Granny’s mean pot of bushmeat stew

Grannies
Left to right, Granny Beck, my Grandma June, and Great-Great Grandma Bertha, circa 1961. Who knows what was on the menu that day.

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.

Deer assortment
Various deer parts brought over by my neighbor this weekend.

 

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?

Prominent magazines run pictures of butchered meat and primates with headlines that are intended to scare and “other.”

People judge harshly, partly because of bush meat consumption:

“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.

Finally, while people malign “bushmeat” hunters in Africa, let’s not forget that almost any source of food can be contaminated with potential pathogens. Even in the United States, 1 in 6 Americans (48 million people) get sick, 128,000 are hospitalized, and 3,000 die of foodborne diseases. Every year. And that’s with our “high standards” for animal husbandry and processing.

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.

Additional readings

The long and ugly tradition of treating Africa as a dirty, diseased place

If you can’t be a good example, be a warning. How EcoInternet’s #Scicomm #Fail can make you a more culturally aware science communicator

 American Bushmeat

It’s not a freaking spider bite

Over at White Coat Underground, Pal has the post that I’ve been meaning to write. Earlier this summer, a family member posted on Facebook that a friend of her daughter was nursing a “nasty spider bite” that she got while camping in Michigan. Her post claimed it was a Brown Recluse bite. Being my usually buttinski self, I posted and told her that it was really, really unlikely to be a brown recluse bite, and that the friend-of-the-daughter-of-the-relative should hie thee to her physician and get the “bite” checked out. I told her that rather than a spider bite, it could be a Staph infection and may require antibiotics.

Now, I should note that few people in my family really “get” just what it is that I do, and even fewer of them realize that I spend my days researching bacterial infections, and that Staph in particular is my specialty. So I didn’t take it personally when she pooh-poohed my suggestion and told me I had no idea what I was talking about, and that FOTDOTR’s doctor had already seen the bite and proclaimed it to be due to a brown recluse. Okay, whatever, northern Michigan is completely the wrong place to get a bite from one of these critters and many research papers say the same thing–that “spider bites” usually aren’t bites at all. I pointed this out (and linked some Google images of supposed spider bites in comparison to Staph infection images) and then left the conversation.

A day later, relative posted an update in the thread–FOTDOTR ended up going back to the doctor as the “bite” was getting worse. As I suspected, she had now officially been diagnosed with a staph infection–and yet they were still trying to determine “what kind of spider bit her.” A few hours later, relative asked “What is MRSA? FOTDOTR was just diagnosed with that from the spider bite.”

This is when I started pulling out my hair, since I’d linked info about MRSA several days prior by this point. There was no spider bite, damn it!

Anyway, FOTDOTR got treatment (though relative probably still believes it’s from a spider bite) and I know at least a few people on the thread now may at least think “staph” when someone says “spider bite”–so overall, a good ending.

Pal notes:

Despite this widespread belief, most “spider bites” in my part of the country [Michigan, ahem–TS] aren’t caused by spiders, and probably aren’t bites at all. (The feared “brown recluse” does not live naturally in my part of the country, although importations have been reported. They do not generally survive through the winter.) The distinction is important for a few reasons. First, many of us are guilty of wanton arachnicide propelled by our unwarranted fears. Second, many “bites” are probably bacterial infections and should be treated properly. Finally, there’s my own bias that we shouldn’t assume things that aren’t so.

Indeed.

The case of the missing smoking sprouts

Maryn McKenna has a great update today on the E. coli situation, looking at where we are as far as unanswered questions about the outbreak and the strain. It’s been a messy day; more evidence seems to point to the sprout farm, but CIDRAP also notes that another contaminated cucumber was found in the compost bin of a family sickened by the bacterium (this one had the correct serotype–O104), but it’s impossible to tell at this point whether the cucumber was the source of that bacterium or it ended up there from one of the sickened family members. Twists and turns abound in this investigation. I’ve not seen any confirmation that the remaining sprout isolates tested negative yet, either.

One thing I want to emphasize and expand upon, from the CIDRAP article:

Most of the investigation findings point back to a sprout source, and microbiological testing a month after the fact doesn’t change that, Hedberg said. “Negative micro results cannot negate positive epi results. This is an important principle that we cannot state too strongly.”

