For those unable to participate on PFI Forum as commentors, I offer this thread. If I am unable to comment on PFI Forum, for whatever reason, I will attempt to post on this thread.
The following projection involves estimates based on media accounts of reported cases as well as estimates of unreported cases.
First some assumptions:
1 HCW is needed for every 10 Ebola patients
There are 10,000 to 20,000 patients not receiving care currently.
By mid-November, this number will jump to 100,000-200,000, without immediate intervention.
By some time in January, this number will reach 1-2 million.
Second, some math:
1,000 to 2,000 additional HCWs are needed immediately, as in, on this very day. This number could be reasonably be acheived if it was made a priority.
If additional HCWs are delayed until mid-November, 10,000 to 20,000 HCWs will be required. Although technically possible, it is unlikely that this number could be mobilised.
If additional HCWs are delayed until January, 100,000 – 200,000 will be needed. This number almost certainly will not be acheived.
Plans to plan, plans to meet to plan, speeches about plannning, speeches about potential deployments, promises to deploy at some point in the future are all equally useless. Either HCWs deploy within the next few weeks or Africa is doomed. Plan B will be to let the virus burn through the continent and attempt to limit it to there while more developed countries develop vaccine for their own populations.
That is all.
Recently, a paper describing the sequencing of many samples from patients in Sierra Leone with Ebola was published in Science by Gire et al.:
There have been many headlines referring to this paper with variants of this phrase: “Ebola rapidly mutating!” The meaning and implications of such statements is not always clear due to an incomplete understanding of evolution. Therefore, I think it is worth defining some terms and explaining how viruses evolve generally and how Ebola may be evolving specifically.
First, I should like to clarify the difference between the rate at which mutations occur and the rate at which mutations are observed. Mutations are changes in the genetic sequence. They can occur for several reasons including mistakes which occur during replication of viruses. The rates at which these mutations occur thus depend in part on how accurately enzymes copy genetic sequence. This mutation rate is unlikely to change for a given species unless there is a change in the enzymes involved in copying genetic material. This is a very rare occurence. However, changes in the rate at which mutations are observed is much more common because another important force, selection, affects this process.
Many mutations occur but are never observed. How can this be? If a mutation occurs which is deleterious, it will decrease the likelihood that an organism will survive. Such mutations are common in viruses. However, although unfavorable mutations have always been occuring in Ebola, they were unlikely to be observed because the individual viruses which possesed them did not produce many additional viruses. We say that such viruses were selected against.
One of the key concepts of evolution is that selection can change. If the environment of an organism changes, then what constitutes a “bad” mutation, from the viewpoint of the organism, can also change. For a virus, the host is the environment. If the host for Ebola changes from, say, a fruitbat, to a human, then the environment has changed and the effect of a mutation on the ability of the virus to survive and replicate may change. In fact, a mutation which was selected against in fruitbats may be selected for in humans if it helps the virus survive in its new environment – humans. This will lead to a change in observed mutations in viruses which have colonised a new host even if the rate at which mutations actually occur has not changed.
Thus far, this has been a relatively academic discussion. But now we come to the public health implications of the Science paper. One interpretation of these results is that Ebola is adapting to its new host, humans, by acquiring new genetic sequences which allow it to replicate and spread person to person more effectively. Indeed, given that the virus has apparently been spreading human to human since December 2013, it would be surprising if this were not occuring.
In the past, Ebola would spread from its animal host to humans, pass human to human a few times, and then die out. It never had a chance to adapt to humans. The current outbreak is different. Because Ebola now has had many “passages” through the novel human environment, it has had many more opportunities to adapt to humans. This may be reflected in some of the changes in genetic sequence observed in the Science paper. It may also be reflected in changes in the ability of the virus to replicate and spread in humans. People who expect Ebola to remain unchanging in its new human host are ignoring evolution. If mutations can occur which will allow the virus to spread more efficiently in humans, then, given enough time, such mutations will occur.
Ebola was an animal virus.
It is becoming a human virus.
1. “Good” Scenario.
Good is in quotes because although this is the best case scenario, a lot of people still suffer and die.
Massive influx of aid from the West decreases the number of new cases in Guinea, Sierra Leone and Liberia. Contact tracing in Nigeria is effective in limiting spread in that country. New treatments prove effective and are used first for HCWs and then, as supplies increase, for all patients. An effective vaccine becomes available 6 months from now and is used in Africa to end the outbreak. West Africa suffers severe economic hardship and comes close to complete societal breakdown but narrowly escapes this fate.
