Are we *sure* Ebola isn’t airborne?

Since yesterday’s post, several people have asked me on various social media outlets about the airborne nature of Ebola. Didn’t I know about this paper (“Transmission of Ebola virus from pigs to non-human primates“), which clearly showed that Ebola could go airborne?

Indeed I do–I wrote about that paper two years ago, and it in no way changes my assertion that Ebola doesn’t spread between people in an airborne manner.

Let me back up. The paper in question was an experimental study done in the wake of the 2008 finding of the Reston Ebola virus in pigs and a previous study looking at the Zaire virus in pigs. In the air transmission study, they inoculated pigs with Ebola and examined transmission to macaques (who were not in direct contact with the infected pigs). They did find aerosolized Ebola in air samples, and some of the macaques did come down with symptoms of Ebola. So, it looked like pigs could spread Ebola through the air, which is something that had already been suggested by the epidemiology of the 2008 pig Ebola outbreak. It’s always nice when experimental data matches up with that observed during a real-life occurrence of the virus.

*However*, the kicker was not that Ebola is transmitted by air in human outbreaks, but rather that there may be something unique about pig physiology that allows them to generate more infectious aerosols as a general rule–so though aerosols aren’t a transmission route between primates (including humans, as well as non-human primates used experimentally), pigs may be a bigger threat as far as aerosols. Thus, this may be important for transmission of swine influenza and other viruses as well as Ebola.

So unless you’re sitting next to an Ebola-infected pig, seriously, airborne transmission of Ebola viruses isn’t a big concern. (Perhaps this corollary should be added to this handy diagram examining your risk of Ebola).

 

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Ebola is already in the United States

It’s odd to see otherwise pretty rational folks getting nervous about the news that the American Ebola patients are being flown back to the United States for treatment. “What if Ebola gets out?” “What if it infects the doctors/pilots/nurses taking care of them?” “I don’t want Ebola in the US!”

Friends, I have news for you: Ebola is *already* in the US.

Ebola is a virus with no vaccine or cure. As such, any scientist who wants to work with the live virus needs to have biosafety level 4 facilities (the highest, most secure labs in existence–abbreviated BSL4) available to them. We have a number of those here in the United States, and people are working with many of the Ebola types here. Have you heard of any Ebola outbreaks occurring here in the US? Nope. These scientists are highly trained and very careful, just like people treating these Ebola patients and working out all the logistics of their arrival and transport will be.

Second, you might not know that we’ve already experienced patients coming into the US with deadly hemorrhagic fever infections. We’ve had more than one case of imported Lassa fever, another African hemorrhagic fever virus with a fairly high fatality rate in humans (though not rising to the level of Ebola outbreaks). One occurred in Pennsylvania; another in New York just this past April; a previous one in New Jersey a decade ago. All told, there have been at least 7  cases of Lassa fever imported into the United States–and those are just the ones we know about, who were sick enough to be hospitalized, and whose symptoms and travel history alerted doctors to take samples and contact the CDC. It’s not surprising this would show up occasionally in the US, as Lassa causes up to 300,000 infections per year in Africa.

How many secondary cases occurred from those importations? None. Like Ebola, Lassa is spread human to human via contact with blood and other body fluids. It’s not readily transmissible or easily airborne, so the risk to others in US hospitals (or on public transportation or other similar places) is quite low.

OK, you may say, but Lassa is an arenavirus, and Ebola is a filovirus–so am I comparing apples to oranges? How about, then, an imported case of Ebola’s cousin virus, Marburg? One of those was diagnosed in Colorado in 2008, in a woman who had traveled to Uganda and apparently was sickened by the virus there. Even though she wasn’t diagnosed until a full year after the infection (and then only because *she* requested that she be tested for Marburg antibodies after seeing a report of another Marburg death in a tourist who’d visited the same places she had in Uganda), no secondary cases were seen in that importation either.

And of course, who could forget the identification of a new strain of Ebola virus *within* the United States. Though the Reston virus is not harmful to humans, it certainly was concerning when it was discovered in a group of imported monkeys. So this will be far from our first tango with Ebola in this country.

Ebola is a terrible disease. It kills many that it infects. It *can* spread fairly rapidly when precautions are not carefully adhered to: when cultural practices such as ritual washing of bodies are continued despite warnings, or when needles are reused because of a lack of medical supplies, or when gloves and other protective gear are not available, or when patients are sharing beds because they are brought to hospitals lacking even such basics as enough beds or clean bedding for patients. But if all you know of Ebola is from The Hot Zone or Outbreak, well, that’s not really what Ebola looks like. I interviewed colleagues from Doctors without Borders a few years back on their experiences with an Ebola outbreak, and they noted:

“As for the disease, it is not as bloody and dramatic as in the movies or books. The patients mostly look sick and weak. If there is blood, it is not a lot, usually in the vomit or diarrhea, occasionally from the gums or nose. The transmission is rather ordinary, just contact with infected body fluids. It does not occur because of mere proximity or via an airborne route (as in Outbreak if I recall correctly). The outbreak control organizations in the movies have no problem implementing their solutions once these have been found. In reality, we know what needs to be done, the problem is getting it to happen. This is why community relations are such an issue, where they are not such a problem in the movies.”

So, sure, be concerned. But be rational as well. Yes, we know all too well that our public health agencies can fuck up. I’m not saying there is zero chance of something going wrong. But it is low. As an infectious disease specialist (and one with an extreme interest in Ebola), I’m way more concerned about influenza or measles many other “ordinary” viruses than I am about Ebola. Ebola is exotic and its symptoms can be terrifying, but also much easier to contain by people who know their stuff.

 

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Repost: What’s it like to work an Ebola outbreak?

In the light of the current Ebola outbreak, I thought this post from 2007 was once again highly relevant. 

