better. “We started him swimming as soon as he had had his vaccinations at four months – he went every week. We’d chuck him up and down in the air and throw him around to mimic a trampoline. He trampolined every week from the age of two until he was 16. He was going to learn the trumpet but the hospital said woodwind would be better, so he went straight onto the saxophone at about eight years old.”
The trumpet was my instrument, and I got to know Rob playing in the same student soul band. He was the boy with an infectious laugh who shared my enthusiasm for Motown, not the boy-who-has-a-genetic-disease. The only outward indication of his condition still happens at meal times, when he subtly pulls out a medicine jar and, with a skill that comes from decades of practice, swiftly swallows a handful of pills in a single gulp.
These capsules contain the digestive enzymes Rob needs to process food properly. They are only a hint at the burdensome and repetitive regime he follows every day. But they are also a symbol of how continual improvements in medication and treatment throughout Rob’s life have made it easier to live with his condition – and hugely increased his life expectancy.
Alison and her husband, Andy, were called into a crowded room in the hospital. Six days after a difficult birth and still recovering from her caesarean, Alison perched on Andy’s knee on the only unoccupied chair in the room, surrounded by some six or seven doctors and nurses. Their son lay in intensive care with pneumonia and gastroenteritis. They were told that he had cystic fibrosis.
Cystic fibrosis (CF) is caused by a genetic defect, inherited from both parents. After sickle-cell anaemia, it is one of the most common life-shortening genetic diseases for Caucasians – in the UK, five babies are born with CF every week, and every week two people die from it. There are approximately 70,000 people with the condition worldwide. The defect makes the body produce a thicker than normal mucus in the lungs – mucus that normally helps protect and lubricate internal organs. The heavier, stickier variety causes an array of symptoms, including diabetes, brittle bones, infertility and liver disease.
The CF defect is caused by any of nearly 2,000 possible mutations that affect a protein, CFTR (cystic fibrosis transmembrane conductance regulator), on the outside of cells that make mucus, sweat and saliva. The most common mutation – called delta F508 – causes people to lose a small bit of genetic sequence in each of the genes that makes CFTR. This leads to one crucial building block being left out. As a result, the protein doesn’t fold properly and is destroyed by the body, leaving its cells short of CFTR.
In the 1960s, a British child with CF was lucky to live past five years old. Rob is now 26, and half of all people in the UK with CF are now expected to live beyond the age of 41. The prospects for babies born with CF today are even better. When I talked to Rob, he told me that the staggering size and pace of these improvements render life expectancy estimates practically meaningless to him.
CF affects different people with different severity. Most people with CF die from chronic bacterial infection of their lungs long before they reach old age.
“That’s pretty much what happens if you ever tell anyone about CF,” says Alison, “that it’s something to do with the lungs and that you hit them.” This beating of the chest is the physiotherapy that becomes a constant drudgery in the lives of people with CF, a time-consuming regime necessary for preventing their lungs from becoming blocked, which can cause permanent lung damage.
As a baby, Rob’s physiotherapy would take about 15 minutes, followed by 10 to 15 minutes of holding a nebuliser up to his face to inhale medication – all of which had to be done before he could be given any milk for a feed. He would also be in and out of hospital with chest infections and bouts of gastroenteritis. At four months old, Rob had spent nearly half his life in hospital.
At their family home in London, we sit with piled-up photo albums on the dining-room table. The earliest show a very small and thin newborn baby. Problems with the pancreas, which normally produces a mix of enzymes for digesting food, mean that people with CF have difficulty breaking down and absorbing fat, carbohydrates and proteins. Alison had to feed Rob milk mixed with powdered extracts of pig pancreas. She remembers it as having a distinctive farmyard-type smell that stuck in the back of her throat. “The problem was that the moment you added it to food, it started digesting the milk. This looked, and probably tasted, horrible, but it meant the food was breaking down before reaching the right part of his digestive tract.” She would hurry to feed Rob the bottle of disintegrating milk before the mix had completely broken it down.
Then, in 1988, Alison’s and Rob’s lives changed, thanks to Creon. Made by Abbott Pharmaceuticals (now AbbVie), these capsules replaced the missing lipase, protease and amylase enzymes in Rob’s digestive system, allowing him to digest his food without the need for stomach-churning substances extracted from animals.
