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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Ebola reemerges from the forest

Ebola has surfaced again. After a hiatus of over a year without any new identified outbreaks, the virus has reemerged in western Africa, in the first-ever multi-country outbreak of the Zaire strain of Ebola. As of this writing, there have been 122 suspected cases of the disease in Guinea (24 laboratory-confirmed per the WHO) and 80 deaths (66% mortality rate). Most of these cases have been in Guekedou and Macenta in rural Guinea, about 35 miles apart, but what’s really concerning is that at least 11 cases have also been identified in Guinea’s capital of 2 million people, Conakry. Conakry is over 400 miles away by the main road and contains the only major hospital in the country (and even that hospital is certainly less than ideal). A direct route from Guekedou to Conakry as the crow flies takes one right through Sierra Leone. It’s probably not too surprising then that this country has also reported 8 possible cases of Ebola, and another neighbor, Liberia, suspects 6 cases of the disease. Guinea’s northeast neighbor, Mali, has also just reported 3 potential cases, but these have not yet been confirmed. Senegal has closed its border to prevent importation of the virus.

Nurses tend to a patient during the 1976 Ebola outbreak in Zaire (now DRC). From Wikipedia.

All evidence points to Ebola having a reservoir in fruit bats. The virus can spread to other species when they come into contact with bats, and has caused massive great ape die-offs in addition to human outbreaks. Humans can become infected in a few suspected ways: direct contact with bats (such as visiting bat-infested caves or working in factories where large numbers of bats roost); butchering or consuming animals (particularly non-human primates, who can also acquire the infection via bats); consuming the bats themselves, as has been suggested may play a role in the current outbreak. Finally, once humans have been infected, human-to-human transmission can also spread the infection via contact with viral-laden body fluids (blood, saliva, feces). 

Though Ebola has a very high mortality rate, the one good thing is that it’s really not easily transmitted between people. Though there have been some experimental evidence that it could be airborne, in epidemiologic studies during outbreaks, no airborne transmission has been confirmed. Instead, most people who contract it from another person have very close contact with that patient: they’re hospital workers, or caretakers of infected family members, or are preparing a body for burial and are exposed to fluids during cleansing rituals. It may also be transmitted via semen and has been found in breast milk.  Casual contact doesn’t seem to readily spread the virus. That fact also makes the ongoing outbreak that much more tragic: new infections and deaths can be minimized if money, supplies, and education are provided.

Many of the more recent outbreaks in the Democratic Republic of Congo and Uganda have had much smaller numbers of cases than earlier outbreaks in these countries (Wikipedia has a nice summary here). Early detection and the use of basic personal protective equipment (gloves, etc.) and environmental disinfection stem transmission of the virus fairly effectively. Outbreaks in the 1970s and 1990s were amplified in hospital settings due to close contact between patients, shared/reused needles, and spread to healthcare workers who were inadequately trained and protected. Unfortunately, this is happening now as well, with 14 healthcare workers infected and 8 killed to date.

Though this is the first significant outbreak in West Africa, it’s not the first time Ebola has been found. One of the types of Ebola, Tai Forest ebola virus, originated in Ivory Coast after a primate researcher became infected while carrying out a necropsy on a chimpanzee. However, this is the only known case of that type of Ebola, and the current outbreak is caused not by the Tai Forest strain, but by the Zaire strain–which is the most virulent of the bunch. This strain has been most commonly found in Central Africa (Democratic Republic of Congo, Republic of Congo, Gabon), and based on analyses of these outbreaks, it was suggested that the Zaire strain had originated near Yambuku, DRC in the early 1970s, and had spread/diverged since then. However, it looks like this outbreak would be too distal for that model. Sequence data could clear that up but is not yet available.

 While every outbreak of Ebola represents a golden opportunity to study this rare virus in nature, it’s an opportunity that no one wants or relishes. This one went almost 6 weeks before a definitive diagnosis was made, and now has the distinction of becoming the largest Ebola outbreak in at least 7 years–possibly more, depending on how quickly they can but the brakes on new cases. Unfortunately because these outbreaks start in rural, resource-poor areas, one thing we can be confident about is that we’ve not seen the last of this virus.

Student guest post: Cancer isn’t contagious…or is it??

