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At what point is a disease deemed to be a global threat? Here’s the answer
Whenever there is an outbreak of a disease in the world – such as monkeypox – it is up to the World Health Organization (WHO) to consider what sort of weight to give it, including whether or not it constitutes a public health emergency of international concern.
Global efforts to manage epidemics are documented as far back as the black plague in Europe in the 14th century. Since that time, rules have been developed and honed to keep up with the emergence of new diseases as well as with the growing complexities of a world that’s increasingly connected.
There are many diseases that can affect large numbers of people. But not all diseases are considered public health emergencies.
These include the degree of contagiousness and potential for rapid spread, severity of infection, case fatality rate (the number of infected people who die), availability of vaccines or treatment (it’s more serious if there are none), impact on travel and trade, and the socioeconomic context.
What it triggers
Declaration of a “public health emergency of international concern” by the WHO triggers a number of things.
The first is that it signals a commitment to provide international resources for the response.
The second is that it enables other provisions of the International Health Regulations. These originated from the International Sanitary Regulations of the mid 1900s, which were used to control cholera epidemics. At this time, there was increasing awareness of the social and economic effects of epidemic diseases across borders, as well as concern about undue interference with trade.
In 1969 the regulations were renamed the “International Health Regulations” by the WHO. They were then modified in 1973 and 1981. But even then they provided a framework for only 3 diseases – cholera, yellow fever and plague. The principles behind them was
maximum security against the international spread of diseases with a minimum interference with world traffic.
In 1995, formal revision commenced to expand the scope of the regulations with six proposed categories of reportable syndromes:
acute haemorrhagic fever syndrome,
acute respiratory syndrome,
acute diarrhoeal syndrome,
acute jaundice syndrome,
acute neurological syndrome, and
other notifiable syndromes.
In addition, five factors were proposed to determine if a cluster of syndromes was urgent and of international importance. These were rapid transmission in the community, unexpectedly high case fatality ratio, a newly recognised syndrome, high political and media profile, and trade or travel restrictions.
The last revision to the regulations was done in 2005 following the SARS epidemic of 2003.
The five substantive changes from the prior version were:
a dramatic expansion of the scope of the regulations,
the creation of obligations on states to develop minimum core surveillance and response capacities,
granting WHO the authority to access and use non-governmental sources of surveillance information,
granting WHO the power to declare a public health emergency of international concern and to issue recommendations on how states-parties deal with it; and
the incorporation of human rights concepts into the implementation of the regulations.
The regulations set down how an emergency will be managed. This includes setting up a roster of experts appointed by the Director General of WHO in all relevant fields of expertise. Then an emergency committee is drawn from this roster for advice. The committee has to decide on a range of issues to do with managing the epidemic. This includes whether an event constitutes a global emergency and when it should be ended.
More than a health issue
But the regulations can only go so far. Many countries cannot comply with them due to lack of resources.
Many of the problems of global emergencies are not specific health problems, but relate to civil society, community engagement, law and order and border control. In the 2014 Ebola epidemic, for example, a health promotion team was massacred in Guinea because local people were fearful of outsiders coming to their village. During COVID-19 we also saw civil unrest in some countries. All of these issues are considerations for the WHO when deciding whether to declare a public health emergency of international concern.
This is a revised extract from an article previously published by The Conversation Africa written by C Raina MacIntyre and Obijiofor Aginam.
C Raina MacIntyre, Professor of Global Biosecurity, NHMRC Principal Research Fellow, Head, Biosecurity Program, Kirby Institute, UNSW Sydney and Obijiofor Aginam, Principal Visiting Fellow & Former Deputy Director, International Institute for Global Health (UNU-IIGH), United Nations University
You’re probably inundated with news and messages about coronavirus at the moment. But how do you know if you’re consuming evidence-based information or just speculation and myth?
There’s still a lot we don’t know but here’s what the evidence tells us so far about the coronavirus, called SARS-CoV-2, and the disease it causes, COVID-19.
How does it spread?
COVID-19 is transmitted through droplets generated via coughing and sneezing.
This means it can spread during close contact between an infected and uninfected person, when it’s inhaled, or enters the body via the eyes, mouth or nose.
Infection can also occur when an uninfected person touches a contaminated surface.
What are the symptoms?
COVID-19 causes similar symptoms to the flu. Fever is the most common symptom, occurring in almost 88% of cases, while a dry cough is the next most common, affecting almost 68% of those with the virus.
Yes, you can still have coronavirus if you don’t have a fever. This occurs in about 12% of cases.
How long does it take to get sick?
The incubation is the period from when you’re infected to when you become sick. For COVID-19, the range is 1-14 days, with an average incubation period of 5-6 days.
How sick do people usually get?
Most people who get sick (80%) have a mild illness which rarely involves needing to go to hospital. They recover after about two weeks.
But just over 20% of people sick with COVID-19 will need to be hospitalised for severe difficulties with breathing.
