called “deer ticks,” were abundant in the forests of eastern Connecticut and surrounding areas. In the early 1980s, a microbiologist named Willy Burgdorfer found a new bacterium in the guts of some Ixodes ticks, a likely suspect as the causative agent. It was a spirochete, a long spiral form, closely resembling other spirochetes of the genus Borrelia. After further research confirmed its role in the arthritis-like syndrome, that bacterium was named Borrelia burgdorferi in honor of its principal discoverer. Lyme disease is now the most common tick-borne disease in North America and one of the fastest-increasing infectious diseases of any sort, especially in New England, the mid-Atlantic states, and Wisconsin. Part of what makes it problematic is that the life history of Borrelia burgdorferi is very complex, involving much more than ticks and people.
Lyme disease, psittacosis, Q fever: These three differ wildly in their particulars but share two traits in common. They are all zoonotic and they are all bacterial. They stand as reminders that not every bad, stubborn, new bug is a virus.
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Parrot fever was recognized as far back as 1880, when a Swiss physician named Ritter described a household outbreak, of something resembling typhus, in which seven people got sick and three died. Because the illness showed certain pneumonia-like aspects, suggesting airborne transmission, Dr. Ritter called it “pneumotyphus,” but he was groping. Although he couldn’t identify what caused it, he did manage to pinpoint the site of common exposure: the house’s study. The only thing remarkable about that room was that it happened to contain a dozen caged birds, including finches and parrots.
A larger outbreak occurred in Paris in 1892, after two animal dealers received a shipment of five hundred parrots imported from Buenos Aires. The dealers became infected, several of their customers became infected, and then so did relatives, friends, and one doctor in attendance. Sixteen people died. Soon the disease had cropped up also in Germany, in New York, and at a department store (which sold birds) in Wilkes-Barre, Pennsylvania. In 1898 it struck the annual exhibition of the Berlin Union of Canary Fanciers, demonstrating that parrots and their kin weren’t the only birds capable of carrying this “parrot fever” microbe, whatever it was. (Canaries belong to the order Passeriformes, not to the Psittaciformes.) Half a dozen canary fanciers fell ill and, by an account in a Berlin newspaper, “three died in agony.”
Then came a hiatus, if not in the incidence of parrot-borne infections at least in the attention they received. The Great War, followed immediately by the great influenza, gave people a surfeit of death and disease to engage their sorrows and fears. The 1920s were decidedly more cheerful and carefree, until they weren’t. “The year 1929 marked a turning point in the revival of interest concerning the etiology of human psittacosis,” according to one historical survey of the disease. Etiology, that was the crux. Outbreaks might come and go. What differed in 1929, besides the Crash and a general lowering of spirits, was a sufficiency of parrot-fever cases to make studying the cause not only more practical but also more urgent.
Lillian Martin of Annapolis had been among the first of this new wave, and though she eventually recovered, others weren’t so lucky. The Washington Post continued to track the story, reporting parrot-fever fatalities in Maryland, Ohio, Pennsylvania, New York—and Hamburg, Germany. On January 13, the Surgeon General telegraphed health officials in nine states, asking for help in tracking the situation. Two weeks later, with cases now reported also from Minnesota, Florida, and California, President Hoover declared an embargo against imported parrots. The director of the Bureau of Bacteriology within Baltimore’s health department, who had been doing necropsies on infected birds, got sick and died. A laboratory technician at the Hygienic Laboratory, which was part of the US Public Health Service, got sick and died. That technician had been assisting a researcher, Charles Armstrong, with bird-to-bird transmission experiments in the laboratory basement. Their working conditions were less than ideal: two small basement rooms full of distressed parrots held in garbage cans, wire mesh over the tops, feathers and bird shit flying out, curtains soaked in disinfectant to contain the airborne drift. It wasn’t BSL-4. Charles Armstrong got sick but did not die. Nine other personnel of the Hygienic Laboratory also became infected, none of whom had even entered the basement bird rooms. The laboratory director, realizing that his building was broadly contaminated with whatever wafting agent caused psittacosis, closed the place down. Then he descended