As you’ve probably seen, unless you’ve been living in a cave, Zika virus is the infectious disease topic du jour. From an obscure virus to the newest scare, interest in the virus has skyrocketed just in the past few weeks:
I have a few pieces already on Zika, so I won’t repeat myself here. The first is an introductory primer to the virus, answering the basic questions–what is it, where did it come from, what are its symptoms, why is it concerning? The second focuses on Zika’s potential risk to pregnant women, and what is currently being advised for them.
I want to be clear, though–currently, we aren’t 100% sure that Zika virus is causing microcephaly, the condition that is most concerning with this recent outbreak. The circumstantial evidence appears to be pretty strong, but we don’t have good data on 1) how common microcephaly really was in Brazil (or other affected countries) prior to the outbreak. Microcephaly seems to have increased dramatically, but some of those cases are not confirmed, and others don’t seem to be related to Zika; and if Zika really is causing microcephaly, 2) how Zika could be causing this, whether timing of the infection makes a difference, and whether women who are infected asymptomatically are at risk of medical problems in their developing fetuses.
The first question needs good epidemiological data for answers. This can be procured in a few ways. First, babies born with microcephaly, and their mothers, can be tested for Zika virus infection. This can be looked at a few ways: finding traces of the virus itself; finding antibodies to the virus (suggesting a past infection–but one can’t know the exact timing of this); and asking about known infections during pregnancy. Each approach has advantages and limitations. Tracking the virus or its genetic material is a gold standard, but the virus may only be present in body fluids for a short time. So if you miss that window, a false negative could result. This could be coupled with serology, to look at past infection–but you can’t be 100% certain in that case that the infection occurred during pregnancy–though with the apparently recent introduction of Zika into the Americas, it’s likely that infection would be fairly recent.
Serology coupled with an infection in pregnancy that has symptoms consistent with Zika (headache, muscle/joint pain, rash, fever) would be a step up from this, but has some additional problems. Other viral infections can be similar in symptoms to Zika (dengue, chikungunya, even influenza if the patient is lacking a rash), so tests to rule those out should also be done. On the flip side, about 80% of Zika infections show no symptoms at all–so a woman could still have come into contact with the virus and have positive serology, but she wouldn’t have any recollection of infection.
None of this is easy to carry out, but needs to be done in order to really establish with some level of certainty that Zika is the cause of microcephaly in this area. In the meantime, there are a few other possibilities to consider: that another virus (such as rubella) is circulating there. This is a known cause of multiple congenital issues, including microcephaly. This could explain why they’re seeing cases of microcephaly in Brazil, but none have been reported thus far in Colombia. Another is that there is no real increase in microcephaly at all–that, for some reason, people have just recently started paying more attention to it, and associated it with the Zika outbreak in the area–what we call a surveillance bias.
This is a fast-moving story, and we probably won’t have any solid answers to these questions for some time. In the interim, I think it’s prudent to take this as a possibility, and raise awareness of the potential this virus *may* have on the developing fetus, so that women can take precautions as they’re able. Public health is about prevention, and there have certainly been cases in the past of links between A and B that fell apart under further scrutiny. Zika/microcephaly may be one, but for now, it’s an unfortunate case where “more research is needed” is about the best answer one can currently give.
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?
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.
I’ve been involved in a few discussions of late on science-based sites around yon web on antibiotic resistance and agriculture–specifically, the campaign to get fast food giant Subway to stop using meat raised on antibiotics, and a graphic by CommonGround using Animal Health Institute data, suggesting that agricultural animals aren’t an important source of resistant bacteria. Discussing these topics has shown me there’s a lot of misunderstanding of issues in antibiotic resistance, even among those who consider themselves pretty science-savvy.
I think this is partly an issue of, perhaps, hating to agree with one’s “enemy.” Vani Hari, the “Food Babe,” recently also plugged the Subway campaign, perhaps making skeptics now skeptical of the issue of antibiotics and agriculture? Believe me, I am the farthest thing from a “Food Babe” fan and have criticized her many times on my Facebook page, but unlike her ill-advised and unscientific campaigns against things like fake pumpkin flavoring in coffee or “yoga mat” chemicals in Subway bread, this is one issue that actually has scientific support–stopped clocks and all that. Nevertheless, I think some people get bogged down in a lot of exaggeration or misinformation on the topic.
So, some thoughts. Please note that in many cases, my comments will be an over-simplification of a more complex problem, but I’ll try to include nuance when I can (without completely clouding the issue).
First–why is antibiotic resistance an issue?
Since the development of penicillin, we have been in an ongoing “war” with the bacteria that make us ill. Almost as quickly as antibiotics are used, bacteria are capable of developing or acquiring resistance to them. These resistance genes are often present on transmissible pieces of DNA–plasmids, transposons, phage–which allow them to move between bacterial cells, even those of completely different species, and spread that resistance. So, once it emerges, resistance is very difficult to keep under control. As such, much better to work to prevent this emergence, and to provide conditions where resistant bacteria don’t encounter selection pressures to maintain resistance genes (1).
In our 75-ish years of using antibiotics to treat infections, we’ve increasingly found ourselves losing this war. As bacterial species have evolved resistance to our drugs, we keep coming back with either brand-new drugs in different classes of antibiotics, or we’ve made slight tweaks to existing drugs so that they can escape the mechanisms bacteria use to get around them. And they’re killing us. In the US alone, antibiotic-resistant infections cause about 2 million infections per year, and about 23,000 deaths due to these infections–plus tens of thousands of additional deaths from diseases that are complicated by antibiotic-resistant infections. They cost at least $20 billion per year.
But we’re running out of these drugs. And where do the vast majority come from in any case? Other microbes–fungi, other bacterial species–so in some cases, that means there are also pre-existing resistance mechanisms to even new drugs, just waiting to spread. It’s so bad right now that even the WHO has sounded the alarm, warning of the potential for a “post-antibiotic era.”
This is some serious shit.
Where does resistance come from?
