ST398 carriage and infections in farmers, United States

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 meat products; 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. aureus which 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 and others 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.

Reference: Wardyn SE, Forshey BM, Farina S, Kates AE, Nair R, Quick M, Wu J, Hanson BM, O’Malley S, Shows H, Heywood E, Beane-Freeman LE, Lynch CF, Carrel M, Smith TC. Swine farming is a risk factor for infection with and high prevalence of multi-drug resistant Staphylococcus aureus. Clinical Infectious Diseases, in press, 2015. Link to press release.


Superbugs rising

It’s a parent’s worst nightmare. Your healthy child is suddenly ill. The doctors you’ve trusted to treat him are unable to do anything about it. Drugs that we’ve relied upon for decades are becoming increasingly useless as bacteria evolve resistance to them. New drugs are few and far between. Old drugs, shelved because of their toxic side-effects, are being brought in as last resorts–kidney failure, after all, is better than certain death.

Unfortunately, this is increasingly the state of medicine today, and people are dying from it. The World Health Organization even recently sounded the alarm, noting that “the world is headed for a post-antibiotic era”–and it takes a lot of consensus to get the WHO to act, so this is a Big Deal.

I was in Washington, DC last week for two days to discuss the issue with other “supermoms” and dads (farmers, physicians, researchers, and parents whose children had experienced antibiotic-resistant infections), and to share information with legislators and government agencies. (I also brought William, 4 months old, for an extra dose of adorableness).

Superbabies against Superbugs
Superbabies against Superbugs

Some of the “super” attendees might be familiar to readers. I had the pleasure of meeting Russ Kremer, who has been profiled in several articles and documentaries. Russ raised pigs in confinement, dosing them with antibiotics from birth to slaughter until he was gored by a boar, resulting in a very difficult-to-treat infection that almost cost him his life. David Ricci was also present. His story was profiled in the Frontline documentary, “Hunting the Nightmare Bacteria.” He contracted an infection with bacteria carrying the NDM-1 genes, making them resistant to almost all known antibiotics, and required multiple surgeries and treatment with some of these last-line drugs over many months.

There were also participants you may not have read about previously, like Amanda Hedin and Everly Marcario, who both lost children to antibiotic-resistant infections. I’ve written before about the immense sadness that comes at times when studying infectious disease, noting that I have a freezer full of bacterial isolates that, while important for study, frequently mark someone’s illness or death. It’s important work, but heart-wrenching at times.

However, we have very little funding to study such infections. My colleague Eli Perencevich recently estimated the amount of money spent on antibiotic-resistant infections versus HIV/AIDS, and the answer is that it’s vastly less. Antibiotic resistance needs to be a priority on many fronts. The FDA has recently made some headway into possibly reducing antibiotic use on farms, though optimism is mixed regarding how much that will actually help things. Hospitals and clinics are working with physicians to encourage and enforce best practices for antibiotic prescribing in these settings.

We need to be responsible with antibiotics. Drugs in development are scarce, and none are ready for prime time. It’s almost unimaginable that we may return to a time when an infected scrape could mean the death of a healthy young man, but we’re closing in on that every day. The WHO wrote in their report:

“A post-antibiotic era, in which common infections and minor injuries can kill, far from being an apocalyptic fantasy, is instead a very real possibility for the 21st century.”

We need action, not promises. And we need it now.

The microbiology of zombies, part III: “We’re all infected”

Warning: here be spoilers

In many latter-day zombie movies, books, and TV shows, zombie-ism has a biological cause. In 28 Days Later, the infection is caused by the “Rage” virus, which escaped from a lab when animal rights activists break in and release a group of infected chimpanzees. Of course, one of the animals promptly bites one of its “liberators,” and the infection spreads rapidly throughout Great Britain. In Zombieland, it’s a mutated form of “mad cow” disease. The Crazies, it’s the Trixie virus; World War Z, the Solanum virus; Resident Evil, the T virus. I could go on and on. Zombie causation has clearly evolved from the early days of radiation or curses, and has become a biological phenomenon in most modern zombie tales.

