HIV’s “Patient Zero” was exonerated long ago

The news over the past 24 hours has exclaimed over and over:

HIV’s Patient Zero Exonerated

How scientists proved the wrong man was blamed for bringing HIV to the U.S.

Researchers Clear “Patient Zero” from AIDS Origin Story

H.I.V. Arrived in the U.S. Long Before ‘Patient Zero’

Gaetan Dugas: “patient zero” not source of HIV/AIDS outbreak, study confirms

HIV’s supposed “Patient Zero” in the U.S., Gaetan Dugas, is off the hook! He wasn’t responsible for our outbreak!

This is presented as new information.

gaetan_dugas
Gaetan Dugas, from Wikipedia.

It is not, and I think by focusing on the “exoneration” of Dugas, a young flight attendant and one of the earliest diagnosed cases of AIDS in the U.S., these articles (referencing a new Nature paper) are missing the true story in this publication–that Dugas was really a victim of Shilts and the media, and remains so, no matter how many times the science evidence has cleared his name.

First, the idea that Dugas served to 1) bring HIV to the U.S. and 2) spark the epidemic and infect enough people early on that most of the initial cases could be traced back to him is simply false. Yes, this was the hypothesis based on some of the very early cases of AIDS, and the narrative promoted in Randy Shilts’s best-selling 1987 book, “And the Band Played On.” But based on the epidemiology of first symptomatic AIDS cases, and later our understanding of the virus behind the syndrome, HIV, we quickly understood that one single person in the late 1970s could not have introduced the virus and spread it rapidly enough to lead to the level of infections we were seeing by the early 1980s. Later understanding of the virus’s African origin and its global spread made the idea of Dugas as the epidemic’s originator in America even more impossible.

When we think of Dugas’s role in the epidemiology of HIV, we could possibly classify him as, at worst, a “super-spreader“–and individual who is responsible for a disproportionate amount of disease transmission. Dugas acknowledged sexual contact with hundreds of individuals between 1979 and 1981–but his numbers were similar to other gay men interviewed, averaging 227 per year (range 10-1560). And while Shilts portrayed Dugas as a purposeful villain, actively and knowingly spreading HIV to his sexual partners, that does not jibe with both our scientific knowledge of HIV/AIDS or with the assistance Dugas provided to scientists studying the epidemic. Dugas worked with researchers to identify as many of his partners as he could (~10% of his estimated 750), as the scientific and medical community struggled to figure out whether AIDS stemmed from a sexually-transmitted infection, as several lines of evidence suggested. There’s no evidence Dugas was maliciously infecting others, though that was the reputation he received. Dugas passed away from complications of AIDS in March of 1984–weeks before the discovery of HIV was announced to the general public.

Furthermore, the information in the new publication is not entirely novel. Molecular analyses carried out in part by Michael Worobey, also an author on the new paper, showed almost a decade ago that Dugas could not have been the true “Patient Zero.” The 2007 paper, “The emergence of HIV/AIDS in the Americas and beyond,” had the same conclusions as the new paper: HIV entered the U.S. from the Caribbean, probably Haiti, and was circulating in the U.S. by the late 1960s–when Dugas was only about 16 years old, and long before his career as a flight attendant traveling internationally. So this 2007 molecular analysis should have been the nail in the coffin of the Dugas-as-Patient-Zero ideas.

But apparently we’ve forgotten that paper, or other work that has followed the evolution of HIV over the 20th century.

What is unique about the new publication is that it included a sample from Dugas himself, via a plasma contribution Dugas donated in 1983, and other samples banked since the late 1970s. The new paper demonstrated that Dugas’s sample is not in any way unique, nor is it a “basal” virus–one of the earliest in the country, from which others would diverge. Instead, it was representative of what was already circulating among others infected with HIV at that time. In supplemental information, the authors also demonstrated how notation for Dugas in scientific notes changed from Patient 057, then to Patient O (for “Outside California”) to Patient 0/”Zero” in the published manuscript–which Shilts then named as Dugas and ran with in his narrative.

patient-zero-graphic
Graphic of sexual network of early AIDS cases, from Auerbach et al., Am J Med 1984.

 

The media then extended Shilts’s ideas, further solidifying the assertion that Dugas was the origin of the U.S. epidemic, and in fact that he was outright evil. The supplemental material notes that Shilts didn’t want the focus of the media campaign initially to be about Dugas, but was convinced by his editor, who suggested the Dugas/Patient Zero narrative would result in more attention than the drier critiques of policy and inaction in response to the AIDS epidemic by the Reagan administration.

And the media certainly talked about it. A 1987 edition of U.S. News and World Report included a dubious quote attributed to Dugas: “‘I’ve got gay cancer,’ the man allegedly told bathhouse patrons after having sex with them. ‘I’m going to die, and so are you.’” NPR’s story adds “The New York Post ran a huge headline declaring “The Man Who Gave Us AIDS. Time magazine jumped in with a story called ‘The Appalling Saga Of Patient Zero.’ And 60 Minutes aired a feature on him. ‘Patient Zero. One of the first cases of AIDS. The first person identified as the major transmitter of the disease,’ host Harry Reasoner said.”

