Movin’…

As several others have already noted, after almost 12 years, Scienceblogs is shutting down at month’s end. Though I’ve done most of my writing elsewhere over the last few years, I’d certainly like to keep the archives of this blog up somewhere, and maintain it as a place to post random musings that don’t fit anywhere else. But admittedly, the primary thing that has kept me here has been inertia–moving is just so hard, y’all. So throwing this out there to anyone who would like to assist in a move. I have a domain and so can set up another WordPress blog elsewhere and export/import the contents, but when Scienceblogs initially moved to WordPress it was…not smooth, and that was with a professional. Which I am not, at least in this area. If anyone with experience wants to help me out (yes, paid), please leave a comment or drop me a line.

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.

 

BLS4 entry/exit procedures

The first person to enter the lab in the morning, has to complete a check of all equipment that makes the lab operational. There is a checklist and you go through all floors of the facility and document the status of every piece of equipment and levels on every pressure gauge. Then you do a visual inspection by walking around the lab in what’s called the buffer corridor.

While in the buffer corridor you can look through windows into the lab to make sure all status lights are green etc. Once you’ve documented that everything on the list is as it should be, then you sign it and enter it into a binder in what is basically the antechamber of the facility.

After that you can enter the lab, which has its own set of protocols. If you’re not the first one in that day, you check the binder to make sure the checklist was done and the lab is operating normally. Then you need to go through the buffer corridor and look through the windows to see if anyone who is already in there needs anything. There are dry erase boards leaning against the buffer corridor walls by each window, as well as inside the lab, so you can communicate that way. If someone needs something, it’s not too late for you to go get it and bring it in with you.

The next step is to get generic coveralls, socks, and a bath towel from a shelf in the buffer corridor. You take those into a locker room. Each door you enter has special security measures. Once in the locker room, you flip a switch that turns a light on on the outside of the room, so anyone in the buffer corridor can see the light and know that someone is in there. The light also indicates if you’re male or female so that no one of the opposite sex comes in uninvited.

In the locker room you get naked, put your clothes in your locker, and then put on the coveralls and socks. Then you grab your shower supplies from your locker and head into the personal shower. Entry into, and exit from, the BSL4 suit-change room is only through the personal shower, which also has special security measures. So you enter the shower, set your shower supplies down and then exit the shower (without showering) into the suit-change room – the place where you don the BSL4 suit. Sometimes there are a few people in the suit-change room. Coordinating entrance with others can save time for everyone.

So, in the suit-change room you put on a hair cap and nitrile gloves. Then you get your suit off the hanger and examine the seams and valves and look for obvious holes, tears or any signs of compromised integrity. Every so often you are required to also test the suit by sealing the exhaust valves, connecting to an air hose and filling with air. Then you spray the suit with a soap mixture that will form bubbles if there is any air leak. This test, while important, can’t be done every time you wear the suit because being filled with air stresses the seams. So it’s a balance.

Once the suit is ready to go, you put earplugs in, connect the air hose and put it on. Entrance to, and exit from, the actual BSL4 lab is through a chemical shower, so you disconnect the air hose and access the chemical shower. You are not showered on the way in, you just move to the other side of the shower and move through the door into the lab. Each of these doors takes some time to open due to pressure differences between the rooms.

By the time you get into the BSL4 lab, you usually don’t waste too much time getting connected to an air hose. Once in, you do what you went there to do. When you leave, you do the whole process in reverse and at each shower you actually shower. The chemical shower is several minutes of a detergent/disinfectant shower, so you connect to an air hose for the duration.

While showering you use large scrub brushes to scrub your suit. You also have to dip your gloved hands and booted feet into a large container of the same disinfectant. Then the shower switches to a water rinse and you do your best to rinse all the disinfectant off of the suit. Once done, you disconnect the air hose and exit the shower. No one can enter or exit the lab while the shower is running, so scheduling is critical.

After the shower you remove the suit and dry it off, then you remove your nitrile gloves and hair cap and put them in the trash. Then you move to a private area outside the personal shower and remove the coveralls and socks and they go into a designated bag to be autoclaved later. Then you walk naked into the personal shower, where you are required to use soap on everything and shampoo your hair. Before leaving the personal shower you have to clean it with disinfectant and a mop/squeegee to help dry the floor so the next person walking through isn’t grossed out. Then you exit into the locker room to dry and get dressed so you can exit.