Resistant bacteria can be bred anytime an antibiotic is used. As such, researchers in the field tend to focus on two large areas: use of antibiotics in human medicine, and in animal husbandry. Human medicine is probably pretty obvious: humans get drugs to treat infections in hospital and outpatient settings, and in some cases, to protect against infection if a person is exposed to an organism–think of all the prophylactic doses of ciprofloxacin given out after the 2001 anthrax attacks, for example.
In human medicine, there is still much debate about 1) the proper dosing of many types of antibiotics–what is the optimal length of time to take them to ensure a cure, but also reduce the chance of incubating resistant organisms? This is an active area of research; and 2) when it is proper to prescribe antibiotics, period. For instance, ear infections. These cause many sleepless nights for parents, a lot of time off work and school, and many trips to clinics to get checked out. But do all kids who have an ear infection need antibiotics? Probably not. A recent study found that “watchful waiting” as an alternative to immediate prescription of antibiotics worked about as well as drug treatment for nonsevere ear infections in children–one data point among many that antibiotics are probably over-used in human medicine, and particularly for children. So this is one big area of interest and research (among many in human health) when it comes to trying to curb antibiotic use and employ the best practices of “judicious use” of antibiotics.
Another big area of use is agriculture (2). Just as in humans, antibiotics in ag can be used for treatment of sick animals, which is completely justifiable and accepted–but there are many divergences as well. For one, animals are often treated as a herd–if a certain threshold of animals in a population become ill, all will be treated in order to prevent an even worse outbreak of disease in a herd. Two, antibiotics can be, and frequently are, used prophylactically, before any disease is present–for example, at times when the producer historically has seen disease outbreaks in the herd, such as when animals are moved from one place to another (moving baby pigs from a nursery facility to a grower farm, as one example). Third, they can be used for growth promotion purposes–to make animals fatten up to market weight more quickly. The latter is, by far, the most contentious use, and the “low hanging fruit” that is often targeted for elimination.
From practically the beginning of this practice, there were people who spoke out against it, suggesting it was a bad idea, and that the use of these antibiotics in agriculture could lead to resistance which could affect human health. A pair ofpublications by Stuart Levy et al. in 1976 demonstrated this was more than a theoretical concern, and that antibiotic-resistant E. coli were indeed generated on farms using antibiotics, and transferred to farmers working there. Since this time, literally thousands of publications on this topic have demonstrated the same thing, examining different exposures, antibiotics, and bacterial species. There’s no doubt, scientifically, that use of antibiotics in agriculture causes the evolution and spread of resistance into human populations.
Why care about antibiotic use in agriculture?
A quick clarification that’s a common point of confusion–I’m not discussing antibiotic *residues* in meat products as a result of antibiotic use in ag (see, for example, the infographic linked above). In theory, antibiotic residues should not be an issue, because all drugs have a withdrawal period that farmers are supposed to adhere to prior to sending animals off to slaughter. These guidelines were developed so that antibiotics will not show up in an animal’s meat or milk. The real issue of concern for public health are the resistant bacteria, which *can* be transmitted via these routes.
Agriculture comes up many times for a few reasons. First, because people have the potential to be exposed to antibiotic-resistant bacteria that originate on farms via food products that they eat or handle. Everybody eats, and even vegetarians aren’t completely protected from antibiotic use on farms (I’ll get into this below). So even if you’re far removed from farmland, you may be exposed to bacteria incubating there via your turkey dinner or hamburger.
Second, because the vast majority of antibiotic use, by weight, occurs on farms–and many of these are the very same antibiotics used in human medicine (penicillins, tetracyclines, macrolides). It’s historically been very difficult to get good numbers on this use, so you may have seen numbers as high as 80% of all antibiotic use in the U.S. occurs on farms. A better number is probably 70% (described here by Politifact), which excludes a type of antibiotic called ionophores–these aren’t used in human medicine (3). So a great deal of selection for resistance is taking place on farms, but has the potential to spread into households across the country–and almost certainly has. Recent studies have demonstrated also that resistant infections transmitted through food don’t always stay in your gut–they can also cause serious urinary tract infections and even sepsis. Studies from my lab and others (4) examining S. aureus have identified livestock as a reservoir for various types of this bacterium–including methicillin-resistant subtypes.
How does antibiotic resistance spread?
In sum–in a lot of different ways. Resistant bacteria, and/or their resistance genes, can enter our environment–our water, our air, our homes via meat products, our schools via asymptomatic colonization of students and teachers–just about anywhere bacteria can go, resistance genes will tag along. Kalliopi Monoyios created this schematic for the above-mentioned paper I wrote earlier this year on livestock-associated Staphyloccocus aureus and its spread, but it really holds for just about any antibiotic-resistant bacterium out there:
And as I noted above, once it’s out there, it’s hard to put the genie back in the bottle. And it can spread in such a multitude of different ways that it complicates tracking of these organisms, and makes it practically impossible to trace farm-origin bacteria back to their host animals. Instead, we have to rely on studies of meat, farmers, water, soil, air, and people living near farms in order to make connections back to these animals.
And this is where even vegetarians aren’t “safe” from these organisms. What happens to much of the manure generated on industrial farms? It’s used as fertilizer on crops, bringing resistant bacteria and resistance genes along with it, as well as into our air when manure is aerosolized (as it is in some, but not all, crop applications) and into our soil and water–and as noted below, antibiotics themselves can also be used in horticulture as well.
So isn’t something being done about this? Why are we bothering with this anymore?
Kind of, but it’s not enough. Scientists and advocates have been trying to do something about this topic since at least 1969, when the UK’s Swann report on the use of Antibiotics in Animal Husbandry and Veterinary Medicine was released. As noted here:
One of its recommendations was that the only antimicrobials that should be permitted as growth promotants in animals were those that were not depended on for therapy in humans or whose use was not likely to lead to resistance to antimicrobials that were important for treating humans.