At this late date, it’s hard to say whether we’ll be able to definitively trace this back to its source–too much time may have passed for there to be any remaining contaminated source material left. This means we might not ever find the “smoking gun” (or smoking sprouts, as the case may be). With such a severe outbreak–725 cases of hemolytic uremic syndrome, over a quarter of those infected–that’s bad news if we can’t confirm the vehicle, as it may make it more difficult to find the ultimate source of this strain. However, as Hedberg notes, we do still have the epi. This was used long before we had today’s molecular typing techniques, or even before we had microbiology culture ability, for that matter. Think John Snow’s cholera investigations, where he didn’t even know about bacteria and yet was able to determine the water as the vehicle for infection. So while confirmation may not happen, it’s still looking like most lines of evidence point to the implicated farm.

Maryn also brings up a great point that what we’re seeing as far as cases may be over-estimating the actual severity of the infection. I’ve talked about this previously regarding influenza infections, particularly H5N1. Right now H5N1 has a high mortality rate–but is it artificially high, because mild or asymptomatic infections are being missed?

With O104, as with any food-borne infection, surely this is happening. Mild diarrhea or stomach cramping isn’t something people frequently go to their healthcare provider over, so inevitably cases are missed. However, it probably happens with any E. coli outbreak, yet in most others we still see HUS rates between about 2-7% of the confirmed infections, while this one is at about 26%. So it doesn’t seem (to me, at least) that missed mild infections are the whole story. Is this acting like the novel Clostridium difficile strains, which have a mutation in a regulatory gene that leads them to pump out higher levels of toxin than “regular” strains? More than just genetic analysis will be needed to investigate that–some basic microbiology will also be needed. If nothing else, this outbreak has given us much research fodder over the coming years.

Getting the whole story- attempting to make sense of disease through evolutionary medicine

Student guest post by Anne Dressler

The idea of evolutionary medicine is new to me and my understanding is quite shallow but it has piqued my interest. Currently, the book “Why We Get Sick” by Randolph M. Nesse and George C. Williams has been satisfying my curiosity during the 15 minutes of intellectual thought I have left at the end of the day while reading before bed. From what I’ve read, I’m finding how useful it can be to consider disease in light of evolution and I’m left wondering how I haven’t heard of it before. I’m guessing I’m not the only one interested, so let’s talk evolutionary medicine, starting with some of the basics and finishing with why I find this particularly interesting for the nexus between infectious and chronic disease.

If basic biology and traditional medicine make up the plot of our disease “stories”, evolutionary medicine would be somewhat like the moral. My roommate is a medical student and when asked, she can tell you how just about anything in the human body works and what is happening when things go wrong. When asked why things go wrong, her answer will refer to a proximate cause, such as certain foods leading to plaque build up which can lead to heart disease. If the question of why is rephrased, as in why does the disease even exist at all, then she’s stumped. This is the question considered by evolutionary medicine. Why aren’t our bodies able to repair clogged arteries? Why are we prone to infections? Why are our bodies so good at some things but so inept at others? At first I found theses questions strange- after studying epidemiology’s risk factors for the past year, I had started viewing them as the sole reason for the existence of disease. And that kind of makes sense…if you completely ignore evolution. Enter famous and ubiquitous Dobzhansky quote:

“Nothing in biology makes sense except in the light of evolution.”
-Theodosius Dobzhansky

It is through the perspective of evolution that one can consider why a disease exists beyond the obvious.

In their book, Nesse and Williams propose six categories for evolutionary explanations of disease: infection, novel environments, genes, design compromises, evolutionary legacies, and defenses. The basis for all these explanations is evolution through natural selection thus I think it is wise to keep in mind some key points. First, natural selection occurs when survival and reproduction are affected by genetic variation among individuals. Genes are only passed on by the organisms that survive to reproduce. Note, surviving to reproduce doesn’t necessarily have anything to do with health or survival later in life nor does it necessarily mean good health before reproduction either.