Student guest post by McKenzie Steger

Off the southeastern coast of Australia lies a small island that in the 1700 and 1800’s was inhabited by the very worst of Europe’s criminals and is now the only natural home in the world to a species named after the devil himself. Decades later beginning in 1996 Tasmanian devils were going about their nocturnal lifestyle in normal devilish fashion feasting on small mammals and birds, finding mates and reproducing, occasionally fighting with one another and so on. (1) Just as criminals divvied up their booty hundreds of years before, the devils were sharing something of their own—only something of much less value. It turns out they were transmitting to one another a rare and contagious form of cancer known as Devil Facial Tumor Disease or DFTD. Once infected, facial tumors developed and the devil faced 100% mortality most often due to inability to eat or airway obstruction. Over the last 17 years the result of this highly contagious and fatal cancer has been the elimination of over half of the devil population throughout Tasmania. (2)

mckenzie picture


DFTD is not alone when it comes to transmissible forms of cancer. For over six thousand years dogs, jackals, wolves, and coyotes across the globe have experienced their own “contagious” cancer in the form of canine transmissible venereal tumor—C TVT and also called Sticker’s sarcoma. (2) CTVT is generally considered the first known cell line to be malignant having been described in the mid 1800’s. These unique growths like DFTD can spread from one individual to the next, but in the case of CTVT this most commonly occurs during coitus, licking, and biting infected areas. CTVT lesions usually establish in the genitals or in close proximity as a result. CTVT is unique in that only an estimated 7% of cases metastasize unlike in DFTD cases where 65% of them result in metastasis. CTVT rarely results in severe clinical illness but instead nearly always regresses on its own. (3)

So what is it that makes DFTD and CTVT so “contagious”? Essentially it boils down to host immunity. In the case of DFTD, devils pass on tumor cells when they are in close physical contact with others during mating or fighting. The Tasmanian devil population simply lacks the genetic diversity to be able to immunologically recognize and ward off the tumor and thus, these highly virulent and metastatic cells set up camp in the new host tissue and invade in no time. Interestingly, studies have shown that the DFTD cells are unique, containing only 13 pairs of chromosomes instead of 14 like most cells. Technology has also shown the very same cell line that began the DFTD devastation—thought to be of Schwann cell origin—is the very same one being transmitted throughout devil populations today. (2)

In contrast, CTVT, a histiocytic tumor (4), affects mammals rather than marsupials which have much greater diversity within the population and a more advanced capability to detect foreign and potentially invasive cells. This is due to the MHC-1 molecules or multiple histocompatibility complexes that help the body’s immune system to recognize foreign substances. CTVT is so effective in transmission because it down regulates these MHC-1 molecules effectively “hiding” the invasive cells from the body’s immune system. At some point however, this mechanism is overcome and the CTVT is recognized and killed by the body in animals that are immunologically sound. (2)

What about transmissible cancer in humans? The good news is that no comparable strain of such a killer contagious cancer has been recognized in humans compared to what devils in the “land down under” are experiencing. The bad news is that there are technically forms of cancer affecting man that result from contagious agents. Estimations attribute 15% of tumors world-wide to contagious pathogens including mainly viruses but also bacteria and parasites as well. Most documentation of cancer transmission cases in humans are reported in individual case reports, however, highlighting the rarity and unlikelihood of this occurrence. (2) Nonetheless, it still occurs. Hepatitis B and C viruses, herpes viruses, human immunodeficiency virus (HIV), and papilloma viruses are just a few examples of viruses that can develop into cancer in patients or predispose them to tumor formation. Bacterial etiologies include members of the Chlamydia, Helicobacter, Borellia, and Campylobacter families. There are also a few select parasites classified as Group I and Group II carcinogens including members of the Schistosoma, Opisthorchis, and Clonorchis families. So really, “contagious cancer” in humans is due to contagious or infectious etiologies and not necessarily direct contact transmission. Although there are documented and potential exceptions including cancer spread through tissue grafts, organ transplants, papillomavirus transmission during sexual intercourse and other isolated events. (1)

At the end of the day, the presence, history, transmission, and pathogenesis of transmissible cancers in Tasmanian devils, dogs, and the few cases documented in humans provides insight regarding the immune mechanisms that do and those that do not allow cancer to develop. The key difference here is mammals verses marsupials and the reality that mammals have a more advanced immune system allowing them to better overcome cancer and other foreign invasions. A better understanding of both CTVT and DFTD has and will likely continue to allow researchers better insight into mechanisms of immune system invasion of various types of cancer. (1)



(2)   Welsh JS. Contagious Cancer. Oncologist. 2011 January; 16(1): 1–4. Published online 2011 January 6.

(3)   Belov K. Contagious cancer: Lessons from the devil and the dog. BioEssays: Volume 34 (4), pages 285–292, April 2012.



Student guest post: Chirp, Chirp, Sneeze!