As another Ebola outbreak simmers in Uganda (and appears to be increasing), I recently was in touch with Zoe Young, a water and sanitation expert with Médecins Sans Frontières (MSF*, known in the US as Doctors without Borders), who was working in the Democratic Republic of Congo during the DRC Ebola outbreak earlier this fall (and blogging it!)

Regular readers know of my interest in this virus, but I’m obviously geographically removed from any of the outbreaks. As such, Zoe and her colleague, physician Armand Sprecher, were generous enough to answer my questions about their work with MSF and the Ebola outbreak in particular.

First, just a bit of background on Zoe and Armand. Armand is a native of Philadelphia, and received his Bachelor’s degree in cognitive science from Brown University. He followed that with his MD from Jefferson Medical College, then headed west for a residence in emergency medicine at the University of Missouri Kansas City, then back to the east coast for a degree in public health from Johns Hopkins. He’s worked in the field with the International Medical Corps (IMC) in Bosnia, and with MSF in Sri Lanka, East Timor, Uganda, and Burindi. He’s been working in the headquarters of MSF’s Operational Center of Brussels (OCB) as the medical department’s public health support person since 2004.

From 1997 to 2001, while not in the field, he worked in emergency rooms in Wisconsin, Nebraska, New Jersey, and Wyoming.

Zoe is London born and bred. She graduated from the University of Manchester with a BSc in Biology and Geology and received an MSc from Edinburgh in Environmental Protection and Management. She has extensive field experience, having worked for Action Against Hunger (ACF) in Sierra Leone in 1996-7 and in Burma from 1997-98. She worked with Oxfam in Sierra Leone 1999 and in Eritrea 2000; with International Federation of Red Cross and Red Crescent Societies (IFRC) in El Salvador in 2001, and with International Rescue Committee in East Timor in 2002. She started work with MSF headquarters in the medical department as part of the water, hygiene and sanitation unit in 2004.

Zoe also worked elsewhere when she wasn’t in the field, including stints with Interact Worldwide, a sexual and reproductive health organization in London. She also helps to run a web-based fair trade business importing recycled items and silver.

I asked them first how they both ended up working with MSF, and in the DRC on Ebola:

Armand: During my emergency medicine residency, I spent my elective time in Bosnia with IMC. The medical coordinator there was a former MSF expat and his recommendation led me to volunteer when I finished my residency. As for the DRC, it was both a matter of assignment and choice (as are most MSF postings). I had experience and interest in filovirus outbreaks, and MSF needed me there.

Zoe: A friend of mine sent me the link to the job when it was advertised and I applied – never really thinking that I would get it and move to Brussels! A few months after I started I took over as the focal point for haemorrhagic fever from one of my watsan (water and sanitation) unit colleagues when he left – he had made it all sound very interesting and challenging.

Can you describe your previous experience with outbreaks of this type?

Armand: I worked with MSF in the Ebola-Sudan outbreak in Gulu in 2000 as their isolation ward physician. This is where I met my wife, who was the field coordinator at the time. She went to the Gabon outbreak in 2002 while I was at Hopkins, and the problems with that outbreak led me to do my masters thesis on health communication in Ebola outbreaks. Once in headquarters, I went to the Marburg outbreak in Angola in 2005 as medical coordinator. Since then, I have been working on, among other things, revision of MSF’s filovirus outbreak management manual.

Zoe: I went to join the team in Angola for the Marburg outbreak. I was lucky as there were several watsans there including my former colleague, so I got a very good job briefing. Then in July this year I went to Uganda to help do some training for a very small Marburg outbreak, which was a good refresher for the DRC Ebola outbreak in September.

What was the situation like when you arrived in the DRC?

Armand: I arrived in the first week of October, so things were almost over by then. The last patient was hospitalized shortly before my arrival (though of course we did not know that then). Many of the people who had been there from the beginning were ready to leave. The project coordinator was tired, so I replaced her in addition to being the medical coordinator for the ensuing two and a half weeks. The community was happy with our presence and the general feeling was that things had improved. Though there was still fear of the disease, this was not interfering with outbreak control.

Zoe: I arrived about a week after the first teams had got there. Basic isolation was in place with disinfection procedures, but it was a bit chaotic. As more medical staff were arriving, it needed to be improved because otherwise with all these new people moving about, it would have been difficult to ensure correct procedures. It was good that there was something in place to build on because it made it much easier to make big improvements very quickly. Also, we were lucky in that there was plenty of space and the local administrator was happy for us to extend the perimeter of the isolation to make a better flow.

What was a “typical” day like (if there was one?) How long were each of you there?

Armand: I was there for two and a half weeks. These interventions are many-headed hydras, and coordinating means spending the day touching base with everyone to make sure that they know what needs to be done and provide any necessary support. It also means keeping in touch with the other organizations (MoH, WHO, CDC, Public Health Agency of Canada, Médecins du Monde, etc.). In practice, this means sitting down with team members or people from other agencies individually, or collectively in MSF team meetings or WHO coordination meetings (quite the change from Gulu, where I spent all day in personal protective gear with patients in the isolation ward). It is fascinating though. It requires that one have a good understanding of epidemiology, clinical medicine, infection control, health promotion, medical anthropology, etc.

Zoe: I think that the typical day changes during the outbreak. To begin with, it was much more about trying to get everything correct and safe in the isolation. Training of staff for burials, collecting patients, disinfection, etc. Sometimes training is a bit by osmosis because there just isn’t time to talk to everyone about every aspect, or it is ad hoc, talking in the car to the drivers about procedure, etc. Then of course activities depend on the number of patients and whether they have died or not. Some days were a bit more fraught than others. There was one day with three burials that I mentioned in my blog (which was edited because it was so awful) where we were literally trying to match the body with coffin – get the body into the small coffin, then to the grave – perhaps not yet dug, back to pick up the next body, etc. Some days, there were reasonably healthy patients in the ward, so perhaps improvements in flow planned and then everything in the air because new patients coming in or people dying outside the isolation. I found the whole experience really tiring but very enjoyable and it certainly kept everyone on their toes.