“If tendencies to anxiety, heart failure, nearsightedness, gout, and cancer are somehow associated with increased reproductive success, they will be selected for and we will suffer even as we ‘succeed,’ in the purely evolutionary sense.”
-Randolph M. Nesse and George C. Williams, Why We Get Sick

Also, think Richard Dawkins and “selfish genes”- selection doesn’t consider populations, but rather benefits genes. With this in mind, let’s go over one of the proposed categories for explaining disease- infection (even if it is just skimming the surface).

Infectious agents have long been a cause of human disease. As we have evolved means to avoid infection, pathogens have evolved means to counter us leaving us prone to infection. Due to their relatively rapid reproduction, pathogens can evolve much more quickly than we can. One way we attempt to make up for this deficiency is by using antibiotics. Interestingly, by using antibiotics we are essentially taking advantage of the evolutionary advantages of another organisms. Toxins produced by fungi and bacteria are a result of millions of years of selection to combat pathogens and competitors. Dangerously, many believed that with antibiotics we would finally be in control of infections. Unfortunately, that was an underestimation of evolutionary forces and while almost all staphylococcal strains were susceptible to penicillin in 1941, today nearly all are resistant. This pattern is standard for most newly introduced antibiotics

The concept seems simple enough, but it’s not the only thing we’ve misunderstood about the evolution of pathogens. A common misperception is that a pathogen will evolve from being virulent to being more and more benign in order for the host to live long enough for the pathogen to pass on offspring to new hosts. This makes sense, yet doesn’t fully take into account the need to pass on offspring. Being able to disperse offspring to new hosts may mean it is most beneficial to the pathogen for the host to be sneezing, coughing, or laying prostrate. Another force behind pathogens evolving increased virulence is within-host selection. Simply, if there is more than one strain of a pathogen within a host, the one that uses the host’s resources most effectively will be the one to disperse the most offspring.

So if infections are one evolutionary explanation for disease, what’s an example? I recently came across an interesting article about infection and it’s relation to premenstrual syndrome. In the article Premenstrual Syndrome: an evolutionary perspective on its causes and treatment, Doyle et al. propose premenstrual syndrome is due to an exacerbation of a set of infectious diseases during cyclic changes of immunosuppression by estrogen and progesterone. While genetics and non-infectious environmental influences have been examined and found largely unable to explain PMS, infectious causes have been overlooked. However, it is know how immune function varies throughout the menstrual cycle in such a way that there could be less effective control of fungi, viruses, and intracellular bacteria, so making the leap to a persistent infection contributing to PMS doesn’t seem too difficult. Supporting this hypothesis is a long list of chronic diseases with suspected infectious causes that are exacerbated premenstrually including Crohn’s disease with Mycobacterium avium and juvenile onset OCD with Streptococcus pyogenes.

I think the most important point to take from this article is that there may be many other chronic diseases we don’t yet fully understand that are caused by infectious agents.

Yet even while the who, what, when, and where of some diseases may already be understood, the why of a disease is usually ignored. With an evolutionary perspective, we can try to answer the question of why diseases arise and persist under the forces of selection. These insights could help answer some old questions, such as those regarding unknown causes of chronic diseases, and ask some new ones, such as how could PMS be treated if it’s cause really is infectious. Finally, while guiding health care practices to improve health is the ultimate goal, at the very least evolutionary medicine reminds us to keep thinking about things in new ways.

Sources:

Doyle, C., H. A. Ewald, and P. W. Ewald. “Premenstrual Syndrome: An Evolutionary Perspective on its Causes and Treatment.” Perspectives in biology and medicine 50.2 (2007): 181-202.

Gammelgaard, A. “Evolutionary Biology and the Concept of Disease.” Medicine, health care, and philosophy 3.2 (2000): 109-16.

Nesse, Randolph M., and George C. Williams. Why we Get Sick. New York: Vintage Books, 1994.

Nesse, R. M. “How is Darwinian Medicine Useful?” The Western journal of medicine 174.5 (2001): 358-60.

Stearns, S. C., and D. Ebert. “Evolution in Health and Disease: Work in Progress.” The Quarterly review of biology 76.4 (2001): 417-32.

Williams, G. C., and R. M. Nesse. “The Dawn of Darwinian Medicine.” The Quarterly review of biology 66.1 (1991): 1-22.