The Walking Dead is no exception. Though the claim is made in season 1, episode 6 (“TS-19”) that the outbreak could be caused by just about anything–bacteria, virus, parasite, act of God–I call shenanigans. In the previous episode (“Wildfire”), Jenner, the CDC scientist, is processing tissue taken from Test Subject 19, and the visualization under his microscope looks very viral. Of course, take this with a few pounds of salt, since he’s using a light microscope and can also see the nice alpha-helical DNA strains within the pathogen (in real life, things just don’t look like this) and unless you’re one of the giant viruses, you can’t see viruses, much less DNA, under the microscope Jenner uses anyway. But still, it looks pretty viral-y to me, which is why I typically refer to it that way:

screenshot wildfire virus

Microbial zombification makes sense in today’s culture. My colleague Brooks Landon notes: “…zombies represent a better monster for the modern, post-9/11 world. They provide a release for feelings of being overwhelmed by abstract and intractable events like global economic crises, terrorism, and pandemics.” In the past decade or so, we’ve seen the emergence of SARS, multiple outbreaks of influenza including a new pandemic strain, the continuing HIV crisis, Nipah, Hendra, more Ebola, just to name a handful. Infectious diseases are commonly in the news, and many times are unfortunately over-hyped, leading to a collective nervousness of all things microbial.

The infected zombie is further boosted by a number of recent studies, largely in insects, that demonstrate a type of pathogen-directed “mind control:” zombie ants, zombie grasshoppers, and zombie cockroaches, just to name a few. A recent video game has exploited the ant fungus idea, mutating it into a form that infects humans. Even rodents (and possibly humans) can have their behavior apparently influenced by a parasite called Toxoplasma gondii, which makes rodents lose their fear of cat scents and may influence the development of schizophrenia in humans, or more controversially, even affect sexual inhibitions. If germs are already controlling our minds–why couldn’t they turn us into zombies?

And certainly, there are some candidate microbes which could, in theory, cause at least the “living” form of zombie-ism, even if they couldn’t necessarily raise you from the dead. The Trixie virus, for example, is supposed to be a weaponized rhabdovirus–the family of viruses that includes rabies. Rabies virus infection certainly causes aggression and biting. The virus is spread via saliva, so biting is the main way it is transmitted between animals. In a recent book, Rabid, the authors trace rabies through history, and note that it may be at the root of many zombie (and vampire) tales. Rabies can also hide out in the body for awhile before showing symptoms, as the virus travels up the nerves toward the brain. This is why a bite near the head progresses to symptoms much faster than, say, one to the foot. Typical time from bite to symptoms is in the neighborhood of 6 weeks, depending on the location of the bite and dose of virus one receives, but extreme cases have been documented, with symptoms not showing up for as long as 8 years. And, like has been done on The Walking Dead, one of the ways that bitten victims would try to avoid symptoms would be to cut off the affected limb before the infection spread. (Ouch).

Could something like the “we’re all infected” scenario used in the Walking Dead occur in real life? Maybe. With rabies, victims could appear physically fine for months to years. Even more extreme, there are a number of germs which can remain with people throughout their entire life. The virus that causes chicken pox, for example, doesn’t ever really go away. Your body fights it off enough to keep it in check after the initial rash, but it hides out  in your nerves and can come back in later years as shingles. Other herpes family viruses have a similar lifestyle: symptoms can come and go, but the virus never really leaves. The human papilloma virus (HPV) can also persist for years in some people (most infected people appear to clear this one, though). A bacterium called Helicobacter pylori can live very happily in a person’s stomach–sometimes causing ulcers, but going completely undetected and causing no symptoms in most people. And of course, HIV, which does not go away except in a few notable and high-profile cases. So the concept is, as they say, biologically plausible.

The problem isn’t necessarily with the microbiology, then, but with the epidemiology. How did everyone get infected so quickly? We know that the plague took an incredibly short time to spread (Jenner says less than 200 days in the first season, and “less than 63 days” since it went pandemic)–but how? That’s a missing link in this scenario. We know the pathogen can certainly be spread by bites and then cause zombification that way, but other forms of inoculation (such as getting sprayed in the eyes or nose with zombie blood) don’t seem to have that effect. Is it in the water? If so, that would be some damn rapid spread, since early on Jenner noted that this appeared to be a true pandemic–present around the world. How would that happen?

In the air? Possibly, but even most airborne microbes don’t hang out indefinitely; they’re dispersed by wind to levels below those able to cause infection, or killed by sunlight or other environmental conditions. So even if you had a herpes- or HIV-like virus that could hide out in the body for an extended period of time without causing symptoms, how did *everyone* get it in such a short timeframe? Some scenarios in other books and movies put the blame on bioterrorism. The above-mentioned Trixie virus, for example, was a bioweapon which was only accidentally released when the plane carrying it crashed. Spread of Trixie in the movie ended up being only local, but transmission beyond that is hinted at the end. A true bioterrorist attack could, theoretically, account for simultaneous outbreaks all over the world.