This was a miracle. When Rob was born, the poor treatments available meant that children with CF struggled to digest and process fat, so low-fat diets were recommended. “This is why CF children were always really scrawny,” Alison remembers. But access to better enzymes so early in Rob’s life meant he could switch to a higher-fat diet, with more calories. Thanks to this, Rob today does not have the thin, undernourished look that used to be characteristic of people with CF. Instead he looks just like any other man in his mid-20s, only with three times as much enthusiasm.
© Bruno Drummond
While others are snoozing or reading the paper over breakfast, Rob will be inhaling hypertonic saline to loosen the mucus in his lungs. Next comes 20 minutes of percussion physiotherapy. “I go through a cycle of breathing exercises, and hit myself on the chest to loosen things up,” he explains. “There is a knack – you have to sort of cup your hand, which also makes it less painful.” He uses this vigorous series of exercises to loosen and then bring up mucus from his lungs, preventing it from blocking his airways and harbouring dangerous bacterial infections. “The breathing exercises are supposed to reach different depths of your lungs, and some of them involve expelling air very quickly to induce coughing, which is quite a strange thing to do to yourself.”
After the saline and the physio comes an inhalation of the asthma drug salbutamol, which helps open up those airways, followed by a daily regimen of antibiotics to help keep the bacteria that have already colonised his lungs under control. Ideally, he does the whole thing again in the evening.
Such a routine is “just not realistic” twice a day, says Rob, now a full-time maths teacher, an accomplished musician and an avid bridge player. “I don’t know whether people sometimes underestimate how impressionable a child is,” he says. “I remember when I found out in primary school that not all of my friends did 20 minutes of physio and a nebuliser every morning. I just thought that was what everyone did.”
As a child, Rob sat at least twice a day for 20 minutes, inhaling from something the size of a briefcase. “I had a compressor thing that was plugged into the wall. It was linked to a hand-held chamber that I had to hold to my face. I was a nine-year-old child, having to keep the thing level, just trying to watch TV.”
This massive piece of kit was a nebuliser, a container that converts liquid medications into a mist, attached to a compressor that would blow air through this mist, allowing it to be breathed in. Available since the early 1980s, nebulisers allow medications to be taken in to exactly where they are needed, the sticky, clogged-up, bacteria-infested lungs. People with CF use them to inhale antibiotics (to keep bacterial populations at lower levels) and strong salt solutions (to loosen mucus) directly into their lungs.
As Rob grew up his briefcase-sized nebuliser was gradually replaced by something smaller than a shoebox, yet more powerful at pushing drugs into his lungs. By his late teens, he had upgraded to an even more compact nebuliser, about the size of a large camera, that can easily be held within his hands and takes just nine minutes to use.
Thanks to advances like this Rob was able to go to university, Alison adamant that he needed to leave London – “I wanted him to start learning to look after himself.” He could choose any university but no more than two-and-a-half hours away, so she could still get to him quickly if needed.
Rob remembers being a bit nervous, saying that it is well known for “CFers” to degenerate when they leave home for the first time. But he was reassured by the gradual handover of responsibilities throughout his teens. “By the time I was in sixth form I was managing my own drugs, but with helpful reminders from mum.”
For Alison, managing her son’s symptoms had been a full-time job. During his first six months, Rob’s parents gave him physio four times a day, resting his tiny body beneath a towel on a cushion, and carefully hitting him to loosen the mucus in his young lungs. Sometimes they would need to do this in a public place. “I think at least twice I was threatened with being reported to social services by members of the public,” she laughs.
Rob was nearly two years old when scientists discovered the CFTR gene, and its role in CF, in 1989. The breakthrough was heralded as a milestone. Some believed a genetic cure was just around the corner.
Ever since scientists began to understand the genes that are linked to diseases, and the mutations that cause them, gene therapy has been a tantalising prospect. If a mutation is the cause, why can’t we just fix it by replacing the broken part?
On the face of it, CF is a perfect candidate for gene therapy. It’s literally a textbook genetic disease – if you were taught about inherited disease at school in the last 25 years, you’ll likely have studied CF as the example of a simple, one-gene, recessive disease that happens to be relatively common in the Western world. Mutations in the CFTR gene lead to faulty versions of an important protein being made, but only people who have two mutated copies, one from each parent, suffer from CF. People who have only one mutated copy are carriers with no symptoms, approximately one in every 22 people in the UK.