Treatment of Chronic Otitis Media: Guidelines versus Practice

First of five student guest posts by Kristen Coleman

Every morning as I prepare for class, I go through the same internal dialogue, “to wear or not to wear my hearing aide.” I am forced to do this because when I was a child I, like most American children (about 80% by age 3 as estimated by the American Academy of Family Practitioners, AAFP), suffered from otitis media and my treatment resulted in hearing loss. The treatment I underwent was called tympanostomy with ventilation tube insertion, which has rapidly become the most common reason for general anesthesia in children in the United States. However, the AAFP reports that meta-analysis of studies exploring the effectiveness of this procedure indicate that benefit is only marginal at best. So why is it that our children are being exposed to this potentially quality of life altering procedure, if there is little benefit? In order to explore the reasons, we must delve further into the disease in question.

Previously, it had been commonly thought that chronic otitis media was characterized by a virus-laden sterile effusion behind the ear drum; meaning that bacteria were not thought to be present and thus, antibiotic therapy was not indicated. Now we know that chronic otitis media is most commonly due to infection of the middle ear by Streptococcus pneumoniae, Haemophilus influenza, Moraxella catarrhalis, (all of which are bacteria) or respiratory viruses. The organisms contribute to the buildup of fluid and pus behind the ear drum that is characteristic of this disease. Dr. Kim Stol and collaborators have reported findings that demonstrate that immune inflammatory response, measured through the presence of immune mediators called cytokines, may play a role in the damage to the ear during bacterial infection that commonly results in hearing loss or diminishment. As demonstrated by the research of Dr. Lusk of the University of Iowa, this immune-mediated damage can persist even after surgical intervention if bacteria persist in the middle ear, making medical management of the bacteria through antibiotic therapy even more essential.

Due to this evidence, the AAFP and other leading organizations that publish guidelines for treatment recommend antibiotic therapy as the gold standard of care for children suffering from chronic otitis media. These guidelines indicate rigorous treatment with high doses of antibiotics such as amoxicillin/clavulanate, cephalosporins and macrolides. If these antibiotics do not offer relief, clindamycin and tympanocentesis (removal of fluid from behind the ear drum with a needle) are then warranted. It is only when all of these medical treatments fail that tympanostomy tubes may be an appropriate option. However, it has been reported by researchers at Mount Sinai School of Medicine in New York City that of the 682 children who received tympanostomy tubes as treatment for chronic otitis media in their study in 2002, only 7.5% did so in accordance to the guidelines set forth by these organizations, and that most of these operations occurred before adequate attempts at antibiotic management of the disease could be utilized. In the study performed by Dr. Stol, it was reported that of the 116 participants in the study who were suffering from chronic otitis media, only 6.9% had received a recent antibiotic prescription, despite the fact that 53% of these patients were suffering from a bacterial form of the disease that may have responded favorably to antibiotic therapy.

As for me and my story, I had an initial round of ventilation tubes places in my ear drums when I was 6 years old, along with an adenoidectomy which was thought to help diminish my ear infections. My family was told that my disease was due to a virus and I was not prescribed any antibiotics prior to my surgical procedure. These tubes fell out the next year, and my chronic otitis media still had not resolved. More permanent tubes were placed in my ears at age 8 and these became lodged in my ear drums until college, all the while I suffered from chronic fluid and pain in my ears. When I had the tubes removed at age 19, my ear drums were permanently scarred and I had to undergo a bilateral tympanoplasty in which a surgeon tried to patch the holes in my ear drums, to no avail. All of this resulted in me having to wear a hearing aide in order to hear adequately at the age of 28.

As the report from Mount Sinai Medical School indicates, the discrepancy between practice and guidelines, as well as the overuse of surgical management in lieu of less-invasive medical management cannot be in the best interest of the children suffering from this disease, and steps need to be taken in order to educate physicians and families alike as to the most appropriate steps for treatment of this chronic disease in order to save our children from having stories like mine.

References:

1. Stol, Kim et al. Inflammation in the Middle Ear of Children with Recurrent or Chronic Otitis Media is Associated with Bacterial Load. The Pediatric Infectious Disease Journal. Volume 31, Number 11, pages 1128-1134. November 2012.

2. Lusk, Rodney P. et al. Medical Management of Chronic Suppurative Otitis Media Without Cholesteatoma in Children. Layngoscope: February 1986.