Finally, though the “infected zombie” is now the most common type, it should be noted that this isn’t really new. George Romero, widely recognized as the grandfather of the modern zombie, acknowledges that he “ripped off” his idea for Night of the Living Dead from Richard Matheson’s I am Legend–a vampire story from 1954. The cause of that vampirism?

Bacillus vampiris–a bacterium.


See also:

Part I: the microbiology of zombies

Part II: ineffective treatments and how not to survive the apocalypse

Part IV: hidden infections

Student guest post: A taste of Lyme

Student guest post by Kyle Malter

In many areas of the country there is a vile blood sucker that lurks in our forests, our parks and even our backyards.  What concerns us is not what this creature takes but rather what it leaves in our body after it bites us:  corkscrew shaped bacteria called spirochetes and with the name Borrelia burgdorferi.  When the bacteria invade our bodies and cause problems along the way we call it Lyme disease.

It is Lyme, not “Lymes” disease, and here’s how it got that name. In the early 1970’s a large number of cases emerged involving children with a “bulls-eye” rash followed by arthritis and they were concentrated in a small area in and near Lyme, Connecticut.  Initially, the cause of the disease was unknown.  A clue to the mystery was that most of the kids lived near a wooded area.  After more investigation, ticks that feed on deer were identified as likely suspects.  The medical community learned that the “deer tick” transmitted the spirochete bacteria which was likely infecting the children and causing symptoms.  A researcher named Willy Burgdorfer helped identify the organism and in honor of his contribution the bacterium was named Borrelia burgdorferi. [1]  Wouldn’t it be fun to have a nasty bacteria named after you?

Signs of Lyme disease can vary from a mild rash to serious pain and disability. If infected, a “bull’s-eye” rash occurs in most people because of the inflammation left in the trail of the migrating bacteria. They move from the bite site away leaving the classic target appearance.  When this bug spirals though your joints, organs and tissues it can cause damage and a wide range of symptoms including fever, headache, lethargy, stiffness and general soreness.   In some cases, more serious and long-term problems with swollen joints, arthritis, Bell’s palsy, and even heart disease can result.   The symptoms can come and go and may last a lifetime.  [1] This is one serious problem if you have the disease-spreading tick in your environment.  Most people refer to the species as the “deer tick” or the “black-legged tick” although the proper name is Ixodes. Don’t forget about your dogs either.  They are also commonly infected in endemic states, can get permanent arthritis, and can rarely even die from the disease. [2]

Lyme disease has been diagnosed in all 50 states but is heavily concentrated in the northeast and upper Mid-West. [3] Approximately 96% of cases come from only 13 states. [4] CDC data by state, maps and disease forecast models show a clearly increasing trend.  Why such a steep increase in the number of cases?  There are probably many reasons.  First, surveillance is probably higher now than it was 15 years ago.  We simply weren’t looking for it as much then.  Another contributor is the increased population of the white-footed mouse in some regions. [5] This rodent is a reservoir for the bacteria meaning they harbor the bug until the tick larva come for a meal.  They are like a bank filled with Borrelia ready for every tick to make a withdrawal.  Once the tick has the bug in its gut, it is a loaded gun.

The recent increase in the white-footed mouse population may be the result of a cascade of events. “Change one thing. Change everything.”[6] Ohio reported two recent “banner years” for acorn production with a 36% increase in white oak acorns between 2011 and 2012.[7] A more abundant supply of “mouse food” in the way of acorns could result in more mice because they replicate much more efficiently.  More white-footed mice means more banks filled with Borrelia.  Ticks have a much better chance of making a withdrawal with every meal.  More ticks with Borrelia means more animals and humans infected.   So that’s how more acorns could mean more Lyme disease.

If you are unsure if Lyme bacteria are in your area just ask your dog.  Some studies suggest that dogs that live in your area may be able to predict your risk level. [8] [9] [10]  For those in the northeast and upper Mid-West you don’t have to ask.  It is ubiquitous in these parts of the country. Veterinarians in many non-endemic states are now screening dogs yearly to see if they have ever been infected with Borrelia.   If some dogs in your region are positive you should be more vigilant.  The CDC will keep track as well so check their Lyme page annually.

