Saturday, 20 September 2014

MERS risk reduction and signs of illness to watch for during hajj and umrah...

I love a good infographic and this one ticks a lot of boxes for getting a clear message out about the Middle East respiratory syndrome (MERS) disease and how to avoid catching and spreading the MERS-coronavirus (MERS-CoV).

Thanks World Health Organization.

World Health Organization poster describing risk of infection
 and how to identify when you might have MERS.
Of course, I'd be happier if the poster specifically suggested putting more distance between people and potentially infected camels, rather than just avoiding "close contact".

Granted, close contact can include spending time in the close, but not physically connected, "personal space" of a camel. But "close contact" is, in my opinion, one of those infectious disease terms that needs to be made more simple and clear. Like "aerosol" and "airborne", "close contact" gets a little lost when translated to the people who are at actual risk from infection.

Friday, 19 September 2014

To the Saudi Arabian Ministry of Health: A request for missing data on retrospective MERS-CoV detections

From: Ian M Mackay

To: The Office of the Minister of Health, Kingdom of Saudi Arabia

I write to humbly ask for your help on a matter of infectious disease communication. I ask that you please consider completing the already near-complete public data picture for all retrospectively confirmed cases of Middle East respiratory syndrome coronavirus (MERS-CoV) that have occurred on your soil. I ask that this be publicly released for analysis, and suitably acceptable citation, by all. The Ministry of Health has already made a number of advances in tracking and communicating new cases of MERS-CoV, addressing criticisms along the way. But there remain some small but epidemiolgically important gaps in an otherwise complete set of data that could be easily closed.

Today, the 19th of September, I make note of the Command and Control Center announcement of the discovery of 19 MERS-CoV cases, identified after retrospective analysis of cases.[1] This adds to the 113 MERS-CoV detections announced 3rd June 2014.[2] I also note the reference to removal of a duplicate case and two false positive cases. In addition to these items, there have been many identified deaths that cannot be linked to publicly announced cases because key date data are no longer published along with the time of death announcements, as they once were (see example [3]).

So I ask if it is possible for you to publish a minimum set of deidentified details from cases that have not been fully described by the World Health Organization Disease Outbreak News reports. I suggest an open access spreadsheet on the CCC website.  I do not ask that any compromising or identifying data be included nor do I believe there is a need for identification of hospital or treatment facility. I would be happy to help identify these cases if that could be of use. 

These data include:

  • Age
  • Sex
  • Date when symptoms began
  • Date of hospital admission
  • Date when a fatal case was first reported (allowing a link to be made)
  • City where case likely acquired

The Command and Control Center website and its updates on contemporary MERS cases have evolved into an essential global asset for many international researchers and for the global public, each of whom are still trying to understand this emerging virus. What I suggest here would add even more reach and value to your efforts to keep us all informed. 

As the custodian of over 90% of MERS case data, the world wholly relies upon your transparency, good will, expertise and willingness to openly share it. I believe a complete set of MERS-CoV data have great potential to engage more researchers from around the globe. These links may help identify new and interesting patterns that could be of use to Saudi Arabia and other Middle East and African nations trying to improve control of MERS-CoV now and in the future.

Thank you for reading this.

Yours sincerely,

Ian M. Mackay, Ph.D.
Science communicator (at)


Thursday, 18 September 2014

Updating a model of a modern Ebola epidemic...

Professor David Fisman, University of Toronto, Canada published one of the excellent recent models designed to estimate where Ebola virus disease case numbers might be heading.[1] He has updated his model using the latest World Health Organization EVD data that includes up to 13-Sept.

This morning I awoke to find the fruits of his labour generously presented to the world via Twitter.

I'm constantly impressed by how much info can and is being provided for everyone to share, discuss and  constructively mull over. This is just the latest fantastic effort.

Prof Fisman's (@DavidFisman) model has provided a very close estimate when compared to the real figures on which it is, of course, based (Figure 1.). His estimates have not changed with the latest data. He calculates an overall R0 of 1.75, and 'd' (a value that can indicate the level of control; when d is zero, you have uncontrolled exponential growth) is at 0.0078. The d values for different countries in the outbreak, differ.

Figure 1. Showing that the model (black line) fits extremely well
to actual reported case numbers (red bars) to date
The projected end date is November 2016 with a final size of approximately 480,000 cases. (Figure 2) This is just based on current numbers and without knowing what interventions are coming not how successful they will be. Prof Fisman says his model currently predicts an epidemic peak in June-2015 at which time there could be 227,000 cases. By Jan-2015, projected case counts reach 28,450.