3. Keyhani, et al. Overuse of tympanostomy tubes in New York metropolitan area: evidence from five hospital cohort. Mount Sinai Medical School. BMJ: 2008.

4. American Association of Family Practitioners. www.aafp.org/afp/2007/1201/p1650.html

Going out with a Bangs: Control of Human Brucellosis by means of an Animal Vaccine

This is the thirteenth of 16 student posts, guest-authored by Jessica Ludvik. 

One Disease, Many Species

Brucellosis, more commonly known as undulant fever in humans or bangs disease in cattle, is one of the oldest bacterial scourges of livestock-producing nations, especially those in which the animals live in close proximity with the human population.  The disease is caused by bacteria of the genus Brucella.  Within this category are many species of bacteria, each almost exclusive to a particular animal species.  A few of the most common seen in veterinary and human medicine today are listed in Table 1.  Of these, all but B. ovis has been shown to be transmissible to humans [1].

Why Should I care about Brucellosis?

            The presence of Brucellosis in a region is catastrophic to the economy and animal and human health.  In many livestock species, the bacteria elicits its major effects on the reproductive system, leading to late term abortions and stillbirths in females, weak newborns leading to death soon after birth, and inflammation of the testicles and testicular abscesses in males [2].  Abortion storms of 30-80% have been documented in cattle herds infected by B. abortus [2].  B. abortus and B. melitensis are the most common of the strains associated with human infection, and the World Health Organization (WHO) estimates that 500,000 new cases of human cases of human Brucellosis occur annually, making it the most common zoonotic disease in the world [3].  Its importance has earned it a spot on the Center for Disease Control’s (CDC) 2012 list of Nationally Notifiable Conditions.  To view this list visit the CDC’s website at http://www.cdc.gov/osels/ph_surveillance/nndss/phs/infdis.htm.

Symptoms include fever, profuse sweating, headache, fatigue, depression, loss of appetite, irritability, cough, chest pain, and upset stomach [1].  It can also affect bones and joints causing arthritis [1].  If untreated, symptoms may recur after a latent period of many years [1].  For the official case definition, click http://www.cdc.gov/osels/ph_surveillance/nndss/casedef/brucellosis_current.htm. 

What’s the Risk?

            Most human cases of Brucellosis are a result of occupational exposure to the bacteria [2].  It can penetrate mucus membranes of the digestive or respiratory tract, or can enter through skin wounds or abrasion after contact with reproductive fluids, aborted fetus or placenta, or aerosolized particles from the aforementioned [2].  Brucellosis can also be contracted by people via accidental injection with the cattle vaccine or by ingestion of unpasteurized dairy products of infected animals [2].

Most people diagnosed with Brucellosis recover fully with treatment, which usually consists of a six to eight week antibiotic regimen [4].  Less than 2% of untreated individuals die, however chronic complications such as endocarditis and meningitis may occur [2].

On the Global Scale….

Figure 1: Worldwide incidence of human Brucellosis [5] Click to enlarge.

As the major mode of human infection is through direct contact with infected animals otr through the consumption of products from those animals, the most logical means of disease prevention in the human population has been through the prevention of the disease in animals.  Many developed regions such as North America, Australia, and Northern Europe have dramatically reduced the prevalence of brucellosis in livestock through widespread vaccination efforts [5].  The United States Department of Agriculture (USDA) implemented an eradication program in 1934, which involved the testing and identification of diseased animals, slaughter of infected animals, and trace back and investigation of their herds of origin [2].  In 1951, Animal Plant Health Inspection Services (APHIS) made compliance of all states mandatory [2].   Currently, RB51 vaccine is the standard in cattle and Rev-1 vaccine in goats.  Both of these are attenuated live vaccines, which are strains of bacteria that cause a similar but less severe infection in the vaccinated individual, so the animal’s immune system will respond to and eliminate the agent.  Immune cells then remember the bacteria, so that if the animal is exposed to the wild type strain of bacteria, it will destroy it before it becoming infected.  One of the advantages of the RB51 vaccine that has helped to make testing for the disease effective is that the vaccine strain lacks a specific surface molecule that the wild type strain of bacteria possesses, so tests can distinguish between diseased cattle and those vaccinated with RB51 [1].  The Program has decreased the number of infected herds in the US from 124,000 in 1957, to 2 as of December 2003 [2].  These vaccines are not approved for human use, and as mentioned before may actually cause clinical illness if accidently injected into the handler [1].