Student guest post by Julia Wiederholt

I don’t think there is a single person that can claim to have never had the joyous experience (sarcasm intended) of suffering from the influenza.  We all recognize the common symptoms that accompany this infectious little virus taking up residence in our bodies: the chills accompanying a fever, the total body ache, the nausea, and overall feeling of malaise.  Typically this virus comes and goes within a week without serious side effects.  When novel strains of the influenza pop up however, there can be more serious complications as your body lacks a sufficient immune recognition of the virus.  An example of a new strain of influenza that presents a great risk for the human population is the H7N9 influenza, also known as Avian Influenza A.

H7N9 was first recognized earlier this year in China and thankfully has yet to be reported in the US. The majority of the people infected have had direct contact with poultry or an environment that has contained infected poultry.  Some of the people diagnosed however, report having had no direct contact with poultry opening up the possibility of human to human transfer of the disease.  The infected poultry have shown no obvious symptoms of being infected, but when humans become infected it can cause severe respiratory problems and fever.  As of May this year, LiveScience reported that there have been a total of 131 reported human cases of H7N9 with 32 reported deaths.

While all of that may not sound too impressive, here’s what makes H7N9 such a concern as an emerging infectious disease.  The first major concern regarding this specific influenza is the fact that it is the first time the H7N9 virus has been reported in humans.  The H in the name H7N9 stands for hemaglutinin, which is the attachment protein found on influenza viruses.  This protein not only enables the virus to attach to the cells it is trying to infect, it also is provides the host’s immune system a way of recognizing the virus as a foreign threat.  The fact that this is the first time this specific virus has been found to infect humans means that we lack any prior immunity to it and are therefore, more susceptible.

Another factor that raises the alarm for this influenza is the fact that the infected poultry that have been found so far have shown no outward signs of being sick.  This is a huge concern because it makes controlling the spread of the disease much more difficult.  When poultry and livestock exhibit obvious signs of being infected, it allows the infected to be separated out from the healthy and either isolated or culled to prevent further spread of the disease.  In some cases, the disease may have already spread amongst all of the animals in the vicinity requiring the entire herd or flock to be culled.  When it is difficult to distinguish between healthy and infected animals however, any evidence that the disease has been found within the animals will more than likely lead to the entire herd or flock being culled.  This not only results in greater economic losses for the poultry farmers but also a higher number of people being exposed to infected animals before realizing the danger that is present.

Possibly the greatest concern with H7N9 is the fact that it could be jumping from person to person.  The original thought was that the only way it had been spreading was from direct contact with sick poultry, which would limit the at risk human population to people coming into contact with the infected birds.  Some of the people who have been diagnosed with H7N9 however, are claiming to have had no contact with poultry suggesting that the disease may be capable of human to human transmission.  This would greatly increase the reproductive rate of the disease because people would no longer need to come into contact with poultry to be exposed to it.  The reproductive rate, commonly referred to in scientific communities as the Ro, is a way of measuring the predicted number of new infections that one infectious case is likely to create.  Another factor that suggests the possibility of human to human transfer is the fact that there have been three reported family clusters of H7N9.  While this does not necessarily mean that the virus is capable of sustained human to human transfer, it is highly suggestive that human to human transmission has occurred in these particular instances and that with the right (or depending on how you look at it, wrong) mutation, it could transfer between humans with ease.

While all of these things explain why H7N9 is being watched so closely and why it is important to have a healthy respect for just how dangerous it could be, there’s no reason for people to start panicking quite yet.  As mentioned earlier, this strain of influenza has only been reported in people that either live in or have recently traveled to China.  Unless you are planning to travel out of the country in the near future, there is no reason to become overly concerned about H7N9 at the moment.  Also, the majority of the cases have either had direct contact with infected poultry or close contact with someone who has had contact with poultry.  This means that unless the virus becomes proficient at human to human transmission, the majority of the population is at a low risk.

For the germaphobes out there that are still freaking out over the possibility of catching H7N9, there are several ways to reduce the risk of catching it, or any other influenza for that matter.  Good hygiene practices such as frequently washing your hands and avoiding touching your face will help minimize the risk of introducing the influenza virus into your body.  Eating a well-balanced diet and getting plenty of rest will help keep your immune system in tip top shape in the event of a virus managing to get past your innate defense mechanisms.  In regards to reducing the risk of catching a zoonotic strain of influenza, practices such as thoroughly washing your hands after handling any animals and avoiding contact with sick poultry or livestock will reduce the risk of transmission.  So rest at ease, the world isn’t coming to an end due to H7N9…at least not yet.


Cong Dai, Min Jiang, “Understanding H7N9 Avian Flu,” BMJ, Available online 3 May 2013.  <>.

