By Marcel Salathé, Pennsylvania State University

The measles outbreak traced back to Disneyland has spread to eight states, with as many as 95 cases reported by January 28. Media outlets are highlighting the rise of anti-vaccination sentiments. Scientists are expressing their dismay at people who reject sound medical advice and put their families and communities in harm’s way.

Measles was considered eliminated in the United States in 2000. But if the first month of 2015 is any indication, this year will easily beat the record number of measles cases recorded in 2014.

The narrative during this outbreak, or any measles outbreak really, is that measles is a highly transmissible disease. So transmissible in fact that 90–95% of people must be vaccinated in order to protect the entire population, or achieve what is called herd immunity.

That is partly true. Measles is highly transmissible, not least because people can be contagious days before symptoms develop. But there are three problems with this line of reasoning about vaccination rates.

First, the numbers are based on calculations that assume a world of random mixing. Second, the vaccination coverage is not a perfect measure of immunity in the population. Third, and most problematic in my view, it gives people a seemingly scientific justification for not getting vaccinated – after all, if not everyone needs to get vaccinated in order to attain herd immunity, can it really be so bad if I opt out of it?

What exactly is herd immunity?

Let’s look at the concept of herd immunity first. The basic idea is that a group (the “herd”) can avoid exposure to a disease by ensuring that enough people are immune so that no sustained chains of transmission can be established. This protects an entire population, especially those who are too young or too sick to be vaccinated. But how many people need to be immune to achieve this?

In order to calculate the number of people who need to be immune for herd immunity to be effective, we need to know how many people will get infected, on average, by an infectious person.

Imagine that a newly infected person will on average pass on the disease to two other people. Those two will each infect another two people, who will themselves pass it on, and so on, resulting in the classical pattern of an exponentially growing outbreak.

In order to stop the growth in the number of transmissions, we need to ensure that each individual case causes, on average, less than one new infection. So, let’s say that one case leads on average to two more infections, but instead we want that number to be less than one. That means at least 50% of the population needs to be immune, so that at most, only one of the two people who might have been infected by an individual will be.

How many people need to get vaccinated to achieve herd immunity?

So, how do we calculate what fraction of a population needs to be immune to reach herd immunity? First, we need to know what the reproduction number, or R, is. That’s how many new cases a single case of an infection will cause.

Imagine that you are infected in a completely susceptible population, and you pass on the infection to five other people (ie R=5). In order to prevent an outbreak, at least four out of those five people, or 80% of the population in general, should be immune. Put differently, 20% of the population may remain individually susceptible, but the population would still remain protected.

So if you can estimate the reproduction number for a given disease, you can calculate the fraction of the population that needs to be immune in order to attain herd immunity.

For influenza and Ebola, the number R is about two. For polio and smallpox, it is around five to eight. But for measles it is much higher, somewhere between 10 and 20. And because of that, the goal for measles vaccination coverage is typically around 90-95% of a population.

But there’s a problem with this calculation.

The population is not random

The assumption underlying the calculation for herd immunity is that people are mixing randomly, and that vaccination is distributed equally among the population. But that is not true. As the Disneyland measles outbreak has demonstrated, there are communities whose members are much more likely to refuse vaccination than others.

Geographically, vaccination coverage is highly variable on the level of states, counties, and even schools. We’re fairly certain that opinions and sentiments about vaccination can spread in communities, which may in turn lead to polarized communities with respect to vaccination.

And media messages, especially from social media, may make the problem worse. When we analyzed data from Twitter about sentiments on the influenza H1N1 vaccine during the swine flu pandemic in 2009, we found that negative sentiments were more contagious than positive sentiments, and that positive messages may even have back-fired, triggering more negative responses.

And in measles outbreak after measles outbreak, we find that the vast majority of cases occurred in communities that had vaccination coverages that were way below average.

The sad truth is this: as long as there are communities that harbor strong negative views about vaccination, there will be outbreaks of vaccine-preventable diseases in those communities. These outbreaks will happen even if the population as a whole has achieved the vaccination coverage considered sufficient for herd immunity.

If negative vaccination sentiments become more popular in the rest of the population as well, we may start to see more sustained transmission chains. Once those chains are sufficiently frequent to connect under-vaccinated communities, we may again be in a situation of endemic measles.