Of the 20% who need to be hospitalised, 6% become critically ill with either respiratory failure (where you can’t get enough oxygen from your lungs into your blood), septic shock, and/or multiple organ failure. These people are likely to require admission to an intensive care unit.
It appears to take about one week to become severely ill after getting symptoms.
How often do people die of it?
The case fatality rate refers to the number of deaths among those who have tested positive for coronavirus. Globally, the case fatality rate today stands at 4%.
But this rate varies country to country and even within countries. These variations may partially be explained by whether hospitals has been overwhelmed or not.
The case fatality rate in Wuhan was 5.8% (although one model says it may be lower at 1.4%). In the rest of China, it was at 0.7%.
Similarly in Europe, Italy’s case fatality rate is (8.3%), greatly surpassing that of Germany (0.2%).
However the case fatality rate only includes people who are tested and confirmed as having the virus.
Some modelling estimates suggest that if you calculated the number of deaths from the total number of cases (those confirmed with tests and those that went undetected) the proportion of people who die from coronavirus might be more like 1%.
How infectious is it, and how does that compare with the flu?
COVID-19 and influenza are probably fairly similarly infections.
A single ill person with COVID-19 can infect more people than a single ill person with influenza. COVID-19 has a higher “reproduction number” of 2.0-2.5. This means one person will infect, on average, 2 to 2.5 people.
But this is balanced by influenza’s ability to infect more quickly. It takes, on average, 3 days to become sick with the flu, but you can still transmit it before symptoms emerge.
It takes 5-6 days to become sick with COVID-19. We still don’t know if you can be infectious before getting coronavirus symptoms, but it doesn’t seem to be a major driver of transmission.
So influenza can spread faster than COVID-19.
The case fatality rate of COVID-19 is higher than that of seasonal influenza (4% versus 0.1%), although as noted above, the true fatality of COVID-19 is still not clear.
It’s too early to know if someone infected with COVID-19 can get it again.
On the basis of what we understand about other coronaviruses, it is likely that infection will give you long-term immunity. But it’s unclear whether that will mean one year, two years or lifelong immunity.
Still have more questions? We might have you covered in this video.
Amid the chaos of an epidemic, those who survive a disease like COVID-19 carry within their bodies the secrets of an effective immune response. Virologists like me look to survivors for molecular clues that can provide a blueprint for the design of future treatments or even a vaccine.
Researchers are launching trials now that involve the transfusion of blood components from people who have recovered from COVID-19 to those who are sick or at high risk. Called “convalescent-plasma therapy,” this technique can work even without doctors knowing exactly what component of the blood may be beneficial.
For the pioneering work of the first treatment using therapeutic serum in 1891 (against diphtheria), Emil von Behring later earned the Nobel Prize in medicine. Anecdotal reporting of the therapy dates back as far as the devastating 1918-19 influenza pandemic, although scientists lack definitive evidence of its benefits during that global health crisis.
The extraordinary power of this passive immunization has traditionally been challenging to harness, primarily due to the difficulty of obtaining significant amounts of plasma from survivors. Due to scarce quantities, infusions of plasma pooled from volunteers were reserved for those most vulnerable to infection.
Fast forward to the 21st century, and the passive immunization picture changes considerably, thanks to steady advances in molecular medicine and new technologies that allow scientists to quickly characterize and scale up the production of the protective molecules.
Immune system’s defense workers
The immune systems of COVID-19 survivors figured out how to combat and defeat the invading SARS-CoV-2 virus.
Neutralizing antibodies are one kind of immunological front-line response. These antibodies are proteins that are secreted by immune cells called B lymphocytes when they encounter an invader, such as a virus.
Antibodies recognize and bind proteins on the surface of virus particles. For each infection, the immune system designs antibodies that are highly specific for the particular invading pathogen.
An enlarged 3D model of a single spike protein in the foreground; in the rear is a model of a SARS-CoV-2 virus covered with many of these spike proteins.NIH, CC BY
For instance, each SARS-CoV-2 virus is covered by distinctive spike proteins that it uses like keys to unlock the doors to the cells it infects. By targeting these spikes – imagine covering the grooves of a key with tape – antibodies can make it nearly impossible for the virus to break in to human cells. Scientists call these kind of antibodies “NAbs” because they neutralize the virus before it can gain entry.
A holy grail for vaccinologists is figuring out how to spark the production of these ingenious antibodies. On first infection, your B lymphocytes train themselves to become expert producers of NAbs; they develop a memory of what a particular invader looks like. If the same invader is ever detected again at any time, your veteran B lymphocytes (known as memory B cells by this stage) spring into action. They rapidly secrete large quantities of the potent NAbs, preventing a second illness.
Vaccines capitalize on this ability, safely provoking an immune response and then relying on the immune system’s memory to be able to fend off the real pathogen if you ever encounter it.
Passive immunization is a process in which neutralizing antibodies from one individual can be used to protect or treat another. A clever example of this process exploited by nature is breastmilk, which passes protective antibodies from the mother to the infant.