This is the real scandal and lingering tragedy of Dugas. His story was used to stoke fear of HIV-infected individuals, and especially gay men, as predators seeking to take others down with them. His story was used in part to justify criminalization of HIV transmission. So while science has exonerated him again and again, will the public–and the media–finally follow?

 

 

 

 

Just how long does the Ebola virus linger in semen?

The 2013-2016 West African Ebola virus outbreak altered our perception of just what an Ebola outbreak could look like.

While none of the three primary affected countries–Liberia, Sierra Leone, and Guinea-have had a case since April 2016, the outbreak resulted in a total of over 28,000 cases of Ebola virus disease (EVD)–65 times higher than the previous largest EVD outbreak, and more than 15 times the total number of cases of all prior EVD outbreaks combined, from the virus’s discovery in 1976 to a concurrent (but unrelated) outbreak in the Democratic Republic of Congo in 2014.

In March 2016, cases were identified once again in both Liberia and Guinea, just after the outbreak had been declared over. Both countries were declared Ebola-free in June 2016; Guinea for the second time and Liberia for the fourth time. The last series of cases in these countries demonstrated just how different this epidemic was from prior ones, changing what we thought we knew about the virus:

Previous research suggested Ebola could persist in the semen for 40 to 90 days. But that window has been eclipsed in this epidemic by a considerable amount. A probable case of sexual transmission occurred approximately six months after the patient’s initial infection last year in Liberia. Another study found evidence of Ebola in the semen of 25% of surviving men tested seven to nine months after infection. And it takes only a single transmission to kick off a fresh recurrence of the disease.

A recent paper extended this window of virus persistence in the semen even longer–over 500 days. It also explains how the outbreaks began in both countries after being declared Ebola-free–so where did the virus come from?

In a convergence of old-fashioned, “shoe leather” epidemiology/tracing of cases and viral genomics, two converging lines of evidence led to the identification of the same individual: a man who had been confirmed as an EVD case in 2014, and had sexual contact with one of the new cases. Author Nick Loman discussed via email:

The epidemiologists told us independently that they had identified a survivor and we were amazed when we decoded the metadata to find that case was indeed the same person. The sequencing and epidemiology is tightly coordinated via Guinea’s Ministry of Health who ran National Coordination for the Ebola outbreak and the World Health Organisation.

It shows that the genomics and epidemiology works best when working hand-in-hand. If we’d just had the genomics or the epidemiology we’d still have an element of doubt.

The sequencing results also suggested that it was likely that the new viral outbreak was caused by this survivor, and unlikely that the outbreak was due to another “spillover” of the virus from the local animal population, according to author Andrew Rambaut:

If the virus was present in bats and jumped to humans again in 2016, it might be genetically similar to the viruses in the human outbreak but not have any of the mutations that uniquely arose in the human outbreak (it would have its own unique mutations that had arisen in the bat population since the virus that caused human epidemic).

It might be possible that the virus jumped from humans to some animal reservoir in the region and then back to humans in 2016 but because we have the virus sequence from the patients acute disease 15 months earlier we can see that it essentially exactly the same virus. So this makes it certain the virus was persisting in this individual for the period.

So the virus–persisting in the survivor’s semen for at least 531 days–sparked a new wave of cases. Ebola researcher Daniel Bausch noted elsewhere that “The virus does seem to persist longer than we’ve ever recognized before. Sexual transmission still seems to be rare, but the sample size of survivors now is so much larger than we’ve ever had before (maybe 3,000-5,000 sexually active males versus 50-100 for the largest previous outbreak) that we’re picking up rare events.”

And we’re now actively looking for those rare events, too. The Liberia Men’s Health Screening Program already reports detection of Ebola virus in the semen at 565 days following symptoms, suggesting we will need to remain vigilant about survivors in both this and any future EVD epidemics. The challenges are clear–we need to investigate EVD survivors as patients, research participants, and possible viral reservoirs–each of which comes with unique difficulties. By continuing to learn as much as we can from this outbreak, perhaps we can contain future outbreaks more quickly–and prevent others from igniting.

The Zika conspiracies have begun

Like cockroaches, the conspiracy theorists suggesting the Zika virus outbreak is anything but a normal, naturally-occurring event have begun to come out of the woodwork. To be expected, the theories they’re espousing make no sense scientifically, and each theory is incompatible with the others, but why should anyone expect that conspiracy theorists would actually use logic?

Claim One: the current Zika virus outbreak is due to the release of genetically-modified mosquitoes by British company Oxitec. The suggestion is that GMO mosquitoes were released in the same area of Brazil now experiencing Zika outbreaks, and somehow these mosquitoes caused the outbreak. The mosquitoes are engineered to require the antibiotic tetracycline in order to survive development in the wild, so when a wild female mosquito breeds with a male GMO mosquitoe, it’s essentially is a death sentence to the female’s offspring. Theorists argue that livestock use of tetracycline leaves this antibiotic in the environment, allowing some offspring to survive. Somehow, Zika is inserted into this.

Who’s claiming this? Stories at Natural News, the Daily Mirror, The Ecologist, and Antimedia, among others. Alex Jones brings in the Bill Gates connection.