During an outbreak like this, I know there are many responsibilities: patient care, education of both local people and your co-workers, contact tracing, diagnostics, scientific research, and I’m sure many others. I also know you wear many hats while you’re there as well, doing everything from setting up isolation wards to burying the dead. I’m wondering about the logistics of all this–do you all work together, or is it more that everyone does their own thing?

Armand: So now you get to why coordination is important. Everyone has their principle domain of responsibility, but there needs to be communication within the group. If the epidemiologist doing case investigation finds a novel transmission method of importance (such as a local traditional medical practice), then this would need to be passed to the people doing health promotion. If the team in the isolation ward notes that the patients have been receiving little in the way of visits or inquiries from the patients’ families, this bodes ill for the welcome that survivors may receive when discharged, and how they are treated may have an impact on the willingness of those who become ill to be detected and isolated themselves. This would be something to discuss with the mobile teams working in the community, that they may investigate further. Even PCR has false negatives, and interpretation of a negative result that should result in a patient’s discharge from isolation needs to be interpreted in light of their clinical appearance and epidemiologic risk. These are just a few examples of how people need to work together. I have not been involved in another sort of intervention that had people so interested in each other’s work. It is also the reason why poor coordination can be so detrimental to outbreak control (as, alas, it has been too frequently the case).

Zoe: Also every evening we had a kind of round up of the days’ events, like hearing about the road making [a road between villages was built while they were there–TS] or meetings or what the CDC was planning to get a general overview, not just the specifics. It was a great team as well and as Armand says, everyone is very interested in the whole process, not just their speciality.

Ebola is a pathogen that’s been so mythologized in the media and popular press. How does working during an actual epidemic like this contrast with what’s been shown in movies such as “Outbreak?”

Armand: As for the disease, it is not as bloody and dramatic as in the movies or books. The patients mostly look sick and weak. If there is blood, it is not a lot, usually in the vomit or diarrhea, occasionally from the gums or nose. The transmission is rather ordinary, just contact with infected body fluids. It does not occur because of mere proximity or via an airborne route (as in Outbreak if I recall correctly). The outbreak control organizations in the movies have no problem implementing their solutions once these have been found. In reality, we know what needs to be done, the problem is getting it to happen. This is why community relations are such an issue, where they are not such a problem in the movies.

Zoe: As Armand says, there is not as much blood as you think there will be, although I also think that I have been lucky when I hear about some patients that colleagues have dealt with where there was more blood and horror. I haven’t seen Outbreak; perhaps I will save that for viewing during the next outbreak as those sorts of films are great tension reliever and also useful educational tools (how not to……….).

I’d like to ask about a few quotes from your posts, Zoe. The first, from here, regarding workers’ appearances in their protective gear:

“What really struck me was how un-human she looked, completely dressed up, making strange jerky movements and impossible to see her face. I saw, really for the first time, how we might be perceived by the patients.”

How *do* you feel you were perceived by the people there, both patients and not? You mention in another post about a driver (I think it was a policeman) who no longer wanted to help once he saw you had a body under a sheet. Was that a common reaction?

Armand: I cannot say much about Zoe’s experiences, but I will add what I can from my own. When I was in Gulu, the outfits were a bit different, but not too much so. It was important that people have their names written on their aprons, or we would have had a hard time recognizing each other. I can imagine what this meant for the patients. This is one of the reasons that maybe face shields would be better than goggles and masks, if the protection were similar.

In the community, we have made an effort to keep people from overusing protective gear so that we do not give the impression of mysterious invaders from another planet coming to take people away as we spray chlorine solution everywhere.

Zoe: In fact it was a soldier who wanted a lift. There were quite often policemen and soldiers by the sides of the road who wanted to be dropped at the next guard post or town. The rule is that we don’t pick up people that we don’t know to take in the cars and certainly not someone from the army. So, we passed this guy without slowing down (we were going pretty slowly because of the road and because of the body in the back) so the driver spoke to him as we passed. A hundred yards or so further on there was a big pothole and one of the spray machines in the back tipped over so we stopped to get out and right it. The soldier thought we had stopped for him and came running up to jump in. More difficult now, since we had stopped, not to take him but luckily at the mention of the body under the plastic sheeting he backed right off.

I think that most people were happy that we were there. Quite often there were comments about that and of course for the staff it was the opportunity for work as well. But, of course the people didn’t want to touch anything contaminated and even the drivers to begin with would be very careful about washing the whole surface of their cars, not just the back that had had the patient in it.

Because of the set up it was possible to see the patients and talk to them without all the protective gear on which was nice – of course they didn’t necessarily realize that you had been the one in the space suit standing next to them 10 minutes before. But it did mean that they could see that they were being taken care of by (friendly) human beings.

Zoe, you wrote, regarding contact follow-up:

“When I went out this morning with the team one of the first houses we visited belonged to one of the patients that we buried last week. His wife was sitting there, looking extremely desolate. I asked how she was and she said, ‘not sick’. Of course, I hadn’t meant that. What was very difficult was that it wasn’t really possible to touch her arm or take her hand to show a bit of empathy. She is a contact and has to be monitored.”

Many of the stories you shared on your blog ended badly, with the death of the patient. But as you note, you stayed removed, even though it was difficult for you. These outbreaks must be hugely emotional–how do you cope?

