Spillover: Animal Infections and the Next Human Pandemic

For Quammen’s next zoonosis tale, he goes back to Australia and also back in time to the 1930s—to a mysterious flulike illness later christened “Q fever.” Unlike previous diseases Quammen has examined, Q fever is a zoonotic bacterium, not a virus. Like Hendra, Q fever has particular ties to Australia, while psittacosis first attracted major attention after parrots that were brought to the United States sickened people in Annapolis, Maryland. The disease causes a variety of symptoms, described as “fever, aches, chills, pneumonia, and sometimes death” (212). Newspapers popularized it as “parrot fever.” The third subject of this section is Lyme disease, so named after parents in Lyme, Connecticut, noticed their children were developing arthritis-like symptoms after being bitten by ticks. All three diseases are bacterial, which Quammen points to as a sign that “not every bad, stubborn, new bug is a virus” (213).

The first recorded outbreak of psittacosis was discovered in the 1880s by a Swiss physician who notice that the symptoms of a mysterious new “pneumotyphus” were traceable to the household’s pet birds. Another outbreak in Paris was caused by a large shipment of parrots, while a cluster of cases in Germany showed that canaries could also transmit the illness. Public interest declined during WWI, but the 1929 Annapolis outbreak renewed interest as it spread to many more states. Then-president Herbert Hoover banned the import of parrots. Government researchers at a US Public Health service laboratory conducting bird necropsies also became ill, leading the laboratory head, George W. McCoy, to euthanize all the remaining animals.

About a month after this, a bacterium was identified as the cause of the disease and called Rickettsia psittaci (in the same family as typhus). Eventually it was determined that California parrots raised for domestic pets also had the disease. Because parakeets are native to Australia and that country was thought to be “psittacosis free,” American scientists proposed repopulating the United States bird market with Australian ones. Some American researchers received permission to import Australian birds and infect them with psittacosis as part of an experiment. Before they could begin, one bird died and was found to already have it, while others had “latent infection.”

Quammen introduces an Australian microbiologist and virologist named Frank Macfarlane Burnet, a somewhat eccentric figure who trained as a doctor but soon decided academia was a better fit. Macfarlane Burnet discovered that many of the parrots he tested from all over the country carried the disease. He surmised that Australian people were also likely experiencing the disease but were simply being misdiagnosed. His investigations found 29 bird owners who experienced similar symptoms. All of them had purchased animals from a bird dealer Burnet dubbed “Mr. X” and whose family members and neighbors also became ill. Burnet hypothesized that most animals were infected young and might carry the infection but rarely suffered from it unless they were kept in unsanitary conditions.

After noting that government action to guarantee sanitary living conditions for birds was necessary but unlikely, Burnet began to study Q fever. The typhus-like illness was common among Australian abattoir workers, and its first investigator was a director of microbiology in the Queensland Health Department. He isolated the mysterious pathogen but couldn’t culture it or see it, so he turned to Burnet for help. Staining samples from infected animals proved that what was once thought to be a “filterable virus” was in fact a very small bacterium. It eventually became “Q fever,” and its scientific name, C. burnetii, was in Burnet’s honor (220).

Back in the United States, scientists at the Rocky Mountain Laboratory in Montana found another Rickettsia agent in ticks. This one was distinct from Q fever but resembled it. Burnet’s further research revealed that Q fever had gone global and infected troops in WWI and domestic animals in North Africa and Greece. The disease was easily transmitted by various routes: As he [Burnet] said, it was versatile” (222).

Q fever is not just a historical episode. A 2007 outbreak in the Netherlands occurred in a small bedroom community called Herpen, home to some limited agriculture in the form of dairy goats. At first only goat farmers noticed the problems—fewer pregnancies were carried to term, and the kids who were born seemed less healthy. That spring was unusually dry and windy. The local doctor and his colleagues soon saw many patients mysteriously ill and in need of antibiotics. Eventually, the Municipal Health Service was notified, and the disease identified as Q fever. This led to more serious national attention to the disease. Scientists in the Netherlands focused on the fact that Q fever was “capable of airborne transmission” and began to investigate the wider environment of the goats in the area (225).

At this point, Quammen moves forward in time a few years to recount his own visit to Herpen and his meeting with the local physician Rob Besselink. Besselink noted a long-term change in the region that helped explain the outbreak: a shift away from cow dairy farming and toward goats because of European community “quotas on cow milk” (225). Goats being kept indoors did little to prevent spread, as the disease “is also excreted in milk, urine, feces, and during normal deliveries of kids carried to term” (226). When straw bedding and feces are used as fertilizer, wind is sufficient to transmit the disease to neighboring areas.

In Herpen, a large commercial farm was found to be the outbreak’s source. Quammen met with a molecular biologist from the Dutch team of scientists named Arnout deBruin. Their results revealed that many people in the area, over a hundred, had been infected recently or sometime in the past. Relatively few of these people actually worked on farms—because of the manure in fields and the weather, “windborne transmission” was the primary cause. Laboratory teams, including de Bruin’s, became more concerned with becoming infected themselves—but even getting out of a car required breathing in the wind before a mask was on.