Example of Ebola virus disease
In addition to their potential preventative role, neutralizing antibodies are starting to prove beneficial in novel treatments for viral disease. Harnessing their protective power has been challenging, though, primarily because isolating enough antibodies to be effective is laborious.
Recent advances in the technology of molecular medicine at last allowed the kind of scale-up that enabled researchers to test the immunological principle. In 2014-15, Ebola virus disease surfaced in West Africa, triggering an epidemic that raged for over a year, killing more than 11,000 people. About 40% of those infected died. There were no treatments and no vaccine.
By the time Ebola again emerged from the rainforest, this time in 2018 in the Democratic Republic of Congo, the science was ready. In November 2018, doctors launched three parallel trials comparing three different antibody cocktails. Nine months later, spectacularresults allowed for an immediate end of the experimental trials so the cocktails could be used in the field.
While ZMapp did not work as well as anticipated, the trials identified two other antibody-based therapies from two different companies that did suppress Ebola symptoms in infected patients. The earlier in their infection that patients received therapy, the better the protection.
At that time last fall, it would have been difficult to imagine that within six months there’d be an even greater need for the powerful strategy of passive immunization.
A doctor who has recovered from COVID-19 holds up a bag of his own donated plasma in Wuhan, China.STR/AFP via Getty Images
While the rapid move to evaluate this novel treatment is a moment for celebration, the science must keep moving. Convalescent plasma, which is isolated from recently recovered survivors, is in too short of a supply to be broadly useful. The most potent neutralizing antibodies must be quickly characterized and then produced efficiently in large quantities. Several companies, as well as a number of powerhouse academic labs, aim to meet the challenge of identifying and generating these life-saving NAbs.
At the fore isRegeneron, the pharmaceutical company that designed the effective Ebola treatment. Although targeting a different virus, their overall strategy remains the same. They’ve isolated and characterized NAbs and plan to engineer a cocktail of the most potent molecules. The viral target of these antibodies is the SARS-CoV-2 spike protein; the NAbs work by preventing the virus from entering cells.
Clinical trials are planned for early summer, essentially three months’ time. It is a breakneck pace for the development of such a sophisticated tool of intervention.
As the U.S. enters the exponential phase of COVID-19’s spread, this treatment cannot come soon enough.
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The race is on to identify an effective vaccine for the COVID-19 virus. Once discovered, the next challenge will be manufacturing and distributing it around the world.
My research group has developed a novel method to stabilize live viruses and other biological medicines in a rapidly dissolving film that does not require refrigeration and can be given by mouth.
Since the ingredients to make the film are inexpensive and the process is relatively simple, it could make vaccine campaigns much more affordable. Large quantities could be shipped and distributed easily given its flat, space saving shape.
Globally, vaccination rates have improved over the past decade, but are still too low – 13.5 million children were not vaccinated in 2018. This new technology, recently published in the journal Science Advances, has the potential to dramatically improve global access to vaccines and other biological medicines.
Inspired by hard candy
Not your grandmother’s vaccine. Maria Croyle, CC BY-ND
My research team began developing this technology in 2007, when the National Institutes of Health asked us to develop a needle-free, shelf-stable delivery method for a vaccine.
The idea of developing a film was inspired by a documentary about how the DNA of insects and other living things can be preserved for millions of years in amber. This got us thinking about hard candy, like my grandmother used to make.
It was a simple idea, yet no one had tried it. So we went to work mixing a variety of formulations containing natural ingredients like sugars and salts and testing them for their ability to form a solid amber-like candy.
Initially, many of the preparations we tested either killed the organism as the film formed or crystallized during storage, shredding the virus or the bacteria we were trying to preserve.
Vaccines like those for measles, polio, influenza, hepatitis B and Ebola, as well as many of the therapeutic antibodies used to treat infections and cancer, can be carefully sandwiched between protective layers. Stephen C. Schafer, CC BY-ND
But finally, after about 450 tries over the course of a year, we found a formulation that could suspend viruses and bacteria in a peelable film.
As we gained more experience with the production process, we worked to simplify it so extensive technical training would not be needed to make it. Additionally, we tweaked the ingredients so they would dry faster, enabling one to make a batch of vaccine in the morning and ship it after lunch.
I’m involved with a startup aiming to get this technology to market within the next two years.
More benefits
All stored vaccines lose their potency over time. The rate at which they do so mostly depends on the temperature at which they are kept. Keeping vaccines continuously refrigerated is difficult and expensive – and in some parts of the world, nearly impossible. So creating a vaccine that can be stored and transported at room temperature is a huge advantage.
The biggest breakthrough for this project came when we were finishing up our Ebola vaccine project and found films containing virus made three years ago, stored in a sealed container on the lab bench. On a whim, we rehydrated them and tested them to determine if the vaccine was still capable of inducing an immune response. To our surprise, more than 95% of the viruses in the film were still active. To achieve this kind of shelf-life for an unrefrigerated vaccine was astonishing.