Armand: When I was doing clinical care, I focused on treating what I could (i.e. other infections that resembled Ebola enough to get the patient isolated – dysentery, malaria, etc.), keeping the patients comfortable, keeping the staff safe, and making sure the survivors recovered well. That worked well enough, but that was Ebola-Sudan, so we had a few more survivors. Coordination removes one from the patients, so it is easier in that regard.

Zoe: In a way the openness of the structure made it all more difficult because all the time, even when inside, it was possible to look out and see the family members and see their sadness. Also, because we were at the end of the epidemic there were not that many patients there at any one time so you build up a bit of a relationship with them–especially the ones that come in earlier on in the disease, and who are talking and walking about. But there are plenty of things to think about and ways to improve what we are doing, so it is not possible to spend too long dwelling on things – and of course there were lots of fun and funny people working in the team so there was lots of laughter and joking as well.

Regarding local conditions and infrastructure, you wrote:

“The man in the isolation unit at the moment comes from Kalombayi. This is a village which has had no road access, just a track for bicycles and motorbikes. Martin has had hundreds of people clearing a path so that cars can pass and so that patients can be collected if necessary. He has also had to make three bridges.”

You make it sound like building roads and bridges is old hat. How much of this has to be done in outbreaks such as these? How widely scattered were the cases you were dealing with?

Armand: I think Martin’s road work impressed even the experienced MSF folks. That being said, we do what needs doing. Zoë didn’t mention the airstrip that he did? The cases and their villages where we traced contacts were within a 1-1½ hour drive by Landcruiser (under 30 kilometers, I think).

Zoe: Yes, as Armand says Martins’s road work was amazingly impressive and now that I read the paragraph I wrote again, I certainly didn’t do him justice. I think that the total length of that particular road was 20km. He also improved the road to Luebo, which was a relief as there was a lot of to-ing and fro-ing for meetings and trainings. Although it was fun to be on such an excitingly precarious road on the first day, it is exhausting to travel like that every day. And of course Martin found a forgotten airstrip and remade it with waiting area and latrine, Kampungu International. All this work involved hundreds of labourers scraping and shoveling the road surface and cutting back trees and bushes, and Martin and his assistants would supervise all of it every day.

Finally, can you give the readers some information about where things stand now? You mention an overlapping outbreak of typhoid, which I also read about in the news; was that confirmed? Do they know anything about the subtype of virus (I assume Zaire strain…?)

Armand: It was Zaire. The typhoid was confirmed, as were some cases of Shigella. However, it is not clear that these were above their normal incidence, so I would hesitate to say there were parallel epidemics (as has been said). The outbreak was declared over on the 19th of November.

Zoe: Yes, that’s over and the next one has begun!

The epidemic was confirmed rather late and was winding down when we arrived, so our impact may not have been great. However, it was a useful experience for us, as is each outbreak, in preparation for the next.

We had good relations with the community, which has not always been the case. It would be nice to know if it was something that we did, which could be repeated, or a result of contextual factors.

Many thanks to Zoe and Armand for taking the time to respond to my questions–and best of luck to them as risk life and limb taking on new epidemics.

*MSF has built considerable experience in previous outbreaks of hemorrhagic fever, especially caused by Ebola or Marburg: in Angola (2005), Gabon (1997 and 2002), Uganda (2001), Congo-Brazzaville (2003/2004), southern Sudan (2004). In DRC, MSF responded to a big Ebola outbreak in Kikwit, capital of the neighbouring province of Bandundu, in 1995. This epidemic killed 244 people between May and August 1995.

 

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A conversation on smallpox and vaccination with Dr. William Foege

I can hardly do Dr. William Foege justice with a short introduction. He is one of the scientists who led the global smallpox eradication efforts. He developed the concept of ring vaccination, which targeted vaccination to those individuals around a known case of smallpox. This concept really made eradication possible, as it eliminated the need for universal vaccination.  Following the success of the smallpox campaign, he has worked tirelessly to increase global vaccination rates.  He led the effort to provide low-cost treatments for river blindness, resulting in an immense reduction in that disease in Africa. To read some of his amazing stories of his time in the field, check out his autobiography and chronicle of smallpox’s demise, “House on Fire: The Fight to Eradicate Smallpox.” He’s currently a fellow at the Gates Foundation after serving with the Carter Foundation and spending time as the director of the CDC. I could go on and on about his positions and awards, but suffice it to say, he’s a man who knows his stuff.

Dr. Foege was generous enough to answer my questions on vaccination and on smallpox in particular, after I ran across a particularly egregious anti-vaccine article which suggested that use of the vaccine actually increased smallpox cases, and did nothing to eradicate the virus. He also discusses what vaccine supporters can do to promote vaccination.

TS: You have certainly encountered resistance to vaccination in your day, and much misinformation about and fear of vaccinations. How did you overcome this misinformation and fear when working to eradicate smallpox, and later in your career to increase rates of vaccination overall in the developing world?

WF: The first anti-vaccination movements appeared immediately after Edward Jenner introduced smallpox vaccine in 1796.  I start from the premise that parents want to do the right thing for their children, and when they don’t it is because of misinformation rather than evil intent.  While resistance was found in many countries, the fear of smallpox overcame many of the problems.  When people observed a decreased risk of the disease in those vaccinated it was a powerful message.  Now parents don’t always see the disease impact and therefore have a harder time weighing risks.

An overwhelming concern in recent years has been the concern about autism.  We know the studies are good showing no increased risk in children who have been vaccinated, but parents are often left with the first impression when that concern was voiced some years ago and have no way of following the literature.  They have been poorly served by Andrew Wakefield.  We now know that his article in the Lancet was more than poor science.  He fabricated and received money from a lawyer.  He lost his license and yet he continues to give talks to parents looking for an answer to autism.  So he not only lost his license but he lost his way.

The research, by the way, is pointing to something that happens in the second trimester of pregnancy as a cause of autism, not something that happens after birth.