“Frequently Asked Questions on Human Infection Caused by the Avian Influenza A (H7N9) Virus.”

World Health Organization. WHO, 30 Apr. 2013. Web. 12 June 2013. <


Guang-Wu Chen, Michael M.C. Lai, Suh-Chin Wu, Shih-Cheng Chang, Li-Min Huang, Shin-Ru Shih, “Is avian influenza A (H7N9) virus staggering its way to humans?”, Journal of the Formosan Medical Association, Available online 3 June 2013, ISSN 0929-6646, 10.1016/j.jfma.2013.04.015. <>.

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Student guest post: A Push for Pasteurization

Student guest post by Molly Stafne

Nothing could be worse than watching your seven-year-old lying in a hospital bed fighting for his life after being diagnosed with hemolytic uremic syndrome. Unfortunately, Mary McGonigle-Martin experienced it first hand as her son, Chris, fought for his life after being poisoned by E. coli 0157:H7 found in contaminated raw milk. Like many mothers, Mary was coerced into believing the inaccurate “facts” given to her by the farm she purchased raw milk from. Too often across the US, parents are given incorrect information about the safety of the milk they drink and unfortunately, it is often children that pay the price.

Few people today know of a time when they didn’t have the choice to drink anything but raw milk. Now there is an overwhelming argument that pasteurization is decreasing the nutritional value and safety of the milk. During the 1800s, Louis Pasteur developed the germ theory which claimed that germs outside the body, like those found in raw milk, have the ability to cause infection. As a result, he developed the process of pasteurization which is used in many foods we consume today, including milk, to kill bacteria. In the past couple decades, many consumers have decided that they would rather consume more natural and organic foods rather than those that were produced by more modern methods. It is frequently believed that these natural foods, such as raw milk, are healthier which is not the case.

Pasteurizing milk has had many benefits through history. One of its major contributions is the massive reduction in human tuberculosis cases as the bacteria that causes bovine tuberculosis can also infect humans. Bovine tuberculosis can be spread to humans through contact with an infected animal but most commonly through ingestion of raw milk. Although the prevalence of tuberculosis in humans in the US has significantly reduced since pasteurization began, there are still a number of other zoonotic pathogens that can be transmissible from milk to humans including salmonella, campylobacter, listeria, and E. coli 0157:H7, all of which can have dangerous or unpleasant consequences or even potentially be fatal. E. coli is possibly the most dangerous since it only needs less than 100 organisms to cause infection. It can lead to a dangerous condition called hemolytic uremic syndrome (HUS) which may cause kidney failure. According to the CDC, there have been 148 dairy product-associated outbreaks from 1998 – 2011 that were a result of consumption of raw milk or cheese which resulted in 2,384 illnesses, 284 hospitalizations, and 2 deaths. Today, milk is heated to 161°F for 15 seconds to destroy the bacteria. This is called high temp, short time pasteurization. Another form of pasteurization is low temp, long time, 145°F for 30 minutes.

Proponents of raw milk often argue it has a greater nutritional value than pasteurized milk. There have been numerous studies that have de-bunked this myth according to the CDC. Many factors are involved when determining the nutritional value of a product. One thing that is analyzed is how readily a body breaks down and utilizes a nutrient. If a mineral or vitamin is passed through the body quickly, any loss would be irrelevant. A second analysis would be the percent contribution of the nutrient to the recommended daily intake. If people don’t rely on a certain product as the main source of an essential nutrient, the loss of the nutrient is almost negligible. It is true that some nutrients or enzymes are slightly reduced during pasteurization. For example, lysine is the most relevant essential amino acid found in milk. After heating the milk, only 1-4% loss of the amino acid was observed1,5,7. But like what was previously alluded to, reduction of nutrients like vitamin C is not considered a significant concern as milk is not a major source of vitamin C. It would take 20 liters of milk to consume the daily requirement of vitamin C, regardless if it was raw or pasteurized milk3. The availability of nutritionally relevant vitamins such as B2 or B12 were found to be affected minimally or not at all by most common heat treatments2,5. Finally, while milk is a significant source of calcium and phosphorus, neither were affected by heating the milk3.

Another raw milk marketing tool some farmers use is to claim that their cattle are grass fed. When cattle were first domesticated, they were raised on a grass diet. As the understanding of animal nutrition grew, farmers discovered that cattle would gain weight faster if they fed them grain which is economically beneficial. Proponents of grass fed cattle argue that grain is not their natural food and the growth at a faster than normal rate is unhealthy. A grass-fed animal does not mean the animal is healthier. Nutritionally speaking, it was hypothesized that grass fed cattle have a lower milk fat content. The amount of grain does play some role in the fat development but energy and dietary protein intake and the current state of pasture the cattle are being grazed on must also be accounted for. In addition, milk fat content is also determined by the genetics of the individual animal, whether or not it currently has or had infections in her udder, and her stage of lactation3.