In February of 2008, all States in the US were classified as disease-free [6].  In September of that year however, the states of the Greater Yellowstone Area (GYA), Montana, Wyoming, and Idaho lost their disease-free status [6].  For more information on this, see APHIS’s website at http://www.aphis.usda.gov/newsroom/content/2009/10/printable/brucellosis_concept_paper.pdf.  What was the source of the infections that triggered this revocation?  Brucellosis is endemic in the herds of elk and bison in the area.  8-60% of elk herds and 11-75% of bison herds were positive for B. abortus by serologic tests [7].  Studies of mapping the molecular profiles of the isolates from this area show that cattle are more likely to be infected by elk than bison, and indicate that there may be a possibility of transmission between cattle and feral pigs, though it is unclear of the direction [7].  These wild reservoirs pose another significant barrier to the complete eradication of the disease in the US.

In the Future

The issue of wildlife reservoirs for Brucellosis will need to be addressed to prevent transmission of the disease to people, especially those at particularly high risk of infection by this route, such as hunters, hikers, and campers.  Some proposed strategies include the daunting tasks of selectively culling bison herds and vaccinating elk and bison [7].

Control of human Brucellosis through vaccination of livestock has been successful thus far because it virtually eliminates our exposure to the infectious agent, so it is a sort of indirect prevention. But how will we prevent disease outbreak should we be exposed by a different means?  There is no human vaccine for Brucellosis, it can be aerosolized, and it only takes 10-100 organisms to cause disease in humans [1].  All these characteristics make it a possible agent of bioterrorism [1].  Although the mortality rate is low, the morbidity rate is high, so an outbreak would cause a tremendous consumption of money and resources to treat the affected, and a dramatic decrease in workforce and morale. Control of human Brucellosis is another area in which we must not allow ourselves to fall victims to our own success.  We must continue to support the vigilant monitoring and livestock vaccination efforts and encourage efforts in the development of a vaccine that is safe and effective for use in humans.

 References

[1]         Ficht, TA, and LG Adams. Brucellosis. Vaccines for Biodefense and Emerging and Neglected Disease. Elsevier Inc. 2009. Ch 42.

[2]         http://www.cfsph.iastate.edu/DiseaseInfo/disease.php?name=brucella-abortus&lang=en. Accessed 9 June, 2012.

[3]         Atluri, VL, MN Xavier, MF de Jong, AB den Hartigh, RM Tsolis. Interactions of the Human Pathogenic Brucella Species in Their Hosts. Annual Review of Microbiology. 2011. 65:523-41.

[4]         Solis Garcia del Pozo, J, J Solera. Systematic Review and Meta-Analysis of Randomized Clinical Trials in the Treatment of Human Brucellosis. PloS One. 2012. 7(2):e32090.

[5]         Pappas, G, P Papadimitriou, N Akritidis, L Christou, EV Tsianos. The New Global Map of Human Brucellosis. Lancet Infectious Disease. 2006. 6:91-99.

[6]        http://www.aphis.usda.gov/newsroom/content/2009/10/printable/brucellosis_concept_paper.pdf. Accessed 9 June, 2012.

[7]         Higgins, J, T Stuber, C Quance, WH Edwards, RV Tiller, T Linfield, J Rhyan, A Berte, B Harris. Molecular Epidemiology of Brucella abortus Isolates from Cattle, Elk, and Bison in the United States, 1998 to 2011. Applied Environmental Microbiology. 2012. 78(10):3674-84.

Coexisting with Coyotes

This is the twelfth of 16 student posts, guest-authored by Stanley Corbin.

Disease in wildlife is an important concern to the health and safety of humans and domestic animals. The expanding growth of our nation and resultant land use changes with urbanization has resulted in a shrinking habitat and fragmentation for all animals, including humans. The effects of ecological disruption are universally recognized and adversely effects wildlife through multiple mechanisms.

Hand it to the coyote (Canis latrans) for its ability to exist with humans. The resilience of this animal can be attributed to its natural instincts, remarkable intelligence and survivability. Opportunistic is another word that can be used to define them. Once an animal roaming the mid-west prairies, their territory has expanded throughout the North American continent and beyond. Coyotes demonstrate their wily nature by meeting the challenges of the American landscape.  

Progression of coyote range expansion throughout North America and Mexico. (7) Click to enlarge. 