Scientists still do not know exactly how CFTR is responsible for causing the symptoms of CF. The leading theory is that, in people with CF, ions and water do not move across the epithelium, the thin layer of tissue that lines all parts of the body. This makes it harder for tiny hair-like structures called cilia to wave around or ‘beat’, which would normally move mucus and the airborne bacteria it traps out of the lungs and airways.
Yet, theoretically, CF is one of the easiest genetic conditions to fix. Healthy copies of the CFTR gene could be delivered to cells in the lung in much the same way that people with CF already inhale treatments through nebulisers. Once they got into the lung cells, the healthy copies of the gene could make functioning CFTR proteins.
“It was very alluring at the beginning to say I have a gene, I have a delivery device, surely I can get it in,” says Eric Alton, professor of gene therapy and respiratory medicine at Imperial College London. People expected that once you’d identified the broken gene and what it did, you could do gene therapy by adding the normal gene. “Neither of those [discoveries] have been forthcoming rapidly,” he reflects.
The 25 years since CFTR’s discovery seems an awfully long time to wait – and still be waiting. The disease has “contributed much more to science than science has contributed to the disease”, Jack Riordan, one of the gene’s discoverers, told the journal Nature in 2009.
Alton says there is only one barrier to gene therapy – delivery. The difficulty is “you’re trying to put a gene into a lung that is extremely well-defended,” he says. “Your lungs have evolved to keep things out, and we’re trying to put something in. I think it’s no more complicated than that.”
Alton began working on CF the year Rob was born. When a CFTR protein works properly, negatively charged chloride ions move through it, while positively charged sodium ions pass through another channel. This movement of negative charges can be detected as electrical current within the body. Working at the Royal Brompton Hospital in London, Alton began developing a tube that could be inserted into the nose or a lung to measure this electricity. His tool is today used around the world to diagnose people who get indeterminate results from the standard diagnostic tests. “The CF gene was identified in 1989, and then there was the possibility that we could use this diagnostic test as a way of measuring whether gene therapy was successful or not.” He’s been trying to develop a genetic therapy for CF ever since.
The “$64 million question”, as Alton puts it, is how much CFTR function do you have to have for you to be healthy? Someone with two normal copies of the gene, and 100 per cent fully functioning CFTR, will have no lung disease. But the same is true for someone who is a carrier of CF – who has only one normal working copy of the gene and thus 50 per cent CFTR function – they’re still perfectly healthy. This suggests that to cure CF, we don’t need to completely fix it, we just need to fix it enough. The crucial question is how much.
To answer this, Alton points to another related disease, congenital bilateral absence of the vas deferens. Men with this condition are missing the tube that carries sperm from the testes to where they become part of semen, and are thus infertile. This missing part relates to the CFTR gene, and many men who have the disease have CFTR mutations, leaving them with just 10 per cent CFTR function. But these men do not have lung disease.
Alton plots an imaginary graph in the air, of CFTR function versus lung health: people with severe CF on the left, healthy people with two normal copies of CFTR on the right. People with really severe CF who have bad lung disease typically have about 1 per cent CFTR function. “The next point on your graph is CF patients with mild mutations – these patients have quite reasonable lung function, and about 5 per cent CFTR function,” says Alton. The vas deferens condition is associated with about 10 per cent CFTR function, and these men have healthy lungs, just like CF carriers and people with two normal copies of the gene, who have 50 per cent and 100 per cent CFTR function, respectively. “So if you draw a graph, you’ll see you’ve got a sharp slope to start with, and when CFTR function reaches 10 per cent, that should be enough to keep your lungs healthy.”
This makes all the difference. The chances of fully compensating for a broken gene or fully fixing all of a person’s misshapen proteins are slim – to mimic naturally occurring levels of 50 or 100 per cent would be a gargantuan task. But boosting CFTR function from 1 to 10 per cent could be all that is needed to protect from lung disease.
Alton and his collaborators have hit upon a way to get through the lung barrier and deliver those healthy genes to the lung’s cells. DNA cannot enter living cells on its own, but it can be packed inside fatty parcels and smuggled inside. The team use liposomes, microscopic bubbles with an outer layer of fatty molecules that mix easily with the make-up of a cell’s surface. Once inside, the CFTR gene finds its way to the cell’s nucleus, where the genetic material is kept, though exactly how it gets there is still unclear.