The film can stabilize the vaccine in a space-saving format, making it easier to ship and distribute around the globe. Stephen Schafer and Maria Croyle, CC BY-NC-SA
The ecological footprint left by global immunization campaigns is not often considered. The 2004 Philippine Measles Elimination Campaign, which immunized 18 million children in one month, generated 19.5 million syringes, or 143 tons of sharps waste and nearly 80 tons of nonhazardous waste – empty vials, syringe wrappers, caps, cotton swabs and packaging. The implications for a larger campaign are significant.
Our film, by contrast, can be distributed by health workers equipped with only an envelope containing the vaccine. Once taken, it will leave no trace, except for a healthy global population.
Cases of the Wuhan coronavirus have increased dramatically over the past week, prompting concerns about how contagious the virus is and how it spreads.
According to the World Health Organisation, 16-21% of people with the virus in China became severely ill and 2-3% of those infected have died.
A key factor that influences transmission is whether the virus can spread in the absence of symptoms – either during the incubation period (the days before people become visibly ill) or in people who never get sick.
On Sunday, Chinese officials said transmission had occurred during the incubation period.
So what does the evidence tell us so far?
Can you transmit it before you get symptoms?
Influenza is the classic example of a virus that can spread when people have no symptoms at all.
In contrast, people with SARS (severe acute respiratory syndrome) only spread the virus when they had symptoms.
No published scientific data are available to support China’s claim transmission of the Wuhan coronavirus occurred during the incubation period.
However, one study published in the Lancet medical journal showed children may be shedding (or transmitting) the virus while asymptomatic. The researchers found one child in an infected family had no symptoms but a chest CT scan revealed he had pneumonia and his test for the virus came back positive.
This is different to transmission in the incubation period, as the child never got ill, but it suggests it’s possible for children and young people to be infectious without having any symptoms.
This is a concern because if someone gets sick, you want to be able to identify them and track their contacts. If someone transmits the virus but never gets sick, they may not be on the radar at all.
It also makes airport screening less useful because people who are infectious but don’t have symptoms would not be detected.
How infectious is it?
The Wuhan coronavirus epidemic began when people exposed to an unknown source at a seafood market in Wuhan began falling ill in early December.
Researchers and public health officials determine how contagious a virus is by calculating a reproduction number, or R0. The R0 is the average number of other people that one infected person will infect, in a completely non-immune population.
Different experts have estimated the R0 of the Wuhan coronavirus is anywhere from 1.4 to over five, however the World Health Organisation believes the RO is between 1.4 and 2.5.
If the R0 was higher than 2-3, we should have seen more cases globally by mid January, given Wuhan is a travel and trade hub of 11 million people.
How is it transmitted?
Of the person-to-person modes of transmission, we fear respiratory transmission the most, because infections spread most rapidly this way.
Two kinds of respiratory transmission are through large droplets, which is thought to be short-range, and airborne transmission on much smaller particles over longer distances. Airborne transmission is the most difficult to control.
SARS was considered to be transmitted by contact and over short distances by droplets but can also be transmitted through smaller aerosols over long distances. In Hong Kong, infection was transmitted from one floor of a building to the next.
Initially, most cases of the Wuhan coronavirus were assumed to be from an animal source, localised to the seafood market in Wuhan.
We now know it can spread from person to person in some cases. The Chinese government announced it can be spread by touching and contact. We don’t know how much transmission is person to person, but we have some clues.
Coronaviruses are respiratory viruses, so they can be found in the nose, throat and lungs.
The amount of Wuhan coronavirus appears to be higher in the lungs than in the nose or throat. If the virus in the lungs is expelled, it could possibly be spread via fine, airborne particles, which are inhaled into the lungs of the recipient.
How did the virus spread so rapidly?
The continuing surge of cases in China since January 18 – despite the lockdowns, extended holidays, travel bans and banning of the wildlife trade – could be explained by several factors, or a combination of:
increased travel for New Year, resulting in the spread of cases around China and globally. Travel is a major factor in the spread of infections
asymptomatic transmissions through children and young people. Such transmissions would not be detected by contact tracing because health authorities can only identify contacts of people who are visibly ill
increased detection, testing and reporting of cases. There has been increased capacity for this by doctors and nurses coming in from all over China to help with the response in Wuhan
substantial person-to-person transmission
continued environmental or animal exposure to a source of infection.
However, with an incubation period as short as one to two days, if the Wuhan coronavirus was highly contagious, we would expect to already have seen widespread transmission or outbreaks in other countries.
Rather, the increase in transmission is likely due to a combination of the factors above, to different degrees. The situation is changing daily, and we need to analyse the transmission data as it becomes available.
C Raina MacIntyre, Professor of Global Biosecurity, NHMRC Principal Research Fellow, Head, Biosecurity Program, Kirby Institute, UNSW
The World Health Organization has declared COVID-19 a pandemic. This is a landmark event. As an epidemiologist listening to the steady stream of conversation around the coronavirus, I’m hearing newscasters and neighbors alike mixing up three important words my colleagues and I use in our work every day: outbreak, epidemic and pandemic.
Simply put, the difference between these three scenarios of disease spread is a matter of scale.
Outbreak
Small, but unusual.