TS: Unfortunately, there is rampant misinformation today even in developed countries. A common anti-vaccine message is that “vaccines didn’t reduce” measles, polio, etc. A recent post even claims that “Small pox had greatly declined before the vaccine, increased after the vaccine in westernized countries, and was effectively eradicated in third-world countries due to the surveillance and containment quarantine program. The small pox vaccine was actually flawed, deadly, and ineffective, killing many and inflicting even more with serious adverse reactions. Small pox eventually exterminated itself when people had access to clean water, good food, clean living conditions, and proper hygiene.” (Source) As one who led smallpox eradication efforts in Africa and India, can you address the claim that what led to the elimination of smallpox was hygiene and quarantine rather than vaccination?

WF: I would never speak against clean water, good food, clean living conditions and proper hygiene, but that is not what eradicated smallpox.  Smallpox was almost a universal disease in Europe at the time the vaccine was developed in 1796.  Even in the 20th century there were an estimated 300 million deaths from smallpox worldwide.  The surveillance/containment strategy was based on using vaccine and getting it to the people at immediate risk because they were in the vicinity of people with smallpox.  Quarantine of smallpox patients in their homes was part of the strategy in order to reduce the number of people they could expose.  Visitors were allowed into their homes but only after being vaccinated.  The science of vaccine preventing smallpox is so abundantly clear that it is difficult to imagine one looking at the evidence and reaching the conclusions cited above.  The same is true of measles and polio.  Measles killed large numbers of children in Africa and Asia before vaccine was introduced.  The number of measles deaths was over 3 million a year in the early 1960’s and has been reduced by over 90% with the introduction of vaccine.  The people who ascribe the reductions of cases in measles, polio and smallpox to hygiene provide proof to Mark Twain’s comment that people who don’t read have no advantage over people who can’t read.

TS: Another common anti-vaccine claim is that “herd immunity is a myth.”  Would smallpox eradication have succeeded if this was the case? 

WF: Herd immunity is a complex subject.  There is no percentage of protection that will automatically protect others.  For example, 90% smallpox vaccination in a state such as Bihar, India, would still allow more susceptible people per square mile than 10% smallpox vaccination in most of the United States.  Measles virus is so contagious that it seeks out susceptible children with tenacity.  Introduce a person with smallpox to a room of susceptible children and only about a third will have smallpox one incubation period later.  Do the same with a case of measles and 80% will have the disease one incubation period later.

However, the concept is correct that increasing the number of persons protected in the population will decrease the chances that an organism will be passed on.  Not only is the vaccinated person protected but they can’t pass on the disease to others.  At high levels of coverage the remaining population receives great protection.  With surveillance/containment in smallpox eradication, our objective was to vaccinate all contacts of a person with smallpox and in that sense attempt to get 100% of close contacts protected, a form of herd immunity in a small defined group.

TS: You were instrumental in increasing vaccination rates in developing countries in years past. What are your thoughts on those who sit in a position of privilege in the U.S., eschewing vaccines and declaring vaccine-preventable diseases “harmless” while many of them have never seen a case of polio or measles?

WF: It would be nice to be protected from both the diseases and the small risks of vaccine.  But it doesn’t work.  The social contract requires that we all participate or the diseases will come back.  Every pregnant woman in this country should be aware that their child will not have Congenital Rubella Syndrome.  Why?  Because other children have been vaccinated against rubella and while they get no direct benefit, they have stopped the transmission of the virus to a fetus.  It is a social contribution they can be proud of providing.  Parents who withhold vaccines from their children are doing their children a disservice. They put others at risk if their children get a vaccine-preventable disease and they have also put their children at increased risk if they want to travel abroad as students or later as adults.  It has turned out to be a heavy burden for parents who have lost their children in recent measles outbreaks.  Indigenous measles has disappeared in this country so every case can be traced to importations.  But we have continuous importations and at times we have had large outbreaks because of the many children are unvaccinated.

TS: In your campaigns against smallpox, for global vaccinations, and for the distribution of ivermectin to treat river blindness, it seems like you have frequently played the role of diplomat in addition to scientist/physician: bringing together people from opposing “turfs” to come to a mutually beneficial understanding and outcome. Do you have any advice for those of us working on raising vaccine awareness in the current U.S. climate, and how we can work to better play the role of diplomat as well?

WF: First, know what we all want.  Our children to be healthy.  Both sides can’t be right (although as Lincoln pointed out they could both be wrong!) so what information is needed to reach a decision?  Immunization rates have improved on Vashon Island because parents got together to try and understand why the difference of opinion.  My belief is that Andrew Wakefield so poisoned the well that the facts have to be explained before there can be common ground.

I often tell students that health leadership today is found not in a title but in a person that can make a coalition work effectively.  We need many coalitions to discuss this at local levels to discover what do the anti-vaccination people need in the way of information.  There has been a movement by some pediatricians to say they can’t care for children who are not immunized.  I understand the feeling but feel those are exactly the children who need care because they already have a strike against them because of parents not understanding the science.

You can make a great contribution by making the science clear, encouraging feedback and providing reassurance to the parents who need support.  Autism is such a difficult burden for parents that they want answers.  They need help in getting what is known about the science.  They are not helped by erroneous information.

 

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Is there such a thing as an “evolution-proof” drug?

Eleven years ago, two scientists made a bet. One scientist wagered that a new type of antimicrobial agent, called antimicrobial peptides, would not elicit resistance from bacterial populations which were treated with the drugs. Antimicrobial peptides are short proteins (typically 15-50 amino acids in length) that are often positively charged. They are also a part of our body’s own innate immune system, and present in other species from bacteria to plants. It is thought that these peptides work primarily by disrupting the integrity of the bacterial cell, often by poking holes in them. Sometimes they work with the host to ramp up the immune response and overwhelm the invading microbe. Because the peptides are frequently targeted at the bacterial cell wall structure, it was thought that resistance to these drugs would require a fundamental change in membrane structure, making it an exceedingly rare event. Therefore, these antimicrobial peptides might make an excellent weapon in the fight against multiply drug-resistant bacteria.