What’s wrong with it? There’s absolutely nothing that makes sense to relate this to Zika. Even if these GMO mosquitoes can reproduce, that doesn’t mean they’re suddenly infected with the Zika virus. This article probably lays it out the best as far as a suggested mechanism, but even then it’s a convoluted mess, suggesting a transposon* (a “jumping gene”) moved from the mosquito into Zika virus (but where did the Zika come from in the first place though? was it already in Brazil?), then that transposon made Zika more virulent and gave the virus “an enhanced ability to enter and disrupt human DNA” (what??), which then leads to microcephaly. All without absolutely any citations from the scientific literature to back up this scenario, of course.

And that’s even assuming that the area where the testing occurred was the same as where the mosquitoes were released. It’s not, as both The Mad Virologist and Christie Wilcox point out. Both have many more details taking down this theory as well.

Claim Two: a program encouraging pregnant women to get the Tdap vaccine led to the presumed increase in microcephaly in Brazilian babies. Because, toxins?

Who’s claiming this? Really credible places, like Brazilian Shrunken Head Babies (not even joking).

What’s wrong with it? Pretty much everything. First, the vaccine isn’t recommended until relatively late in pregnancy; even one of the links cited by the “shrunken heads” page notes that it’s suggested in the 27th to 36th week of pregnancy. This is very late in pregnancy to have such a severe effect on brain/skull development. For other microbes that cause microcephaly (such as cytomegalovirus or rubella), infection occurring in the first half of the pregnancy (before 20 weeks) is usually associated with a higher likelihood of adverse developmental outcomes, not one very late like Tdap. And of course, this theory completely contradicts the “Zika-GMO mosquito” one, which suggests that Zika is the cause.

Biologically, this makes zero sense–and furthermore, why wouldn’t other countries be seeing this spike, if Tdap is truly the cause? Women in the U.S. and other countries also receive this vaccine during pregnancy, but we haven’t seen an increase in microcephaly cases. Furthermore, a recent study has demonstrated yet again that Tdap is very safe during pregnancy.

Claim Three: Rockefeller something something bioterrorism something, maybe. They’ve taken the fact that an organization, the American Type Culture Collection (ATCC), has Zika virus available on their website, and twisted that into apparently some kind of deliberate release, maybe? It’s all pretty shadowy. [Updated: this site very clearly says the Rockefellers invented it to kill people. If that were true, they did a pretty shitty job].

Who’s claiming this? Chemtrails Global Skywatch and The Freethought Project.

What’s wrong with it? Even the Freethought Project post basically unravels its own conspiracy theory, but still posted this for some reason, noting “It seems that while the virus is available online, it is not extremely easy to get, and would likely require some extremely creative fraud in order to make it happen,” but concluding that “…it definitely does seem that it would be possible for a group or individual that is determined enough to make their way through the website’s security measures.”

I seriously doubt that.

For those of you who don’t know, ATCC is basically a global clearinghouse for biological samples–they offer tissue culture lines, bacteria, viruses, etc. Researchers need these for a number of reasons, such as having positive controls for assays, or to be sure they’re using the same cells as another investigator whose work they want to replicate or expand upon. I’ve used them many times to get both bacteriophage as well as isolates of bacteria for my research projects. And they won’t ship to just some random person.

When I moved institutions and set up my new laboratory, on my first ATCC order, they contacted the director of biosafety at my institution to be sure my lab was equipped and ready to handle the organisms I had requested. When that was assured, we still had to establish a Material Transfer Agreement in order for the items to actually be shipped–a legal document between ATCC and my university, signed by an “authorized representative” of my institution. It was only after jumping through all of these hoops that I was finally able to get the requested samples.

Even if someone had chosen to order Zika, an obscure, mostly-asymptomatic virus that until this outbreak was not associated with any serious ill effects, and perpetuated the “extremely creative fraud” mentioned by the Freethought Project…why? They’d need to initially infect themselves or others in order for the mosquitoes to subsequently become competent vectors of the virus. The mosquitoes would feed on them when there was adequate virus in the blood, and presumably the insects would then be released–to what end? To spread a previously-thought-relatively-harmless virus into a new population? Again, nonsensical.

[Updated: this doesn’t mean that “Rockefeller owns the patent on Zika virus,” as sites like this are claiming. As far as I can ascertain, there are no patents involving Zika. What it means is that the virus was deposited by Jordi Casals, who was an eminent virologist and had a large collection of viruses that he accumulated throughout his career, including Zika (but many others, as a search of ATCC shows). Rockefeller makes no money on this–in fact, now some journals require deposition of strains to ATCC or similar banks as a condition for publishing.]

Claim four: Zika simply doesn’t exist and/or isn’t causing microcephaly, and the “outbreak” is a ploy to push the not-yet-extant Zika vaccine/get people to blindly obey the government. (hat tip to Mary Mangan for this one).

Who’s claiming this? HIV denier and anti-vax advocate Jon Rappoport, among others (another post of his here on the topic). A very common sentiment in the comments pages on anti-vaccine pages.