The important thing is that the therapy seems to work. The team’s early studies in the late 1990s found that gene therapy could boost CFTR’s electrical activity to 25 per cent on average, a level that Alton believes should theoretically be more than enough to protect a person’s lungs.
After testing the potential of gene therapy, Alton’s team needed to explore how large a dose would be safe but effective enough to use on a long-term basis. In 2009, Rob, then in his final year at Oxford University, enrolled alongside 36 other eager people with CF to take a single dose of the gene treatment. Although this experiment was mainly intended to check the safety of the drug, the researchers got tantalising glimpses of its power. “Some people showed fantastic changes. Some people completely corrected their electrical defect – whilst some didn’t show any change,” cautions Alton, keen not to get too carried away.
It has been such a long time coming that many outside the project – not just scientists but also people with CF and their families – are sceptical. Alton has no doubt that gene therapy will work. “It’s only a question of delivering a gene into a nucleus – it’s not rocket science,” he says. “I have complete scientific faith that it will work at some point.” But the practicalities of such a task are more difficult. Not only must the gene be read by the cell’s own machinery to make the right protein, it must do this on a large enough scale to make a difference to the disease. And over time, as lung cells repair and replicate themselves, repeated doses of the therapy need to be just as effective as the first to be able to sustain any benefits in the long term.
The key test now is to see whether the improvements seen by Alton and his team produce real changes in CF symptoms. “We can get quite reasonable changes in electrical measurements… The question is does that mean anything? If we get 25 per cent restoration of CFTR function, does that mean we’re sitting on the therapy we’re looking for, or that we are a million miles away? You won’t know until you do something repeatedly.”
His aim is to develop something that takes off, even a little, and go from there. “We always say to the patients that we have modest aspirations… like I think the Wright brothers had for the first aeroplane that flew. It didn’t fly every day, it only flew 50 yards, but it proved that powered flight can happen.”
© Bruno Drummond
Like many people with CF, Rob manages to keep abreast of the latest research into his disease using the internet. Twitter, blogs and mailing lists make it easy for him to stay up-to-date, although a favourite gripe of his is how much harder it’s been to keep plugged into the CF online community since Google Reader was shut down. But ivacaftor was hard to miss.
An American team had developed the first ever drug to directly and successfully fix the broken protein causing CF. After all the focus on gene therapy – with limited results – this new way to tackle the disease seemed to come out of left field. But ivacaftor was the result of more than a decade of work.
It began almost ten years after the CFTR gene had been identified in 1989. Frustrated and disappointed by the slow progress, the CF Foundation, a charitable funder of research in the US, decided it was time to try something else. One suggestion was to stop trying to fix the faulty gene factory, and instead fix the broken products. “It was kind of a crazy idea,” says Paul Negulescu, a researcher at Vertex Pharmaceuticals, over the phone from San Diego. “It was unprecedented – there were no examples of drugs that could restore the function of a defective protein in people.”
It was 1998. Rob was getting ready to start secondary school. The Human Genome Project would soon be complete and the first ripples of its impact were being felt through biological science. Amid the buzz, there was a lot of interest in applying the new technologies involved to drug discovery. “There was this atmosphere, that there are new tools to begin to find drugs for targets,” Negulescu recalls.
Negulescu had first come across CFTR while he was studying for his PhD in a gastrointestinal physiology lab at the University of California, Berkeley. He’d thought about what the protein normally does in transporting ions and water across the gut lining, but moved on to other scientific questions when he was unable to secure funding. He was working at a biotech start-up in San Diego when the CF Foundation came knocking. Negulescu, with his ion channel expertise, was brought in on a project that would provide the first ever direct treatment for CF.
His team screened hundreds of thousands of molecules in tiny wells on plates able to host up to 384 experiments at a time. In each well they put mouse cells with defective CFTR and added a different compound to each one. These were the high-throughput screening methods of the post-genomics age. If a cell successfully passed ions through its CFTR, it would light up thanks to a fluorescent marker. Eventually, one did.
During a second round of screening in 2003, they found ivacaftor. “If you think of the [CFTR] channel as a little bit like a door… in CF the hinges are rusted and the door can’t open and close. Ivacaftor loosens those hinges,” Negulescu explains. The exact way that ivacaftor works is still unknown but it seems the small molecule helps the CFTR protein find a different way to open and close.