Additionally, the remarkable diversity of these peptides, combined with the presence of multiple types of peptides with different mechanisms of action present at the infection site, rendered unlikely the evolution of resistance to these molecules (or so some reasoning went). However, evolutionary biologists have pointed out that therapeutic use of these peptides would differ from natural exposure: concentration would be significantly higher, and a larger number of microbes would be exposed. Additionally, resistance to these peptides has been detailed in a few instances. For example, resistance to antimicrobial peptides has been shown to be essential for virulence in Staphylococcus aureus and Salmonella species, but we didn’t *witness* that resistance develop–therefore, it might simply be that those species have physiological properties that render them naturally resistant to many of these peptides, and were never susceptible in the first place.

The doubter of resistance, and the bet instigator, was Michael Zasloff of Georgetown University, who wrote in a 2002 review of antimicrobial peptides:

Studies both in the laboratory and in the clinic confirm that emergence of resistance against antimicrobial peptides is less probable than observed for conventional antibiotics, and provides the impetus to develop antimicrobial peptides, both natural and laboratory conceived, into therapeutically useful agents.

Certainly in the short term, resistance may be unlikely to evolve for reasons described above. However, if these peptides are used over an extended period of time, could the mutations necessary to confer resistance accumulate? This was the question asked in a new study by Dr. Zasloff along with colleagues Gabriel Perron and Graham Bell. Following publication of his 2002 paper where he called evolution of resistance to these peptides “improbable,” Bell challenged Zasloff to test this theory. Zasloff took him up on the offer, and they published their results in Proceedings of the Royal Society

The result?

Zasloff had egg on his face. Resistance not only evolved, but it evolved independently in almost every instance they tested (using E. coli and Pseudomonas species), taking only 600-700 generations–a relative blip in microbial time. Oops.

Well, everything old is new again. A very similar claim has been making the rounds recently, originating from the press release for a new paper claiming to have found bacteria’s “Achilles’ heel,” advancing the claim that “Because new drugs will not need to enter the bacteria itself, we hope that the bacteria will not be able to develop drug resistance in future.”  A grand claim, but history suggests otherwise. It was argued that bacteria could not evolve resistance to bacteriophage, as the ancient interaction between viruses and their bacterial hosts certainly must have already exploited and overcome any available defense. Now a plethora of resistance mechanisms are known.

Alexander Fleming, who won the 1945 Nobel Prize in Physiology or Medicine, tried to sound the warning that the usefulness of antibiotics would be short-lived as bacteria adapted, but his warnings were (and still are?) largely ignored. There is no “magic bullet;” there are only temporary solutions, and we should have learned by now not to underestimate our bacterial companions.

Part of this post previously published here.

I went to college in Connecticut. Deal with it.

Perhaps because it’s college graduation and reunion time, L.V. Anderson at Slate has written a column entitled “People Still Say They ‘Went to College in Boston,’ Meaning Harvard? Please Stop Doing This.” She claims that by giving such an evasive answer, one “buy[s] into the overblown mythos of Harvard and the presumption of Ivy League superiority.” Or worse, it “functions as an elitist dog whistle,” and that those who may “react inelegantly” upon hearing one went to Harvard/Yale/Princeton and others are “insecure people who perhaps have not yet learned that Ivy League schools confer degrees on plenty of idiots every year.”

Um, wow.

Here is why I usually say “Connecticut” or “New Haven” when I’m casually asked about college  by passing acquaintances: it’s just so much fucking easier in almost all situations. Perhaps because Anderson lives in Brooklyn, and as she notes, works with colleagues who “have degrees from universities that rank highly on U.S. News and World Report’s annual list,” she runs in circles with many of those who do understand that Ivy League schools confer degrees on plenty of idiots every year. Great for her. This is not universal. 

Let me suggest that she spend some time in flyover country. Where I come from in rural Ohio, very few people give a shit about Yale, or Harvard, or MIT. At my high school, way more people aspired to attend universities in the Big Ten than in the Ivy League. I’d not even heard the term “safety school” until my first week at Yale, or realized that so many in my Yale class considered institutions like Wellesley and Swarthmore to be such. (To be honest, I’d never heard of those colleges, and didn’t even know where Yale was precisely located until I applied. Somewhere out east was my best approximation). My alternate schools were both institutions in Ohio rather than the typical Ivy backups.

The Ivies just aren’t on the radar for many of us outside of the coasts, even those who could be prime Ivy material. Even Yale acknowledges this, as I wrote before–calling students in these states “low-hanging fruit” and claiming that we are tough to find. Over the years, even though I’ve enjoyed attending reunions and keeping up with my classmates, I’ve felt increasingly distant from my alma mater. Anyone surprised that there’s no “Yale Club of Cedar Rapids”?

So when I’m here  in “flyover country” and discussing college, I’ve found in my 20-year-experience as a student and alumna that to bring up Yale in many circles is to do just what Anderson is accusing those who say “Boston” or “New Haven” of doing: buying into the overblown mythos of Harvard and the presumption of Ivy League superiority. Really, what conceivable reason do I have to name-drop? To many here, Yale might as well be Mongolia–people travel there about as frequently, and understand it about as much. It’s practically mythical, and those who’ve gone there may as well be unicorns when it comes to the frequency of encountering an Ivy alum in many areas. The Ivies are places of Romneys and Bushes and Kennedys, where people shit gold bricks and dress like this:

How Ivy Leaguers probably look on campus, to an average Midwesterner.