What’s wrong with it? Pretty much everything. Rappoport has made a meta-conspiracy theory, claiming the increase in microcephaly is caused not by Zika, but by a combination of pesticide use and manufacturing, the Tdap and GMO mosquitoes mentioned above, mosquito sprays, and poverty/sanitation/malnutrition (the boogeymen of every anti-vaccine advocate). While he’s correct that the link between Zika and microcephaly isn’t yet 100% confirmed (as I mentioned yesterday), he’s taking at face value the claim that there actually is an increase in microcephaly at all–something which is also not been confirmed. So like many science deniers, he’s taking the parts of the research that fit his biases (look at how toxic Brazil is! Of course it’s causing health problems in babies!) and ignoring the parts he doesn’t–that if there is an increase in microcephaly, Zika might be a driving force. In his mind, the virus is irrelevant and just a mechanism to make the public into “sheep” who will fall in line with government recommendations.

I’m sure this will not be the last of the conspiracy theories. Like those we saw with Ebola, these have the potential to cause real harm. Outcry over the GMO mosquito program can curtail use of another agent to control the Aedes aegypti mosquito–the primary vector not only of Zika, but also yellow fever, chikungunya, and dengue. I know those who benefit from these type of conspiracies will never stop churning them out (Mike Adams, I’m looking at you), but we need to bring them to the light and show just how little scientific support any of this has. It won’t inoculate everyone against these ideas, but hopefully it will provide enough community immunity that they’re unable to spread far and wide.

*Christie Wilcox pointed out another great observation on just how implausible this is–that the potential to insert a 8.4kb double-stranded DNA transposon into a 10.8kb single-stranded RNA virus is…not possible. So, yeah, just to add to the ridiculousness of that idea.

Preparing for the zombie apocalpyse

I have a paper out in the Christmas issue of BMJ on the coming zombie apocalypse.

You read that right. And yes, it was peer-reviewed.

I’ve discussed previously how I’ve used the attention paid to zombies to talk about infectious diseases with children and other audiences; and to bring some science to the Walking Dead and other zombie tales. I even include a zombie lecture as part of the talks I give in my position as an American Society for Microbiology distinguished lecturer.

Why?

Like them or hate them, zombies are part of the zeitgeist. The Walking Dead is still one of the highest-rated programs on television, and its spin-off, Fear the Walking Dead, has been renewed for a second season. Early 2016 will bring us Pride and Prejudice and Zombies on film. Even Aaaahnold Schwarzenegger did a zombie movie. The Girl with all the Gifts was a sleeper hit, and a movie version of the zombie fungus video game The Last of Us is supposedly on the way.

So that’s what the BMJ paper was all about. Of course, it’s ridiculous at its core–no one really expects a zombie outbreak. *But*, we do see new diseases emerging all the time. MERS. Zika virus. Chikungunya. Hendra. Nipah. Pandemic influenza. Other, novel influenzas. And of course, the Ebola virus disease outbreak that is still ongoing in Guinea and Liberia (though cases have finally slowed to a mere trickle).

And we’re still unprepared for them when they become explosive, as Ebola did in 2014. Analyses have showed that the delayed response to that outbreak cost lives. And that’s for a virus that is not particularly easy to transmit, as it’s only spread late in the illness via direct contact with infected bodily fluids. If that had been another virus that was airborne instead of bloodborne, the world could have been in a much worse situation. Now imagine that it was the Solanum virus of World War Z (the book version), slowly incubating in infected individuals as they move all over the globe. Definitely unprepared.

Furthermore, even with our handful of cases in the U.S., we saw that the hype and misinformation about Ebola was out of control. We saw this with H1N1 in 2009 as well, and H5N1 before that. We’re still, as a whole, pretty bad at communicating about infectious disease threats–striking that correct balance of assurance that we know what we’re doing, but acknowledging the gaps in our data and how we’re working to address those. It’s not an easy thing to do, but we need to continue improving. Because again, that’s how it always starts in zombie movies, right?

All-Im-saying-is-Zombie-movie

Ebola and zombies also lead to ethical dilemmas. As I noted in the paper, for a zombie outbreak, there would remain the question of quarantine (for those exposed/bitten but not yet sick), and isolation (for those who are ill)–how would those be handled? What if quarantining the healthy-but-exposed led to essentially a death sentence, as the bitten would inevitably “turn”, and possibly start chowing on the still-living who were quarantined with them? Again, ridiculous on its face, but it has parallels in real-life outbreaks and the legality and ethical quandaries of when to use such measures (and, of course, used with the assumption that they would be effective–which doesn’t always hold). There are accusations that these were violated last year, when individuals coming back from working the Ebola outbreak were quarantined–lacking in scientific justification for sure, and potentially illegal as well.

Using zombies in lieu of real diseases gives researchers, public health professionals, policy makers, and laypeople the ability to discuss these heavy issues without getting bogged down in one specific outbreak or pathogen, because many of the problems we’d face during the zombie apocalypse are similar to those that come up in any serious epidemic: coordination. Funding. Communication. Training. Access to treatment or prevention. Though I didn’t discuss it in this particular article, proper personal protective equipment (PPE) is another issue–both access to it (lacking in developing countries), and being sure to choose the right gear for the outbreak (“overprotection” is not always better). Further, it encourages individuals to put together their own zombie (disaster) preparedness plan, which is how the CDC has used the zombie phenomenon.

In short, it’s way more fun for the average person to shoot the shit about zombies than to have a more serious discussion about influenza, or Ebola, or whatever the infectious disease du jour may be–and maybe even learn a bit of science and policy along the way.