In addition, grass-fed cattle don’t necessarily carry a lower bacterial load. Even at the most sanitary facilities, milk is often contaminated by fecal material carrying pathogens during the milking process. According to Dr. Jim Kazmierczak, a Public Health Veterinarian with the Wisconsin Department of Health Services, there have been numerous studies that proved grass-fed cattle shed E. coli 0157:H7 in the feces longer than grain-fed cattle4 and that “cattle fed a forage diet were 0157:H7 culture-positive longer and with higher numbers of bacteria in their feces than cattle fed a grain diet.6” This means that E. coli 0157:H7 remained alive in their feces longer than grain-fed cattle.  In addition to being found in fecal material, E. coli 0157:H7 can be found where cattle are grazing, can live on different environmental reservoirs for many months, such as gates, walkways, or water troughs, and is found more frequently during the summer.

We are blessed in the US to have a relatively safe food supply. Sure there will be occasional food-borne illness outbreaks but we are fortunate to have the technology, sanitary methods, and capabilities to keep the food we consume free from diseases to the best of our abilities. The invention of pasteurization reduced the number of illnesses and deaths caused by contaminated dairy products while maintaining the integrity and nutritional value of the milk. But there is a misconception of pasteurized milk across the country that has led to people making deadly decisions. Mary McGonigle-Martin would have never given her child raw milk had she known that it had the potential to harm or kill him. The risks are high when consuming raw milk and people need to be properly informed before their put their families and themselves in unnecessary danger.

1. Andersson, I., and Öste, R. (1995). Nutritional quality of heat processed liquid milk. In P. F. Fox (Ed.), Heat-induced changes in milk (2nd ed.) (pp. 279e307). Brussels: International Dairy Federation.

2. Burton, H. (1984). Reviews of the progress of dairy science: the bacteriological, chemical, biochemical and physical changes that occur in milk at temperatures of 100e150 _C. Journal of Dairy Research, 51, 341e363.

3. Claeys, W. L., et. Al (2013). Raw or heated cow milk consumption: Review of risks and benefits.

4. Hovde, C. J., et al. (1999). Effect of cattle diet on Escherichia coli O157:H7 acid resistance. Appl Environ Microbiol 65:3233–32

5. Schaafsma, G. (1989). Effects of heat treatment on the nutritional value of milk. Bulletin of the International Dairy Federation, 238, 68e70.

6. Van Baale, M. J., at al. (2004). Effect of Forage or Grain Diets with or without Monensin on Ruminal Persistence and Fecal Escherichia coli O157:H7 in Cattle. Appl Envir Microbiol 70:5336-5342.

7. Walstra, P., and Jeness, R. (1984). Dairy chemistry and physics (p. 467). New York: John Wiley & Sons.

Plague in Victorian San Francisco–lessons for public health communication

I have a post up today at the Scientific American Guest blog, discussing how an earthquake and denial led to prairie dog plague. It details an outbreak of plague in Victorian San Francisco–the first time plague hit the United States–and the many downstream consequences of that outbreak (which began in 1900 and wasn’t really contained until 1908). While the story is over at SciAm, here I wanted to talk more about why the outbreak became such a public health disaster.

The outbreak was first recognized by Dr. Joseph Kinyoun, a bacteriologist who had been, until his transfer to San Francisco, heading up the United States Hygienic Lab, the precursor to the National Institutes of Health. Charged with inspecting incoming ships, Kinyoun had the power to quarantine ships and their crew in harbor, in an effort to keep plague out (which was already circulating in port cities of Honolulu, Sydney, and Tokyo, amongst others). When Kinyoun first suspected a case of plague, San Francisco merchants quickly banded together to deny any such pestilence in their city. What followed was a mess of ineffective quarantines, fights over scientific data, accusations of “spiking” corpses with plague samples Kinyoun had brought with him from Washington, D.C., and an eventual call for Kinyoun’s execution.

History shows that Kinyoun was right–San Francisco had plague cases, and the plague would continue to smolder for almost a decade. As I note in the post, it still lingers today in squirrels and rodents from the Pacific Ocean inland to the Great Plains. So what went wrong, if Kinyoun clearly had the facts on his side?