The solution often proposed is that we should do a better job of convincing people that vaccines are safe. I’m all for it. But I would also suggest that we should stop basing our vaccination policies on models that made sense in a world of constrained vaccine supply, and aim for 100% vaccination coverage among those who can get vaccinated.

This would also solve another problem, often glanced over: There are many people who cannot get vaccinated for medical reasons, either because they are too young, or because they have other conditions that prevent them from acquiring immunity through vaccination.

Herd immunity against measles requires that 90-95% of the entire population are immune, whereas vaccination coverage is measured as the percentage vaccinated of the target population – which only includes people who are eligible for vaccination. This means that to achieve 95% immunity in the population for measles, vaccination coverage needs to be higher than 95%. This is the scientific argument for a public health policy that aims at 100% vaccination coverage.

More importantly, there is an ethical argument to be made for the goal of 100% vaccination coverage. It sends the right message. Everyone who can get vaccinated, should get vaccinated – not only to protect themselves, but to protect those who can’t, through herd immunity.

This article was originally published on The Conversation.
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By Connor Bamford, University of Glasgow

The world has been keeping a very close eye on the Ebola virus for nearly a year now following the extraordinarily large outbreak seen in Western Africa, which has so far killed more than 8,000 people. One of the things that scientists and public health officials look at is how the genetics of the virus changes. This is because Ebola virus gene sequences have in the past allowed scientists to work out patterns of spread during an outbreak and when and where it likely originated.

While we would like to predict how the virus behaves directly from its gene sequences, we do not yet have the ability to do this. So when the BBC reported that “scientists tracking the Ebola outbreak in Guinea say the virus has mutated,” what did it really mean? Is the virus now more contagious and therefore better able to spread and even more of a worry for those fighting to stop it?

The answer is probably no. Of course the virus is mutating – mutation is a fundamental living process and all viruses do it. The news article contained no new surprising information but it did highlight a lack of understanding – or appreciation – of mutation in viruses and other organisms.

The truism

Mutation refers to the process of genetic change. Naturally, genetic information is encoded in a genome, which is made of either DNA or, in some organisms, a similar molecule called RNA. Genomes are important because they control almost every function of an organism: whether a human has blue or brown eyes; whether a fly has two or four wings, or whether a virus is sensitive to a drug or is resistant.

Genetic information is specified by strings of letters: A, T (U in RNA), C and G. If one sequence has ATCG and then changes to AGCG then we say it has mutated. This is one example of mutation and is referred to as a “single nucleotide change”. It is one of the most simple and common occurrences, especially in viruses such as Ebola.

Mutation is one of the most important processes in living things and is a central feature of things with genomes; without mutation there would be no life on this planet. This is because mutation supplies genetic diversity that can be acted on by evolutionary processes, such as natural selection, to change a particular function of an organism. This only happens when there is a selective advantage to the mutation and its change in function.

For example: a bacteria has a mutation that makes it resistant to an antibiotic that is used commonly – but under conditions without that antibiotic present, it will be no more adapted than its non-resistant cousin. But when you add the antibiotic into the mix then the resistant one will grow more than its sensitive cousin. Therefore it is said that mutation fuels evolution.

The importance of mutation

Some organisms mutate and can evolve at a much greater rate than other organisms. Viruses with genomes composed of RNA, like the Ebola virus, have especially high mutation rates. As it turns out, some other of these RNA viruses also pose a great threat to human health, including the influenza viruses, human immunodeficiency virus (HIV), Hepatitis C virus (HCV) and the measles virus.

One of the more pressing consequences of mutation is in a health setting. There are lots of known examples of mutations affecting human health, including the appearance of antiviral resistance in the influenza A virus, HIV, and HCV; the evasion of vaccine immunity of the influenza A virus between flu seasons, and the emergence of novel pathogens, namely in the origins of influenza pandemics, such as that of the H1N1 virus in 2009-10.

One of the other ways that mutation could do harm is by altering our capacity to diagnose an infection. Viral diagnostics is now commonly based on sequence-specific approaches, such as the polymerase chain reaction (PCR) and sequencing. If a mutation made a virus unable to be picked up by our lab diagnostics then it would be invisible to us.

