Zoobiquity

Authors’ Note

Acknowledgments

Notes

Works Consulted

A Note About the Authors

Although this work is a journalistic collaboration between two authors, we chose for stylistic reasons to write the book from Dr. Natterson-Horowitz’s point of view. We felt her journey from focusing solely on human medicine to a broader, species-spanning approach demanded a first-person narrative structure. Most interviews in the book were conducted by both authors, although in a few cases only one author did the questioning. The final book is the result of a true partnership not just between Dr. Natterson-Horowitz and Ms. Bowers but among the many physicians, veterinarians, biologists, researchers, other dedicated professionals, and patients (whose names we’ve changed where necessary) who so generously shared their time, scholarship, and experiences with us.

In the spring of 2005, the chief veterinarian of the Los Angeles Zoo called me, an urgent edge to his voice.

“Uh, listen, Barbara? We’ve got an emperor tamarin in heart failure. Any chance you could come out today?”

I reached for my car keys. For thirteen years I’d been a cardiologist treating members of my own species at the UCLA Medical Center. From time to time, however, the zoo veterinarians asked me to weigh in on some of their more difficult animal cases. Because UCLA is a leading heart-transplant hospital, I’d had a front-row view of every type of human heart failure. But heart failure in a tamarin—a tiny, nonhuman primate? That I’d never seen. I threw my bag in the car and headed for the lush, 113-acre zoo nestled along the eastern edge of Griffith Park.

Into the tiled exam room the veterinary assistant carried a small bundle wrapped in a pink blanket.

“This is Spitzbuben,” she said, lowering the animal gently into a Plexiglas-fronted examination box. My own heart did a little flip. Emperor tamarins are, in a word, adorable. About the size of kittens, these monkeys evolved in the treetops of the Central and South American rain forests. Their wispy, white Fu Manchu–style mustaches droop below enormous
brown eyes. Swaddled in the pink blanket, staring up at me with that liquid gaze, Spitzbuben was pushing every maternal button I had.

When I’m with a human patient who seems anxious, especially a child, I crouch close and open my eyes wide. Over the years I’ve seen how this can establish a trust bond and put a nervous patient at ease. I did this with Spitzbuben. I wanted this defenseless little animal to understand how much I
felt
her vulnerability, how hard I would work to help her. I moved my face up to the box and stared deep in her eyes—animal to animal. It was working. She sat very still, her eyes locked on mine through the scratched plastic. I pursed my lips and cooed.

“Sooo brave, little Spitzbuben …”

Suddenly I felt a strong hand on my shoulder.

“Please stop making eye contact with her.” I turned. The veterinarian smiled stiffly at me. “You’ll give her capture myopathy.”

A little surprised, I did as instructed and got out of the way. Human-animal bonding would have to wait, apparently. But I was puzzled. Capture myopathy? I’d been practicing medicine for almost twenty years and had never heard of that diagnosis. Myopathy, sure—that simply means a disease that affects a muscle. In my specialty, I see it most often as “cardiomyopathy,” a degradation of the heart muscle. But what did that have to do with capture?

Just then, Spitzbuben’s anesthesia took effect. “Time to intubate,” the attending veterinarian instructed, focusing every person in the room on this critical and sometimes difficult procedure. I pushed capture myopathy out of my mind to be fully attentive to our animal patient.

But as soon as we were finished and Spitzbuben was safely back in her enclosure with the other tamarins, I looked up “capture myopathy.” And there it was—in veterinary textbooks and journals going back decades.
There was even an article about it in
Nature
, from 1974. Animals caught by predators may experience a catastrophic surge of adrenaline in their bloodstreams, which can “poison” their muscles. In the case of the heart, the overflow of stress hormones can injure the pumping chambers, making them weak and inefficient. It can kill, especially in the case of cautious and high-strung prey animals like deer, rodents, birds, and small primates. And there was more: locking eyes can contribute to capture myopathy. To Spitzbuben, my compassionate gaze wasn’t communicating, “You’re so cute; don’t be afraid; I’m here to help you.” It said: “I’m starving; you look delicious; I’m going to eat you.”