Figure 2. Extending the model into 2017.
Red curve (right y-axis): incidence by 15-day generation.
Blue curve (left y-axis): cumulative cases.
Keeping in mind that these numbers do not include deaths. The proportion of fatal cases (PFC) requires some further mathematical wizardry in order to account for the time between when cases present to a treatment facility, and when they die. 

Figure 3. Ebola virus disease cumulative curve for Nigeria.
The proportion of fatal cases is markedly lower than for
 the more overwhelmed countries. This does
not appear to be an artefact as most cases have
been laboratory confirmed.
It's not a simple division of deaths and total cases at the same time point (these are the crude percentages I report on VDU and which the WHO report-this reporting may change in the future). 

The addition of that calculation spikes the PFC to >80% at times (see the post by @maiamajumder post on HealthMap), but seems to vary to lower figures depending on country and population for example, in Nigeria (Figure 3). But whatever way you look at it, many people will die from Ebola virus infection, as well as all the other diseases and medical care needs that going with sufficient attention.


  1. Early Epidemic Dynamics of the West African 2014 Ebola Outbreak: Estimates Derived with a Simple Two-Parameter Model

Monday, 15 September 2014

Happy 2nd birthday Middle East respiratory syndrome coronavirus (MERS-CoV)...

Its been 2-years since Prof. Ali Mohamed Zaki sent his email to ProMED notifying them of a novel coronavirus. That email was published 20-Sept 2012.[1] 

A year ago we had 138 cases and 58 deaths. Today we have 856 cases with perhaps 306 fatal (36%).

I won't rehash what I said a year ago - I invite you to check that out over at the 1st birthday post.[2]

Suffice to say the past year has been, to my mind anyway, mostly about:

  • Camels
  • High level job "shuffling"
  • Controversial parallel publications
  • Very problematic infection prevention and control issues.
The latter leading to the relatively huge number of MERS-CoV detections and deaths in Saudi Arabia and to some exported detections and cases. The one constant over both years has been that the MERS-CoV is a pitiful spreader among humans. MERS-CoV is nonetheless a virus that is very capable of inducing fatal outcomes, especially among older males with underlying diseases.

Has MERS-CoV gone away? No. Of course it hasn't. MERS has, mostly. That's the disease, not the virus. For now anyway MERS cases are sporadic, although still geographically widespread. 

MERS cases fell to zero cases per week for a number of weeks this year following containment of the Jeddah-2014 outbreak. Nonetheless, this is a virus of camels that seems to  spread, rarely, to humans and when in us, it has not been in any rush to mutate into the pandemic SARS-like threat many once worried about. 

Camels are where this virus likely remains. And there have been no signs that that has in any way changed. The latest information suggests camels have been harbouring MERS-CoV for at least 30-years.[3] This, as with a great deal of the research to date, is knowledge gained mostly thanks to the efforts of international research teams and their funding

So Happy 2nd Birthday you opportunistic, spiky little killer. I'm once again wishing Dr Zaki well and congratulating him on co-parenting the birth of this novel coronavirus. This year I also wish Prof. Ziad Memish well and congratulate him on seeing the infant virus through to toddler age.

Oh, and 2-years on, I still see no sign that the contentious patenting issues were any sort of hindrance to diagnostics or actual research. Just sayin'.


  2. Happy 1st birthday Middle East respiratory syndrome coronavirus (MERS-CoV)
  3. MERS Coronavirus Neutralizing Antibodies in Camels, Eastern Africa, 1983–1997

Sunday, 14 September 2014

The proportion of fatal cases (PFC)...

This is excerpted and altered a little, from a more influenza A(H7N9) virus slanted article to be found here. But I think it deserves its own page.

In July 2013 I coined a term on VDU to avoid the use of the term Case Fatality Ratio/Rate/Risk (CFR). 

My term was the Proportion of Fatal Cases (PFC). I use the term on VDU and have published it an article.[1] I have no expectations that anyone else will use it although I notice it made an appearance in a HeathMap story[2] by Maia Majumder.

The PFC is a percentage calculated as the currently known number of fatalities divided by the number of total lab-confirmed cases including fatalities, regardless of whether surviving cases are inpatients (hospitalized) or outpatients.