And some baby steps have been made previously, restricting use of some important types of antibiotics. More recently in the U.S., Federal Guidelines 209 and 213 were adopted in order to reduce the use of what have been deemed “medically-important” antibiotics in the livestock industry. These are a good step forward, but truthfully are only baby steps. They apply only to the use of growth-promotant antibiotics (those for “production use” as noted in the documents), and not other uses including prophylaxis. There also is no mechanism for monitoring or policing individuals who may continue to use these in violation of the guidelines–they have “no teeth.” As such, there’s concern that use for growth promotion will merely be re-labeled as use for prophylaxis.
Further, even now, we still have no data on the breakdown of antibiotic use in different species. We know over 32 million pounds were used in livestock in 2013, but with no clue how much of that was in pigs versus cattle, etc.
We do know that animals can be raised using lower levels of antibiotics. The European Union has not allowed growth promotant antibiotics since 2006. You’ll read different reports of how successful that has been (or not); this NPR article has a balanced review. What’s pretty well agreed-upon is that, to make such a ban successful, you need good regulation and a change in farming practices. Neither of these will be in place in the U.S. when the new guidance mechanisms go into place next year–so will this really benefit public health? Uncertain. We need more.
So this brings me back to Subway (and McDonald’s, and Chipotle, and other giants that have pledged to reduce use of antibiotics in the animals they buy). Whatever large companies do, consumers are demonstrating that they hold cards to push this issue forward–much faster than the FDA has been able to do (remember, it took them 40 freaking years just to get these voluntary guidelines in place). Buying USDA-certified organic or meat labeled “raised without antibiotics” is no 100% guarantee that you’ll have antibiotic-resistant-bacteria-free meat products, unfortunately, because contamination can be introduced during slaughter, packing, or handling–but in on-farm studies of animals, farmers, and farm environment, studies have typically found reduced levels of antibiotic-resistant bacteria on organic/antibiotic-free farms than their “conventional” counterparts (one example here, looking at farms that were transitioning to organic poultry farming).
Nothing is perfect, and biology is messy. Sometimes reducing antibiotic use takes a long time to have an impact, because resistance genes aren’t always quickly lost from a population even when the antibiotics have been removed. Sometimes a change may be seen in the bacteria animals are carrying, but it takes longer for human bacterial populations to change. No one is expecting miracles, or a move to more animals raised antibiotic-free to be a cure-all. And it’s not possible to raise every animal as antibiotic-free in any case; sick animals need to be treated, and even on antibiotic-free farms, there is often some low level of antibiotic use for therapeutic purposes. (These treated animals are then supposed to be marked and cannot be sold as “antibiotic-free”). But reducing the levels of unnecessary antibiotics in animal husbandry, in conjunction with programs promoting judicious use of antibiotics in human health, is a necessary step. We’ve waited too long already to take it.
(1) Though we know that, in some cases, resistance genes can remain in a population even in the absence of direct selection pressures–or they may be on a cassette with other resistance genes, so by using any one of those selective agents, you’re selecting for maintenance of the entire cassette.
(2) I’ve chosen to focus on use in humans & animal husbandry, but antibiotics are also used in companion animal veterinary medicine and even for aquaculture and horticulture (such as for prevention of disease in fruit trees). The use in these fields is considerably smaller than in human medicine and livestock, but these are also active areas of research and investigation.
(3) This doesn’t necessarily mean they don’t lead to resistance, though. In theory, ionophores can act just like other antibiotics and co-select for resistance genes to other, human-use antibiotics, so their use may still contribute to the antibiotic resistance problem. Studies from my lab and others have shown that the use of zinc, for instance–an antimicrobial metal used as a dietary supplement on some pig farms, can co-select for antibiotic resistance. In our case, for methicillin-resistant S. aureus.
(4) See many more of my publications here, or a Nature profile about some of my work here.
Long-term readers of the blog know of my interest in HIV denialism, especially as it is maintained and spread via the Internet. In my online travels, I recently met John Strangis via this blog post. John has an interesting story to tell regarding his experiences with HIV denialism and subsequently, his turn to patient and science activism. Many thanks to John for sharing it here.
TS: Can you tell the readers a bit about yourself?
JS: My name is John Strangis. I was born in the United States from Italian parents but lived for fifteen years in Italy when I was brought there at 10 years old after my dad retired; I lived there for 15 years before moving back to the States. I have a technical degree in network engineering and computer tech support and have worked in this field until I was laid off in 2010. After my layoff I developed a love for cooking, self taught myself in culinary arts and discovered I was quite talented so I decided to start my own cooking show on youtube. Along with my youtube channel I run a blog where I post HIV/AIDS information, recipes or anything else I may feel like writing about. I also have a passion for science and medicine, which are topics I love to study on my own as a hobby and also because as an HIV/AIDS activist, I find it important to be knowledgeable about certain issues so I can do a better job informing people about HIV through my activism work which I do through my blog and social media. I am a Social Ambassador for Get Tested Coachella Valley; a region wide public health campaign dedicated to dramatically reducing HIV by making voluntary HIV testing standard and routine medical practice and ensuring linkage to care. I believe it is important for people to see that the H in HIV stands for human and being a heterosexual man living with HIV and a public figure, my work can show others that HIV is a condition that affects us all, can help reduce the stigma and discrimination against people living with HIV and encourage others to get tested and treated.
TS: When were you diagnosed as HIV positive? What was your initial reaction?JS: I was diagnosed with HIV in 2011 after learning that my partner, Jessica was living with HIV. I met her in 2007 and she didn’t disclose her status to me out of stigma and fear of being rejected and although I already knew she was living with HIV because I found her prescriptions for HIV medicines, I decided not to hold it against her because I cared for her deeply. When we started seeing each other she made the mistake of throwing her antiretrovirals away and when I discovered she did so, I strongly urged her to tell me the truth because if she was living with HIV as I believed, the last thing I wanted was for her to fall ill because she was not on treatment. Well, my concern became a reality when after four years, she ended up in the hospital with pneumocystis pneumonia. Fortunately she got better and returned on treatment and I reassured her that if after testing, I was also found to be positive, we would deal with it together and I would never leave her side because of it. It did happen that I tested positive for HIV but my initial reaction wasn’t one of fear; I was aware that HIV today is a manageable chronic condition and just viewed my new status as another bump in the road of life and started researching HIV/AIDS to learn as much as possible for us to be able to live a long and healthy life regardless of living with HIV.