Preventing Lyme disease can be a very big challenge.  For dogs, very effective vaccines are available to protect them. [11] [12] So if this is such a potentially devastating disease in people why don’t we have a vaccine for humans?  Well, we did.  In the late 1990’s a vaccine was approved by the FDA to aid in the prevention of Lyme disease in humans.  While the safety and efficacy during the approval studies were good, there were skeptics and strong opponents in the public and medical community.  Some people claimed that the vaccine caused Lyme disease rather than prevent it.  Ultimately, the vaccine manufacturer withdrew it from the market citing poor demand. [12] Allen Steere, the man who discovered Lyme disease, also led one of the SmithKline Beecham (SKB) Lyme vaccine trials.  He said, “the withdrawal of the SKB vaccine . . . represents the most painful event in our Lyme disease history . . . the vaccine was really withdrawn because of fear and lawsuits, not because of scientific findings” [13]  Some advocates are attempting to rekindle efforts to make a vaccine for Lyme disease available again while others are opposed to the idea.

Tick prevention is our best strategy to prevent Lyme disease. Without a tick bite you cannot get Lyme disease.  In fact, even if an Ixodes tick bites you, it takes at least 24-48 hours of attachment to transmit the bacteria into your body. The National Institutes of Health suggest that you follow their fashion advice and tuck in your shirt into your light colored pants, tuck your pants into your socks and then put tape around the bottom. [1] I’ve never seen this method utilized in a public place but I’m sure you will end up on the “People of Wal-Mart” site if you try it.  The CDC recommends pyrethrins on your clothing and DEET on your skin and clothing to repel ticks. [4] The EPA also has a nice online tool.  Check yourself everyday for ticks during peak months.  Deer ticks are tiny so take some time and inspect your nooks and crannies.  The nymph stage, the second smallest tick in this picture,  is the one that usually infects people.  Again, don’t forget about your dog. While he can’t give you Lyme disease, he is also susceptible to it. Ask your veterinarian which flea and tick preventative is right for your pets.

Kyle picture

Lyme disease is no longer just a Lyme, Connecticut problem.  If it is not yet in your backyard, it could be soon. Lyme disease can have lifelong, debilitating consequences. Arm yourself with information and your body with tick protection.  We are not defenseless.  Protect yourself.   Protect your dog.  Please.


[1] NIH Website

[2] Littman MP. Lyme nephritis. J Vet Emerg Crit Care (San Antonio). 2013 Mar-Apr;23(2):163-73

[3] Smith BG, Cruz AI Jr, Milewski MD, Shapiro ED. Lyme disease and the orthopaedic implications of lyme arthritis. J Am Acad Orthop Surg. 2011 Feb;19(2):91-100

[4] Centers for Disease Control and Prevention

[5] National Science Foundation

[6] Townsend, Tracy A., “Change One Thing, Change Everything: Understanding the Rhetorical Triangle” (2013). Rhetoric Unit. Paper 3.

[7] Ohio DNR

[8] J M Lindenmayer, D Marshall, and A B Onderdonk.  Dogs as sentinels for Lyme disease in Massachusetts. American Journal of Public Health November 1991: Vol. 81, No. 11, pp. 1448-1455.

[9] Olson, Canines as Sentinels for Lyme Disease in San Diego County, California, Journal of Veterinary Diagnostic Investigation March 2000 vol. 12 no. 2 126-129

[10] Faith D. Smith, Rachel Ballantyne, Eric R. Morgan, Richard Wall Estimating Lyme disease risk using pet dogs as sentinels Comparative Immunology, Microbiology and Infectious Diseases, Volume 35, Issue 2, March 2012, Pages 163–167

[11] Levy et al. Use of a C6 ELISA test to evaluate the efficacy of a wholecell bacterin for the prevention of naturally transmitted canine Borrelia burgdorferi infection. Vet Ther. 2002 Winter;3(4):420-4

[12] Aronowitz RA. The rise and fall of the lyme disease vaccines: a cautionary tale for risk interventions in American medicine and public health. Milbank Q. 2012 Jun;90(2):250-77.

[13] Steere, A.C. 2006. Lyme Borreliosis in 2005, 30 Years after Initial Observations in Lyme Connecticut. Wien Klin Wochenschr 118(21–22):625–33.