The PFC is just a number - it's not meant to imply that every case that ever happened is included - it never could. It does not account for those cases who will die later on, either directly or indirectly, as a result of their infection but who may be alive at the time of calculation. 

The PFC is a snapshot to be used before an outbreak is done and dusted. It is meant as a guide to what is happening right now using the data we can get our hands on. Sometimes that means lots of data and sometimes they are very limited or just plain behind closed doors.

The CFR makes use of the number of recovered cases in its denominator.[3] So it's important to know survivor numbers. As suggested above, this requires that all the people who will recover from their infection, have recovered (and been discharged) from their infection. 

Using the CFR early in an emerging virus/disease outbreak, when what usually brings in outbreak to our attention is death, is great for selling papers, but not helpful realistic in a bigger picture sense. 

The CFR is most useful at the end of an epidemic/pandemic, but not so much when data-in-hand is poor during the early days of many outbreak. 

Of course, some will take a PFC and multiply it by the world's population as an estimate of how many are going to die if the virus reaches pandemic levels. That's not helpful or accurate. Just accept it as that snapshot of what's happening now.

  1. J. P. Dudley and I. M. Mackay. Age-Specific and Sex-Specific Morbidity and Mortality from Avian Influenza A(H7N9). J. Clin. Virol. 2013. Nov;58(3):568-70. ePub Sept.

Saturday, 13 September 2014

The wind beneath my Ebola virus.... [UPDATED]

Only a couple of weeks ago the report in Science presented 99 genomes representing some of the thousands of those circulating in Sierra Leone this year.[1] I say thousands because each infected person has a range of subtley different viral variants among the billions of viruses per millilitre of blood that all compete to be the champion. The words "mutant" and "ebolavirus" are now hard to avoid. And of course as soon as you talk mutations, you can only see one endgame - a virus that is easily transmissible and turns us all into zombies. spreads across the world in a pandemic and kills as many as 80% of those it infects. Yes, its seems the proportion of fatal cases (PFC) in West Africa may not be as simply calculated as most of us were thinking these past months. When we take into account that Ebola virus disease deaths occur in people that were part of a case tally days earlier (if they were counted of course) when the total case numbers were smaller, the PFC inflates. How much, we don't really know.

And so the story of mutants was brought full circle today thanks to Dr. Michael T. Osterholm. In a very nicely written piece for the New York Times,[2] Dr. Osterholm, ventured behind the scenes to crack the door into the world of whispered discussions, shadowy frappé meetings by chino and beige blazer-wearing figures, many of whom were men with with thinning hair. Yes, he found where the real virologists hang out and what were they discussing at length? Why they were talking about how soon it would be until Zaire ebolavirus was going to mutate and become an airborne killer virus identifiable only through watching big wall-mounted LCD screens as they are rendered in red because of the fusion of rapidly growing dots, spreading across a map of a world filling rapidly with infected hosts. Or red dots. Or something. Okay, some of that was from me.

Only problem is, I think he may have entered the tinfoil hat room next door to the (but very similarly attired) room full of virologists. Maybe not. Hard to tell sometimes. But seriously.

For sure, a virus changes over time. It will change randomly through mutations that happen because viruses, especially those with genes/a genome made of RNA, are always making errors in their gene/genome copying and sometimes those errors make the virus better at something. Viruses may hold on to those changes in response to all sorts of pressures on them. These genetic sequence changes sometimes results in change to the proteins that make their structures and enzymes. Sometimes the changes may revert back as pressures go away or new ones come to be. It's a constant micro-environment of change; evolution on fast forward.

We should also keep in mind ebolaviruses didn't come down in the last shower. They are viruses that are happy in their own envelopes...and natural host(s). But mutational changes can impact on how the viral "bits" assemble and release from the cell and perhaps on how the virus causes disease, where virus replicates in the body, how it interferes with the host immune system's attempts to interfere with it, how hardy it is, how well it replicates in response to temperature and so on. 

A virus doesn't "think" about any this of course. It doesn't plan to do the nastiest thing to us that we can imagine when it jumps into us from an animal (a zoonosis). Headlines might make you think otherwise. These changes happen because, in a new host species producing many subtley different viral variants all vying for supremacy, the virus with the mutation(s) that allow it to get out from under some sort of controlling pressure or to do something better than the earlier viral versions, wins the day. The winner thrives, makes more of itself or does it better, and passes to new hosts.

