In a month, they won't need cash…
Posted on 08/10/2014 12:46:23 AM PDT by Smokin' Joe
Keep in mind that the average incubation period of Ebola is 7 or 8 days, with the limits being 3 and 21 days.
I have seen a few stories that suggest that it is very difficult to fly in or out of the affected countries right now: Fear spreads, borders close as Ebola restricts travel in West Africa, Travel restricted within Ebola-affected West African countries
It is conceivable that illegal immigrants would try to stow aboard a cargo ship, but I think that those are being scrutinized, as well. Malta rejects ship with suspected Ebola case. I think it takes several days for a cargo ship to cross the ocean, so anyone infected with Ebola would probably start showing symptoms before the ship arrived.
Illegal immigration is not going to bring Ebola into this country, IMO. If an Ebola victim arrives, it will be via air travel.
EarlyBird, you should appreciate this. Yesterday, I was supposed to attend a VTC. I went to the VTC room with another PhD scientist and a Masters level colleague. We stared at the black VTC screen, looked at each other, asked each other what was wrong (Did we get the room wrong? What about the time?). Finally, the woman with a Masters called for IT support. The IT guy came and determined that the equipment had been turned off...
The histology photos are quite interesting. Did you notice the staining of the cell (presumably Langerhans') in figure 3A?
See, it's quite easy to have an adult conversation. If I find an update on the skin factor I'll post it.
Without playing parsing games, this would be an act of terrorism, not an accidental infection.
In that case, the southern border is a superhighway of invasion.
The ones coming in the airport will have their papers, and likely be either students, government officials, missionaries, or expatriate/visiting workers and will probably not know they are infected..
While it is possible to think up any number of scenarios by which terrorists would attempt to use Ebola, I will not engage in that exercise. I will continue to limit my comments to my area of expertise, the natural course of infection.
From there, infection would be likely along natural pathways through human contact, and the outbreak would build from there.
Unless, of course the sick jihadi picked a crowded venue to blow themselves up in.
Then you'd have aerosols, direct fluid contact, piece to person contact, and fomites all in one mess, and with the addition of shrapnel, plenty of open wounds among the initial survivors, and contamination of medical personnel and first responders, among others.
That precedent exists, at least in attempt, sans pathogen. (http://www.freerepublic.com/focus/f-news/1497194/posts)
"The race is not always to the swift, nor victory to the strong. But that's the way to bet." Damon Runyan.
I questioned your claim regarding epithelial infection because the ZMAPP drug began as an effort to transport modified alleles to treat cystic fibrosis. The researcher used Ebola glycoproteins due to the virus' efficient transduction of lung tissue. Your claim doesn't jibe with the ZMAPP work.
On the epithelial issue:
Intracellular Events and Cell Fate in Filovirus Infection Viruses 2011 (PDF pg 4)Indeed, MARV or ZEBOV can be isolated from any organ or tissue. Besides the typical target cells for ZEBOV and MARV infection in non-human primates, additional target cells were occasionally found in individual animals. These cells included alveolar epithelial cells, bronchial epithelial cells and the cells of endocardial layer.
Ebola haemorrhagic fever Lancet March 2011Target cells and tissues
Ebola virus has a broad cell tropism, infecting a wide range of cell types. In-situ hybridisation and electron microscopic analyses of tissues from patients with fatal disease or from experimentally infected non-human primates show that monocytes, macrophages, dendritic cells, endothelial cells, fibroblasts, hepatocytes, adrenal cortical cells, and several types of epithelial cells all lend support to replication of these viruses.