By tracking diseases over time and geography, epidemiologists learn to predict how many cases of an illness should normally happen within a defined period of time, place and population. An outbreak is a noticeable, often small, increase over the expected number of cases.
Imagine an unusual spike in the number of children with diarrhea at a daycare. One or two sick kids might be normal in a typical week, but if 15 children in a daycare come down with diarrhea all at once, that is an outbreak.
When a new disease emerges, outbreaks are more noticeable since the anticipated number of illnesses caused by that disease was zero. An example is the cluster of pneumonia cases that sprung up unexpectedly among market-goers in Wuhan, China. Public health officials now know the spike in pneumonia cases there constituted an outbreak of a new type of coronavirus, now named SARS-CoV-2.
As soon as local health authorities detect an outbreak, they start an investigation to determine exactly who is affected and how many have the disease. They use that information to figure out how best to contain the outbreak and prevent additional illness.
Epidemic
Bigger and spreading.
An epidemic is an outbreak over a larger geographic area. When people in places outside of Wuhan began testing positive for infection with SARS-CoV-2 (which causes the disease known as COVID-19), epidemiologists knew the outbreak was spreading, a likely sign that containment efforts were insufficient or came too late. This was not unexpected, given that no treatment or vaccine is yet available. But widespread cases of COVID-19 across China meant that the Wuhan outbreak had grown to an epidemic.
COVID-19 was first noticed in Wuhan, China, but quicky spread across the globe. This map show the 110 countries with confirmed cases as of March 11.
CDC
Pandemic
International and out of control.
In the most classical sense, once an epidemic spreads to multiple countries or regions of the world, it is considered a pandemic. However, some epidemiologists classify a situation as a pandemic only once the disease is sustained in some of the newly affected regions through local transmission.
To illustrate, a sick traveler with COVID-19 who returns to the U.S. from China doesn’t make a pandemic, but once they infect a few family members or friends, there’s some debate. If new local outbreaks ensue, epidemiologists will agree that efforts to control global spread have failed and refer to the emerging situation as a pandemic.
The WHO has declared only two pandemics in history – for influenza in 1918 and for influenza H1N1 in 2009. For weeks, epidemiologists like me have been calling the coronavirus a pandemic. From an epidemiological perspective, the WHO’s declaration is overdue. As of March 11, the official numbers count an excess of 120,000 cases in at least 114 countries. Eight countries, including the U.S., have more than 1,000 cases each, and community spread has been documented in several U.S. states.
Pandemic is the highest level of global health emergency and signifies widespread outbreaks affecting multiple regions of the world. However, the WHO statements remain hopeful that the pandemic can be controlled and the damage minimized by taking immediate aggressive steps.
The formal declaration of COVID-19 or any other infectious disease as pandemic tells governments, agencies and aid organizations worldwide to shift efforts from containment to mitigation. It has economic, political and societal impacts on a global scale, and the WHO takes extreme care when making this determination.
This formal declaration needn’t incite fear or cause you to stockpile surgical masks. It doesn’t mean the virus has become more infectious or more deadly, nor that your personal risk of getting the disease is greater. And it doesn’t mean that efforts to fight COVID-19 are being abandoned. But it is an historical event.
This is an updated version of an article originally published on March 5, 2020.
The measles virus has been a part of human life for thousands of years. A recent study suggests that it appeared about 4,000 years ago, originating from a virus affecting livestock. That was also the time when cities were reaching population sizes above 250,000 – enough to keep the virus spreading even though people who have had measles don’t ever get it again.
As recently as the mid-20th century, before the development of a vaccine, nearly every person could expect to be infected with the measles virus in their lifetime. The introduction of a vaccine in the mid-1960s has dramatically cut the incidence of measles. Fewer than seven million cases were estimated in 2017. But those improvements have not been evenly spread. The incidence of measles is concentrated in low-income countries. And the risk of death or severe complications is disproportionately high in marginalised populations with poor access to health services.
The risk of mortality due to measles infection is 5-times higher in low- compared to high-income countries and can be greater than 10% when outbreaks overwhelm health systems. There were over 1,000 measles deaths in Madagascar in 2019 and there have been over 6,000 deaths so far in an outbreak in the Democratic Republic of Congo (DRC). The long-term effects of these outbreaks on immunity to other diseases has yet to be seen, and may be substantial.
Measles is very easily transmitted from person to person in the droplets created when an infected person coughs or sneezes. These droplets can stay in the air for hours.
The disease often begins with a runny nose, runny eyes and a cough, followed by a rash. The virus infects cells throughout the body, but specifically kills cells of the immune system which the body uses to fight infection. This makes it harder to fight off common infections that cause pneumonia or diarrhoea. During and just after measles infection, individuals are more likely to get very ill or even die from secondary infections that would otherwise be relatively harmless.
Recent research has uncovered a new mechanism suggesting that this effect may persist for over a year. This new research suggests that measles infection not only weakens the immune system, but in some cases resets it. It can make people susceptible again to infections they were previously immune to. In rare cases, measles infection can lead to neurological complications that result in deafness or blindness.