The Dutch outbreak was several years long. By the end of 2009, “3,525 cases had been recorded” (229). Quammen visited the Dutch Central Veterinary Institute to learn more about what made Q fever unique. Because the bacteria took over cells and reprogrammed them, much like a virus does, it was able to evade standard “immune response” (230). The conditions goats were raised in aided in bacterial growth, and the Netherlands’ high population density and weather conditions likewise made it easy for the bacteria to spread. Some data also suggested that C. burnetii had mutated in the Netherlands, as one particular type of the bacteria was frequently found to be responsible for outbreaks there.

The Dutch government took a variety of preventative steps as the outbreak continued into 2009. First, it required notification of any large clusters of goat abortions that would likely indicate disease. Then, it implemented a mandatory vaccination program for goats and sheep. When this did not halt the spread, it established a mandatory “culling” of all pregnant goats was established. Eventually, the outbreak tapered off, but experts remained wary.

Quammen returns to 1930s Australia to detail another of Burnet’s contributions to our understanding of the science of disease. After his discovery of Q fever, Burnet turned to the problem of disease in general. As doctors, the individuals who had discovered germ theory, like Pasteur, had been mostly concerned with public health. Their focus on prevention obscured that bacteria are also living, with “their own histories in the wild” (235).

As he considered this, Burnet compared “parasites” (his term for bacteria) to “predatory carnivores” feeding off their hosts as large animals feed off small ones. Diseases also seek transmission so that new hosts provide new opportunities to survive and reproduce. Like some of his mathematically minded predecessors, like Cormack and McKendrick, Barnet emphasized that diseases benefit from population growth of susceptible hosts, and also from population density. Burnet also noted that while we naturally focus on disease outbreaks in people, these are often only one episode in a bacterial life cycle. For him, psittacosis illustrated that human activity was constantly influencing where diseases spread and how they evolved.

Quammen turns back to the United States and moves forward in time to introduce his last bacterial zoonosis: Lyme disease. He notes that this particular zoonosis may seem more familiar than others, declaring, “You probably know someone who has had it; you may well have had it yourself. By any standard, it’s the most commonly reported vector-borne disease in the United States” (238). One enduring controversy between patients and scientists is the existence of chronic Lyme disease—patients whose symptoms persist want ongoing treatment, while experts are deeply skeptical of their claims.

Physicians as early as 1910 found patients with infections after insect bites and noted that the rashes resembled some symptoms of syphilis patients (the bacteria are somewhat related) and caused symptoms resembling meningitis (240). A Swedish doctor published some of his findings in the United States, and in 1970 an American doctor identified a patient with the same symptoms.

This research history resurfaced when a rheumatologist named Allen Steere in Lyme, Connecticut became troubled by an apparent “cluster” of rheumatoid arthritis cases. Eventually, a field biologist was bitten by a tick and developed symptoms, and he brought the tick for sampling. The deer tick or “Ixodes scapularis” was suspected as the animal carrying the disease. The actual bacterium was discovered by a Swiss microbiologist named Willy Burgdorfer who grew the bacteria, tested it against antibodies from Lyme patients, and infected rabbits with it to look for the typical rash. When both occurred, he was credited with discovery of the agent, and it was named Borrelia burgdorferi.

A more consequential naming occurred when the tick carrying the bacteria became colloquially known as the “deer tick,” which led to assumptions that the insect commonly fed on deer. This led to the assumption that Lyme levels must correlate with deer population. An ecologist named Richard Ostfeld untangled this mystery in 2011, but not before several misguided efforts to reduce deer population throughout New England.

Quammen calls Ostfeld “a heretic with data” (247). A small mammal expert, Ostfeld found that the white-footed mouse was infested with the so-called deer tick. Using “trap and release,” he and his team became experts in detecting and examining ticks, then returning the mice to their habitat (248). White-footed mice host the ticks in their “larval stage” prior to adulthood (250), because the smaller ticks seek hosts they can access easily. Adult ticks do feed on deer, but infection occurs only at the larval stage. The mice are known as “competent reservoirs” because they have high rates of carrying and transmitting the disease to other ticks (251). Deer and humans, by contrast, are “incompetent,” since the disease does not spread well from either (252).

Quammen visits the woods of Duchess County, New York, with Ostfeld and his team of postdoctoral researchers and laboratory assistants. After observing some catch and release, Quammen asks Ostfeld what precautions concerned people should take to prevent Lyme. Ostfeld asserts that “biodiversity” is critical—if there are enough predators to keep mouse and small-animal populations down, Lyme is less likely. (255-56). Less diverse forests correlate with recent human settlement— in other words, human habitat disruption influences the spread of Lyme just as it does viral zoonosis. Borrelia Burgdorferi also attempts to defend itself against bacteria—it transforms into “round bodies” that “are resistant to destruction and very difficult to detect” and may be responsible for the mystery of chronic Lyme (258-59).