Precise population estimates of coyotes in the United States are not available and unclear at best. However, to put it in perspective, the California Department of Fish and Game estimates a population range of  250,000  to 750,000 animals.(1)  The greater metropolitan area of Chicago estimates home to between 200-2000 coyotes. (3) The coyote population in New York during the summer is approximately 20,000-30,000. (2)  In March 2010, a lone coyote led a police chase through lower Manhattan, deep in New York City.

Coyotes can thrive in suburban settings and even some urban ones creating a concern for public health. A study by wildlife ecologists at Ohio State University yielded some surprising findings in this regard. Researchers studied coyote populations in Chicago over a seven-year period (2000–2007), proposing that coyotes have adapted well to living in densely populated urban environments while avoiding contact with humans. They found, among other things, that urban coyotes tend to live longer than their rural counterparts. (3)

As with most all wild animals, the coyote population represents a reservoir for diseases. Zoonotic (animal to human) diseases in particular are on the rise, comprising 75% of emerging infectious diseases. Viruses, bacteria, fungi, internal and external parasites, and other pestilence are only the headings for what’s out there.

Fortunately, the rabies virus is rather uncommon in coyotes as reported. The only exception was the 1974-1998 rabies epizootic (epidemic in animals) in south Texas. The world’s largest wildlife oral rabies vaccine (ORV) drop, 11.6 million doses covering over 189.6 square miles, was performed beginning in 1995 and led to the total elimination of the domestic dog-coyote (DDC) variant by 2006. (4) A study performed by the USDA, APHIS, Wildlife Services, National Wildlife Research Center concluded; “In Texas, the use of the ORV stopped the northward spread and led to the progressive elimination of the DDC variant of rabies in coyotes”. (5) This campaign was a win for our tax dollars as well. The economic evaluation study yielded “total estimated benefits of the program approximately ranged from $89 million to $346 million, with total program costs of $26,358,221 for the study period”. This represents benefit-cost ratios that ranged from 3.38 to 13.12. (5)

Coyote rabies surveillance reported by the Center for Disease Control (CDC) for 2010 declared 10 confirmed cases. None of these cases were DDC variant, which remains non-detected from the populations. The raccoon variant and skunk variant represented 8 (AL, GA, NC, NJ, NY, NYC) and 2 (CA, CO) cases respectively. (6)These coyote rabies cases were diagnosed from New York City (1) on the east coast to California (1) in the west, confirming the widespread distribution of this terrestrial carnivore. An interesting fact that comes from this data is that the coyote is not a player in the zoonotic rabies front. From a public health concern, a human has a significantly greater chance of contracting the disease from the backyard domestic cat.

Canine Distemper Virus is an enzootic disease (prevalent in an animal population) in the coyote. The neurological form is rightfully confused with a rabies infection as the two appear similar clinically. Humans are not susceptible to the disease, however it is highly contagious to dogs. Greater Yellowstone Park has a dynamic management study to assist with the surveillance of the disease enzootic in the parks coyote population.

The parasitic disease Sarcoptic mange is what gives the animal the “mangy” look. Caused by the mite Sarcoptes scabei, the disease in humans is called Scabies. Severely affected coyotes are unsightly and are perceived as threatening by their appearance. The compromised condition may explain the increased frequency of nesting and scavenging in suburban areas, especially in daylight hours. Coyotes with extensive mange infections are not considered aggressive as concluded by The Cook County, Illinois, Coyote Project.(7) Human infections from animal sources are short-lived and self-limiting due the highly host species-specific nature of the bug.

A recent hot epidemiological study conducted in Santa Clara County, California, identified coyotes as a wildlife reservoir for a disease caused by Bartonella vinsonii subsp. Berkhoffii .(8) The disease in humans is characterized by endocarditis, an inflammation of the interior lining of the heart. The study was prompted by the coyote bite of a child who developed symptoms compatible with Bartonella infection. Among 109 coyotes sampled, 31 animals (28%) were found to be bacteremic and 83 animals (76%) had Bartonella vinsonii seropositve antibodies. The disease is thought to be transmitted by insect vectors (ticks, biting flies, fleas), however further studies are necessary to elucidate additional modes of transmission to humans.(8) Bartonellosis in domestic cats is commonly called “cat scratch fever”, caused by a different species variant of Bartonella. The role coyotes play in this emerging infectious zoonose and public health concern are yet to be resolved.

Additional diseases exist in the coyote populations warranting public health attention. Anyone concerned with coyote interaction and communicable diseases will need to seek information relative to their geographical location. The ubiquitous nature of this animal and the corresponding diseases posing risks to humans and domestic animals respectively are regionally specific.