Like many scientific issues today, it wasn’t the facts that ended Kinyoun’s career in San Francisco, but his messaging. Admittedly, he was acting without all the knowledge of plague transmission that we have today–it wasn’t confirmed in 1900 that rat fleas were the main vector of the disease from rodents to person, and so Kinyoun couldn’t have been sure his attempts to quarantine Chinatown would be ineffective. Furthermore, in some cases, he was merely obeying orders from his superiors. His boss, Surgeon General Walter Wyman, had recently published a monograph on plague, endorsing the idea that plague selectively targeted Asians due to their particular diets and their poverty.

Still, the way Kinyoun went about attacking those most affected in the initial outbreak–the Chinese immigrants–only served to terrify them and drive plague cases underground. Indeed, when public health officers went door-to-door searching for plague cases, one anecdote notes that a game of dominoes was set up in a home, and all the men stayed perfectly still with dominoes in their hands while officers searched the home for anyone with plague symptoms. Little did they know that a plague corpse was sitting at the card table, “Weekend at Bernie’s” style (1). Other Chinese fled Chinatown, bunking with friends and relatives elsewhere when possible. Threats were made to burn Chinatown (as had recently happened in Honolulu); Kinyoun tried to bar travel by any “Asiatics” on trains or boats leaving the city, clearly a race-based order. Furthermore, even when cases of plague were identified in Chinatown, the very practice of carrying out autopsies was offensive to the Chinese, giving them even more reason to hide their sick and dead rather than cooperate with Kinyoun and other public health authorities.

Kinyoun left the city in 1901, and eventually Rupert Blue was brought in to control the outbreak. Taking lessons from those who’d been there prior (and were unsuccessful), Blue took a much more diplomatic tack. He secured the assistance of a Chinese translator, Wong Chung, and worked within the Chinese community to gain their support. He often downplayed the outbreak–never suggesting it wasn’t happening or wasn’t important, but trying to differentiate hype from supported fact. He worked to clean up Chinatown, both in its housing and in rat infestations, rather than to quarantine infected areas. He noted that plague could occur in many different races, and avoided scapegoating one particular ethnic class. He also reached out to businessmen to educate them, and show how important cleaning up the city was for their bottom lines. He worked with the facts as Kinyoun did, but he recognized the importance of grassroots support in his campaign, and targeted reasons why various factions should support his various anti-plague measures.

In the end, while Kinyoun was practically run out of town on a rail, Blue was given banquets and numerous accolades. He served as the Surgeon General from 1912-1920, and his methods for cleaning up the city led to a decrease not only in plague, but in many infectious diseases. While Kinyoun’s science was sound, Blue managed to break down barriers and work with those who could help him spread his message, and take ownership of the work that needed to be done. He framed* the threat in terms that meant something to the populations he was working with: businessmen and threat to their incomes; immigrants’ threat to health, with promises to respect their culture and help them make their homes cleaner places to live; city and state government, noting the threat to the very reputation of California and San Francisco in the US and around the world. His tactics served him well in 1902-08, and should serve as a reminder to science communicators today as well.

(*I know that term is somewhat tainted in some circles, but bear with me…)

Further reading and references

Chase, “The Barbary Plague”.

Echenberg, “Plague Ports: The Global Urban Impact of Bubonic Plague, 1894-1901.”

Ebola: Back in the DRC

August, 1976. A new infection was causing panic in Zaire. Hospitals became death zones, as both patients and medical staff succumbed to the disease. Reports of nightmarish symptoms trickled in to scientists in Europe and the US, who sent investigators to determine the cause and stem the epidemic. Concurrently, they would find out, the same thing was happening hundreds of miles to the north in Sudan. In all, 284 would be infected in that country, and another 358 in Zaire–over 600 cases (and almost 500 deaths) due to a mysterious new disease in just a few months’ time.

The new agent was Ebola, but remarkably, the outbreaks were unrelated, at least as far as any direct epidemiological links go. No one had brought the virus from Sudan to Zaire, or vice-versa. Molecular analysis showed that the viruses causing the outbreaks were two distinct subtypes, subsequently named for their countries of origin, Ebola Zaire and Ebola Sudan.

While Uganda is currently battling another outbreak of Ebola Sudan, rumors in the past week have suggested that this virus may have spread to former Zaire (now the Democratic Republic of Congo), where Ebola has reappeared 4 additional times since the first discovery there in 1976. It’s now been confirmed that Ebola is again present in the DRC, with an (unconfirmed) 6 deaths. However, it’s not related to the Uganda outbreak. Reminiscent of 1976, the strain that’s circulating currently in the DRC is the Bundibugyo subtype, which was first identified in Uganda in a 2007-8 outbreak in that country, rather than the Sudan type causing the current Ugandan epidemic. Interestingly, every previous outbreak of Ebola in the DRC has been caused by the Zaire type of Ebola, so the appearance of Bundibugyo is a first–though not altogether surprising given that the outbreak province borders Uganda.