It’s not a complete cure – of the many CFTR gene mutations that can cause CF, ivacaftor can only treat those where faulty CFTR proteins manage to get out to the surface of the cells, meaning it isn’t of use where the proteins are degraded before they reach the surface, or where no proteins are made at all. But where it works, it is extremely effective. The team have had particular success using ivacaftor to treat a mutation known as G551D – which around 4 per cent of people with CF have. In 2006, they began a trial of the drug on 20 people who carried the G551D mutation. Despite the small size of the study, the results were clear – ivacaftor improved CFTR function in people with G551D.
“Every end-point that we looked at… we saw marked changes,” says Negulescu. “People with CF have abnormally high levels of chloride in their sweat… but when we looked at that the levels dropped dramatically to below the cut-off point for where you get diagnosed for CF.” Although that first study lasted only two weeks, the team also saw improvements in the lung function of participants. A key measure in people with CF is the volume of air they can force out of their lungs in one second. After 14 days taking ivacaftor, this volume increased by an average of 10.1 per cent, around 220 millilitres.
In 2009, the team began a larger trial, with 200 patients from the US, Europe, Canada and Australia – over 10 per cent of all the CF patients with the G551D mutation in the world. After 48 weeks, the participants could push an average 10.6 per cent more air out in a second, and their sweat was much less salty. The success meant that by 2012, the US Food and Drug Administration approved the use of ivacaftor within three months, one of the fastest drug approvals ever to have taken place in the US. A year later, patients with G551D in the UK began to receive the drug.
Nick, a 38-year-old businessman in London, was one. For him, the effects of ivacaftor, now sold under the trade name Kalydeco, were near-instant. “It’s absolutely amazing. I felt there was a difference within about 24 hours.”
“Once you start coughing, it’s really hard to stop until you get rid of the phlegm, and, because you cough a lot at night, it disrupts your sleep,” he says. “I used to be in board meetings or on a date, and I would never know when I was going to start coughing.” Since he began ivacaftor in March 2013, Nick has been getting used to living a more normal life, which he says he “hadn’t really felt before”. He’s much healthier too, needing less daily physiotherapy. “I discovered that I now put weight on. The doctor would think this is great, but – I know it sounds vain – it used to be really easy for me to eat a lot of chocolate and still have a six-pack!”
We don’t yet know what the long-term effects of a life of taking ivacaftor will be, and it’s still too early to say whether the striking difference it makes to people’s lives will last. Until patients have been taking ivacaftor for more than a few years, it won’t be known for sure whether the drug has toxic effects. And while Nick felt some effects instantly, it will be some time before researchers know if ivacaftor successfully treats the slower, subtler symptoms of people with CF, such as their gradual loss of bone density.
Yet at the time of writing, it is the only drug ever to have been discovered and approved that directly acts upon the cause of CF, rather than just alleviating the symptoms. This, says Negulescu, is in part thanks to the close interest of the CF patient community worldwide. “It is remarkable that we were able to recruit over one in ten [G551D] patients into our study for an experimental medicine like this,” he says. “Patients, physicians and caregivers were very aware of the small study. Word got around very quickly to the patient groups… and they came forward. I think the fact that it was such an active, well-connected patient community was really key.”
Negulescu’s team know these patients not just as research subjects, but as people. “We had a young lady on the G551D trial here in San Diego,” Negulescu remembers. “The day the drug was approved, it was on the news… She rushed right over after work to share the excitement about the surprise early approval with us. She took a couple of her enzyme pills, and then shared our celebration cake.”
Rob is an endearingly positive person. He doesn’t have the time or the inclination to moan about the small stuff – he’d much rather talk music or movies, or swap anecdotes. He credits this in part to how Alison and Andy raised him, describing his regular hospital check-ups as “just a fact of my life”. He says he tries hard to limit his more downbeat feelings and concerns to those days only. While he will talk about his lung health in general terms, he doesn’t go further. “The more specific details of what goes on are, to me, incredibly private.”
Rob’s genetic CF combination is a tricky one. One of his CFTR genes produces no protein at all, and nothing short of gene therapy is likely to fix that. But his other CFTR gene has a mutation called delta F508, which means it is missing an important protein building block. This results in a misshapen CFTR protein that is destroyed by his own cells before it can get to the cell surfaces where it is supposed to act. Of all people with CF worldwide, around 47 per cent have two copies of this mutation, with a further 39 per cent having one copy of delta F508, like Rob.