 

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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“Spillover” by David Quammen

Regular readers don’t need to be told that I’m a bit obsessed with zoonotic disease. It’s what I study, and it’s a big part of what I teach. I run a Center devoted to the investigation of emerging diseases, and the vast majority of all emerging diseases are zoonotic. I have an ongoing series of posts collecting my writings on emerging diseases, and far too many papers in electronic or paper format in my office to count. Why the fascination? Zoonotic diseases have been responsible for many of mankind’s great plagues–the Black Death, the 1918 “Spanish” flu pandemic, or more recently, HIV/AIDS. So you can imagine my delight when I read about Spillover, a new book by David Quammen on zoonotic diseases.

I’ve previously highlighted some of Quammen’s work on this site. That link goes to a 2007 story he wrote for National Geographic on “infectious animals,” which really serves as a preview to “Spillover,” introducing some of the concepts and stories that Quammen elaborates on in the book.

“Spillover” is wide-ranging, tackling a number of different infectious agents, including viruses like Nipah, Hendra, and Ebola; bacteria including Coxiella burnetii and Chlamydia psittaci; and parasites such as Plasmodium knowlesi, a zoonotic cause of malaria. HIV is a big part of the story; Quammen devotes the last quarter or so of the book to tracing the discovery and transmission of HIV from primates to humans, and from 1900 to present-day. He even takes the time to explain the basic reproductive number–something that’s not always a page-turner, but Quammen manages to do it well and without being too tangential to the rest of the story; much more of a Kate-Winslet-in-Contagion than Ben-Stein-in-Ferris Bueller delivery.

Indeed, “Spillover” is somewhat unique in that it doesn’t read quite like your typical pop science book. It’s really part basic infectious disease, part history, part travelogue. Quammen has spent a number of years as a correspondent for National Geographic, and it shows. The book is filled with not only well-documented research findings and interviews with scientists, but also with Quammen’s own experience in the field, which gives the book a bit of an Indiana Jones quality. In one chapter, he details his adventure tagging along with a research team to capture bats in China, entering a cave that “felt a little like being swallowed through the multiple stomachs of a cow.” This was after an earlier dinner in which he describes his encounters with the an appetizer of the “world’s stinkiest fruit” (I’ll keep the description of the smell to myself) with congealed pig’s blood for a main dish (bringing to mind the scooping out of monkey’s brains in “Temple of Doom”–and the various zoonotic diseases that could be associated with those, come to think of it).

Quammen’s book is an excellent, and entertaining, overview of the issues of zoonotic disease–why do they emerge? Where have they come from? How do they spread? The only thing that’s missing is more of a cohesive discussion about what to do about them. However, that’s rather understandable, as we certainly have less of a grasp of this question than we do about the others (and even with some of those, our knowledge is spotty at best). I hope “Spillover” will inspire another generation of future germ-chasers, as “The Coming Plague” did almost 20 years ago.

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.

Wait, the infamous “Black Death” still plagues the United States?

This is the eighth of 16 student posts, guest-authored by Michelle Formanek. 

For many of us in the scientific world, particularly budding infectious disease epidemiologists like myself, the Plague (or, more dramatically, the “Black Death”) is a prime example of the rapid and devastating spread of an infectious disease. So devastating, in fact, that it wiped out nearly one-third of the population in Europe in the mid-1300’s. That’s roughly equal to 25 million people. It then persisted and has caused various outbreaks throughout history, most notably the Great Plague of London in which 1 in 5 residents died.

So why should be care about the Plague today? Isn’t that old news?

While I will go into more detail about the history of the plague a little later, I first want to mention what prompted me to write about what many people consider to be a no-longer-relevant disease. In order to gauge modern perceptions of the plague, I took a very unofficial survey of friends and family from various backgrounds about what they knew about the Plague. While the knowledge base ranged quite a bit, most were very surprised to hear that we still have cases of the Plague here in the United States.

Yes, you heard me right. The Plague still exists in the United States.

Of course, due to increased knowledge and antibiotic therapy, we no longer see the sweeping epidemic that caused so much turmoil throughout history. Nevertheless, an Oregon man is currently suffering from a rare case of the “Black Death.”

According to reports, a stray cat bit the unidentified man while he was trying to pull a mouse away from the cat. (I won’t even begin to speculate as to why this man was attempting to steal a mouse away from what was likely a very hungry stray cat, but that’s another story.) Several days later the man began to feel ill and presented to the hospital with symptoms typical of the Plague. These included fever, swollen lymph nodes and stomach pain. It has since progressed to bleeding mouth, nose and anus, and dying tissue.  Although the CDC has yet to confirm the diagnosis, all signs point to the Plague.

Only 10-15 people report becoming ill with the disease each year in the United States; this man is the fifth person in Oregon since 1995.

The Plague is caused by the bacterium Yersinia pestis., a rod-shaped bacillus that can live in various species of animals including rats, mice, squirrels, cats, prairie dogs, camels, and rabbits, among others. Yersinia pestis can then be transferred to humans through direct contact with infected animals, bites from fleas that have previously fed on infected animals (this is most common), or human-to-human through the air. Historically, the high population of small rodents and their flea friends in urban areas were attributed to the rapid spread of the disease.