TS: How did you become introduced to HIV denialism? Can you describe your involvement with this movement?
JS: It was during my research on HIV/AIDS that I stumbled upon the denialist information; information which is quite easy to find when doing a search for HIV on google. I was into conspiracy theories at the time and the thought of HIV being a conspiracy was something I found pretty interesting to say the least. I asked questions about the denialist information on official HIV/AIDS websites and was banned for doing so by moderators who told me that I was parroting denialst propaganda. This censorship reinforced my belief that perhaps the denialist information had some truth behind it, without knowing that the reason I was banned was because this information can be and is a danger to public health. I searched for denialst groups to attempt to make contact with these people in order to learn more and this led me to joining the Facebook group “Rethinking AIDS”. Eventually, I decided to become a vocal speaker for the denialists because I believed at the time that their information was genuine and I wanted to do the best I could to spread this information in the hopes of helping other people.
During my time with them I was advised not to speak to certain people from the “orthodox side” because they’re all lying shills and sociopaths or not take seriously scientific information on HIV because according to the denialists it’s all propaganda from the “AIDS establishment”. Once I lifted my confirmation bias and decided to disassociate myself from Rethinking AIDS and denialism in general, it caused a wave of attacks, anger, disbelief and insults with some members even alluding to the fact that I was the leader of Rethinking AIDS at the time. Of course I wasn’t and I always reminded them that I was and independent even if I was supporting their point of view regarding HIV/AIDS. You can say I was very involved with the movement; I spoke on radio shows about denialism, filmed my own youtube videos, wrote my own articles about denialism and attempted to inform every person I could about the denialist information.
TS: You mentioned the notorious HIV denialism documentary “House of Numbers” in your blog post. What did you find so compelling about that movie?
JS: The most famous denialist documentary happens to be “House of Numbers” and denialists recommend the viewing of this film to everyone they speak to because according to them, this documentary and others like it prove their allegations that HIV is a scientific fraud. It does so by attempting to show people how HIV tests are unreliable, HIV has never been isolated, HIV drugs are the cause of peoples’ illness and death, etc. I can honestly say I believed the same until I viewed the youtube series “Debunking the AIDS Denialist Movie House of Numbers” by Myles Power. His series deconstructs “House of Numbers” to show you that the film is nothing more than a biased piece of denialist propaganda. I was aware of Myles’ series when I was still a denialist and never took it seriously because for me and others, his series was nothing other than propaganda from the “AIDS establishment”. Once I disassociated from denialism and lifted my confirmation bias, I decided to give Myles’ videos another watch and this time I could see clearly how deceptive the movie “House of Numbers” is. The film contains interviews with scientists that have been edited in such a way to make people believe these scientists support the idea that HIV is a fraud, when in reality many of their statements were taken out of context and some have even released statements to clarify their real position on HIV/AIDS. People to this day are being misled into believing “House of Numbers” is proof that HIV is a fraud, when in reality it’s a cleverly designed tool of denialist propaganda.
TS: What caused you to modify your stance?
JS: During the last year with the denialists, Jessica and I had a son who was born negative for HIV because my she and my child received the appropriate treatment to avoid vertical transmission. I was still entrenched in denialism during the birth of my son and was not too happy about the doctors wanting to give AZT to my wife and newborn child but decided to do so for two reasons. The main reason was the worry that the authorities would force treatment on my son but the second reason was a thought that crossed my mind: What if I was wrong? We opted for the treatment and hoped for the best and although everything worked out fine for us; the denialists chastised us for our decision. The final blow which led to my disassociation from denialism was when months after our son’s birth, my wife Jessica fell ill with pneumocystis pneumonia again; this time so severe she almost died. Jessica restarted treatment after falling ill the first time in 2011 but only stayed on treatment until we joined the denialists; we both stopped treatment during our time with them because as they preach, we believed the medications were toxic poisons and the real cause of AIDS. Something was definitely not right here and I decided to end my time as and HIV/AIDS denialist. Fortunately Jessica recovered and we are back on treatment but this choice and our disassociation from denialism caused us to be attacked, insulted, unfriended on Facebook by many people I was associated with; something akin to being thrown out of a cult, actually.
TS: What has been the response you’ve gotten from the denialist community? How have you and your wife handled it?
JS: As I previously mentioned, we were attacked, insulted and even my son was brought into the filth they spewed against us. The president of the group “Rethinking AIDS”, David Crowe, accused me of selling my soul to the devil, many others continued to harass me and even told me that our decision to get back on treatment will result in the death of my whole family. My wife and I have pretty thick skins and while she ignores them and is happy she is doing better now, I use my knowledge to help other people avoid the same trap we fell into in the hopes that perhaps I can do some real good this time and avoid people’s suffering because they were fed and believed incorrect medical information. The best example I can make of how we were treated by the denialist community after our disassociation would be how a member of Scientology is treated once he or she decides to abandon the church. To the denialists we are nothing more than human garbage. I was called a shill and a sellout, and they accuse me of leading people to the death camps because today I promote HIV/AIDS awareness instead of pseudoscientific nonsense. The denialists in my eyes are a cult; too bad I did not see this before becoming entrenched into their dogma and becoming a voice for their agenda.
TS: How do you feel others can avoid being miseld (potentially dangerously so) by the denial movement?