A virus may keep more of these mutational changes while it is "settling in" to a new animal host species if they help that process. It may be under more pressure to adapt to slightly different environments, different receptor structures, temperatures, immune responses - all sorts of things may created a different environment from the one the virus came from and so it may need to make use of more mutations in order to "find its footing". Or fail and not find a home in the new host.

There can be all sorts of new and negative pressures to try and avoid or adapt to for a virus. So ebolaviruses seem to naturally infect bats, not us, and in bats the infection does not seem to cause a whole lot of disease. Of course we don't know a whole lot about how bats spread virus among themselves. Perhaps they do it via an airborne route. The theory then goes that humans or other forest animals including chimpanzees, gorillas, porcupines and antelopes may eat the bats or bat/virus-contaminated fruit. We, and those animals, do get sick.

Another unsure thing, a sizable knowledge gap you might call it, is whether an ebolavirus would actually be under any pressure at all to keep the mutations that change its proteins, site of replication and disease course which result in it being:

  • More stable in dried droplets
  • Shed in higher concentrations from the upper respiratory tract
  • Able to trigger more coughing or sneezing.
Each and all of these major changes might be necessary to create the mythical airborne Ebola virus. The outcome? Creation and propulsion of more droplets from an infected human, that dry down and linger in the air (the airborne part) while still containing infectious ebolavirus, and enough of it to result in human infection and disease. Phew. That is an unbelievable series of huge changes, even for a "sloppy" replicating RNA virus. 

I think we all understand that a virus doesn't "know" that these changes would provide better spreading outcomes and we now know that Ebola virus already spreads very well between bats and in humans (see the West Africa outbreak numbers which have not at any time been linked to a different or unusual spread of virus compared to any earlier outbreak[11]). To date, airborne spread has never been found to happen naturally in the dissemination of Ebola virus disease in humans. That is some kind of significant considering it does not take a lot of virus to start an infection through direct contact and considering there have been non-human primate transmission chains in the forests for a long time.

Each of those changes to the virus and the host's disease might happen by a series of accumulating mutations over time. But is their pressure to keep each of them? And really to be airborne, these changes would need to co-occur and do so without any trade-offs that meant the 'new airborne virus' was negatively impacted in some other area of its attachment, cell entry, replication, interference with the immune response enzymatic efficiencies etc. 

We do already know that in the lab, under laboratory conditions, with lab animals, lab equipment, plenty of lab-grown virus and a closed space with a lot of aerosol (probably some of which is wet droplets, not just droplet nuclei, meaning not truly airborne conditions), an Ebola virus can be forced to infect non-human primates. I've written about that previously.[3] 

And yet even when it was sought, no sign of such airborne infection has been found to occur naturally among humans. Direct. Contact. 

So I think it was a stretch to expend so many words on the chances of an airborne virus emerging rather than one that causes more bleeding, or less diarrhoea, or more vomiting, or more shedding in sweat, or having lower viral loads, more rash, more hiccups etc. 

Many additional things could result from mutational changes. We know next to nothing about the mutations recorded from the 99 genomes in Sierra Leone.[1] So why all this focus on one specific yet really quite complex outcome of viral air travel instead of many/any others? I don't know. But hey, now we have indeed been able to talk about this aspect some more, so good one Dr O! 

Others have come out to comment too. 

  • Dr Anthony Fauci, director of the National Institute of Allergy and Infectious Diseases in the US noted that "it’s fundamentally unlikely"[9]
  • Dr Amesh Adalja, University Pittsburgh said "it may not be the best path for the virus to take"[10]
  • Dr Derek Gatherer of Lancaster University in the UK noted an airborne Ebola virus would need a "conjunction of coincidental, unlikely events" [10] 

  • Dr David Heymann, Chair of the Health Protection Agency in the UK stated "No one can predict what will happen with the mutation of the virus", reminding us that "The virus's epidemiology is consistent with transmission via bodily secretions and excretions, which is exactly the same as other past epidemics".[11]
  • Prof Vincent Racaniello, a virologist at the College of Physicians and Surgeons at Columbia University stated "We have been studying viruses for over 100 years, and we've never seen a human virus change the way it is transmitted."[12]

Dr Osterholm did hit some other nails flush with the timber though. West Africa needs fewer promises to defeat Ebola virus and more plans that include actual rapid mobilization and on the ground experienced leadership to make inroads into getting beds for sick people and tracing contacts. Two key items on a long list of things to do better (in my opinion).