Mutation and Ebola

During this outbreak, the Ebola virus has infected more than 20,000 people and led to the deaths of around 40% of those people. Recently the strategy to tackle Ebola has been three-fold: diagnose cases and isolate them; treat those confirmed cases, in isolation, using standard care and targeted antiviral drugs; and work to develop preventative strategies, such as a safe and effective vaccine. These strategies appear to have been effective at controlling the outbreak.

But no Ebola antiviral drug has so far completed phase III clinical trials, nor have any of the vaccines, although trials are due to begin in the affected countries.

If the Ebola virus were to mutate would this inhibit this current positive response? Or even one in the future? This is an important and valid point because it could impact our ability to control this epidemic and a similar one in the future, which is critical to save human lives.

Studies that have looked at genome mutations of the virus have shown changes in the genes that are also the targets for antiviral treatments, including those for vaccination. They build a strong case that we should be keeping an eye on these sequences now and into the future. But this is as far as our predictive capacity goes. Without testing how these mutations function in the virus under controlled experimental conditions we will not able to say for certain. However, studies of this sort have not yet been published.

Is Ebola becoming more contagious?

One big concern is whether or not the Ebola virus might evolve to become more contagious in the human population. Two ways this might be achieved is through the virus causing a less incapacitating disease that allows it to be shed more; or spreading via the airborne route rather than via bodily fluids.

Anavaj Sakuntabhai, a geneticist at the Institut Pasteur in France, which put out the warning about Ebola mutating, said they had now seen several cases where people didn’t have any symptoms at all – asymptomatic cases. “These people may be the people who can spread the virus better, but we still don’t know that yet,” he said. “A virus can change itself to less deadly, but more contagious and that’s something we are afraid of.”

But as yet, and this is something which Sakuntabhai admits, we have no evidence that the first is happening and that the virus is evolving to make people less sick. Increased detection of cases with less pronounced disease may be a function of our greater ability to diagnose Ebola in general. And it has been suggested that asymptomatic cases of Ebola virus infection may be more common than once thought.

It is still very unlikely that the Ebola virus is evolving to become airborne, despite the headlines. There is no precedent for a virus changing its mode of transmission and considering how many chances the Ebola virus has had to make such a change during this outbreak and previous ones, without doing so, suggests that evolution of this property might be one step too far.

Putting an end to the outbreak

Recently, the number of cases of Ebola has begun to drop across the three affected nations. This suggests that our interventions have begun to work. This positive response is thus most likely due to the excellent job that front line clinicians and lab staff have done in diagnosing, isolating and treating those patients with the standard care available. If this response continues then we may see the last case in this outbreak appear by the end of 2015.

So despite all of the worries around mutation, this outbreak is being controlled successfully and without targeted antiviral treatments in place. Our focus should be to finish the job in hand and put a stop to this epidemic using what we know works.

Read more about how the outbreak in West Africa began here.

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By Arinjay Banerjee, University of Saskatchewan and Grant Hill-Cawthorne, University of Sydney

The conflicts in Syria and Iraq are straining public health systems and public health efforts meant to prevent and detect the spread of infectious diseases. This is generating a “perfect storm” of conditions for outbreaks. Among the infections raising concern is Middle East Respiratory Syndrome, caused by a type of coronavirus, which emerged in 2012.

Infection with the MERS virus can cause fever, cough and shortness of breath, and is particularly dangerous in older people or people with weakened immune systems or other illnesses. In severe cases it can cause respiratory failure and occasionally lead to kidney failure. As of January 27 the MERS virus has infected 956 individuals and killed 351. Cases have been reported throughout the Middle East, but also in Asia, Africa, Europe and North America.

The MERS virus belongs to the coronavirus family. Even if you haven’t heard of coronaviruses until now, you have probably heard of some of the illnesses different types of coronaviruses can cause, like Severe Acute Respiratory Syndrome (SARS). And if you’ve been coughing and sneezing thanks to a cold, then you could have had a bout of infection with a coronavirus. They aren’t new, or even that rare, but we still don’t know very much about them.

Why are some coronaviruses more lethal than others?

Coronaviruses infect humans on a regular basis and are one of a number of viral groups that lead to symptoms that we clump together and call the common cold: coughing, sore throat, runny nose, sneezing and fever. While this may leave you feeling unwell for a few days, they are rarely lethal. The common cold-causing coronaviruses have been with humans for some time and therefore we have natural immunity to them, reducing the risk of lethal infections.