While the Bubonic plague may be the most well known form of the disease, there are actually three different types of the Plague.  The Bubonic plague is the most common form and is characterized by buboes – painful, swollen lymph nodes – in the groin, armpit or neck. Septicemic plague occurs when the bacteria begins to spread in the bloodstream. Lastly, the most infectious form of the disease is Pneumonic plague. This advanced stage strikes when the bacteria can be passed from person to person through airborne droplets coughed up from the lungs. Bubonic plague is fatal roughly half the time, while Septicemic and Pneumonic are almost uniformly fatal without antibiotic treatment.

The man in Oregon was first believed to be suffering from Bubonic plague, but is now beginning to show signs of Septicemic plague, meaning it has entered his bloodstream and is able to reach all different parts of the body.  Luckily, antibiotics are effective in the treatment of the Plague if given early enough. Without antibiotics, 1 in 7 people infected end up dying.

So you may be asking yourself, as I did, where a deadly disease like this came from in the first place. The puzzling start of the epidemic went something like this:

“The Black Death arrived in Europe by sea in October 1347 when 12 Genoese trading ships docked at the Sicilian port of Messina after a long journey through the Black Sea. The people who gathered on the docks to greet the ships were met with a horrifying surprise: Most of the sailors aboard the ships were dead, and those who were still alive were gravely ill. They were overcome with fever, unable to keep food down and delirious from pain. Strangest of all, they were covered in mysterious black boils that oozed blood and pus and gave their illness its name: the “Black Death.” The Sicilian authorities hastily ordered the fleet of “death ships” out of the harbor, but it was too late: Over the next five years, the mysterious Black Death would kill more than 25 million people in Europe–almost one-third of the continent’s population.”

Unfortunately, the cause of the disease was not discovered until 1894, long after it swept through Europe with alarmingly high death rates. People had their ideas about what was causing the Black Death, but no one could actually figure it out. Some believed it was the spirit escaping the eyes of a sick man and infecting the nearest healthy person, others believed it was God’s way of punishing those who had sinned.  Citizens were so panicked that they went to extreme lengths to avoid contracting the disease, even so far as to completely abandon loved ones who got sick. More details here.

As mentioned before, antibiotics can be extremely effective in fighting this bacteria. As of right now, the Oregon man is still fighting for this life, but thanks to modern medicine, his chances of living are fairly high. The man likely contracted the disease from the cat; however, the cat died shortly after and its remains have since been sent to the CDC for testing.  Who knew that a stray cat in the Northwest U.S. could have possibly been harboring bacteria that once had the potential to wipe out entire cities. Fortunately, modern medicine is on our side.

So is the re-emergence of the Plague something that we should really be concerned about? Probably not. But it never hurts to be informed.

References:

http://www.cdc.gov/ncidod/dvbid/plague/index.htm

http://ocp.hul.harvard.edu/contagion/plague.html

http://science.nationalgeographic.com/science/health-and-human-body/human-diseases/plague-article/

http://www.cbsnews.com/8301-504763_162-57452519-10391704/oregon-man-diagnosed-with-black-death-plague/

http://www.mayoclinic.com/health/plague/ds00493/dsection=symptoms

http://www.cdc.gov/ncidod/dvbid/plague/bacterium.htm

http://www.cdc.gov/ncidod/dvbid/plague/qa.htm

http://www.who.int/mediacentre/factsheets/fs267/en/

http://www.history.com/topics/black-death

Raw milk. Raw deal?

This is the sixth of 16 student posts, guest-authored by Anna Lyons-Nace. 

Natural…unprocessed…raw.  These terms are often used by consumers, nutritionists and health experts to denote the most healthful, high-quality food options available for consumption. However, when pertaining to the recent increasing trend in raw milk consumption, can consumers be confident that they are choosing the safest and most healthful option?  Statistical data and health studies would suggest otherwise.

Before we delve into the discussion any further, we should first establish what is considered raw milk and what is not raw.  Raw milk is considered any animal milk, most often from cows, sheep and goats, which is not pasteurized, but still utilized for human consumption. Keep in mind that raw milk can also be used for producing other dairy products such as cheese and yogurt. Raw milk may also undergo a straining process, but it is otherwise unprocessed.  Sources of raw milk are typically local farming operations.  In fact, the interstate sale of raw milk for direct consumption has been prohibited in the U.S. by federal law since 1987, due to safety concerns regarding shelf life and disease risks.  However, there are many states that allow the intrastate sale of raw milk, while a few states prohibit it completely.  This means that the vast majority of what we see in our local grocery stores will have undergone the process of pasteurization, which will be clearly stated on the label.  Pasteurization involves heating the milk to very specific temperatures for short time frames in order to kill potentially harmful germs. Pasteurization was introduced in the U.S. during the first part of the 20th century, at a time when millions of people were contracting life-threatening illnesses such as typhoid, diphtheria and tuberculosis, often through milk consumption. Applying the simple process of pasteurization, along with other health advances, led to a dramatic decline in such diseases, and is considered a major public health triumph.  Decreasing or eliminating potentially harmful microbes through pasteurization, not only makes the product safer for consumers, it also increases shelf life.