Though this was my first encounter with the diagnosis, parts of it were startlingly familiar.
Cardiology in the early 2000s was abuzz with a newly described syndrome called takotsubo cardiomyopathy.
This distinctive condition presents with severe, crushing chest pain and a markedly abnormal EKG, much like a classic heart attack. We rush these patients to an operating suite for an angiogram, expecting to find a dangerous blood clot. But in takotsubo cases, the treating cardiologist finds perfectly healthy, “clean” coronary arteries. No clot. No blockage. No heart attack.

On closer inspection, doctors notice a strange, lightbulb-shaped bulge in the left ventricle. As the pumping engines for the circulatory system, ventricles must have a particular ovoid, lemonlike shape for strong, swift ejection of blood. If the end of the left ventricle balloons out, as it does in takotsubo hearts, the firm, healthy contractions are reduced to inefficient spasms—floppy and unpredictable.

But what’s remarkable about takotsubo is what
causes
the bulge. Seeing a loved one die. Being left at the altar or losing your life savings with a bad roll of the dice. Intense, painful emotions in the brain can set off alarming, life-threatening physical changes in the heart. This new diagnosis was proof of the powerful connection between heart and mind. Takotsubo cardiomyopathy confirmed a relationship many doctors had considered more metaphoric than diagnostic.

As a clinical cardiologist, I needed to know how to recognize and treat takotsubo cardiomyopathy. But years before pursuing cardiology, I had completed a residency in psychiatry at the UCLA Neuropsychiatric Institute. Having also trained as a psychiatrist, I was captivated by this syndrome, which lay at the intersection of my two professional passions.

That background put me in a unique position that day at the zoo. I reflexively placed the human phenomenon side by side with the animal one.
Emotional trigger … surge of stress hormones … failing heart muscle … possible death
. An unexpected “aha!” suddenly hit me. Takotsubo in humans and the heart effects of capture myopathy in animals were almost certainly related—
perhaps even the same syndrome with different names
.

But a second, even stronger insight quickly followed this “aha.” The key point wasn’t the overlap of the two conditions. It was the gulf between them. For nearly four decades (and probably longer) veterinarians had known this could happen to animals—that extreme fear could damage muscles in general and heart muscles in particular. In fact, even the most basic veterinary training includes specific protocols for making sure animals
being netted and examined don’t die in the process. Yet here were the human doctors in early 2000 trumpeting the finding, savoring the fancy foreign name, and making academic careers out of a “discovery” that every vet student learned in the first year of school. These animal doctors knew something we human doctors had no clue existed. And if that was true … what else did the vets know that we didn’t? What other “human” diseases were found in animals?

So I designed a challenge for myself. As an attending physician at UCLA I see a wide variety of maladies. By day on my rounds, I began making careful notes of the conditions I came across. At night, I combed veterinary databases and journals for their correlates, asking myself a simple question: “Do Animals Get [
fill in the disease
]?”

I started with the big killers. Do animals get breast cancer? Stress-induced heart attacks? Leukemia? How about melanoma? Fainting spells? Chlamydia? And night after night, condition after condition, the answer kept coming back “yes.” The similarities clicked into place.

Jaguars get breast cancer and may carry the BRCA1 genetic mutation that predisposes many Jews of Ashkenazi descent and others to the disease.
Rhinos in zoos get leukemia.
Melanoma has been diagnosed in the bodies of animals from penguins to buffaloes.
Western lowland gorillas die from a terrifying condition in which the body’s biggest and most critical artery, the aorta, ruptures. Torn aortas also killed Lucille Ball, Albert Einstein, and the actor John Ritter, and strike thousands of less famous human beings every year.

I learned that koalas in Australia are in the middle of a rampant epidemic of chlamydia. Yes,
that
kind—sexually transmitted. Veterinarians there are racing to produce a koala chlamydia vaccine. That gave me an idea: doctors around the United States are seeing human chlamydia infection rates spike. Could the
koala
research inform
human
public health strategies? Since unprotected sex is the only kind koalas have (my searches for condom use by animals came up short), what might those koala experts know about the spread of sexually transmitted diseases in a population that practices nothing but “unsafe” sex?