Preventing measles
Vaccination prior to exposure remains the single most effective way to prevent measles disease. The vaccine is a weakened virus which triggers strong immunity to the full-strength virus without causing disease. A successful vaccination against measles in childhood should provide lifetime protection. Two doses are recommended for each child to ensure at least one is successful.
The more similar the structure of the vaccine is to the virus in its natural state, the stronger the protection of the vaccine. The measles vaccine is very similar and conveys strong protection. But this similarity is the vaccine’s greatest weakness as it must be kept in a very narrow temperature regime – not too cold, not too warm – to remain effective. The supply chains to get the vaccine from production to health clinics must have very specific refrigeration equipment throughout. This has been difficult in places where electrification is limited. These communities may only receive effective vaccines during large campaigns every few years, leaving some children unprotected.
The combination of rapid transmission and strong immunity after infection means that measles disease commonly occurs in dramatic outbreaks. Even in places where measles is present year-round, there tends to be large differences between the high and low seasons. It can flare up in periods of increased contact among people, for example due to school or economic cycles. A lot of people will be infected at the same time, and then be immune. After an outbreak, there aren’t many people who are still able to get infected – until more children are born. If vaccination coverage is high enough, it can prevent transmission altogether and eliminate measles, as has been achieved in the Americas.
The impact of measles has changed dramatically over the last half century. What was once a near certain infection for all people has become a distinctly inequitable health risk. Wealthy countries can maintain high rates of vaccination and reduce the risk of exposure. Even within low-income countries where measles is both endemic and common, the risk falls disproportionately on populations that are difficult to reach with effective vaccination. They may be far from vaccination services or otherwise marginalised and unable to access vaccination. Political and military conflict frequently add to the problem.
An analysis prior to the Madagascar outbreak highlighted that declining vaccination coverage (perhaps due to the political crisis in 2009) and failure of supplementary immunisation activities to reach adolescents who had missed routine childhood doses may have increased the outbreak risk. The magnitude of the ongoing outbreak in the DRC reflects long-term, systemic challenges of achieving high vaccination coverage in a large, mainly rural population. The Ebola outbreak in the northeast has placed additional burdens on the routine health system and led to additional declines in vaccination coverage.
Measles infection can be easily managed with prompt health care and symptom management. But in the absence of care, mild symptoms can turn into life-threatening secondary infections or long-term effects such as deafness and blindness.
While measles may be a faint memory in some parts of the world, the impact in the worst-affected populations is a constant reminder of the need for vigilance.
A Victorian teenager was recently reported to be suffering from a Buruli ulcer, an infection caused by the “flesh-eating” bacteria Mycobacterium ulcerans. She was said to have caught it on Victoria’s Mornington Peninsula, where cases seem to be on the rise.
Buruli ulcer, also known as Bairnsdale ulcer, occurs in many areas of the world, including Victoria. Besides the Mornington Peninsula, Australian cases have also been reported in tropical areas, including north of Mossman in Queensland, and the Capricorn Coast of Queensland near Yeppoon.
In Victoria, the number of reported cases has definitely increased over the past two years. As of September 2017, 159 cases have been reported, compared with 182 for the whole of 2016, 107 in 2015, and 89 in 2014.
Buruli ulcer is a major public health problem in West Africa, where cases have been described in 32 countries and untreated ulcers can result in significant disfigurement and disability, particularly in children.
The hallmark of this infection is a non-healing sore, usually on the leg or arm, which slowly enlarges over weeks to months. In the very early stages, the infection may start as a red lump. The edges of the ulcer are often medically described as “undermined”, which means the dead tissue may appear to extend far beyond the actual ulcer on the skin surface.
Ulcers are usually single, but they can be multiple or recurrent. Some patients can get a lot of swelling of the infected area, and sometimes this may affect a whole limb. Extensive tissue damage requiring amputation is rare in Australia, but may be required for very advanced infections.
M. ulcerans is a distant relative of organisms that cause tuberculosis (Mycobacterium tuberculosis) and leprosy (Mycobacterium leprae). It seems that this organism can evade the body’s immune system by producing a toxin called mycolactone, which destroys immune cells. Without control by the immune system, the infection can proceed unchecked and cause progressive tissue death.
When we look down the microscope at tissues infected with other bacteria, we usually see lots of white cells which cause inflammation. But in the case of M. ulcerans, the telltale absence of white cells is often an important clue to diagnosis.
What causes it?
M. ulcerans infection was first recorded in patients in eastern Victoria in the 1930s. But over the past 15 years, cases have been moving westwards along the coast to the Bellarine Peninsula south of Geelong. Since 2012, cases have reversed back to the Mornington Peninsula southeast of Melbourne.
Although cases can present at any time of year, more tend to present between June and November. A few patients only report very transient exposure, such as a weekend trip to the Bellarine Peninsula. From these patients, it is thought the incubation period (the period between getting infected and the ulcer appearing) is around three to five months.