Is this just coincidence that Ebola has twice now broken out in two different places at the same time, but with different viral subtypes? Hard to say. Though we can now say it’s fairly likely that bats are a reservoir host for Ebola and other filoviruses, we can’t say for sure that bats are the *only* reservoir. Indeed, we know that some outbreaks have occurred because the index case was in contact with an infected ape or their meat–were these animals originally infected by a bat, or by another source? How does the ecology of an area affect the chances of an outbreak occurring? Were there reasons that humans might be increasingly exposed to the virus in these different areas–Zaire and Sudan in 1976, DRC and Uganda in 2012–at the same time? Weather conditions? Trade/industry? Host migration or dispersal? We know with another bat-borne virus, Nipah, that changes in farming practices led to increased proximity of fruit bats and farmed pigs–allowing pigs to come into contact with virus-laden bat guano, become infected with Nipah, and subsequently transmit the virus to farmers. Things that may seem completely inconsequential–like the placement of fruit trees–can actually be risk factors for viral emergence. Is there a common factor here, or just bad luck? Only additional hard-won knowledge of filovirus ecology will be able to tell.

Ebola resurfaces in Uganda–history and analyses of Ugandan Ebola

Uganda just can’t catch a break. They’ve recently been hit with nodding disease, a mysterious syndrome where children repeatedly nod their heads and undergo serious seizures, typically leading to death. Now they’re in the grips of another Ebola outbreak. This will be the fourth time the country has suffered through Ebola since 2000, when the virus was first found in the country:

The first occurred in August of 2000; the first case died in Gulu on the 17th of September. Despite an investigation, doctors were unable to determine where or how she had contracted the disease. Her death was followed by the deaths of her husband, two children, and several other family members. This was reported to the Ministry of Health in October of that year, near the peak of the epidemic. An investigation and intervention to control the disease followed, and the epidemic was declared to be over in January of 2001. A total of 425 patients from 3 villages (Gulu, Masindi, and Mbarara) across Uganda were identified based on symptoms and/or laboratory data. 224 of them died, with a resulting mortality rate of 53%; an eerie echo of the 1976 Ebola outbreak in Sudan. Indeed, sequence analysis showed the infecting strain to be the Sudan subtype of Ebola; the first time this type had surfaced since the 1979 outbreak in Sudan. It is hypothesized that Sudanese rebels, who carried out regular attacks around Gulu, may have accidentally introduced the virus in some manner, though this has not been confirmed.

Ebola returned to Uganda in August of 2007, causing 149 illnesses and 37 deaths until the outbreak was declared over in February of 2008. This mortality (36%) was significantly lower than most Ebola outbreaks. Interestingly, when scientists tested this virus, it also reacted strangely with their assays. Therefore, they determined the entire molecular sequence of the virus, and found that it was a whole new strain of Ebola, which they named Ebola Bundibugyo.

The third outbreak occurred just last year, as a single case in a 12-year-old girl, who died of the infection. I’ve not been able to find any follow-up identifying the 2011 strain, but Uganda has been hit previously by both the Sudan and the novel Bundibugyo strains of Ebola, and the current outbreak has been identified once again as Ebola Sudan.

In the current outbreak, which began in the Kibaale district in western-central Uganda, at least 20 have been affected and 14 have died. As of today, an additional six cases are suspected but not yet confirmed, and it appears to be affecting more than one village in the district. One death has also occurred at Mulago hospital in the capital of Kampala. The individual who died was reported to be:

… a health worker who “had attended to the dead at Kagadi hospital” in Kibale, Health Minister Christine Ondoa told reporters.

She is believed to have travelled independently to Kampala — possibly on public transport — after her three-month old baby died, Ondoa added.

Reports also note that other health care workers are in quarantine as a precaution. In Africa, Ebola has really been able to spread in previous outbreaks for two reasons: breakdowns in barrier nursing within hospitals (not wearing gloves/gowns; reusing needles; lack of handwashing/sanitation, etc.) and ritual funeral practices within villages, which put many family members in contact with the virus as they assist with cleansing the victim. Indeed, it appears that 9 of the deaths in this outbreak have come from a single family, so it’s quite possible many were sickened using this type of practice. However, now that Ebola has been confirmed and people are aware of this, stricter controls over these practices can be implemented, and health care workers are being urged to report any cases that may be Ebola to authorities.

