The discovery, Blue wrote Washington, was “perhaps the first demonstration of the occurrence in nature of bubonic plague in the ground squirrel (Citellus beecheyi) of California.” As the animals inhabited the whole state, he added, “the discovery has caused considerable apprehension.”30
In San Francisco, the team was tackling another question. Back at 401 Fillmore Street, Blue ordered the rat trappers to bring rats back alive. Baskets of the wriggling prey were emptied into glass jars with chloroform-soaked gauze.
Once the scrambling rats slowed in their struggle and grew still in their death sleep, district officers combed their fur for fleas—by now also dead. They put the fleas from each rat into glass bottles filled with alcohol. Each bottle was labeled with the date, type of rat, and the district from which it was captured. The flea wranglers then sent their catch to 401 Fillmore Street.
Colby Rucker pored over flea anatomy with a sense of wonder. He marveled that the flea has the largest, most powerful hind legs of any creature its size, enabling it to jump five hundred times its length—a feat equal to a human vaulting over a skyscraper of almost two hundred stories. The flea, he asserted, was responsible for more annual deaths than any monstrous reptile or carnivore in nature.
For an essay entitled “The Wicked Flea,” Rucker peered through the microscope and discovered that the sesame seed—size specks were armed with armadillolike plates, triangular slashing weapons, two lances, and a stiletto with which they pierced their victims’ skin and sucked their blood. Rucker also studied the mating habits of fleas; during their courtship, he watched as the “lordly” males sat back in a passive role, while the females engaged in a frenetic dance of seduction. After coupling, the female laid a clutch of waxy ovoid eggs that, over her lifetime, could produce up to five hundred hungry hatchlings.31
Even less savory were the fleas’ dining habits. With horrid fascination, Rucker observed the suckling parasites in action with his colleague George McCoy. McCoy rolled up his sleeves and, holding the fleas under inverted test tubes, allowed the insects to feed on his bare arms. The men found that, after eating, the flea left a deposit on the skin of its victim. When the victim scratched, this deposit got rubbed into the skin. Scratching helped to inoculate the bacteria with deadly efficiency. The lab fleas, fortunately, were healthy.
Years later, scientists would discover that the material injected by a flea into its victim was actually blood from a previous bite. After several feedings, these previous blood meals collected in the flea’s foregut, welling up like heartburn, to be injected into the bite wound on the next victim’s skin.32
But Rucker and McCoy’s colleague, Carroll Fox, made a curious discovery: In San Francisco, the prevalent flea species was not the Oriental or Indian rat flea, Pulex cheopis. While there were a few of those in the city, the main flea species on the Golden Gate was the northern European rat flea, Ceratophyllus fasciatus.33 Beyond being of academic interest to entomologists, what possible difference could that make?
Plenty, as it turned out.
For San Francisco had had a stroke of dumb luck. The plague flea’s key trait wasn’t its armor or its stiletto, but its gut. Although Fox didn’t appreciate the significance of his findings at the time, scientists now know that the Asian flea cheopis grows a basket of spines in its belly. Inside that basket, a clot of blood collects, forming a potent ball of plague germs. The clot also blocks new blood meals from reaching the flea’s stomach, so it begins to starve. That makes the ravenous flea attack more aggressively, biting any warm-blooded animal that crosses its path. Finally, its frenzied sucking dislodges the ball of germ-laden blood. It is, in effect, this flea heartburn that delivers a lethal dose of plague into its hapless human host.
Fasciatus, the Frisco flea, has a foregut without that spiny basket. So while it is capable of transmitting plague, each injection delivers a less potent—that is, less infectious—dose of the germs. Cheopis, the lethal flea, visited San Francisco, but it remained in the minority. Had it taken over to become the dominant species on the Pacific coast, the toll of the sick and the dead might have been far higher.
Although he didn’t know it at the time, Fox’s finding about local flea species provided a clue to later scientists as to why San Francisco’s plague claimed hundreds, rather than thousands, of casualties. The plague germs were as deadly, the rats as numerous, the fleas as hungry. The only difference may have been a quirk of flea anatomy.
With so much energy funneled into flea studies in the San Francisco laboratory, Indian summer commenced with little fanfare. Warm, sunstruck, and treacherous, September 1908 was ripe for a resurgence of human plague. Blue remained edgy and watchful.
Without warning, word of a setback came from the southern tip of the state. Health officers in Los Angeles, four hundred miles to the south, had a sick ten-year-old boy on their hands. Doderick Mulholland, who lived in the Elysian Park neighborhood of Los Angeles, fell suddenly ill with a fever and tender knobs sprouting from his glands. A dead squirrel was found near his house. The Mulholland boy was biopsied and tested positive for plague. The animal, too, harbored the bacteria. But the young boy lived. To everyone’s relief, his case remained an isolated one. Plague did not establish a foothold in Los Angeles—not yet, anyway.
Managing operations on three fronts, Blue decided that a frontal attack on the squirrels was the fastest way to purge the countryside. But squirrels are wary and lightning-fast, nearly impossible to bait and trap. He wrote to Washington, asking $1.50 a day to rent rifles and buy ammunition. Once more, he tripped over red tape. Washington reproached Blue for sloppy form in making his request, denying him funds.
Colby Rucker had greater woes. One evening, after giving a speech in San Jose, Rucker dined with Annette’s physician. The doctor frankly confided his fears about her cough. “In truth it worries me too,” Rucker wrote in his diary. “But I don’t know what to do.”34
As Annette lay pale and fatigued, her son, Colby, tried to beguile her with a popular new song on the player piano. He inserted the roll, and out pealed the song “Glow, Little Glowworm.” Annette smiled wanly, but a nurse hired to tend her hushed the boy. “Let the boy play,” Annette implored. He was allowed to finish the tune, but he never touched the instrument again, forever hating the song that couldn’t make his mother well.35
With rumors of many squirrels dying, and Washington dragging its feet, Rucker bought himself a $9 rifle and some maps. He packed up his family and ferried them to the East Bay. The warm, dry weather might be good for Annette’s lungs, he thought. He staged a buggy excursion to the East Bay peak of Mt. Diablo, with watermelon picnics by the roadside. Annette gained a bit of strength. When Rucker returned to San Francisco, he marked a birthday and found tufts of gray sprouting over his ears. He was thirty-three years old.36
Meanwhile, the epidemic retreated in San Francisco. The month of September, which had seen fifty-five cases the previous year, ended without a single new case.
By October 1908, Blue counted a lapse of eight months since the last case of human plague in San Francisco. From May 1907 to February 1908, plague had sickened 160 San Franciscans and killed 77 of them. It was a broader and swifter outbreak, more democratic in its choice of victims, but less deadly than the smoldering plague of 1900. That earlier episode in Chinatown took a narrower aim on the Chinese, and case for case, it was far more lethal, with an official count of 121 sick and 113 dead. However, given the suspicion by many white doctors that the community had hidden some of its sick and the dead, the true total would never be known.