So why is raw milk becoming a sought after commodity for many consumers?  This can probably be attributed to such things as a general increase in societal demand for whole, natural and sustainable food products; as well as the perceived benefits of the milk itself. Raw milk drinkers claim that the unpasteurized product is higher in nutrients, protective enzymes and immune boosting probiotics, and can help treat a variety of ailments from asthma to gastrointestinal disorders. Supporters also claim that pasteurization is the cause of milk allergies and lactose intolerance.  It is important to note that these claims remain largely unsubstantiated by published scientific studies.  In many cases these claims have been categorically refuted by direct scientific evidence.  The Food and Drug Administration (FDA) frankly states that “research shows no meaningful difference between the nutrient content of pasteurized and unpasteurized milk”.  Science has also shown that most enzymes of concern by advocates are not altered by pasteurization. For those with allergy concerns, medical experts and research agrees that it is the proteins naturally present in milk (both raw and pasteurized) that are the cause of allergic reactions to milk and have no relationship to the pasteurization process.  In regards to lactose intolerance, it needs to be understood that lactose intolerance is a genetic error of metabolism that some people are born with, and there is lactose present in both raw and pasteurized milk.  So unfortunately for the lactose intolerant, raw milk is not the solution. As for probiotics, milk does not naturally contain probiotics; so if they are detected in the raw milk they are likely from another source such as air exposure or fecal contamination.  But the good news is that we as consumers have many, safer options for experiencing the benefits of probiotics, including yogurt with active cultures and over the counter supplements.

Now that we have explored some of the common myths surrounding raw and pasteurized milk, it is most important to discuss the reality of the risks involved with raw milk consumption. Real world case studies, as well as research by such reputable organizations as the Centers for Disease Control and Prevention (CDC) and the FDA, consistently show that the risks of raw milk consumption far outweigh any real or perceived benefit. A 13 year study by the CDC showed raw milk and raw milk products are 150 times more likely to cause a disease outbreak than are pasteurized dairy products. These risks come in the form of a long list of disease causing germs that can contaminate dairy products, and are the reason that pasteurization was instituted in the first place. Some of the more significant contaminants that can be present in raw milk include such pathogens as Salmonella, E. coli, Listeria, and Campylobacter.  These pathogens can cause a variety of symptoms, but most commonly produce gastrointestinal illness such as vomiting and diarrhea that can range from mild forms to fatal illnesses. The most vulnerable to becoming sick from drinking raw milk include babies, young children, those with weakened immune systems and pregnant women. But “healthy” people can become ill as well, and there are many documented cases. Data collected by the CDC from 1998-2009 documented 93 disease outbreaks due to raw milk and raw milk product consumption.  These outbreaks caused 1,837 illnesses, 195 hospitalizations, and 2 deaths.  It is important to note that for every case that is reported and diagnosed, there are many illnesses that go unreported, which means these case numbers in reality are certain to be much higher.  The most recently reported outbreak occurred in Oregon this past April.  The outbreak involved 19 people, 15 of which were children, with 4 of the children ending up in the hospital undergoing treatment for kidney failure.  Eleven of the cases were confirmed to have been caused by a very dangerous strain of E. coli that was traced back to a dairy farm that supplied the families with raw milk. In reflecting on outbreaks such as these, it is important to remember that these illnesses are preventable.   But hopefully, these sad cases will also serve to educate us as consumers, so that we can make informed and healthy choices for ourselves and our families.

References

  1. Langer AJ, Ayers T, Grass J, Lynch M, Angulo FJ, Mahon BE. Nonpasteurized dairy products, disease outbreaks, and state laws-United States, 1993-2006. Emerg Infect Dis. 2012 Mar;18(3):385-91.
  2. Oliver SP, Boor KJ, Murphy SC, Murinda SE. Food safety hazards associated with consumption of raw milk. Foodborne Pathog Dis. 2009 Sep;6(7):793-806. Review.
  3. Centers for Disease Control and Prevention, Trying to Decide about Raw Milk? Last Updated March 7, 2011, http://www.cdc.gov/foodsafety/rawmilk/decide-raw-milk.html (Accessed June 5, 2012)
  4. Centers for Disease Control and Prevention, Raw Milk Questions and Answers, Last Updated March 22, 2012, http://www.cdc.gov/foodsafety/rawmilk/raw-milk-questions-and-answers.html (Accessed June 5, 2012)
  5. Milk Facts, Heat Treatment and Pasteurization, http://milkfacts.info/Milk%20Processing/Heat%20Treatments%20and%20Pasteurization.htm (Accessed June 8, 2012)
  6. Food and Drug Administration, Raw Milk Misconceptions and the Danger of Raw Milk Consumption, Last Updated November 1, 2011, http://www.fda.gov/Food/FoodSafety/Product- SpecificInformation/MilkSafety/ConsumerInformationAboutMilkSafety/ucm247991.htm (Accessed June 5, 2012)
  7. Food and Drug Administration, Questions & Answers: Raw Milk, Last Updated November 1, 2011 http://www.fda.gov/food/foodsafety/product-specificinformation/milksafety/ucm122062.htm (Accessed June 5, 2012)
  8. Food Safety News, 19 Ill with E. Coli in Oregon Raw Milk Outbreak, Last Updated April 21, 2012, http://www.foodsafetynews.com/2012/04/post-5/ (Accessed June 5, 2012)
  9. International Association for Food Protection, Raw Milk Consumption: An Emerging Public Health Threat? Last updated 2012 http://www.foodprotection.org/events/other-meetings/3/iafp-timely-topics-symposium-raw-milk-consumption-an-emerging-public-health-threat/10/speaker-presentations/ (Accessed June 6, 2012)
  10. International Association for Food Protection, Nutritional Straight Talk on Raw and Pasteurized Milk, last updated 2012 http://www.foodprotection.org/files/timely-topics/TT_02.pdf (Accessed June 6, 2012)

 

 

Things that want to eat your brain

This is the fourth of 16 student posts, guest-authored by Eric Wika.