Coyotes are here to stay. Most every state (excluding Hawaii) has a control program in effect to manage the public health risks and deprivation to human welfare. The Humane Society of the US has issued techniques to resolve coyote conflict and how to discourage coyotes.  Project Coyote champions innovative solutions to live in peace with the coyote despite differences, especially in terms of human policy. (9) A collaborated and integrated management approach is required to maintain a balance of needs for this specie of animal and humans. Wildlife specialist Jeffery Green summarizes; “regardless of the means used to stop damage, the focus should be on damage prevention and control rather than elimination of coyotes”. (10)

Pet owners need to adapt to coyote presence and take precautionary measures in securing their animal’s health and safety. Routine core vaccinations and other preventative health care are effective in stopping the transmission of nearly all the important diseases from the coyote to a pet animal.

Coyote attacks on humans are rare; the coyote human avoidance factor is responsible for the low incidence. In the cases of human attacks, approximately 30% were reported as humans feeding coyotes. (8) Additionally, greater than 50% of the human attack cases were in California, (8) where coyotes have a longer history of habituation with humans.

A person who sees a coyote should feel lucky since they avoid humans and are mostly invisible.

The most important advice to prevent human exposure is: do NOT feed coyotes and ensure your environment is NOT coyote friendly. Any attempt to domesticate or habituate the coyote will surely be a kiss of death for its existence. Survival of coyotes is dependent on living side by side but not together with humans.

The “tricksters still run wild and provoke all sorts of all-too-human difficulties, pitting the spirit of the wild against the sturdy values of our American farmers and their need to protect livestock. Somehow we need both”. (11)

Our Canadian neighbors at The Royal Canadian Geographical Society  conclude; “the more we cut down habitat and build, the happier the scavenging and opportunistic coyote”. (12)

As they say in Texas, “when the human population fails, cockroaches and coyotes will survive”. (13)

References:

  1. L.A. County Department of Animal Care and Control website. Accessed June 15, 2012. Available at: http://animalcare.lacounty.gov/coyote.asp
  2. New York State Department of Environmental Conservation website. Accesses June 15, 2012. Available at: http://www.dec.ny.gov/animals/9359.html
  3. World Science website: Thriving under our noses, stealthily: coyotes.  Accessed June 13, 2012. Available at:  http://www.world-science.net/othernews/060105_coyotefrm.htm
  4. Texas Department of State Health Service website. Accessed June 12, 2012. Available at: http://www.dshs.state.tx.us/idcu/disease/rabies/orvp/statistics/
  5. Stephanie A. Shwiff, PhD; Katy N. Kirkpatrick, BS; Ray T. Sterner, PhD. Economic evaluation of an oral rabies vaccination program for the control of a domestic dog-coyote rabies epizootic: 1995-2006. JAVMA, Vol.233, No.11, Dec.1, 2008. Available at http://www.avma.org/avmacollections/rabies/javma_233_11_1736.pdf
  6. Jesse D. Blanton, MPH; Dustyn Palmer, BA; Jessie Dyer, MSPH; Charles E. Rupprecht, VMD,PhD. Rabies surveillance in the United States during 2010. Vet Med Today: Public Veterinary Medicine. JAVMA, Vol. 239, No. 6, September 15, 2011. Available at: http://avmajournals.avma.org/doi/pdf/10.2460/javma.239.6.773
  7. The Cook County, Illinois, Coyote Project website. Accessed June 13, 2012. Available at: http://urbancoyoteresearch.com/Coyote_Project.htm
  8. Chang CC, Kasten RW, Chomel BB, Simpson DC, Hew CM, Kordick DL, Heller R, Piedmont Y, Breitschwerdt EB. Coyotes (Canis latrans) as the reservoir for a human pathogenic Bartonella sp.: molecular epidemiology of Bartonella vinsonii subsp. Berkhoffii infection in coyotes from central coastal California. J Clin Microbiol. 2000 Nov; 38 (11): 4193-200. Available at: http://www.ncbi.nlm.nih.gov/pubmed/11060089
  9. Project Coyote website. Accessed June 15. 2012. Available at: http://www.projectcoyote.org/programs.html
  10. Jefferey S. Green, Urban Coyotes: Some Summary Thoughts. Proceedings of the 12th Wildlife Damage Management Conference (D.L. Nolte, W.M. Arjo, D.H. Stalman, Eds. 2007
  11. Shake-Spear’s Bible.com website; Coyote: An Instant Classic. Post by Roger Strirtmatter, October 25, 2011. Accessed June 13, 2012. Available at: http://shake-speares-bible.com/2011/10/25/coyote-an-instant-classic/
  12. The Royal Canadian Geographical Society website. Accessed June 13, 2012. Available at: http://www.canadiangeographic.ca/wildlife-nature/?path=english/species/coyote/2
  13. Personal correspondence; James Wright; Tyler Texas. Retired Texas Department of State Health Service official.