JS: In the past, censorship of denialist information was the norm; pretend it doesn’t exist and hope nobody will notice. I believe that people should be informed about the dangers of eschewing necessary treatment for HIV and what can possibly happen to them if they do. I have people writing to me daily asking for help or wanting to hear my story because they got involved in denialism and are falling ill but don’t know what to do. Although I cannot and do not offer medical advice, I share my story in the hopes that they make the best choice for themselves. It’s great to also hear one of these same people write to me again down the road to thank me because their health has improved after returning on or starting treatment. Articles such as this one and many others exposing the denialist agenda are a great help and I will continue to do my part to make sure people understand the risks they are taking when getting involved with HIV/AIDS denialism. Giving people the correct information regarding HIV/AIDS, how today it is no longer a death sentence and that on treatment they should expect to live a long and healthy life comparable to a person not living with HIV is also very helpful. For now me and a few others are the only voices speaking against denialism but there should be more. In some countries it’s illegal to disseminate incorrect medical information and I believe such a law could prove to be of some benefit in this country as well. The article entitled “Can You Inoculate Against Science Denial?” is a great read and explains very well what we are facing today and how to approach this issue.
TS: What message would you pass on to others who are newly diagnosed?
JS: If you’re newly diagnosed, the treatments today can keep you healthy and living a long life comparable to a person not living with HIV and there are many people and organizations that can offer you support; you are not alone. Remember, HIV doesn’t define you, you define HIV. Being newly diagnosed is a life changing experience, but it doesn’t have to be a bad experience. By getting tested and getting into treatment, you are taking control of your health. Become informed as much as you can about HIV. Ask your doctor questions, research, reach out to support groups and if you happen to stumble upon the denialist information, make sure you know what you’re possibly getting yourself into before jumping on the bandwagon. If anyone newly diagnosed is reading this and would like to contact me for information or support, feel free to reach out.
Now another “Frontiers In” journal has stepped in it, publishing a paper that has the anti-vaccine groupies frothing at the mouth. Published in Frontiers in Neurology this time, the paper, “Biopersistence and brain translocation of aluminum adjuvants of vaccines,” is another review article using cherry-picked data to suggest that aluminum in vaccines accumulates in the brain and nervous system, causing “toxic effects.”
The editor of this paper is Lucija Tomljenovic of the University of British Columbia. Tomljenovic is a biochemist who has made a career, with her advisor Chris Shaw, of publishing commentary suggesting that vaccines, and particularly the HPV vaccine and vaccine adjuvants, are unsafe. It probably will not shock readers that Shaw and Tomljenovic are funded in part by the The Dwoskin Family Foundation and the Katlyn Fox Foundation, both of which are big players in the anti-vaccine community (see this post at Harpocrates Speaks for more background info on those foundations). Both appeared at the 2011 Vaccine Safety Conference, with other notable vaccine foes including the NVIC’s Barbara Loe Fisher and Lawrence Palevsky, a doctor who appeared in the anti-vaccine movie “The Greater Good” and apparently spoke on the topic, “Rethinking the Germ Theory.” That should speak volumes about the scientific validity of the movement. Meanwhile, Shaw specifically notes in his bio, “He has two children. The youngest has not been vaccinated.”
Who else appeared at that meeting? The first author of the current paper, Romain K. Gherardi.
Others have alreadyposted stingingcritiques of Shaw and Tomljenovic’s previous papers (even the World Health Organization has criticized them), so I won’t go further into the science–suffice it to say, Shaw & Tomljenovic are cited widely within the review, and several other important citations are self-citations of the first author, Gherardi. It should be noted that Gherardi also receives funding from the Dwoskin Foundation. Further, Tomljenovic served not only as the paper’s editor, but also as a reviewer–and the Frontiers In journals as a whole have a crazy-high acceptance rate of 80-90% in the first place. Another reviewer, Mark Burns, is on FN’s editorial board.
So while the anti-vaccine brigade will count this publication as a victory, it’s really just another case of a poor paper being published in a shoddy journal, shepherded to publication by a like-minded editor–and you could certainly at least argue there was a conflict of interest here, with both Gherardi and Tomljenovic funded by the Dwoskins and running in the same small anti-vaccine circles. Not that it matters to those who will gleefully cite this publication, of course. The only time they really want to “follow the money” or pay attention to such matters is when the money is coming from “Big Pharma” or the government or other such boogeymen in order to allege some kind of conspiracy. Too bad they don’t hold all publications up to such lofty standards, or recognize conspiracy when it’s actually in their own backyard.
I’ve been working on livestock-associated Staphylococcus aureus and farming now for almost a decade. In that time, work from my lab has shown that, first, the “livestock-associated” strain of methicillin-resistant S. aureus (MRSA) that was found originally in Europe and then in Canada, ST398, is in the United States in pigs and farmers; that it’s present here in raw meatproducts; that “LA” S. aureus can be found not only in the agriculture-intensive Midwest, but also in tiny pig states like Connecticut. With collaborators, we’ve also shown that ST398 can be found in unexpected places, like Manhattan, and that the ST398 strain appears to have originated as a “human” type of S. aureuswhich subsequently was transmitted to and evolved in pigs, obtaining additional antibiotic-resistance genes while losing some genes that help the bacterium adapt to its human host. We also found a “human” type of S. aureus, ST5, way more commonly than expected in pigs originating in central Iowa, suggesting that the evolution of S. aureus in livestock is ongoing, and is more complicated than just ST398 = “livestock” Staph.
However, with all of this research, there’s been a big missing link that I repeatedly get asked about: what about actual, symptomatic infections in people? How often do S. aureus that farmers might encounter on the farm make them ill? We tried to address this in a retrospective survey we published previously, but that research suffered from all the problems that retrospective surveys do–recall bias, low response rate, and the possibility that those who responded did so *because* they had more experience with S. aureus infections, thus making the question more important to them. Plus, because it was asking about the past, we had no way to know that, even if they did report a prior infection, if it was due to ST398 or another type of S. aureus.