Let’s face it, it’s a dangerous world to be a brain. The brain is so soft and squishy it cannot even support its own weight. That’s right, even gravity itself is enough to take out an unprotected brain. Besides these passive threats, there are several factions out there that active try to damage your brain! Zombies are an ever present menace which wish to eat our brains. TV will rot our brains, drugs will fry our brains and bullies will offer to “beat your brains in”. It’s no wonder mother nature had to come up with the enormous bone braincase on top of your shoulders, it really is a dangerous place to be a brain!

And now, there’s even a new threat against our brain. Brain eating amoebas. Isn’t mother nature so adorable sometimes?!? Scientist have discovered an amoeba in river water that normally sits quite happily in its own environment eating bacteria. However, when it’s take out of its natural environment and shot up someone’s nose, it starts to eat the food source that’s readily available. That’s right, lunch time for brain eaters.

The amoeba is Naegleria fowleri, and has been reported recently in Louisiana. The Department of Health and Hospitals in the region had this to say about it.

Now if you think you may be infested with these brain loving parasites, let’s take a trip down Webmd.com to review what the natural history and symptoms of this tour of joy are. Remember standard disclaimers apply. If you go to the internet and use it as a replacement for real medical evaluation and treatment, then you are essentially leaving your medical health up to this guy, and come on, this guy can’t even figure out how to ROW.

Luckily there’s a FAQ for brain eating amoebas. The first thing to do is to check your exposure history. This bug doesn’t take the midtown bus and arrive at the steps of your apartment. You have to come to it. It lives in lake water, ponds, untreated pools, well water and the like. If you (or more to the point your nose) hasn’t been to any of these places, then you’re in luck. If your nose doesn’t go to these places, the bug can’t have access to your juicy brain bits. If you use a neti pot   there are some extra precautions to take. (more on this later) If you do get this bug up your nose, that’s where the confusion begins. It’s been postulated that these bugs get confused by the chemicals your brain cells use to communicate with each other. The signal that brain cell 1 uses to say “Hey, let Frank know I smell a hotdog down here” gets to the amoeba and through some massive mess up in communication, that signal is misinterpreted as “hey, Naegleria, get your butt up here for some goodies!!!” Naegleria then does the logical thing and get’s it’s little amoeba butt through the olfactory nerve (the bit that smells stuff) and into your frontal lobe (the smart “decides what you’ll have for lunch” bit) and begins the chow down process. Once you get it it takes about 2 to 15 days to show symptoms, and most people unfortunately die 3 to 7 days after symptoms appear. Symptoms are very similar to that of viral meningitis, including headache, fever, stiff neck, loss of appetite, vomiting, altered mental state, seizures and coma. Luckily these are symptoms that generally get you prompt attention from the local doctors at your hospital.

There have been a few cases of this disease so far. About 400 cases have been reported worldwide, 35 of which have been from the US since 2001. Thankfully, it is pretty rare. Unfortunately that can be a double edged sword as rare diseases tend to take longer to diagnose, if they get diagnosed at all. One of the most common ways to get this disease is through the use of a neti pot. A neti pot for those fortunate enough to not be in the know, is a tool used for pouring water directly into your nose. If you ever get to the point where your sinuses are so bad you start thinking to yourself “wow, having water poured directly into my nose would suck WAY less than this”, then getting a neti pot is for you. Other than medieval torture, a neti pot is a great device for flushing out the sinuses. Using one involves getting water, mixing it with some salt, and pouring it right on in there. Here is a lovely set of instructions coupled with an equally lovely picture of a woman in full nose irrigation mode.

The trick, however, is you have to use CLEAN water. If you’re going to shove something up your nose, whether it’s water or if you’re in Total Recall trying to remove an alien probe from your brain, do yourself a favor and make sure it’s clean.

Now you may be thinking “I’m fine, the only water I stick up my nose is pure, clean tap water. I don’t use dirty well water or go swimming in icky lakes and streams. Unfortunately, in today’s world, that just ain’t good enough. See tap water isn’t sterile. It’s clean, it’s safe to drink, but it isn’t sterile. Drinking tap water with Naegleria in it won’t make you sick, but sticking it up your nose will. You can avoid this easily one of two ways. 1) boil water (don’t forget to cool it!) before using your neti pot, or 2) buy distilled water for use with your neti pot (it costs less that $1 per gallon at most grocery stores).

Remember, the only one who can protect your brain is you! Use your neti pot safely and don’t get your brain eaten!