Thankfully some promising signs are appearing. The scope of this outbreak has now been guesstimated - 20k-100k cases.[4,5,6,7] I list this range rather than extending it to much higher levels [8] because I do still have hope that things will improve and interventions will turn the exponential case growth curves away from the sky and back to the horizon, sooner rather than before entire nations are destroyed. Because that's what is coming without successful intervention.

Money is being freed up and arriving from all over and more resources are slowly moving in to the region. Resources needed just to keep the people safe who have come from all over the world, including the nations of Africa, to care for the overwhelming numbers of sick and sickening people. Not to mention the money needed to prevent more infections. More specific and insistent pleas for defined numbers of healthcare professionals are also being broadcast. Drugs and vaccines are closer than they have ever been to use in humans. They may be our only hope to stop this virus.

If the many thousands of people predicted to die from a virus that is killing 4 in 5 confirmed cases (see the Medicins Sans Frontieres tweet below) is not enough reason for stopping the spread of Ebola virus, then stopping this particular evolving variant before it does change into something worse or more ingrained to the communities all over Africa and beyond, really is. 

While this Ebola virus variant may never make the changes necessary for it to go airborne, it has shown signs of relatively rapid change and that was relatively early in what looks to be a very long chain of human-to-human-to-human-to-human... transmission. Each person allowing the virus to adapt further, if that's what it needs to do.

Such a long transmission chain, from 1 animal>human infection, has never been recorded before and so we are indeed in new territory when it comes to the ebolaviruses. For now at least, the Ebola virus in 5 countries in and around West Africa has the upper hand. This tiny self-assembling unthinking, randomly mutating thing is totally dependent on our cells to replicate itself - and we are not doing enough to starve it of those cells. 

It clearly doesn't "need" to be airborne to spread efficiently.


Saturday, 6 September 2014

Case number changes between Ebola virus disease reports...

This is one of my favourite charts for following the Ebola virus disease outbreak in West Africa because it shows how things are changing from report to report. 

It plots the total number of suspected, probable and laboratory-confirmed cases between reports - which is a measure of change over time that is not cumulative.

That's not to say that understanding this chart is easy for with everything, what you take away from it may be heavily influenced by your own perspective and your background in reading graphs. I have written something about how to read some of the graphs on my blog here, which may be helpful too.

Uses World Health Organization data up to and including the Situation Report from the 5th-Sept, 2014.
Click on chart to enlarge.
I've marked up the last three periods between reports to highlight that the time changes differently. You can see this for yourself if you look carefully at the horizontal or "x" axis (the one that has the dates) and look at where each dot lines up with its date. Some are further apart than others. 

You can also mouse over the dots on the interactive version of the graph here. That will tell you the dates. THe subtraction is up to you though!

The lines joining the dots here suggest what is happening between the WHO Reports, but the line do not actually use any real collected values...because we don't have them to plot. 

Technically, a bar graph would be more accurate, but I find a line graph easier to read at a glance. So do remember - we don't know what is happening between those dots. We're just presuming it.

Friday, 5 September 2014

Editor's Note #20: Tweepidemiology...

Followers of my @MackayIM Twitter account (and this blog which gets promoted through it) since I started tweeting. It shows the cumulative rise and rise of followers and the relationship of rate of that rise to a very active period of infectious disease epidemics over the past 18-months or so.
Click on the graph to enlarge

While its hard to separate whether I pick up followers because of delivery of specific content or because as you pick up followers, they help spread the word and you pick up more followers, to simple old me this cumulative graph looks like MERS-CoV and the West African Ebola virus disease outbreaks have driven people to seek information. And sometimes they've done me the honour of following me on Twitter as I seek to understand what's going on as well. I'm constantly amazed at that, let me assure you.

I thought it worth having a look at the Tweepidemiology of my Twitter account. That is, the epidemiology of my Twitter followers - a bit of a long bow - but you follow me because I talk about infectious disease outbreaks and stuff so, given that I like my new word, I'm keeping with it!

I paid Twitter Counter to get my Twitter data and plotted it in Excel and tidied it using Illustrator and here it is. 

I started Tweeting a little after I started blogging - this Twitter thing is for the young people and their constant need to take selfies and update the world on their lives

Despite VDU blog posts on the emergence of influenza A(H7N9) virus in China dating back further in time, I came to Twitter well after H7N9's Wave 1 was engaged. So the slow burn could have been due to that or just because no-one knew me or that I could generally be trusted and generally don't spout drivel. 