So, in 2011, we started a prospective study that was just published in Clinical Infectious Diseases, enrolling over 1,300 rural Iowans (mostly farmers of some type, though we did include individuals with no farming exposures as well, and spouses and children of farmers) and testing them at enrollment for S. aureus colonization in the nose or throat. Like previous studies done by our group andothers in the US, we found that pig farmers were more likely to be carrying S. aureus that were resistant to multiple antibiotics, and especially to tetracycline–a common antibiotic used while raising pigs. Surprisingly, we didn’t find any difference in MRSA colonization among groups, but that’s likely because we enrolled relatively small-scale farmers, rather than workers in concentrated animal feeding operations (CAFOs) like we had examined in prior research, who are exposed to many more animals living in more crowded conditions (and possibly receiving more antibiotics).
What was unique about this study, besides its large size, was that we then followed participants for 18 months to examine development of S. aureus infections. Participants sent us a monthly questionnaire telling us that they had a possible Staph infection or not; describing the infection if there was one, including physician diagnosis and treatment; and when possible, sending us a sample of the infected area for bacterial isolation and typing. Over the course of the study, which followed people for over 15,ooo “person-months” in epi-speak, 67 of our participants reported developing over 100 skin and soft tissue infections. Some of them were “possibly” S. aureus–sometimes they didn’t go to the doctor, but they had a skin infection that matched the handout we had given them that gave pictures of what Staph infections commonly look like. Other times they were cellulitis, which often can’t be definitively confirmed as caused by S. aureus without more invasive tests. Forty-two of the infections were confirmed by a physician, or at the lab as S. aureus due to a swab sent by the patient.
Of the swabs we received that were positive, 3/10 were found to be ST398 strains–and all of those were in individuals who had contact with livestock. A fourth individual who also had contact with pigs and cows had an ST15 infection. Individuals lacking livestock contact had infections with more typical “human” strains, such as ST8 and ST5 (usually described as “community-associated” and “hospital-associated” types of Staph). So yes, ST398 is causing infections in farmers in the US–and very likely, these are flying under the radar, because 1) farmers really, really don’t like to go to the doctor unless they’re practically on their deathbed, and 2) even if they do, and even if the physician diagnoses and cultures S. aureus (which is not incredibly common–many diagnoses are made on appearance alone), there are very limited programs in rural areas to routinely type S. aureus. Even in Iowa, where invasive S. aureus infections were previously state-reportable, we know that fewer than half of the samples even from these infections ever made it to the State lab for testing–and for skin infections? Not even evaluated.
As warnings are sounded all over the world about the looming problem of antibiotic resistance, we need to rein in the denial of antibiotic resistance in the food/meat industry. Some positive steps are being made–just the other day, Tyson foods announced they plan to eliminate human-use antibiotics in their chicken, and places like McDonald’s and Chipotle are using antibiotic-free chicken and/or other meat products in response to consumer demand. However, pork and beef still remain more stubborn when it comes to antibiotic use on farms, despite a recent study showing that resistant bacteria generated on cattle feed yards can transmit via the air, and studies by my group and others demonstrating that people who live in proximity to CAFOs or areas where swine waste is deposited are more likely to have MRSA colonization and/or infections–even if it’s with the “human” types of S. aureus. The cat is already out of the bag, the genie is out of the bottle, whatever image or metaphor you prefer–we need to increase surveillance to detect and mitigate these issues, better integrate rural hospitals and clinics into our surveillance nets, and work on mitigation of resistance development and on new solutions for treatment cohesively and with all stakeholders at the table. I don’t think that’s too much to ask, given the stakes.
Because of the anti-science views she has expressed, and their chance to do real harm, I’ve noted previously that I’m very uncomfortable with Bialik being used as any kind of an ambassador for science and STEM education. And of course, anti-vaccine advocates have seized on her education and anti-vaccine stance as proof of their own correctness:
i would like to dispel the rumors about my stance on vaccines. i am not anti-vaccine. my children are vaccinated. there has been so much hysteria and anger about this issue and i hope this clears things up as far as my part.
…which is great, from my point of view. I’d really like to see Bialik advocate for vaccines, as she is firmly in the “crunchy” camp that all too often have a reputation as eschewing vaccines.
So did she really change her mind and her stance? If so, why? Or is she just jumping on the “I’m not anti-vaccine” bandwagon like Jenny McCarthy and others who claim not to be anti-vaccine, but at the same time spew vaccine fear and misinformation? Are her kids fully vaccinated, or did they only have the ones she mentioned previously (such as polio for international travel)? Is she walking back statements that are basically anti-vaccine talking points, and removing her support of anti-vaccine doctors like Bob Sears and Lauren Feder (or her own pediatrician, Jay Gordon)?
I really hope so. But I won’t hold my breath, and take her statements that she’s “not anti-vaccine” with a big grain of salt. After all, that statement, itself, is often an anti-vaccine talking point.
Measles has come to the happiest place on Earth. As of this writing, a total of 32 cases of measles have been linked to Disneyland visits that took place between December 17th and 20th. About 75% of the cases identified to date were not vaccinated, either because they chose to forgo vaccines or because they were too young, and at least 6 have been hospitalized.
A measles outbreak is a public health disaster, which can cost into the millions of dollars in health resources. You can be sure that public health workers in California and beyond are working overtime trying to identify cases, educate those who were possibly exposed about how dangerous measles can be, and implement practices so that those who may have been exposed to measles don’t further put others at risk. This includes avoiding public places, and practices such as calling ahead to a doctor’s offices so possible cases can be ushered into private rooms rather than languishing in the waiting room. A clinic in La Mesa recently closed because of a potential measles exposure. An unvaccinated South Pasadena woman, Ylsa Tellez, received a quarantine order after her younger sister was diagnosed with measles. Tellez is fighting the order and “taking immune-boosting supplements” instead.
Why such extreme measures on the part of public health?
Measles is highly contagious. It’s spread by air, and so contagious that if an infected person enters a room, leaves, and an unvaccinated person enters the room hours later, they still can contract measles. Remember a few months back, when that figure was circulating showing that Ebola wasn’t particularly easy to spread? Well, measles very much is. The basic reproductive rate for Ebola is around 2, meaning on average each infected person will cause an additional 2 infections in susceptible individuals.