Regarding the transmission vector issue:
Ebola Hemorrhagic Fever, Kikwit, Democratic Republic of the Congo, 1995: Risk Factors for Patients without a Reported Exposure JID 1999In 1995, 316 people became ill with Ebola hemorrhagic fever (EHF) in Kikwit, Democratic Republic of the Congo. The exposure source was not reported for 55 patients (17%) at the start of this investigation, and it remained unknown for 12 patients after extensive epidemiologic evaluation. Both admission to a hospital and visiting a person with fever and bleeding were risk factors associated with infection. Nineteen patients appeared to have been exposed while visiting someone with suspected EHF, although they did not provide care. Fourteen of the 19 reported touching the patient with suspected EHF; 5 reported that they had no physical contact. Although close contact while caring for an infected person was probably the major route of transmission in this and previous EHF outbreaks, the virus may have been transmitted by touch, droplet, airborne particle, or fomite; thus, expansion of the use of barrier techniques to include casual contacts might prevent or mitigate future epidemics.
If you go back to my first post to you in this thread, I agreed that it's unlikely that Ebola will mutate into the epidemiological definition of an airborne disease. Nor must it undergo such mutation. Fomite, contact, droplet and aerosol are more than sufficient to spread it far and wide, as we're seeing now in West Africa. Much will be learned from this outbreak and much previous work will be upended.
You seem to think that no one should be the least bit concerned about the spread of Ebola to the western hemisphere. That is your right, of course, but your continued insistence that you know all possible epidemiological factors is odd given that the researchers engaged with this virus will not say the same. Every statement I've heard and read regarding vectors is predicated with a statement that much is unknown regarding transmission and pathogenesis.
I suspect continued efforts to communicate with you will not prove fruitful. You appear hell-bent on sticking to your opinion and position, and cannot abide a hint of disagreement, divergence or doubt.
I plan to revisit this thread when this outbreak is over and compare events to predictions. It will be interesting to see how it ends.
Just because somebody does not have permission to enter the US, doesn't mean he does not have money. Coyotes charge $3,000 and up to get somebody over the border, and find plenty of customers.
Now, consider what happens if there are a number of Ebola infections in Mexico, and how much Mexicans who think they may have been exposed would want to get into the US and have access to US medical care?
I work with PPE every day. One of my favorite observations is "for VRE, nobody does it right. For meningococcal meningitis, everybody does it right".
Even given the catastrophic conditions in West Africa, the attack rate among HCWs with access to PPE is extraordinary. I think this is most consistent with transcutaneous (intact skin) infection with an extremely low ID50.
Scary stuff.
There are Ebola cases in Nigeria. Expedia still lists flights from Nigeria to Mexico City. Nigeria to Mexico City is one day. Mexico City to the border is another day. Across the border to the US is a third day.
Yes, it will require money. There are Nigerians with money, or at least the $2K to make the flight to Mexico, and the $4K to pay a coyote.
Yes, travel is officially restricted. But this is West Africa, notorious for the corruption of its public employees. Slip some cash to the border guards, and you can cross. I doubt it would even take a lot of cash.
In a month, they won't need cash…
“Temporal Variations in the Effective Reproduction Number of the 2014 West Africa Ebola Outbreak”
I picked this up via the PANDEMIC FLU INFORMATION FORUM.
Short form, Lancet documented in June 2000 that asymptomatic Ebola Hell exists and it is Coming for Breakfast.
“This study showed that asymptomatic, replicative Ebola infection can and does occur in human beings. The lack of genetic differences between symptomatic and asymptomatic individuals suggest that asymptomatic Ebola infection did not result from viral mutations.”
http://www.ncbi.nlm.nih.gov/pubmed/10881895
The abstract, in full:
Quote:
Lancet. 2000 Jun 24;355(9222):2210-5.
Human asymptomatic Ebola infection and strong inflammatory response.
Leroy EM1, Baize S, Volchkov VE, Fisher-Hoch SP, Georges-Courbot MC, Lansoud-Soukate J, Capron M, Debré P, McCormick JB, Georges AJ.
Author information
Abstract
BACKGROUND:
Ebola virus is one of the most virulent pathogens, killing a very high proportion of patients within 5-7 days. Two outbreaks of fulminating haemorrhagic fever occurred in northern Gabon in 1996, with a 70% case-fatality rate. During both outbreaks we identified some individuals in direct contact with sick patients who never developed symptoms. We aimed to determine whether these individuals were indeed infected with Ebola virus, and how they maintained asymptomatic status.