Student guest post: Mission Impossible: Fighting Zoonotic Infections in Nicaragua

Student guest post by Brandon Woods

A Dangerous Paradise

From jungles with jaguars to crystal blue lakes with freshwater sharks, Nicaragua is one of the most beautiful and dangerous countries in Central America. The brilliant biodiversity attracts millions of tourists each year and the looming volcanoes that pepper the landscape can be an exciting yet unsettling sight. However, in reality much of the danger in Nicaragua comes from the risk of infectious diseases. For example, if you’re planning to travel to this tropical paradise anytime soon, the Center for Disease Control (CDC) states that international travelers are at risk of contracting Typhoid fever, hepatitis A, hepatitis B, Leishmaniasis, malaria, dengue, rabies, and more! As a dual degree veterinary medical and public health student, I am fascinated by these infectious diseases and want to learn how they interact with the environment, people and animals. Many of the diseases that the CDC listed are called zoonotic diseases, or diseases that are transmissible between animals and humans. Other zoonotic diseases you may know include ringworm, Lyme disease, and Cat scratch disease. Whether you own a pet, like to travel, or simply enjoy spending time outdoors, you are at risk of infection because these zoonotic diseases are increasingly emerging worldwide and are becoming a serious public health threat. During the spring break of my first year of veterinary school, I traveled to Nicaragua on a mission trip and got first-hand experiences of these frightening infectious diseases.

 Brandon picture 1

Bed Nets and Bug Spray

Planning for this trip was time-intensive and reminded me of planning for my semester study abroad adventure to Tasmania, Australia. However, unlike my semester Down Under, this trip was coordinated through the national non-profit Christian Veterinary Mission (CVM) whose goal has been to help veterinarians serve others and live out their Christian faith for more than 30 years. Out of all the fundraising and logistics meetings we had, the meeting that stands out the most was when the Iowa State University travel nurse described the laundry list of potential pathogens we could encounter. Our team of 8 veterinary students, 3 veterinarians, and 1 pharmacist would be treating animals in a remote village called Espavel in the jungles of eastern Nicaragua. When I saw that my destination was in the middle of the red zone for malaria on the CDC map, my eyebrows escalated and my stomach dropped.

I was going to fly to an unstable, earthquake-prone country of approximately 5.7 million Spanish-speaking people where malaria was endemic. My Spanish was scarce, but my drive to serve was strong. After I heard that malaria was essentially eliminated from Nicaragua, my blood pressure dropped a few millimeters of mercury. Approximately 84% of the Nicaraguan population is at risk of contracting malaria, according to a UCLA study. However, Nicaragua has experienced a 97% decrease in reported malaria cases between 2000 and 2010. This significant decrease in prevalence was a result of Nicaragua partnering with the Pan American Health Organization (PAHO) in 2006 which heavily implemented stronger surveillance, prevention, vector control, and treatment. Despite this progress, I learned from my undergraduate Lyme disease Honors project that there are always numerous challenges to completely eliminate vector-borne diseases like malaria. For instance, controlling mosquito breeding populations is particularly vexing due to the complex ecology of the parasite life-cycle. In addition, you may have heard about the controversy surrounding toxic pesticides like DDT. My colleagues and I were fortunate for our DEET bug spray and Permethrin treated clothes and bed nets that we brought after skyping our host-country missionaries. I was also relieved that our trip in March 2013 was during the dry season and not during the September-to-January rainy season, when disease transmission is highest.

Rambunctious Rabies

Escaping the endless hours in the frigid, formaldehyde laden anatomy lab and flying to a third-world tropical country to practice preventative medicine was slightly shocking, but totally worth it. On our first day, we drove through the littered streets of Catarina to an outdoor shelter where we set up a temporary clinic. The local children brought their pet dogs and we treated them with Ivermectin and other anti-parasitic medication. Many animals were very thin and infested with fleas and ticks. However, it was rewarding to interact with the children and walk them through a brochure that described both healthy animal care and the Gospel of Jesus Christ. Then suddenly one of my colleagues was bitten by a dog! He was trying to give a rambunctious mixed-breed a pill to protect against heartworm disease and the next thing he knew, the dog bit him in the hand. He quickly washed the wound with soap and water and bandaged it. Fortunately, everyone on our veterinary team was already vaccinated for rabies prior to the trip because it’s a requirement to enter veterinary school. He also followed up with post-exposure rabies prophylaxis when he returned home.Brandon picture 2