And what’s the reproductive number for measles?
Eighteen. Eight. Teen. I’m not exaggerating when I say that it is literally one of the most contagious diseases we know of. On average, if you have 10 susceptible individuals exposed to a measles patient, 9 will end up getting sick.
How do we break the cycle of transmission? Vaccination is one way–if one has been vaccinated for measles, chances are very low (but not zero, because nothing is perfect) that they will contract measles. Beyond vaccination, the next-best intervention is to keep those who are infected away from everyone else. The way we do this is by quarantining them.
In public health terms, quarantine specifically refers to the separation of individuals who have been exposed to an infectious agent, *but are not yet ill themselves,* from the rest of society. That way, they’re unable to spread the infection to others. Quarantine makes the most sense when individuals can transmit the infection before they realize they’re sick, which is exactly the case with measles. Infected individuals can spread the virus fully 4 days before the characteristic rash starts to appear, and continue to spread it for another 4 or so days after the rash begins—potentially infecting a lot of people. The problem is, like Ylsa Tellez, they’ll feel fine while they’re out there in the general population. They don’t even have to be coughing or sneezing to spread it (symptoms which can appear prior to the rash)—they can just be breathing (something many of us like to do on a regular basis), and still contaminate their environment with the measles virus.
The difference in transmissibility also makes measles a very different situation from Ebola. Public health officials almost universally condemned quarantine for Ebola exposures, for two reasons: 1) Ebola wasn’t highly transmissible, and isn’t airborne like measles is; and 2) because Ebola isn’t efficiently transmitted until late in the infection when the patient is very ill and likely bedridden. Quarantining Ebola patients was a political stunt, not a public health necessity.
This is why states have the legal authority to enforce quarantine for infectious diseases: it reduces the risk that asymptomatic, potential disease-spreaders will act as “Typhoid Marys” (another asymptomatic, deadly-disease-spreader), which is in the public interest. And while unvaccinated Tellez feels “attacked” and her mother thinks people are being “not nice” when they demand that Tellez submit to quarantine, their choice not to vaccinate has already put many others at risk of disease and, and is resulting in the quarantine of many other exposed individuals as well. In the 2011 Utah measles outbreak, 184 were quarantined and thousands of contacts traced, at an expense of approximately $300,000. The Disneyland outbreak has already spread into 4 states (California, Utah, Washington, and Colorado). Quarantine is one of our tools to stem the epidemic. In our recent outbreak among Ohio Amish, most willingly submitted to quarantine, and over 10,000 doses of the MMR vaccine were administered. Quarantine is undoubtedly a difficult prospect to face, but perhaps if Tellez and others had been vaccinated in the first place, they, and we, wouldn’t be in this situation.
I’ve been asked several times about this NY Post article on the CDC’s “admission” that a sneeze could spread Ebola. The Post (which, I should note, is the least credible newspaper in New York City, for those not familiar with the paper) suggests that the CDC has changed their tune regarding the spread of Ebola.
Except, they haven’t, and this is a ridiculous, trumped-up non-story, passed along not only by the Post but by others of the typical suspects like conspiracy theorist extraordinaire Mike Adams, aka “The Health Ranger” of Natural News.
Here’s what the NY Post claims:
“Droplet spread happens when germs traveling inside droplets that are coughed or sneezed from a sick person enter the eyes, nose or mouth of another person,” the poster states.
Nass slammed the contradiction.
“The CDC said it doesn’t spread at all by air, then Friday they came out with this poster,” she said. “They admit that these particles or droplets may land on objects such as doorknobs and that Ebola can be transmitted that way.”
Of course, no poster is linked in their article, so I feel like I’m playing a game of telephone, trying to figure out just what has been added.
The NY Post article is basically messing up the definition of “airborne,” as Iand othershave discussed ad nauseum. The kind of contact the NY Post describes above isn’t “airborne,” as measles or chickenpox are, where one can come into a space that had been occupied by an infected person, breathe in the suspended virus, and get ill. With Ebola, you have to have *direct contact* with a person’s secretions. So their entire story (not surprisingly, due to their tabloid-y nature) is based on either a purposeful or accidental incorrect definition of just what it means to be “airborne.”
Adams takes it one step further, suggesting that CDC not only misinformed, but revised history; that a poster was “scrubbed” from CDC’s site because it supported “airborne” transmission.
From what I can tell, Adams claims this poster (which he saved) was removed from the CDC site, and replaced by this file. Adams claims that the latter is “entirely empty,” so he may have tried the link before it went live? I have no idea. In any case, the two documents are almost identical in content. Both note that droplet spread can happen, when “germs traveling inside droplets that are coughed or sneezed from a sick person enter the eyes, nose, or mouth of another person” in the first poster, and “droplets that are coughed or sneezed from a sick person splash the eyes, nose, or mouth of another person” in the second poster.
Wow, that’s a sinister difference there.
You can see that both documents still show a picture of doorknobs as possible fomites for transmission (possible in theory, but they’d have to be heavily contaminated by a person late in the disease). It appears that CDC just did a minor redesign of the poster, with the first having an emphasis just on Ebola and the second version trying to be more of an explainer on “air vs. droplet spread,” with Ebola as the example. The content is almost exactly the same: the first portion defines “airborne” spread; the second “droplet” spread; the third focuses on how one protects oneself from getting sick; and the final one clarifies that Ebola is not spread by air, but it could be by droplets. There are minor wording changes as I noted above, but that’s it.
This is nothing new. There’s never been a conspiracy to suggest that droplet transmission can’t happen–but the CDC and others have tried to emphasize that droplet transmission is still direct contact. That’s what people like Adams don’t want to accept. They assume because those droplets travel via air, it’s “airborne,” taking a layman term instead of one accepted and used by the scientific community. Now, given, I understand this can be a source of confusion as scientific terms frequently are. Virologist Ian Mackay has even solicited ideas for other terms to describe such transmission, and make it more clear to the general public what the difference is. But either way, the usage has been clear from the beginning and I guarantee Adams understands the difference. He just doesn’t care.