The coronavirus is an RNA virus, and can mutate and recombine, producing strains that are different from those that the immune system “remembers.” This is called antigenic drift and is the reason we get colds every year – the virus changes a bit every season.

Drifting creates a virus which differs from its predecessor but some similarities remain, so the body might still be able to recognize it and mount a “memory” response, which would lead to no or milder symptoms.

The reason that the MERS coronavirus can be lethal is because the human immune system has never seen this virus before, and has no “memory” from previous exposure. This is what makes an infection with the MERS virus more severe than the cold-causing coronaviruses.

Where do coronaviruses come from?

Within eight months in 2003, the SARS virus spread to 29 countries, infected 8,098 people and killed 774 of them. And now, a decade after the SARS epidemic, we are facing the ongoing outbreak of another potentially deadly coronavirus – MERS.

The SARS coronavirus led to a new found interest in human coronaviruses. Researchers started looking for coronavirus reservoirs, places where the virus can be maintained in the wild by transmitting between, but not killing, its hosts. Because coronaviruses can mutate and recombine, they can sometimes jump species.

Both SARS and MERS coronaviruses are very closely related to bat coronaviruses, suggesting that both these viruses could have emerged from bats. The SARS virus is believed to have spilled over from bats to civet cats to humans. The MERS virus is believed to have spilled over from Egyptian cave bats to humans, with camels acting as the intermediate host species.

It is the cross-species – called zoonotic – transmission of these viruses that makes them have more severe consequences. Our immune system does not have any remembered immunity to these viruses, and therefore infection is likely to become more widespread before it is controlled. This is a particular problem for older people or those with other health problems – in fact it is these kinds of patients who have experienced the brunt of MERS coronavirus infections.

How do we control the spillover of coronaviruses?

Controlling spillovers is not as easy as it sounds. As humans exploit the virgin forests and come into contact with exotic species of animals, one cannot predict the various different viruses that humans would encounter, some of which have never been seen before. The scientific community has only recently started looking at bats and the viruses that they harbor. They are also trying to explore how bats survive infection by these viruses and extrapolate that knowledge to humans.

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By Colin Brown, King's College London

Ebola virus disease was first discovered in the Democratic Republic of the Congo in 1976, and by 2013 had caused about 20 recorded outbreaks across East and Central Africa. These had been restricted to rural areas and confined to small clusters of villages. In each case containment was achieved within a few months and after fewer than 500 confirmed cases. The world assumed that Ebola was too efficient at killing its hosts, doomed to quickly burn out wherever it arose.

The 2014 West African outbreak has changed everything. It was the “Black Swan” – the inevitable consequence we did not foresee. As we head into mid-January 2015, there have been more than 21,000 reported cases spread across nearly every region in three adjacent countries, and more than 8,000 people are known to have died.

Cases have cropped up in the US, Mali, Senegal and Nigeria. Patients have been treated across Western Europe. Until early November 2014, there was no sign of a reduction in transmission and case numbers were rising exponentially. As we wrote in the journal Tropical Doctor, though numbers are now slowing in Guinea and Liberia, there is still an increase in cases in Sierra Leone where 500 healthcare workers have died. There is no certainty the other affected countries will not again see an upsurge in new cases.

Estimates of how many people could be affected have varied widely and included projections of up to 1.4m, or up to 25,000 cases per day by mid-January 2015. This was a dramatic increase since the World Health Organisation (WHO) projected a maximum of 20,000 cases in August 2014, highlighting how difficult it is to predict the future epidemic direction, though organisations such as Médecins Sans Frontières highlighted their concern as early as March 2014.

Current expert opinion suggests that an overall decline will be likely in the next few months, however the “tail” of the epidemic curve will be protracted and punctuated by many smaller, localised outbreaks.

Mathematical modelling is challenging and cannot easily account for conflict, mass movement of people, or breakdown of civil society, but though the very high case numbers may not be reached, one thing is certain: this will be a terrifyingly large outbreak, something never before faced on a global scale.

Same but more virulent virus

Given Ebola’s appearance in a setting thought solely home to Lassa Fever, there was initial speculation that this was a different virus than had been seen before. The same – but different: more virulent, more transmissible.