Rabies is one of the deadliest and most notorious zoonotic diseases in the world. Rabies is endemic to Nicaragua, often occurs in poor rural communities, and the most common source of transmission is when a dog bites a human and delivers the fatal RNA virus. According to the World Health Organization, potentially any mammal can contract rabies, and common reservoirs in the USA include skunks, foxes, raccoons, and bats. Although rabies cases can be successfully treated, it still persists worldwide killing more than 55, 000 people each year. The Center for Food Security and Public Health (CFSPH) at Iowa State University is an excellent resource that provides more information on rabies and preventing zoonotic diseases. Reducing the prevalence of rabies globally requires a multinational effort and the World Rabies Day Initiative was founded solely for this mission and has already collaborated with 150 countries and vaccinated over 7.7 million dogs.

Tasting Iguana and Tackling Typhoid

It’s a good thing I like rice and beans, because that was the bread and butter of most of my meals every day. Hiking to farms builds an appetite and one day we had to traverse across a narrow blank that stretched precariously over a ravine. After we arrived, we vaccinated over 100 head of cattle for clostridium, anthrax, and Dectomax. Dectomax is an injectable drug used to control parasites like hookworms, round worms, grubs and mites. When we returned to the main village and got out of the blazing 90+ degree sun, the crispy, plantain chips with a glass of freshly squeezed tamarind juice was an irresistible snack. However, the most memorable meal of all was the morning the villagers surprised us with two 5 foot long iguanas! A few hours later, I was savoring some delicious iguana meat seasoned with local spices and vegetables. Cooking wild reptiles is foreign to us in the developed world; likewise, the way many Nicaraguans prepare their food is also different.

Brandon picture 3

Sayings like, “Don’t drink the water,” or ‘Boil it, cook it, peel it or forget it,” come to mind when traveling abroad, and they couldn’t ring more true for my experience. Food-borne illnesses are another great example of how veterinary medicine and public health overlap. I’m enrolled in the dual DVM-MPH degree program at the University of Iowa’s College of Public Health and learned that food-borne epidemics are a major focus of research in epidemiology. From mild cases of spoiled potato salad on romantic picnics to church dinner outbreaks from contaminated home-made ice cream, food-borne illnesses can range in their severity depending on your pre-existing health and the dose and type of microorganism ingested. One of the Nicaraguan diseases that I was vaccinated for before my trip was a food-borne illness known as Typhoid fever. Thankfully I avoided this illness; however, I couldn’t escape the wrath of Montezuma’s revenge, or traveler’s diarrhea, most commonly caused by enterotoxigenic Escherichia coli.

Typhoid fever is transmitted through contaminated food or water and is unique among food-borne pathogens because it only affects humans. In fact, some individuals can unwittingly become carriers of the bacterium and transmit the disease to others through improperly prepared food, like the infamous Typhoid Mary. This disease is caused by the bacterium Salmonella typhi, which is one of over 2,300 species of Salmonella and can be treated with antibiotics, according to the USDA. Other Salmonella species are also common among household, cold-blooded critters like turtles, frogs, iguanas, and snakes, so it’s important to always wash your hands after handling these pets.  Like malaria and rabies, Typhoid fever presents challenges for eradication in developing countries where poverty limits accessibility to clean water, pasteurization, and proper sanitation and hygiene. For example, I had never taken a well-water bucket shower before, and although the murky water felt refreshing after a long days’ work, I came to more deeply appreciate the luxuries of everyday plumbing and electricity.

Collaboration is Key

An empowering lesson that continues to inspire me was when I participated in a humanitarian collaboration. Before our departure, we communicated with another mission team from an Arkansas Baptist church that would work at the same time as our Iowa State Christian veterinary mission team would work over spring break. The goal of the Arkansas team was to provide humanitarian care while the goal of the Iowa State team was to provide veterinary care. For instance, the Arkansas team brought donated shoes and eyeglasses, provided nutrition education and had a dentist and nurse that pulled teeth. On the other hand, the Iowa State team vaccinated dogs, cats, horses, cattle, and pigs, performed surgeries and provided agricultural advice to farmers. Even though the two teams set up separate clinics to work on different species, we still felt united as one team because we traveled together, ate meals together, and worshiped together.