June’s passing

She just bought two pairs of new shoes.

This is the refrain my brain keeps returning to, as if that will make the outcome any different. She hardly ever bought new shoes, or clothes, and especially furniture. Yet in the past year, as she decided she’d go on dialysis and stick around awhile, she purchased all of that. The shoes were just mere weeks ago. So she can’t really be gone.

My Grandma had been preparing for her death for literally decades. She’d occasionally show me things–knick knacks, collectibles, heirlooms, etc.–that she’d tagged with a sticker on the bottom bearing my name. She’d been methodically going through her belongings and identifying who should get what in order to minimize any issues after her passing. She and Grandpa bought their cemetery plots long ago, just a few blocks from their house, and joked that any other moves they made would be to their plots there.

She taught me how to bake, and made the best desserts ever. She was way more precise with her recipes than I am; I tend to dump flour and sugar and use “rounded” everything for measurements; she always meticulously scraped the extra flour off the top of a measuring cup, and laid down spoons as counting devices for large recipes to keep track of how many cups she’d already added. She knew where to go for the “best lard” in the area. She used to make her own strawberry jam and keep a garden; as kids, we’d snap beans at her house and watch the hummingbirds at her backyard feeders.

She was immensely patient. We stayed at her house quite a bit as children when my mom was in the hospital. One day she was making breakfast for myself and my siblings, including my younger brother, who was maybe 4 years old at the time. He wanted “dipping eggs”– basically made over-easy. Every egg she made, she cracked the yolk and he refused to eat it. Finally one came out unbroken–and she said she “could have killed him” when the first thing my brother did was take a piece of toast and break the yolk.

She was a fan of both sports and politics. She loved the Buckeyes and the Indians, and was disappointed when hometown hero Ben Roethlisberger kept screwing up his charmed life. Though she’d never gotten a driver’s license and had only been employed a few weeks out of her life, she was progressive and couldn’t stand the right-wing mouthpieces. She routinely clipped newspaper articles on MRSA and other infectious diseases to mail to me. She still used words like “oleo” and “davenport.” She would have been 86 in just a few weeks, and we were already planning a party for her and my Grandpa’s 65th wedding anniversary in June. Though she was also obsessive about sending everyone birthday and anniversary cards (always written in her neat, small cursive) but I didn’t know until just a few weeks ago that she’d never gotten a card for Grandpa. She figured 65 years was enough time to wait, and just bought him his first birthday card. It was on the mantle yesterday when my sister went over to visit.

She seemed, in many ways, both fragile and invincible. Over the past 20 years, she’d survived breast cancer, Clostridium difficile, a heart attack (and ~5 minutes of death in 2008), and “The E. Coli” as she called it, like it was a person rather than a bacterium. The E. Coli put her in the hospital with hemolytic uremic syndrome. It was this foe, with its subsequent reduction in kidney function, that necessitated her dialysis. She started the latter in late summer of 2011, after feeling incredibly tired for much of that season. Initially she fought it–she “didn’t want to trouble anyone” and there were no transportation options for seniors going to and from dialysis in her county–but after a family intervention (“you need this or you WILL die, and soon”) she decided she wanted to stick around for awhile. Indeed, she’d mentioned more than once that she felt better in the past 6 months than she had in quite awhile. She’d lost 50 pounds, some of it fluid due to the dialysis, and some due to better eating via a “meals on wheels” program she started with Grandpa–and was confident enough to make some purchases, like the shoes and a new sofa.

Two days ago, Grandma June was unable to do dialysis at her clinic as a clot was identified. Yesterday, my aunt took her to a hospital facility to have it checked out and receive dialysis there. I’m not yet sure of all the details; sounds like she had another heart attack (due to the clot?) but this time, there wasn’t any coming back, new shoes and sofa be damned.