And now I just spent a half hour of my life to uncover that vast governmental conspiracy-that-wasn’t. Not that it will stop Adams or the NY Post from misinforming and driving fear of the virus and distrust of the government, because *that’s what they do.* Adams is making a pretty penny, I’m sure, off of his absurd Pandemic Prevention kits (only $99 or $199! Bargain!). Perhaps I should get into a different and more lucrative business, because if you believe shtick from Adams or the Post over the CDC or, hey, a trained epidemiologist like myself, I just may have a shiny bridge to sell you.
My Great-Grandpa and Granny Beck were, in some ways, ahead of their time. My Grandpa’s mom and step-dad, they both went through scandalous divorces and then switched partners with another couple, Granny Orpha marrying Wade and my Grandpa’s dad Lee marrying Wade’s ex-wife, Edna. Orpha and Wade raised 5 of Orpha’s boys together, and had a daughter after the divorce/remarriage.
By the time I was born, my Granny Beck was in her 80s, and I have only vague recollections of going over to visit her at her home. But I remember hearing about her cooking. I was a picky eater anyway, and my mom once told me she was always afraid to eat Granny Beck’s stew, because it could be rabbit, it could be ‘possum, it could be squirrel, it could be groundhog…you just never knew. I never ate anything over there.
Grandpa Beck used to have coon dogs, and would bring home anything that the dogs would catch. My great-aunt affirmed my mom’s recollection of Granny Beck’s cooking (and Grandpa Beck’s eating):
My mom did cook some pretty weird things. We always had wild game such as rabbit and pheasant, but I do remember when she cooked a raccoon (I didn’t try it!). My dad was the one that would eat anything, and I do mean anything! We used to bring him such things as chocolate covered ants, pickled pigs feet, and pickled rooster combs. He loved them!
Over the weekend, my neighbor sent along some meat packages for us. He had recently gotten back from another hunt and bagged his third deer of the season (you’re allowed four per year in my county). He was grilling when my partner stopped over on the way home, and sent some ground deer (I think–I’ve not opened the package yet), deer steaks, and a still-warm hunk of a deer heart, well done.
All of this is to say that we can eat some really weird things here in the “civilized,” first-world, developed United States.
Why bring this up now? The current Ebola outbreak has brought out all kinds of biased to outright racist views of Africa and disease. Because it’s postulated that the outbreak started with the consumption of or contact with an infected animal—possibly a fruit bat, which the index family noted they do hunt—people have come out of the woodwork to pontificate on how those in Guinea and other countries “brought this on themselves” because of their consumption of “bushmeat,” and that they’re so uneducated and backwards to eat that in the first place–because really, how could people eat that stuff, especially when it could be diseased?
“Is it time that we drag ignorant, superstitious third world Africans kicking and screaming into the 21st century or should we stop giving aid to Africa and let them fend for themselves? Would the later propel the former?”
Even though we do the same. damn. thing. in the United States.
“Bushmeat” is the name given to pretty much any kind of wild game hunted in Africa–bats (obviously a concern given their possible role in Ebola spread and maintenance of the virus); primates; birds, duikers, lizards, crocodile, various rodents, even elephant, and more.
What do we call “bushmeat” in the US? Or just about everywhere else?
Just “wild game,” or some variation thereof.
In the U.S., we hunt thousands of deer, elk, pheasant, turkey, rabbit, and other animals every year. There are even wild game restaurants that cater to those tastes (though many “wild game” species are actually farmed to some degree). Yet even the bushmeat page at United States’ Fish and Wildlife Service ignores the hunting that goes on in the United States, noting that:
Here in the United States, we have laws that control the preparation, consumption, and trade of meat, ensuring that animals are treated appropriately, kept healthy, and sold legally. This is not the case in some countries in Africa and other parts of the world.
This seems to refer mostly to domestically-raised meats, as it’s much harder to police the treatment, health, and sale of hunted animals. Though one needs a license to hunt many animals and generally to fish, laws vary from state to state. Here in Ohio, though a hunting license or permit needs to be obtained for most types of hunting or trapping, and there may be limits on the number of animals of certain species one can kill per season (such as deer and turkey), for most animals, there’s merely a daily limit (6 squirrels, 4 rabbits, etc. per day). For other animals, including fox, raccoon, skunk, opossum, weasel, crow, groundhog, and coyote, there is no daily bag limit. So one could, conceivably, feed themselves fairly well on just a diet of wild game if they had the time and inclination to do so.
Of course, most people in the U.S. don’t get our food this way. We look at Daryl Dixon of the Walking Dead and his squirrel-hunting prowess as something that could carry one through the zombie apocalypse, but not school lunches for a family of 4. We think it’s awesome when he finds an opossum in a cupboard and proclaims, “Dinner!” I’m sure many readers have plans for their own apocalypse survival plan, which likely involve some kind of wild source for food.
But in modern-day Africa, such hunting is somehow “barbaric” and “backward,” regardless of whether it is for sustenance or trade.
Though Ebola has not been identified in wild animals in the US, our animals are far from disease-free. No wild (or domesticated) animal is. We certainly can find Tularemia and Pasturella in rabbits; deer can carry tuberculosis, Brucella, Hepatitis E, and maintain transmission of Lyme disease and potentially Erlichia. Other zoonotic pathogens that could be acquired from a variety of wild animals include Campylobacter, E. coli, plague (mainly in the Southwestern United States); Cryptosporidia, Giardia, avian influenza from waterfowl, rabies (more likely from handling than ingestion); hantavirus, Trichinella, Leptospira, Salmonella, Histoplasma, and I’m sure many more from handling or consumption of wild animals.
So perhaps rather than looking to countries in Africa and judging their food consumption habits as they relate to infection, we should turn a mirror to our own. If we don’t judge Granny Beck for her wild game consumption, neither should we judge those a continent away.