As such, it creates an artificial distance between myself and those I’m conversing with. I “other” myself by saying that I graduated from Yale. This might not be important in Anderson’s line of work, coaxing other upper-middle-class foodies to “go ahead and eat the cookie dough,”  but when I’m out speaking with farmers and other community members in the rural Midwest,  or meeting with potential students coming to a state school, you can bet that my background from a farming area in Hancock County, Ohio is way more important and relevant than my four years spent at Yale. 

As Anderson should know, some of these conversations come down to knowing your audience. In Brooklyn, or in workplaces that are Ivy-heavy, I may agree with her. Maybe they’re really being faux-modest if they answer the inquiry about their college with “Boston” or “New Jersey.” In my professional biography I put Yale, and certainly will say that to academic colleagues when the topic comes up. But she’s flat-out wrong when she claims that “there is never any reason to answer the direct question ‘Where did you go to college?’ with an evasive half-truth.” In many of my conversations, I just don’t see the point in going into it, and in the past, it’s made both people involved feel awkward. If this makes me a “patronizing, self-serious jerk,” so be it. I’m the one who gets to claim my identity and own my biography, and I’m fine with being one who went to college in New Haven.

 

What is the harm in agricultural-use antibiotics?

After this post on antibiotic resistance, many of you may have seen an exchange on Twitter calling me out for being “knee-jerk” about my call to action to do something about the overuse of antibiotics. In that post, I focused on antibiotic use in agriculture, giving only brief mention to human clinical use. There are a number of reasons for this, and while I didn’t discuss them extensively on Twitter, I did want to provide an overview here in order to better explain my position and concern about antibiotic use in agriculture.

How are antibiotics used in animal production?

To start, some background on the issues. Antibiotics are used in agriculture in a number of different ways. Like humans, they’re used to treat disease when animals get sick. This type of use isn’t disputed for the most part–no one wants animals to die from treatable disease, nor do they want sick animals to enter the food chain. Antibiotics can also be used to prevent disease, such as when animals are stressed (as when they’re moved from farm to farm) and disease has a tendency to break out, or if a few animals in the herd are sick and owners want to prevent the rest of the herd from falling ill. This type of use is somewhat controversial, and many have argued that this type of use is only necessary because hygienic conditions on farms aren’t up to snuff–and that if better husbandry was practiced, this prophylactic use could also be significantly decreased or eliminated. Others argue that it’s necessary even with good husbandry.

The practice which is most widely disputed is the use of antibiotics for growth promotion. We’ve known for roughly 60 years that animals, when fed antibiotics at low doses (below the level required for disease treatment),  grow to their slaughter weight faster (and therefore, with less food input). This is the “low-hanging fruit;” the practice that even some in industry agree could end with pretty much no (or minimal) side effects to industry; and the practice that the European Union has already ended. It’s also the target of FDA guidance 213, which asks the phamaceutical industry to voluntarily phase out the use of growth promotant antibiotics in feed and water given to livestock. Twenty-five of 26 companies have agreed to this already, so again, there’s really not much dispute that this is a process that will be ending, after over 60 years of use and 45 years after a government report suggested that rising rates of antibiotic resistance in humans was tied to agricultural antibiotic use in the Swann report. (Maryn McKenna has a great timeline of other developments here).

Why am I (and many others) concerned about the use of antibiotics in agriculture?

First, and most compelling to me, is the fact that between 70-80% of all antibiotics used in the United States are used in agriculture. I’m linking to a PolitiFact report because they drill down into the caveats with that number in more detail than I want to go into for this post, but I will note that it’s tough to get good numbers because the industry won’t release them, and that the numbers we do have include drugs that are not used in human medicine–but that doesn’t mean they may not be important. More on that later.

Second, this is my area of expertise. I study antibiotic-resistant pathogens in the agricultural environment, so naturally this is my interest and where I know the literature the best. Third, antibiotic use in agriculture just isn’t as intensively studied when it comes to methods to reduce antibiotic-resistant microbes that may emerge from this setting. In the hospital and clinics, patients need a prescription to get antibiotics. The amount of antibiotics that are prescribed are tracked and those data are available. Hospitals often have stringent infection-control policies put in place to reduce the generation and spread of antibiotic-resistant “superbugs.” Hell, there’s enough research on these policies that my colleagues have a blog devoted just to that topic. In human medicine, no one is ignoring the generation and spread of resistant pathogens.

None of these control and monitoring policies are present on livestock farms as a matter of routine. Rather, as my colleague Lance Price has noted more than once, if he was going to try to create a superbug, farm use of antibiotics–subclinical dosing of thousands of animals at a time–would be an ideal way to create one.

What if we remove “growth promotant” antibiotics?

What remains an issue is what will happen after growth-promotant antibiotic use is stopped. There is already a “natural  experiment” going on in the EU, where such antibiotics were banned back in 2006. As I noted here, the results have been mixed when antibiotics have been removed from agricultural practices. Sometimes resistance persists, sometimes it goes down. A modeling paper examined the use of antibiotics for agricultural use, and suggested that their biggest impact happens before we even realize it via surveillance, and by the time we notice it, it may be too late to make much of a difference, which is depressing.  So even if antibiotics are banned for growth promotion purposes, there is a chance that we won’t see much of a dent in antibiotic resistance overall–or if we do, it may take years to see it decrease. This is an argument against removal of these sub-therapeutic uses–if we can’t 100% guarantee it will help, why change the status quo?–but at this point, even the current status quo is better than an ever-increasing arc of resistant bacteria.

Another concern that persists and muddies the waters is that no meaningful reduction in antibiotic use in animals will occur, but that rather antibiotics used for growth promotion will just be repackaged as “prophylactic” use, which will still be allowed under the new guidance. The industry says this won’t happen, but without meaningful and transparent surveillance, how can we know if it is or not?