METHODS:
Blood was collected from 24 close contacts of symptomatic patients. These asymptomatic individuals were sampled 2, 3, or 4 times during a 1-month period after the first exposure to symptomatic patients. Serum samples were analysed for the presence of Ebola antigens, virus-specific IgM and IgG (by ELISA and western blot), and different cytokines and chemokines. RNA was extracted from peripheral blood mononuclear cells, and reverse transcriptase-PCR assays were done to amplify RNA of Ebola virus. PCR products were then sequenced.
FINDINGS:
11 of 24 asymptomatic individuals developed both IgM and IgG responses to Ebola antigens, indicating viral infection. Western-blot analysis showed that IgG responses were directed to nucleoprotein and viral protein of 40 kDa. The glycoprotein and viral protein of 24 kDa genes showed no nucleotide differences between symptomatic and asymptomatic individuals. Asymptomatic individuals had a strong inflammatory response characterised by high circulating concentrations of cytokines and chemokines.
INTERPRETATION:
This study showed that asymptomatic, replicative Ebola infection can and does occur in human beings. The lack of genetic differences between symptomatic and asymptomatic individuals suggest that asymptomatic Ebola infection did not result from viral mutations. Elucidation of the factors related to the genesis of the strong inflammatory response occurring early during the infectious process in these asymptomatic individuals could increase our understanding of the disease.
However, the report is
1. Trying really hard to conflate/confound that fact with the relative ineffectiveness of enforced quarantine (referred to as cordons sanitaire) in response to that accelerated urban infection spread; and
2. Trying really hard to avoid even the word fomite.
The best they come to touching fomite Ebola spread is mentioning the “Homecare setting.”
See the link for more text and tables.
SEPTEMBER 18, 2014 · RESEARCH
AUTHORS
Sherry Towers
Oscar Patterson-Lomba
Carlos Castillo-Chavez
ABSTRACT
Background
The rapidly evolving 2014 Ebola virus disease (EVD) outbreak in West Africa is the largest documented in history, both in terms of the number of people infected and in the geographic spread. The high morbidity and mortality have inspired response strategies to the outbreak at the individual, regional, and national levels. Methods to provide real-time assessment of changing transmission dynamics are critical to the understanding of how these adaptive intervention measures have affected the spread of the outbreak.
Methods
In this analysis, we use the time series of EVD cases in Guinea, Sierra Leone, and Liberia up to September 8, 2014, and employ novel methodology to estimate how the rate of exponential rise of new cases has changed over the outbreak using piecewise fits of exponential curves to the outbreak data.
Results
We find that for Liberia and Guinea, the effective reproduction number rose, rather than fell, around the time that the outbreak spread to densely populated cities, and enforced quarantine was imposed on several regions in the countries; this may indicate that enforced quarantine may not be an effective control measure.
Conclusions
If effective control measures are not put in place, and the current rate of exponential rise of new cases continues, we predict 4400 new Ebola cases in West Africa during the last half of the month of September, with an upper 95% confidence level of 6800 new cases.
FUNDING STATEMENT
This publication was made possible by grant number 1R01GM100471-01 from the National Institute of General Medical Sciences (NIGMS) at the National Institutes of Health. Its contents are solely the responsibility of the authors and do not necessarily represent the official views of NIGMS. OPL additionally gratefully acknowledges the support of NIH training grant T32AI007358-26. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
INTRODUCTION
Ebola virus disease (EVD) is a severe, often fatal viral infection in humans, with a case fatality risk (CFR) of up to 90% in previous outbreaks 1,2,3,13,14. There have been 13 recorded outbreaks since 2000, associated with at least two distinct strains of the Ebola virus (Ebola-Zaire and the Ebola-Sudan) 23, but the current West African outbreak has spread over the largest geographic area and caused the greatest number of infections and deaths 3,15,16,22,23. Critically, unlike previous epidemics, this outbreak has spread to densely populated areas, increasing the risk of international spread 22; the problem is compounded by lack of resources for effective quarantine and isolation in the under-developed countries that have been affected, and the high mobility of the population in a region with porous borders.