Brandon picture 4

One sunny afternoon, we asked the human dentist to come over to our animal clinic to pull a rotten tooth out of a horses’ mouth. The dentist had hardly been around horses in his life, let alone stuck his hand in one’s mouth before, but after the novelty wore off, he quickly agreed to help our team. The sedated horse was lying on its side surrounded by curious villagers and veterinary students. The dentist was nervous and the 3 inch long decayed molar kept wiggling out of his grip. Finally, he extracted the tooth and everyone was amazed and overjoyed. It’s a simple story like this that showcases the successful collaboration between veterinarians and other medical professionals that is the goal of the One Health Initiative or the new concept of interdisciplinary healthcare collaboration. In order for us to eradicate these infectious diseases and save lives, it is vital that veterinarians, physicians, dentists, and epidemiologists collaborate and communicate to find solutions.

A Future Fighting Infections

Going on this short-term veterinary mission trip put me in harm’s way, but it gave me real-life experience with infectious diseases, deepened my faith, and strengthened my clinical skills. It was bittersweet to say adios to my amigos, but I know I’ll return to that perilous paradise.  I enjoyed the international fieldwork and cross-cultural partnership because it embodies the One Health Initiative that I highly esteem. From hiking in the jungle on my 23rd birthday to taste-testing iguana to teaching children about pet care and the Word of God, this trip was a remarkable adventure that has forged a new trail for me. I don’t believe it’s an impossible mission, and I am committed to pursue veterinary public health as a career and control zoonotic diseases in developing countries.

All photos courtesy and copyright Brandon Woods. 


Student guest post: A Push for Pasteurization

Student guest post by Molly Stafne

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Student guest post: Tuberculosis: A Real Problem With No Real Solution

Student guest post by Jack Hamersky

After successfully completing a job interview I had the opportunity to take the next step in my employment process: taking a Tuberculosis or TB test.  I have received the test before but never really understood the point of testing for a disease no one ever sees in my community. I always thought, “Why not focus all this effort and money on more prevalent infectious agents such as Ebola or HIV?” You know, focus on something important.  So, as the nurse called me in from the waiting room I began to curse that hard little bubble that would soon be forming under my skin, and the inconvenience it would be to have to come back to this same clinic to have it read.

This same type of experience is known throughout the United States and other developed countries.  However, many people like myself, do not know the importance of this test.  They might not know that this test is a crucial part of the much larger goal of eradicating a deadly and common worldwide disease.

What is tuberculosis and why is it even important?

Tuberculosis is a contagious disease that is found in both animals and humans. The human form of the disease is caused by a group of three bacteria: Mycobacterium bovis, Mycobacterium avium, and Mycobacterium tuberculosis.  This disease can come in two forms: latent and active.  The active form of tuberculosis causes pockets of pus called granulomatous lesions in lungs and has a death rate around 50%. It is estimated that TB infects around one third of the human population on earth and is the second leading cause of death by infectious disease, behind HIV, killing around million people annually, according to the Center for Disease Control and Prevention; CDC (4).  The greatest prevalence of TB occurs in developing countries and their low socioeconomic populations.  This is likely due to the limited availability of health care, poor nutrition, and overcrowding conditions these people face on a daily basis.  Immunosuppressed individuals, such as people infected with HIV, are also more likely to contract tuberculosis.  TB is also very hard to treat and many forms of the disease are resistant to antibiotics.

Another reason TB is so dangerous is the threat of Mycobacterium bovis. M. bovis is another strain of tuberculosis that mainly infects cattle, cervids (deer like animals), elephants, bison, etc (7,10). What makes this bacterium interesting is its been known to infect people through the consumption of raw (unpasteurized) milk or products that were made from that raw milk (1,5,7,10). This zoonotic microorganism is responsible for two percent of all new cases of TB in the US (7) with an even a greater percentage worldwide (6).  The zoonotic nature of M. Bovis allows for it to hide in wildlife populations which act as a reservoir for the disease (6,9). The good news is a campaign to eradicate M. Bovis from the US food supply began in 1993(5). The bad news is that TB remains endemic in wildlife and agricultural animal populations worldwide. The program in the United States has been a success and most of the United States is considered Bovine Tuberculosis free.  However some states, such as Michigan, still find M. bovis in their wild deer herds making the continual threat of reemergence a reality.

So what have we done about this problem?