2. Bad Scenario.
Aid from the West is too little, too late. Although the aid helps some people, the virus continues to spread in Sierra Leone and Liberia. Large numbers of cases show up in the West Point slum in Liberia a few weeks from now. Rioting occurs when soldiers shoot people trying to escape. Men with guns from outside Monrovia move in to “liberate” their kinsmen in West Point. Large numbers of cases are revealed in Lagos in October. Government attempts to hide the full extent of the outbreak in this country fail at this time. Nigerians start to flee to Western countries. A few are infected and start outbreaks in the countries they flee to. These are mostly contained but, as the numbers carrying the virus from Nigeria increase, containment starts to fail as ERs are overwhelmed by sick Nigerians as well as secondary contacts. Effective treatments are available but limited quantities lead to violent arguments over who will receive them. An effective vaccine is identified 6 months from now but is available in insufficient quanitities to do much good. Millions die and the world is plunged into economic Depression. The situation doesn’t stabilise until 2016 when there is finally enough vaccine to first slow and then stop the pandemic.
3. Very Bad Scenarios
There are actually several:
A. New Ebola becomes airborne before an effective vaccine can be developed.
B. New Ebola is used by terrorists.
C. It is discovered that New Ebola is a strategic biological weapon.
D. China starts WWIII while the New Ebola pandemic is ravaging the US.
The four Very Bad Scenarios are not mutually exclusive.
From CNN, July 29, 2014
Brantly’s family had been with him in Liberia, according to the Centers for Disease Control and Prevention, but left for the United States before he became symptomatic; as such it is highly unlikely that they caught the virus from him. Out of an abundance of caution they are on a 21-day fever watch, the CDC said.
Nancy Writebol from Charlotte, North Carolina, has also been infected. She is employed by Serving in Mission, or SIM, and had teamed up with the staff from Samaritan’s Purse to help fight the Ebola outbreak in Monrovia when she got sick. She, too, is undergoing treatment.
It is believed one of the local staff was infected with Ebola and came to work with the virus on Monday and Tuesday, Isaacs told CNN. “We think it was in the scrub-down area where the disease was passed to both Nancy and Kent,” he said. That staff member died on Thursday.
Dr. Brantly is a doctor with obvious experience in diagnosing Ebola cases. Yet, he was unable to detect infection in the co-worker who infected both him and Mrs. Writebol. Further, the co-worker was able to function for two days while still being able to infect at least two other people.
This suggests that we are indeed dealing with a “New Ebola” (as Pixie has put it at PFI Forum). This New Ebola apparently leaves people well enough, while they are infectious, to both travel and work without being detected. This makes this new Ebola pandemic-capable.
Here are two possible ways Ebola could become a pandemic:
1. It could slow down.
In the past, Ebola patients were only infectious when they were very ill and obviously infected with this disease. If the virus were to change in such a way that patients were well enough to travel while they were infectious, they could spread the virus to others before they died, especially if it was not obvious that they had Ebola. There are anecdotal reports that this may be happening in the current outbreak in West Africa.
2. It could become airborne.
In the past, Ebola was spread strictly by bodily fluids. If it changed so that it was transmitted through respiratory droplets, Ebola might spread to others much easier. There is no evidence of this in the current outbreak. However, another strain of Ebola, the Reston virus, was shown to be capable of respiratory transmission. So conversion of any Ebola virus to a respiratory form is a theoretical possibility.
From The Conversation, July 2014
The features of MERS-CoV do not suggest an epidemic disease, but rather, a sporadic pattern. This could be an animal source or deliberate release. My paper shows there is slightly more weight to deliberate release than an animal source, although both are possible.
In the case of bioterrorism, if it is not considered at all, it can never be detected, unless it involves an eradicated pathogen such as smallpox. Public health does not have a good track record of correctly interpreting aberrant patterns.
The author is Dr. Raina MacIntyre, Professor, Head of the School of Public Health and Community Medicine at UNSW Australia. She is affiliated with the National Centre for Immunisation Research and the NHMRC Centre for Research Excellence in Immunisation in understudied populations.
The paper she alludes to in the quote above can be found here:
The discrepant epidemiology of Middle East respiratory syndrome coronavirus (MERS-CoV)
Environment Systems and Decisions (2014)