The spread of EVD requires direct contact with infected blood, tissue, or body fluids of either the living ill or the recently deceased, and the disease is particularly prone to transmission in unprotected homecare settings and during traditional burials 24,25. Symptoms typically appear after 2–21 days, and the disease quickly progresses and kills most infected patients within a few days 13,14. No licensed vaccine or specific treatment is currently available 26, leaving improved hygiene, quarantine, isolation, and social distancing as the only potential interventions. In an attempt to quell the outbreak, on August 1st the governments of Guinea, Liberia, and Sierra Leone announced plans to impose a military-enforced mass quarantine of entire regions and villages , in an attempt to prevent spread of the disease (referred to as cordons sanitaire) to other areas 17. The spread of disease within the isolated areas has typically been allowed to run its course 19,20.
Assessing the net positive or negative impact of such attempted intervention measures involves assessment of a complex adaptive system, where the system dynamics are intimately connected to the impact of multiple feedback mechanisms that evolve over time 9. Because the situation in West Africa is rapidly evolving in time, and attempts at intervention measures are far ranging and also rapidly evolving, understanding how best to control the outbreak, and/or assessing whether or not current attempts to contain the spread are working, poses unique challenges.
In this analysis, we examine current outbreak incidence data for Guinea, Sierra Leone, and Liberia up to September 8, 2014, as estimated by the World Health Organization (WHO) 3,4. Using novel methodology, we assess the impact of adaptive response measures by fitting piecewise exponential curves along the data time series to estimate the evolving rate of exponential rise (or decline) in cases. We then use a Susceptible, Exposed, Infected, Recovered (SEIR) model to estimate the temporal patterns of the effective reproduction number for the outbreak in each country. In the following sections, we describe our sources of data, and the statistical and modeling methods used to estimate the effective reproduction number.
[big snip]
Estimation of the effective reproduction number from the local rates of exponential rise
The basic reproduction number, R0, of an infectious disease is the average number of secondary cases a case generates during the course of its infectious period, in a completely susceptible population. The basic reproduction number is affected not only by the ease at which an infection is transmitted upon contact between two hosts, but also by the contact rate between members of the population. Because of heterogeneity in susceptibility, infectiousness, and differing social dynamics, the estimates of for an infectious disease tend to be different across populations. For example, rural and densely populated urban areas are likely to have substantial differences in contact rates 10. Traditionally R0 has been computed under simplifying assumptions, like the existence of a constant contact structure, or under the assumption that interventions like quarantine and isolation are uniformly applied from the very beginning of the epidemic. However, particularly in the case of a disease with high morbidity and mortality, it has been shown that human behaviors adapt to limit spread of the disease 9, thus limiting the usefulness of R0 as a means to assess the efficacy of evolving intervention strategies, and to forecast the future progression of the outbreak.
Given these limitations of R0 , in this analysis we thus instead assess the time evolution of the effective reproduction number, Reff , which is a dynamic estimate of the average number of secondary cases per infectious case in a population composed of both susceptible and non-susceptible individuals during the course of an outbreak. The effective reproduction number is a function of, among other things, the probability of transmission upon contact of the disease, the contact rate within the population, and the number of susceptible individuals in the population, all of which may be time dependent.
In an epidemic, given a short enough period of time, the value of Reff during that time period can be considered to be approximately constant.
[snip]
Typically, if the transmissibility and contact rates in the population remain constant, one expects to see the effective reproduction number decrease in time as the fraction of susceptible individuals in the population decreases. However, if Reff increases, it can signal that, for instance, contact rates within the population have increased, the virus has become more transmissible, and/or that attempted intervention strategies are actually making the outbreak worse.