The reasons for where and in whom infection occurs isn’t clear. Circumstantial evidence seems to implicate mosquitoes, as the bacteria can be found in mosquitoes, occurs on exposed parts of the body where mosquitoes tend to bite, and seems to be associated with outdoor activities. So covering up and using mosquito repellents would seem to be the best preventative measures.
Oddly, cases seem to occur in very specific areas – on the Bellarine Peninsula some towns seem to be “hotspots” whereas others are relatively spared. An intriguing lead that may partly explain this is the discovery that possums, and more specifically possum faeces, appeared to be infected, and sometimes without the possum apparently being unwell. Positive “possum poo” seems to occur where human cases occur.
This suggests that M. ulcerans may be a zoonotic infection – this is where human cases occur as a “spillover” from what is otherwise an animal infection. Clearly this isn’t the whole story, as M. ulcerans infection occurs in regions of the world with different mosquito and animal species.
How is it treated?
Unfortunately, these infections don’t respond to the usual antibiotics for skin infection, and it isn’t uncommon to see patients who have been on several courses of antibiotics before a diagnosis is made.
In the past, it was thought that all cases needed surgery, similar to that for skin cancer. In Australia, surgery to remove the affected tissue is still sometimes required, but most cases can be cured with long courses of antibiotics. The antibiotics used for M. ulcerans are usually reserved for other infections such as tuberculosis, which aren’t the first choice of treatment for skin infections.
The use of treatment solely with antibiotics is being tested in a trial in Africa, and if successful would be good news for patients in regions where surgeons are scarce.
What can I do to avoid it?
Although the effectiveness of preventative measures is not confirmed, avoiding mosquitoes would seem to be the most prudent measure to prevent infection. This includes covering up exposed skin and using mosquito repellents in the warmer months.
Get unexplained lumps and sores checked out, particularly if they persist for weeks or months. There is a long list of other conditions that cause non-healing ulcers which may also require medical attention, such as skin cancers and diabetic foot infections. However, Buruli ulcers are more easily treated before the infection spreads, so early diagnosis is important.
That said, M. ulcerans is very slow growing, so there’s no need to panic. Make sure you let your doctor know if you’ve been in any of the affected areas – while this infection is on the radar of doctors in these areas, it may not be top of the list for those elsewhere.
We’ve probably all heard of mitochondria, and we may even remember learning in school that they are the “powerhouses of the cell” – but what does that actually mean, and how did they evolve? To answer this question, we have to go back about two billion years to a time when none of the complexity of life as we see it today existed.
Where did mitochondria come from?
Our primordial ancestor was a simple single-celled creature, living in a long-term rut of evolutionary stagnation. Then something dramatic happened – an event that would literally breathe life into the eventual evolution of complex organisms. One of the cells engulfed another and enslaved it as a perpetual source of energy for its host.
The increase in available energy to the cell powered the formation of more complex organisms with multiple cells, eyes, and brains. Slowly, the two species became intertwined – sharing some of their DNA and delegating specific cellular tasks – until eventually they became firmly hardwired to each other to form the most intimate of biological relationships. Two separate species became one.
These energy slaves are the mitochondria, and there are hundreds or even thousands of them inside every one of your cells (with the exception of red blood cells) and in every other human alive. They still resemble their bacterial origin in appearance, but we can no longer exist without them, nor they without us. The evolutionary explosion powered by mitochondria is evident by the fact they are found in every complex multicellular organism that has ever existed, from giraffes to palm trees, mushrooms and dinosaurs.
As vestiges of their ancient origin, mitochondria still have their own genome (although some of their DNA has been transferred to our genome). It’s alien in appearance and composition when compared with our own nuclear genome (the DNA inside each of your cell’s nuclei that contains about 20,000 genes). In fact, our nuclear genome shares more in common with that of a sea sponge than with the mitochondrial genome inside our own cells.
Unlike the nuclear genome, the mitochondrial genome is small (containing just 37 genes), circular, and uses a different DNA code. The mitochondrial genome slinks its way across generations by stowing away within mitochondria harboured in each egg, and as such, is passed down from the mother only. This is different to the nuclear genome, half of which is inherited from your father and the other half from your mother.
The mitochondrial genome is vital for the mitochondria’s main role: burning the calories we eat with the oxygen we breathe to generate the energy to power all of our biological processes. But this amazing source of energy is not without its cost.
The mitochondrial genome is passed down from the mother only.
Natalya Zaritskaya/Unsplash, CC BY
Like any powerhouse, mitochondria produce toxic byproducts. Free radicals (highly reactive oxygen molecules with an odd number of electrons that can cause ageing and health problems) can be created by accidents that happen during energy production.
So in essence, mitochondria power and imperil our cells.
Because the mitochondrial genome is in close proximity to the source of free radicals, it’s more susceptible to their damaging effects. And the mitochondrial genome undergoes replication thousands of times more than the nuclear genome, simply because you have so many in each cell. Making copies of copies introduces mistakes.