The United States government has taken a leading role in the fight against TB. It formed the Advisory Council for the Elimination of Tuberculosis to address the growing resurgence of TB in the 1980’s (5). It also passed legislation like the Comprehensive Tuberculosis Elimination Act which called for the increase of federal funding, education, and international collaboration in the fight against TB.  Other non-governmental advancements have taken place over the years too.  A vaccine was created and is now available throughout the world.  Known as BCG, this vaccine is good at protecting children against the disease, however, it loses its effectiveness as children grow older and has not shown promising results in adults (8).  This, coupled with the increasing amount of antibiotic resistant cases (known as Multi Drug Resistant Tuberculosis or MDR TB) once again proves the fight to eradication or even control might be more of an uphill battle then we once thought.

So how is the fight to end TB going?

Over the past few decades we have made progress and in 2011, the World Health Organization reported “The absolute number to TB cases has been falling since 2006”. However, in that same report, the WHO also stated, even though TB cases had dropped, “In 2009 there were almost 10 million children who were orphans as a result of parental deaths caused by TB” (12,13).  As long as there TB is left to reside in our low income populations and in animal reservoirs it will continue to plague millions worldwide.

So where do we go from here?

The continuation and strengthening of surveillance and research projects worldwide is the key to combat tuberculosis.  The more we know about the disease and its ecology the better prepared we will be to face the challenges we may encounter during its eradication process.  Will we ever get to total world eradication of tuberculosis?  This writer thinks so but to quote the great Robert Frost it seems that “we have miles to go before we can sleep”.




















Student guest post: Cholesterol, a bacterium, and gallbladder cancer

It’s time for this year’s second installment of student guest posts for my class on infectious causes of chronic disease. Fourth one this round is by Kristen Coleman. 

If you are anything like me, you have been told countless reasons over the years why we must watch what we eat, keep our cholesterol intake down, and try to work out. It shouldn’t really come as a surprise then that I, since I am a public health student after all, aim to convince you of yet another reason why a healthy diet and exercise are valuable. What is this huge reason to avoid Big Macs and think about taking the stairs instead of the elevator you ask? Well, it may help you to prevent gall bladder cancer, is all.

All of this begins with gallstone formation. Gallstones are hard deposits, usually of cholesterol, that become lodged in your gallbladder over time. Your gallbladder is an organ that helps to aid in digestion through the storage and release of bile which helps to break down fats in your small intestine. The gallbladder is located on the right side of the body attached to the liver. The process of gallstone formation is called cholelithiasis. In this process, cholesterol, which is not very soluble, becomes clustered together in droplets in the bile called micelles. This cholesterol droplet then hardens into the crystals that make up a gallstone. Obesity causes bile to transit the gallbladder less rapidly and increased cholesterol in the diet means there is more cholesterol available to form stones. It does not require and active imagination then, to understand how obesity and high cholesterol intake contribute to stone formation, but how does this all tie into cancer you ask?

It all comes down to infection with a bacterium known as Salmonella typhi. Yes, this is the same bacterium that causes Typhoid fever and was the malady that afflicted the famous Typhoid Mary. While many people may become infected with S. typhi over the course of their lives, those individuals with gallstones are 6-15 times more likely to become carriers of S. typhi in the gallbladder. This is important because those people with a chronic infection of S. typhi have been shown to have 3-200 times higher risk of developing gallbladder cancer then non-carriers. Furthermore, chronic carriers have a 1-6% lifetime risk of developing gallbladder cancer. In fact, gallbladder cancer is so linked to S. typhi infection that gallbladder removal, called cholecystectomy, is recommended for those people with gallstone disease who live in high risk areas. Where is a high risk area? Most developing countries of the world are high risk areas for S. typhi, especially countries in Asia, Africa, and Latin America. This means that travelers from the USA and other developed countries to these regions are at risk for developing the infection. However, even at home in the USA, low risk doesn’t mean no risk, and we should be vigilant against emergence of this bacterium.  

In conclusion for all my gallbladder-containing friends out there (I make this distinction because I, myself, am no longer at risk for gallbladder cancer since I had mine removed in 2006 after a bout with gallstone disease) stay aware of your cholesterol levels and pay attention to making sure you have a healthy diet because, like every health care professional will tell you, it might just save your life….perhaps in a way you don’t expect!


  1. University of Maryland Medical Center. Gallstones and gallbladder disease. Online
  2. Ferreccio, Catterina. Salmonella typhi and Gallbladder Cancer.

Center for Disease Control online source.

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.


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.

Plague in Victorian San Francisco–lessons for public health communication

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

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

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

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

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

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

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

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

Further reading and references

Chase, “The Barbary Plague”.

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