[big snip]
We stress again that our analysis makes no assumptions about whether or not control measures have been employed, and/or when they were employed. We simply examine the local rates of exponential rise to estimate how the effective reproduction number appears to be changing in time. We note that up until mid-August, the values of for Guinea are significantly below the average central value obtained from the fit the the data from July 1st onwards, and were rising (unless otherwise noted, all subsequent statistical tests are Bonferroni corrected one-sided Z tests, with rejection of the null hypothesis occurring when p < 0.05/k, where k is the number of values being compared). The dip in the two recent Guinea data points compared to the central value is not significant. In addition, the dip in the two recent estimates of from the Liberia data are also not significant. However, the estimates of for the three earliest points in the Liberia local time series are significantly lower than the central value, and rising. None of the estimates of from the Sierra Leone data and combined data for all countries are significantly different than the central value.
It is unclear why the transmission rate of the disease apparently rose for both Guinea and Liberia between mid July to mid August, and why the transmission rate in Sierra Leone is systematically lower, although is important to note that the WHO data are obtained from rudimentary surveillance systems in under-developed countries, under the stress of a rapidly evolving outbreak situation. The temporal patterns we observe may thus partly be due to variations in surveillance during the outbreak, under-reporting, and/or reporting delays. In addition, serial passage of the disease as the outbreak progresses may be leading to increased pathogenicity, and a subsequent increasingly larger rate of increase in case counts. However, it also must be considered that otherwise well intentioned attempts at intervention may in fact be making the situation worse, at least in some regions; in a joint meeting of officials from Guinea, Liberia, and Sierra Leone on Aug 1st , it was announced that cordons sanitaire would be implemented, to seal off the villages and regions worst hit by the outbreak, in an attempt to limit its spread outside those areas 17. In addition, at that time Liberia closed all schools and non-essential government offices 18, and two weeks later imposed a military-enforced cordon sanitaire on the West Point slum of Monrovia, sparking riots 19. It must be stressed that cordons sanitaire do not generally attempt to limit disease spread within the quarantined areas, and the implementation of these measures in West Africa has received criticism due to the fact that the quarantined areas are at risk for crowding, lack of medical and basic services, and poor sanitation, potentially increasing the spread of disease within those areas 20. It was around the period of time that the cordons sanitaire were first imposed, and when the outbreak moved to the densely populated cities of Conakry and Monrovia, that the exponential rise in new cases in Guinea and Liberia increased, rather than went down. Again, it is unclear why the rate of exponential rise in Sierra Leone was apparently unaffected by these events.
Based on our estimates of the exponential rise in cases between July 1st to the beginning of September, if this rise is to continue unabated, there will be approximately 4400 new EVD cases in West Africa during the last half of the month of September (95% CI [3000, 6800]), 500, 900, and 3000 of which will be in Sierra Leone, Guinea, and Liberia, respectively.
SUMMARY
We have presented an analysis where piecewise exponential fits are employed to estimate the local rate of exponential rise in cases in the 2014 West Africa Ebola outbreak. We have shown that these local rates of exponential rise can be used in conjunction with a mathematical model to estimate the temporal changes in the effective reproduction number (in the case of this analysis, we employed an SEIR model). Our analysis indicates that the spread of the disease to densely populated cities, and/or the imposition of cordons sanitaire in West Africa may have accelerated the spread of the disease in some regions. Our methodology is novel, and is applicable to any outbreak, and any mathematical disease model.
Transcutaneous transmission would explain the multiple times I’ve heard physicians on the ground insist that not a single square millimeter of skin can be exposed in the treatment wards.
What a nightmare scenario.
And if THAT delightful fact ever appeared in our public transport system the circus would truly begin.
Disclaimer: Opinions posted on Free Republic are those of the individual posters and do not necessarily represent the opinion of Free Republic or its management. All materials posted herein are protected by copyright law and the exemption for fair use of copyrighted works.