Rob still actively participates in CF research with scientists like Alton. Alton coordinates the UK Cystic Fibrosis Gene Therapy Consortium, which unites researchers at Imperial College London with those at the Universities of Edinburgh and Oxford. After 11 years of hard work, the consortium finally embarked upon a multidose clinical trial of their genetic therapy in 2012. Patients received one dose of treatment a month, for 12 months, with the last dose this May. The team are now analysing their data, and will know the results soon.
By the stage of the multidose trial, participation became a large time commitment, difficult for people like Rob, who had now graduated from university and begun his job as a full-time maths teacher, to fit around a normal working life. His working day starts as early as 8.45, and in the evenings he juggles department meetings, parents’ evenings and marking with choir rehearsals, orchestra performances and a couple of bridge games a week. But while many people with CF were unable to take part in such an extensive trial, the CF community has followed its progress with keen interest. “Lots of people ring up every day and ask what the results are,” says Alton.
The consortium plan to reveal their data in early October, at the North American Cystic Fibrosis Conference in Atlanta, Georgia, the world’s most important CF research meeting. “I’m just hoping that some people on some occasions can improve,” says Alton philosophically, “that’s all I’m looking for.”
Regardless of its outcome, the consortium are already pushing forward with a second way of delivering gene therapy to the lungs, using a type of virus they believe could be safer and more effective than other viruses that have been used for gene therapy. They hope to trial it in people with CF in 2017.
Meanwhile, Negulescu’s team in San Diego are working on a second small molecule called lumacaftor – which they believe will help those, like Rob, with delta F508. Lumacaftor helps broken, and normally discarded, CFTR proteins get to the cell surface, where they need to be. At the time of writing, his team were wrapping up a crucial big trial of using lumacaftor and ivacaftor in combination – the drug pair will both put the CFTR door in the right place and then help open it. Negulescu told me the therapy could be approved by the end of 2015.
Yet when the first results appeared in June 2014, I was disappointed. Like so many scientific advances, the results show a significant and important improvement, but not a large and dramatic one. After 24 weeks on the combined treatments, trial participants showed an average improvement in the amount of air they could push out of their lungs in one second of around 2.6–4 per cent. Statistically, this is significant, but it’s only a small improvement in lung function.
In an email, Negulescu told me his team were very excited by these preliminary results. As well as improved lung function, they also found that patients on the drug combination put on weight and suffered fewer bouts of severe bacterial infection and inflammation, an important result for long-term lung health and quality of life. It’s a great result, but still a lot lower than the 10.6 per cent improvement Vertex saw after 24 weeks of using ivacaftor in people with G551D. I was disappointed, both for the team and especially for Rob.
Yet Alton says this is a hopeful time for CF research. Vertex are planning to work on a third molecule to enhance the effects of lumacaftor and ivacaftor. The results of Alton’s big gene therapy trial are due in October 2014, and it is possible that one day, small drug molecules like ivacaftor and lumacaftor could be used in combination with gene therapy to boost CFTR function in the trickiest combinations of mutations. “We know more about the disease, there are pharma companies like Vertex who have done very well… there’s gene therapy… and life expectancy continues to rise,” he says. “In a graph of optimism against time, the trend is very much on the up.”
There is still much to be done in refining treatment of the disease. Research might help to reduce the number of tablets and the frequency of physiotherapy that are needed, Alton says. Until a cure is found, the most crucial studies for Rob and others like him will be those that produce new antibiotics and more effective treatments for removing mucus, so that he can keep his lung infections under control and minimise lung damage. For instance, recent innovations mean that when Rob’s infections get out of control, he no longer has to spend two weeks lying in hospital being drip-fed antibiotics. Now he just visits the hospital to get an intravenous line put into his arm, and can then treat himself from home, using special pressurised rubber balls of antibiotics that drain themselves into his arm, without the need for hypodermics. Instead of having to take sick leave, Rob can continue to go into work, where the pupils he teaches mostly have no idea and no need to know about his condition and treatments. “I think even a lot of my colleagues don’t know. I’m not actively trying to hide it, but I don’t see a need to broadcast it,” he says.
“Every step is a step closer to a cure,” says Rob. “I think we CFers just have to take every inch we can.”