from left: influenza, SARS, Ebola virus, Tuberculosis in sputum
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Those two things are connected. The greater its efficiency in inducing lethal, bug-spreading syndromes (good for the microbe), the faster the microbe kills us (bad for the microbe). Following this logic, a pathogen may end up killing lots of people by one of two routes. In the style of HIV, it can keep the disease carrier alive for a long time, infecting new victims over the course of months or years. Or in the style of smallpox and cholera, it might kill quickly with explosive symptoms that can spread an infection to dozens of new victims within a day.
A microbe’s deadly rampage through humans might stem from an accident of nature.
Searching for the Source
For epidemiologists hoping to stanch such outbreaks, tracking killer germs to the source is key. Do deadly pandemics arise spontaneously in human populations? Or are they “gifts” from other species, mutating and then crossing over to make us ill? Which ecosystems are spawning them, and can we catch them at the start, before they cause too much damage?
Some answers can be found in the history of yellow fever, a virus spread by mosquitoes. The cause of devastating human epidemics throughout history, yellow fever is still rife in tropical South America and Africa. Biologists now understand that yellow fever arose in tropical African monkeys, which, through the mosquito vector, infected (and continue to infect) tropical African people, some of whom unintentionally carried yellow fever with them on slave ships several hundred years ago to South America.
Mosquitoes bit the infected slaves and in turn carried the virus to South American monkeys. In due course, mosquitoes bit infected monkeys and transmitted yellow fever right back to the human population there.
In Venezuela today, the Ministry of Health keeps a lookout for the appearance of unusual numbers of dead wild monkeys, such as howler monkeys. Because the monkeys are so susceptible to yellow fever and can act as a reservoir from which the virus leaps to the human population, an explosion of monkey deaths serves as an advance warning system, signaling the need to vaccinate humans in the vicinity.
This pattern of cross-infection from animals to humans is par for the course in emerging infectious disease. In fact, the big killer diseases of history all came to us from microbes living in other species, overwhelmingly from other warm-blooded mammals and, to a lesser extent, from birds.
On reflection, this all makes sense. Each new animal host to which a microbe adapts represents a new habitat. It is easiest for a microbe to jump between closely related habitats, from an animal species with one sort of body chemistry to a closely related animal species with very similar body chemistry.
In the tropics, disease sources have included a host of wild animals, most notably the nonhuman primates. We can thank our primate cousins not just for yellow fever but also for HIV, dengue fever, hepatitis B, and vivax malaria. Other wild animal disease donors include rats, the source of the plague and typhus.
In temperate regions like the United States, meanwhile, ticks in suburban neighborhoods and domestic livestock living in proximity to humans have posed threats. Mammalian reservoirs like mice and chipmunks carry Lyme disease and tularemia; ticks transmit these diseases to humans. Cattle probably gave rise to the measles and tuberculosis. Smallpox is likely to have come from camels, biologists say, and flu from pigs and ducks.
The Next Wave
Today, with fewer people tending farms and more living in the suburbs, things have certainly changed. The principles of infectious disease are the same as they have always been, but modern conditions, including life in proximity to pets and mammal-filled woods, are exposing us to new pathogen reservoirs and new modes of transmitting disease.
One of us (Nathan Wolfe) has spent much of the last six years in the tropical African country of Cameroon, studying the kinds of interspecies jumps that such conditions might spawn. To examine the mechanisms, I worked with rural hunters who butchered wild animals for food. I collected blood samples from the hunters, from other people in their community, and from their animal prey. By testing all those samples, I identified microbes inhabiting the animal reservoirs and focused on those that showed up in the hunters’ blood, making them candidates for firing up human disease.
One evening I asked a group of hunters if they had ever cut themselves while butchering wild monkeys or apes. The response was incredulous laughter: “You don’t know the answer to that?” Of course, they said. All of them had cut themselves once or more, thereby giving themselves ample opportunity to get infected from animal blood.
