“We lost the Guanay cormorant and a Chilean flamingo here, and the bald eagle over there,” McNamara recalled as we stood by the pool. She pulled her red parka tight, seemingly against the cold March wind but perhaps also against the memory of the virus that blew through the zoo’s bird population. On the morning of September 7, McNamara’s assistant brought her microscope slides bearing brain tissue from the dead flamingo, which looked just like tissue from the dead crows. “I saw the same encephalitis, and my heart just sank,” she said. “Because whatever it was, it was hot, it was bad, and I didn’t know what I had been exposed to.” On her way home that day, McNamara stopped to see a lawyer and drafted her will.
The coincidence was too much for McNamara to ignore. “The fact is,” she said, “I had a bunch of dead birds that had died of encephalitis at the same time that people had encephalitis.” McNamara—a strong personality, candid to the point of abrasion, but scientifically tenacious—refused to take St. Louis encephalitis for an answer, and the growing line of black-lidded specimen jars on a counter in her lab, each filled with the pickled tissue of the virus’s animal victims, gave her plenty of motivation. Before long, it wasn’t just birds. Arhinoceros developed a droopy lip, and a snow leopard became ill. Frantic for help, she sent tissue samples to the National Veterinary Services Laboratory in Ames, Iowa, which ruled out St. Louis encephalitis as well as other likely animal pathogens, and to the CDC’s Fort Collins lab, which declined to analyze her samples. Meanwhile, New York State health officials sent samples from human encephalitis victims to Ian Lipkin, an expert in neurological disorders of viral origin, then at the University of California at Irvine. At the end of September, Lipkin and the CDC (which did test human samples) concluded that the pathogen was not St. Louis encephalitis after all but West Nile virus, a pathogen not previously seen in the Western Hemisphere.
The virus derives its name from the West Nile District in Uganda, where the first human case was identified in 1937. It is found in Africa, the Middle East, Eastern Europe and Asia, where it causes sporadic outbreaks of human disease. Two main lineages of West Nile virus circulate in the world, and the one that reached North America is the more virulent; it’s nearly genetically identical to a strain that circulated in Israel in 1998. Whether it was carried here by an infected person or a bird or a mosquito, no one knows, and probably never will.
But the initial failure of U.S. health officials to quickly identify the pathogen exposed weaknesses in the nation’s ability to detect emerging infectious diseases that occur overseas and then jet to our shores; an even more recent example of how such a disease can spread is Severe Acute Respiratory Syndrome (SARS). Indeed, some experts believe that West Nile virus is more important as a wake-up call about the danger of other jet-setting microbes than a major public health threat. In that spirit, Dominic Travis, a veterinary epidemiologist at Chicago’s Lincoln Park Zoo, and McNamara, with CDC assistance, have organized a network of about 120 zoological parks in the United States to act as sentinels in monitoring the spread of West Nile among zoo animals—and perhaps to serve as an early-warning system for the arrival of other pathogens that affect humans and other animals. “The lessons to be learned from the West Nile outbreak in 1999 is that we received ample warning, at least six weeks before the first human cases,” McNamara said. But because it came from wild birds, she added, “the warning was ignored.”
“West Nile is extraordinarily good at adapting to this new environment,” said Lipkin, who is now director of the Jerome L. and Dawn Greene Infectious Disease Laboratory at ColumbiaUniversity. He takes in the Hudson River and seemingly half of New Jersey from his 18th-floor office. He has long studied bornaviruses, a largely obscure class of pathogens that may play a role in some mental illness. He tested the New York encephalitis samples with a variation of the method known as polymerase chain reaction, which analyzes nucleic acids, and identified the pathogen as West Nile virus, a type of flavivirus. Other flaviviruses include the ones that cause yellow fever and dengue.