So there ya go - Tweepidemiology as a way of looking at when and perhaps why one gains followers through Social Media when used to engage and try and help people understand what's happening with new or emerging viruses and diseases . Perhaps I should check what happens when I post photos of my cat too.

Sunday, 31 August 2014

Ebola: Blood, sweat and tears...

This post follows up the recent one on convalescent semen being able to harbour infectious Ebola virus (EBOV; although I am not aware of any infection resulting from this route of transmission there has been at least one report for Marburg virus [4]).

I thought I'd give the same treatment to tears and sweat which are also fluids intermittently listed as possible sources of EBOV infection for humans. Some examples of the scientific literature which support the risk messaging, follow.


I think we are all pretty clear that the blood of an advanced case of Ebola virus disease (EVD) is heavily laden with virus and is the most serious of the risk factors for acquiring infection by an ebolavirus.

Viral loads (amount of virus in the sample) in blood can be above 106-108 plaque forming units or copies (pfu; a measure of infectious virus present using a lab test that measure the impact of virus on infected cells; copies measure viral genome and cannot prove infectious virus is present) per millilitre of blood in acute phase disease patients and non-human primates.[5,6]


There is not a lot on sweat containing signs of an ebolavirus.
  • Bausch and colleagues found no trace of EBOV in a single acute sweat sample.[1]
  • Jaax and colleagues found that in experimentally infected non-human primates (NHPs; rhesus macaques), that connective tissues next to hair follicles and sweat glands in the skin as well as the cells lining ducts of glands in the skin were sometimes positive for EBOV antigens (proteins).[2]
  • Davis and colleagues infected NHPs (African green monkeys) and found signs of EBOV antigens in the cells lining the sweat gland ducts and in cells in the connective tissues next to hair follicles, but no virus particles by electron microscopy.[3]
  • Zaki and colleagues found heavy signs of EBOV antigens (proteins) in the tissues around the sweat glands, but rarely also within sweat glands and ducts.[8] No virus particles were seen in the sweat glands or ducts when examined by electron microscopy.

There is also very little I have found on this one.

  • Bausch and colleagues found EBOV RNA in tears from 1 sample, but no infectious virus could be isolated.[1]
  • Jaax and colleagues found some signs of virus in macrophages in the ciliary body of the eye of experimentally infected NHPs
  • Bausch and colleagues found infectious EBOV in 1 of 12 acute saliva samples (from 10 patients; none from 4 convalescent samples) and EBOV RNA in 8 of 12 (67%) of acute samples (none from convalescent samples).[1] RT-PCR positivity was significantly associated with fatal outcome.
  • Formenty and colleagues found EBOV antigens and EBOV RNA in oral fluids from fatal cases and those who survived infection.[7]

Saturday, 30 August 2014

The fifth I give you...[UPDATED]

According to it's Minister of Health, Awa Marie Coll Seck[1,2], a case of Ebola virus disease (EVD) has been imported from Guinea and it is confirmed by testing at the World Health Organization's collaboration Centre, the Pasteur Institute in Dakar.

Interesting that this occurred one week after Senegal closed its borders (again) with Guinea.[3,4] The infected 21-year old Guinean student travelled on 21-August to Dakar. On the 23rd he presented to a hospital but did not admit to being in contact with known EVD cases; Guinea issued an alert that a person with EVD contact has escaped surveillance 27-Aug; Senegal closed its borders around 22-August.[5,6,7,8].
[WHO Disease Outbreak News places his movements ahead of the closure of the border, arriving in Senegal 20-Aug [8]]

These borders are leaky and so the effect of "closure" essentially hinders aid, trade and economy (all very important to the region, especially right now) but very clearly does may not stop the spread of human hosts-as we have seen here

Humans are the variable in outbreaks. 

They behave differently each time. 

They respond differently each time. 

This is why no two outbreaks are identical. 

It's why you're a mug to assume this outbreak will be like the last outbreak.

While it looks like this is now a case study in why closing a border is ineffective, I maintain a position that border closures can't contain infectious disease. And please, do not point me to "temperature measurement" as a way to ensure capture of infected individuals. You could easily be harbouring an infection that does not yet express the symptom of fever. 

Click on image to enlarge. 
Graphic lifted from a great CNN video narrated by
Dr Sanjay Gupta. The video describes an example of
contact tracing and its importance to the fight
to contain EVD.[2] 

The contact tracing starts in Senegal now. A 42-day clock starts for the country and a signs and symptoms watch continues on all this case's contacts for 21-days.