A combination of these two effects results in the mitochondrial genome mutating up to 50 times faster than the nuclear genome, which is meanwhile kept safely in the nucleus. These mutations can be passed down to maternal offspring, causing devastating metabolic disorders in the next generation.
What happens when something goes wrong?
Only as recently as 1988 was the first disease caused by such a mutation in the mitochondrial genome identified. Now, we know about many such disorders, called mitochondrial diseases, which can be traced to mutations in the mitochondrial genome. These diseases can manifest at any age and result in a wide range of symptoms including hearing loss, blindness, muscle wasting, stroke-like episodes, seizures, and organ failure.
Despite this, during life, it’s inevitable that mutations will occur in the mitochondrial genome in an individual’s neurons, muscle, and all other cells. Compelling work now suggests that the accumulation of these mistakes may contribute to the progressive nature of late-onset degenerative diseases such as Alzheimer’s and Parkinson’s.
The health of this seemingly alien genome is inextricably linked to that of our own bodies. As we come to grips with mitochondria’s importance in disease, we continue to uncover the intimate secrets of a two-billion-year relationship that has given complex life to the planet.
Hepatitis means inflammation of the liver. While we usually think of hepatitis A to E viruses, anything that causes inflammation or damage to the liver can be considered as a form of hepatitis.
Hepatitis A, B, C, D and E are very different viruses. Hepatitis A is genetically closer to the common cold than it is to hepatitis B, for example. Hepatitis C is closer to the virus that causes dengue fever.
The thing all five have in common is they can cause mild to very severe liver damage.
Viral hepatitis caused around 1.45 million deaths in 2013, making it the seventh leading cause of death world-wide; 96% of these were due to hepatitis B and C.
Hepatitis A
Hepatitis A is spread by contaminated food and water, and from person to person via faecal transmission, particularly in household settings.
Hippocrates first described epidemics of diarrhoea and jaundice as far back as the fifth century BCE.
Although hepatitis A can cause significant illness, the body usually recovers without treatment and becomes immune to future infections.
Vaccines can prevent hepatitis A; these are recommended for travellers and other groups at particular risk of infection. Vaccination given early after exposure can also prevent hepatitis A from developing.
Hepatitis B
This is the most prevalent form of viral hepatitis worldwide. It’s also the leading cause of liver cancer.
An estimated 250 million people live with hepatitis B worldwide. Around 220,000 Australians are thought to be living with chronic hepatitis B.
Hepatitis B can be transmitted from person to person through sex or blood-to-blood contact. But most people living with chronic (long-term) hepatitis B acquired it at birth from their mother, or early in life. Following infection, the chance of developing chronic hepatitis B in infancy is around 90%, but falls to 5% among adults.
A safe and highly effective vaccine has been available for hepatitis B since the 1980s. It has been provided for all infants born in Australia since May 2000.
In China, the proportion of children aged under five who had chronic hepatitis B fell from 9.7% in 1992 to 1% in 2006 after a vaccination program was introduced. The program has prevented millions of deaths from liver cancer and liver cirrhosis in China alone.
Effective antiviral treatments are also available for chronic hepatitis B. These can prevent liver damage and liver cancer from occurring. But even in a well-resourced country such as Australia, only a minority of people needing treatment and care for hepatitis B are receiving it.
Hepatitis C
This is the most common cause of viral hepatitis in Australia; an estimated 230,000 people live with chronic infection.
Hepatitis C is the leading cause of liver cancer and liver transplants nationally.
Most hepatitis C infections in Australia were acquired through unsafe injecting drug use. But in some low-resource countries, ongoing transmission of hepatitis C in health care settings is a major problem.
Around 80% of people infected with hepatitis C develop chronic infection; those who do clear the infection naturally remain susceptible to future infections.
No vaccine for hepatitis C is available.
On March 1, new treatments were listed on the Pharmaceutical Benefits Scheme (PBS). Although expensive, these treatments represent a huge advance and are a cost-effective way to prevent both new infections and deaths due to existing hepatitis C infections. With cure rates of the order of 90% with 8-24 weeks of tablets, and minimal side effects, these agents have the potential to drastically reduce the impact of hepatitis C.
The real key to unlocking this potential is the very liberal access criteria the Commonwealth government has applied to these treatments. As a result, uptake of treatment for hepatitis C in Australia has risen more than 20-fold.
Hepatitis D
Hepatitis D is a satellite virus that can only infect people who also have hepatitis B.
It is estimated that approximately 5% of people living with hepatitis B globally also have hepatitis D, which can lead to more severe liver disease.
Hepatitis E
Hepatitis E, like hepatitis A, is spread through contaminated food and water.
The first outbreak of hepatitis E infection acquired in Australia was reported earlier this year.
While hepatitis E is usually relatively mild, it can cause serious illness late in pregnancy, with a death rate of up to 20% among pregnant women in their third trimester.
A vaccine against hepatitis E has been developed but is currently licensed only in China.
While viral hepatitis remains a substantial public health challenge in Australia and world-wide, with political will, adequate investment and global partnerships, the world can eliminate viral hepatitis by 2030.