Modelling now firmly places the current outbreak strain as belonging to the Zaire strain (EBOV), with entry into the West African animal population around the mid-2000s from central Africa. One discrete contact with one infected animal is responsible for all the disease seen.

Early analysis of some 80 samples from Sierra Leone shows that in one month, 400 mutations were identified. It is unclear if those mutations carry any fitness advantage, or whether this epidemic will evolve differently than those seen before. Currently, Zaire Ebola in West Africa is not behaving differently to what has previously been seen. There is no change in route of transmission, no suggestion of aerosolised spread, no gross differences in disease presentation.

Therefore we know the measures required to control this outbreak: contact tracing, adequate testing and isolation, onward referral for treatment, communications with communities, improved logistics to support a fragile health system. These are the stalwarts of public health control across the last decades.

Why did the situation get so bad?

We cannot attribute the failure of early containment on differences in virulence or transmission of the virus. The reasons for lack of control are complex, multi-factorial and open to debate. Emergence was in Guéckédou, a remote and difficult-to-access area in West Africa, with porous borders across the three post-conflict nations most affected: Guinea, Liberia and Sierra Leone.

As with much of Africa, these boundaries were European-drawn and do not correlate with different community identities or languages. Radio messages were initially in official languages only. Spread between countries was likely.

In this region, where availability of mainstream healthcare was already severely limited, the care of unwell individuals is vastly different to that available in the West. Sick relatives are nursed at home by family members, and further care is often sought from traditional healers, unofficial providers and private pharmacies rather than government health facilities.

Peripheral health units are only equipped to diagnose and treat malaria, pregnancy and a few other key conditions, and if patients do go to hospital, in many settings there is a lack of basic equipment such as gloves, aprons, running water and soap. The number of trained healthcare professionals of all cadres is very low.

Additionally, there is huge stigma associated with Ebola, similar to those seen in the early years of HIV care. The present Ebola outbreak began very close to where civil war erupted in Sierra Leone in 1991, and trust in the government in this region is low. Although acceptance of Ebola is rapidly increasing, there was initially disbelief about its existence, and conspiracy theories about population control were prominent and sometimes roused by media.

This constellation of palpable fear and deep mistrust inhibited early engagement and sound communication about the threat of Ebola. It was understandable, therefore, that families were reluctant to hand over their relatives to treatment centre staff wearing masks and suits. This is particularly true when there was a high likelihood of never seeing their loved ones or their bodies again.

These factors have all increased the risk of transmission of Ebola, both in the community and within hospitals, and lead to a delayed and disjointed response both in-country and internationally. By keeping family members at home to die, burial practices involving body preparation and touching by mourners further facilitated spread.

Early in the outbreak, families also buried their own dead due to insufficient staff to bury bodies safely. Given that many of these factors are present in the settings of Uganda and the Democratic Republic of Congo, where previous outbreaks have centred, the emergence of a disease thousands of miles from where it had been seen previously also contributed to spread. Lassa Fever is endemic and may have led to a false sense of security among healthcare workers regarding the transmissibility and mortality associated with viral haemhorragic fevers. Furthermore, wearing full personnel protective equipment in a humid environment comes with considerable difficulties, with differing opinions on which option is best to use. Safely incinerating waste in the rainy season brings its own challenges.

There is general agreement that a sufficient early international response, when traditional control strategies of case isolation, contact tracing and geographical containment were feasible, were not forthcoming. The WHO were slow to deploy experts, not appreciating the potential seriousness from the outset. Approaches used in smaller outbreaks were followed, and institutions were slow to adapt to new models of care. There was an initial dearth of organisations willing to deploy clinical staff to the field and many traditional health non-governmental organisations withdrew their in-country staff. Fear led to delays as they adapted to the disease. And unlike Severe Acute Respiratory Syndrome (SARS), major travel routes with potential spread into the West were not affected. The world watched but did not engage.

New therapies

Novel therapeutics are on the horizon. TKM-Ebola, ZMapp, Favipiravir, Brincidofovir and other novel agents are being fast-tracked by regulatory authorities and rolled out for testing in clinical settings.

Convalescent plasma (using blood plasma from Ebola survivors) – long thought useful in a variety of viral illnesses including SARS, influenza, Crimea-Congo haemhorragic fever – offers a potential treatment option that can be delivered locally using modified existing transfusion services. Any reduction in circulating and replicating the virus may allow the body vital time to produce immunity; however this has not proved effective for Lassa Fever and needs to be evaluated formally.