Additionally, other sources of low-level antibiotics may still be present on farms and in feed, such as the use of distiller’s grains in animal feed which may still contain some antibiotics. And even if antibiotics that are important for human medicine are removed altogether, resistance still may linger or even climb if we allow for other classes of antimicrobials (such as ionophores, which are part of that group I mentioned above that are used in agriculture but not in human medicine) to still be used on the farms. Why could this be an issue? Right now, we really don’t know if any of these drugs co-select for resistance to important human medicines. For example, in some cases, antibiotic resistance genes are together as cassettes that can move around between bugs, such as on a plasmid or other mobile genetic element. That’s why using tetracycline on a pig farm can select for methicillin resistance–not because the drugs are the same (they’re totally different classes), but because the resistance genes come as a package deal. Is this happening with ionophores? Don’t know. It’s a messy area and makes any clear-cut cause-and-effect research very difficult to carry out.

To make matters even messier, because there’s so much transport of animals across state, national, and international lines, even if antibiotics are reduced in one place, new resistant bugs could be imported from elsewhere where no reduction in antibiotic use has taken place, mucking up the data and making it appear that antibiotic withdrawal has had no effect.

Furthermore, there is no directive for companies to actually track and report antibiotic usage differences after growth-promotant antibiotics are removed. We can’t even get good data on the industry as a whole, much less finer-level data describing how much goes to pigs, how much to cattle, how much on Iowa pig farms versus North Carolina, or for Smithfield versus Hormel farms, etc. It’s a surveillance nightmare. Even if we did have this data, surveillance of resistant pathogens is quite limited, especially on the farms themselves. Most of the data we have comes from NARMS–the national antimicrobial resistance monitoring system, which examines gram negative pathogens in people, meat samples, and live animals (taken at slaughterhouses). It’s a start, but what if we don’t see an effects in these organisms–but might in other commensal pathogens, or in the microbiome as a whole? Or in gram positives like my pet bug, Staphylococcus aureus? NARMS right now would miss those, and so might lead to false impressions of how reduction in antibiotics is really affecting resistance in the bacteria originating on farms.

Soooo….as you can see, this is a messy area. However, as I noted on Twitter, one should look at the totality of the research rather than searching for any particular “smoking gun” publication (a fallacy, I might add, that is employed by many types of science “skeptics”). There have been many, many papers that have shown, usually in ecological studies, that use of antibiotics on the farm is linked to generation of resistant bacteria, and that these bacteria (and associated resistance genes) can spread to humans via food, water, environmental runoff/contamination, air, and other mechanisms. Pew Health has an extensive bibliography of many of these studies here, and it’s barely even scratching the surface when it comes to publications in this field. In the end, though it’s messy, it breaks down to a simple truth: antibiotic use leads to antibiotic resistance, and reduced use is a goal to strive for–be it use in humans or in animals.

Unpacking a bit more

Yesterday’s post was frustrating. However, if anything good came out of it, it was some sharing of stories and mutual affirmations on the Twitters that yes, this happens to women all too frequently; yes, it’s obnoxious; and that hopefully some people viewing it thought about their own internalized biases, and how those may reflect in behavior toward women. I’m reminded at times like these how important social media networks have been to me, both in introducing me to new people (I’ve already found many new scientists to follow because of this) and in having an outlet to discuss and commiserate. So, some thoughts.

1) I hadn’t considered this in the beginning (because it’s my life and all), but from the write-up alone, I probably sound like “just a mom,” especially with my baby’s picture within the post. I mention at one point my colleague and link to a fellow scientist, but let’s be honest–people don’t always read these posts carefully or all the way through. So I was an easy target. Many studies have shown that people still describe scientists as old, white men–the Einstein stereotype. Just google “scientist” and check out the images: a bunch of nerdy, older white guys for the most part, and a handful of women (some scantily dressed, cause that’s exactly how we science, amirite ladies?). I got this type of attitude just the other day, as the driver who picked me up at the Philadelphia airport (a driver who routinely transports scientists!) was still surprised that I was a young woman and doing the work that I do. I’ve gotten that response previously at conferences as well. Women just aren’t accepted as scientists, even at times by other people working in the field.

2) I think many people (especially men) may underestimate or not understand just how frustrating this type of behavior/attitude is to women. Or worse, minimize it or not accept that this happens. I’ve been gaslighted previously by male (and female!) colleagues, telling me that surely my perception of a situation or event was incorrect. I accepted that they were right at the time (this was long before #ripplesofdoubt or other such support and story-sharing). No way would I stand for that now.

3) Blowback. The current situation involved a pseudonymous man on the internet, but all too often in these types of situations where women are dismissed and their expertise minimized people are involved who are more difficult to ignore. They may be senior colleagues in one’s own department or college. People in the field who could be reviewers of your papers or grant applications. Even collaborators who, in theory, should respect your training and value your expertise can try to appropriate your work because they see themselves as more important. (Thankfully this has not happened to me, but it has to several of my female colleagues, with mixed results in the end as far as credit, authorship, etc.)

In the end, much of this type of sexism is not conscious on the part of the one initiating it. I’m sure that people who told me I don’t look like a scientist meant it as a compliment and truly believed it was–because after all, scientists aren’t supposed to be young, or female, or particularly attractive. I’m sure that those that may have assumed I’m “just a mom” and didn’t bother to pay any attention to my professional accomplishments before explaining my field to me don’t think they’re particularly biased against women. Outright, blatant bias against women is much tougher to get away with today (in theory, anyhow), but the more subtle, “everyday” sexist behaviors are still very much amongst us. If it hurts people’s feelings that they get called out on these, well, tough. The only way things change is by shedding light on them. I have a bright spotlight and I’m not afraid to use it.