Kampala is a city of a bit over a million people on Lake Victoria, southeast of the Kibaale district. The 2011 case originated from Luwero district, due east of the Kibaale district and north of Kampala. The 2000 outbreak occurred in the Gulu district in the north of the country, and the 2007 outbreak in the Bundibugyo district, in the west and neighboring Kibaale. It would seem that Ebola reservoirs (likely fruit bats) could very well be spread across Uganda’s central region, occasionally spilling over into the human populations and igniting these outbreaks. One story notes that “The site where most of the cases occurred are close to Kibale forest where there are a lot of monkeys and birdlife,” and while bats are not explicitly mentioned, they presumably would also be present. Non-human primates have also been implicated in previous outbreaks of Ebola as an amplifying species.

The reporting of the current outbreak was delayed, as patients didn’t have any noticeable bleeding–rather, diarrhea and vomiting were the main reported symptoms. However, while many reports I’ve seen are characterizing hemorrhagic symptoms as “typical,” these aren’t seen in all patients, and indeed the diarrhea, vomiting, and even hiccups are common symptoms of Ebola infection. As such, Uganda has been playing a bit of catch-up, but has certainly learned since the first (and worst) outbreak in 2000. Hopefully this one will end fairly quickly.

Using zombies to teach science

With my colleague Greg Tinkler, I spent an afternoon last week at a local public library talking to kids about zombies:

The Zombie Apocalypse is coming. Will you be ready? University of Iowa epidemiologist Dr. Tara Smith will talk about how a zombie virus might spread and how you can prepare. Get a list of emergency supplies to go home and build your own zombie kit, just in case. Find out what to do when the zombies come from neuroscientist Dr. Greg Tinkler. As a last resort, if you can’t beat them, join them. Disguise yourself as a zombie and chow down on brrraaaaiiins, then go home and freak out your parents.

Why zombies? Obviously they’re a hot topic right now, particularly with the ascendance of The Walking Dead. They’re all over ComicCon. There are many different versions so the “rules” regarding zombies are flexible, and they can be used to teach all different kinds of scientific concepts–and more importantly, to teach kids how to *think* about translating some of this knowledge into practice (avoiding a zombie pandemic, surviving one, etc.) We ended up with about 30 people there: about 25 kids (using the term loosely, they ranged in age from maybe age 10 to 18 or so) and a smattering of adults. I covered the basics of disease transmission, then discussed how it applied to a potential “zombie germ,” while Greg explained how understanding the neurobiology of zombies can aid in fleeing from or killing them. The kids were involved, asked great questions, and even taught both of us a thing or two (and gave us additional zombie book recommendations!)

For infectious diseases, there are all kinds of literature-backed scenarios that can get kids discussing germs and epidemiology. People can die and reanimate as zombies, or they can just turn into infected “rage monsters” who try to eat you without actually dying first. They can have an extensive incubation period, or they can zombify almost immediately. Each situation calls for different types of responses–while the “living” zombies may be able to be killed in a number of different ways, for example, reanimated zombies typically can only be stopped by destroying the brains. Discussing these situations allows the kids to use critical thinking skills, to plan attacks and think through choice of weapons, escape routes and vehicles, and consider what they might need in a survival kit.

Likewise, zombie microbes can be spread through biting, through blood, through the air, by fomites or water, even by mosquitoes in some books. Agents can be viral, bacterial, fungal, prions or parasitic insect larvae (or combinations of those). Mulling on these different types of transmission issues and asking simple questions:

“How would you protect yourself if infection was spread through the air versus only spread by biting?”

“How well would isolation of infected people work if the incubation period is very long versus very short?”

“Why might you want to thoroughly wash your zombie-killing arrows before using them to kill squirrels, which you will then eat?” (ahem, Daryl)

can open up avenues of discussion into scientific issues that the kids don’t even realize they’re talking about (pandemic preparedness, for one). And the great thing is that these kids are *already experts* on the subject matter. They don’t have to learn about the epidemiology of a particular microbe to understand disease transmission and prevention, because they already know more than most of the adults do on the epidemiology of zombie diseases–the key is to get them to use that knowledge and broaden their thinking into various “what if” situations that they’re able to talk out and put pieces together.

It can be scary going to talk to kids. Since this was a new program, we didn’t know if anyone would even show up, or how it would go over. Greg brought a watermelon for some weapons demonstrations (household tools only–a screwdriver, hammer and a crowbar, no guns or Samurai swords) which was a big hit. Still, I realize many scientists are more comfortable talking with their peers than with 13-year-olds. Talking about something a bit ridiculous, like an impending zombie apocalypse, can lessen anxiety because it takes quite a lot of effort to be boring with that type of subject matter; it’s entertaining; and kids will listen. And after all, what you don’t know, might eat you.