Food for Thought

When is a zoönosis not a zoönosis? Two new books show how animal diseases have taken advantage of our primitive hunger for protein.

MARIA DE LA O

As a group of passengers disembarked at Logan International Airport in Boston last year, they had a very special shipment of cargo to declare: the remains of 26 primates from the West African country of Guinea, amounting to 300 pounds of meat destined to be the main course at an upcoming wedding reception.

Agents proceeded to confiscate the meat—after donning biohazard suits. Hazmat gear is standard procedure every time U.S. Fish and Wildlife Service agents discover an illegal shipment of wild meat, which, while far from an everyday occurrence, isn’t uncommon.

Not long after the Logan seizure, an Ebola outbreak flared in Central Africa. Although eating primate meat has been implicated in the transmission of Ebola from primates to humans, primates are not the only animals identified as sources of human disease: sars is associated with eating civets, monkeypox can be transmitted through rodent meat, and domestic poultry and livestock are often implicated in flu outbreaks. Transportation and global trade facilitate not only the spread of goods, but also the spread of zoönoses, those diseases that infect both animals and humans.

But there are other kinds of zoönoses, too—diseases that we are just beginning to understand, that are arguably of our own making, and that don’t normally cross the species barrier but will do so under highly unusual conditions, with symptoms that mutate along the way. These “transmissible spongiform encephalopathies,” or TSEs, are the subject of How the Cows Turned Mad, by molecular biologist Maxime Schwartz, and The Pathological Protein: Mad Cow, Chronic Wasting, and Other Deadly Prion Diseases, by Scientific American editor Philip Yam.

Merriam-Webster defines a zoönosis as “a disease communicable from animals to humans under natural conditions.” But what exactly are “natural” conditions? TSEs, which include scrapie and mad cow disease, are thought to be caused by prions, a toxic protein first described in the early ’80s. Prion researchers believe that all TSEs are related, so much so, say experts like Dr. Schwartz, a former head of the Institut Pasteur, that they are simply variants of the same disease. Under the right conditions, “The Disease,” as Dr. Schwartz calls it, can affect sheep, cows, deer, cats, mice, and humans, among other beasts, in the guise of different “avatars.”

How the Cows Turned Mad, first published in France in 2001, and Mr. Yam’s new offering both consider the question, How did TSEs cross the species barrier? To answer that, the books take the reader from scrapie’s first appearance in 18th-century Britain to mad cow disease and the current outbreak of chronic wasting disease among deer in the United States, explaining how prions are highly adaptable and can jump from one animal species to another.