There are three major vaccine developments underway, entering Phase I and II trials, likely eligible for roll-out by early 2015. However, though these offer hope for the future, they are unlikely to shape the control efforts of this outbreak. Earlier trial intervention was hampered by a lack of ability to conduct research given the burden of treatment needs, so we’re still waiting for evidence of their effectiveness from the field. Simple treatment interventions such as aggressive electrolyte replacement and treatment using anti-diarrhoea agents remain untested.

What can be done now?

The only human-to-human transmission of Ebola occurs via direct contact with body fluids of an infected individual. Importantly, the chance of transmission is greatly increased in the advanced stages of the disease, when diarrhoea, vomiting and bleeding can occur and viral load is high. Disease control is therefore aimed at interrupting this transmission and consists of early case identification and testing, effective isolation and contact tracing. None of these were reliably being achieved early in the outbreak: cases were identified in the late stages when substantial exposure had occurred; testing suspects took several days to perform; treatment centres were at capacity; and contact tracing was disorganised.

What was needed in West Africa was a multifaceted international response, integrating different agencies and spanning all affected countries, with the cornerstones of disease control at its heart. As case numbers grew, and more regions were affected, achieving a coordinated response became increasingly difficult. Each new case exponentially increased the workload for clinical and public health staff; hence every case and every day compounded and threatened to overwhelm any response, especially where a fragmented health service was already present.

Hope is on the horizon. We are seeing a redoubling of efforts along with disease spread – international agencies and regional funders have ramped up their response, there are money and material human resources being deployed daily. Governments are stepping up to the challenge. As well as financial commitment, logistical assistance is paramount. Armed forces, who have the responsiveness and capacity to stage a meaningful intervention, are being deployed to deliver infrastructure, logistics and engineering support. In Sierra Leone, holding and treatment centres are being built apace, staffed by local workers with technical support and oversight from international agencies. Most importantly, this response is happening now.

We’re building a robust model of care at King’s Sierra Leone Partnership, which aims to help build Sierra Leone’s health system by strengthening training, clinical services, policy and research. One way we’re doing this is by building units in existing healthcare facilities for testing and holding, allowing these centres to stay open for care of other health needs: paediatric vaccination, maternal care, HIV management. Onward referral to dedicated treatment centres keeps the existing infrastructure and prevents fragmentation of care.

In addition to tried-and-tested control methods, the seriousness of this outbreak represents an opportunity for using new approaches if potential harms and benefits are properly considered. For example, the employment of Ebola survivors as “patient champions” has been proposed, both in advocacy and clinical work within communities and hospitals.

Once numbers begin to fall, complacency must not set in. Control efforts must be maintained until every case has been treated.

Looking to the future

In the event that Ebola is brought under control in West Africa over the coming months, it is paramount to remember how badly damaged the remaining health infrastructure will be. As is the case with humanitarian disasters, there has been a crippling effect on other programmes for communicable and non-communicable diseases alike.

In Sierra Leone we recently observed a reversal of steps to improve health since the civil war ended 12 years ago. Other activity essential to a functioning democracy such as food supply, security, industry (particularly mining) and trade sectors are facing significant challenges. A response that strengthens these institutions in addition to control efforts is needed.

Ever since its discovery, it has been appreciated that Ebola poses a serious risk to global public health. Infectious diseases represent a global threat, not just to those within the country or region of emergence. With the current increase in the movement of people (rural to urban, within countries and across borders), this risk will inevitably increase. While the current priority should be to contain the present outbreak, there is a great need to plan for prevention of future events. The development of an international response group tasked with immediate assessment of and initial response to emerging pathogens is needed, backed by sufficient international political will, clinical expertise and funding. This needs to be agile and responsive, with clear chains of command, and able to engage early.

We may have been fortunate to have avoided an outbreak of this scale before now. Will we be ready next time? And will we succeed now? The upcoming months will be vital in determining the direction of the response. Time is not on our side, but the will and effort is now here for the humanitarian catastrophe of our time. Let it continue.

This article was co-written with Paul Arkell and Sakib Rokadiya, volunteer doctors with the King’s Sierra Leone Partnership

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