Zoonoses and Us

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The explosion in human population over the last couple of centuries has meant, among other things, that we tend to associate more directly and more often with animals that had long been confined alone to forest areas, caves and other habitats. There, animals had lived and died for millennia, the causes of their illnesses largely confined just as they were. But as we move into their homes, cut down their trees, climb through their caves, hunt them, capture them, imprison them, slaughter them, we put ourselves at risk of catching something that can have devastating consequences for us. The last century has seen the outbreak of SARS, Ebola virus, Hendra virus, AIDS and other contagious and deadly illnesses. All of these diseases have zoonotic origins – they spread from their normal environments into new hosts: us. And though we are not clones (well, not most of us), we are all homo sapiens, and thus susceptible as a species to either these known diseases, or ones as yet undiscovered.

The most deadly of these diseases, those which end up killing well over 50% of their victims, have to date been unsuccessful in gaining a strong enough foothold to become truly civilization-threatening outbreaks. The long-mysterious Spanish Flu, which killed some 50 million people over only a couple of years, was zoonotic, an H1N1 virus carried far and wide by its reservoir hosts, the world’s seafaring birds. AIDS has been the most successful of the new breed of zoonotic diseases, despite being relatively difficult to transmit. The more recent SARS and bird flu outbreaks hit hard, spread quickly and then stopped. Scientists can claim some credit for the end of these diseases, but not all.

The determining factor for a successful pandemic, its basic reproductive rate, is referred to as R0 [read “Arrr not”]. This factor is dependent on a pathogen’s rate of transmission \beta, host population size N, lethality \alpha, rate of recovery from infection b and normal death rate of a host population v. In math terms (yay!):

R0 = \betaN / (\alpha + b + v)

Originally described by Roy Anderson and Robert May in 1982, this formula overturned an existing model that a viral or parasitic agent will evolve to co-exist with its chosen host population, weakening its capacity for deadly attack while its host’s immune system adapts to accommodate, often unbeknownst to the host itself. Nope; lethality of a given virus can remain unbelievably high even as the other rates shift, and a seeming “balance” can still be struck between host and invader population, even as R0 stays unchanged. Regardless, the larger R0 gets, the more dangerous the pathogen is to its host population.

The above formula concerns only the basic rate, however, and there are events which can assist the spread of new infections. First and foremost is proximity, density and variation of animal species in a given area. Next are the superspreaders, those people who seem to be ground zero for mass infection, like Typhoid Mary in the early twentieth century, or seafood merchant Zhou Zuofeng, from whom sixty other people directly caught SARS, or Gaetan Dugas and AIDS. And then we have the amplifier hosts, animals that get infected by other animals and then pass them on to humans at much greater rates than otherwise possible. Hendra virus came to us in this way, via sick horses originally infected by the giant bats known as flying foxes.

Grey-Headed Flying Fox

Many of us link AIDS to the 1980s, and with good reason; that decade saw the discovery of both HIV-1 and HIV-2, and many of their variants. Both are zoonotic, with the more geologically confined of the pair originating most likely from the sooty mangabey, and the pandemic that is HIV-1 arising from chimpanzees. Discovery of the disease and viral cause was not its origin, however, and not until the 1990s were dedicated researchers able to locate two samples of HIV-infected blood dating from 1959 and 1960 Zaire/DRC. The fact that these viral samples were significantly different from each other led to a lot of confusion; HIV is a tiny retrovirus made of ribonucleic acid (RNA), and can certainly mutate at a faster rate than DNA, but it’s not *that* fast. By using the genetic clock method I discussed in an earlier post, researchers identified the first (and possibly only) spillover of HIV from a chimpanzee to a human, all the way back to around 1908. It went undetected for so long because the life of the average native Congolese, especially during that era, was already brutal and short, and AIDS simply prevents our immune systems from attacking other invaders. How it spread from the Congo is largely speculation, but it seems quite possible that HIV got a boost from health clinics that opened in the 1920s and 30s, hoping to cure via injection unrelated diseases like syphilis and gonorrhea, using needles that were not always properly sterilized, and shared by hundreds of patients each. This was common practice at the time, and without any knowledge of HIV and many other blood diseases, who could blame them?

Sooty Mangabey

Left unchecked and uncontrolled (if it’s even possible to do so), diseases can decimate populations, even eradicate them completely, as once happened to one of our favorite fruits. Most of us today consume the Cavendish banana, a curved, yellow berry that seems almost as if it were designed to fit directly in the palm of one’s hand. Essentially seedless, plentiful in nutrients and carbohydrates, and safely sheathed in its own protective yet removable scabbard, the banana is ideal. Perfect. One of the oldest of cultivated plants, it is something of a genetic freak that developed by chance intermingling of its relatives in the genus Musa. A mule of the fruit kingdom, bananas are unable to reproduce without the careful work of human handlers. For thousands of years, South Asians successfully cloned the original banana plants, which remain genetically identical, frozen in evolutionary time.

All well and good, but for one pesky little issue. Monocultures are highly prone to infection, and can succumb quite readily to new diseases. The Cavendish, you see, is not the only banana in existence, and it is not even the most popular of all time. That honor goes to the Gros Michel, top banana of markets throughout the developed world straight up until the 1960s. Now largely extinct, it fell victim to Panama disease, a fungus that left a mushy mess of the famed plant, and took it out in only a handful of decades. The Cavendish is doing alright for the time being, but other perils lie in wait, some of which scientists are currently working against, and some of which may yet be discovered.

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We’ve been lucky so far, as the worst diseases of these latter days have failed to maintain their outbreak status. We’re not clones, not like the poor banana, but we are still a single species. As interconnected as we are, even as we move further into the territories of wild animals, it seems only a matter of time before the next Big One hits. That said, we have something going for us that no other animal on Earth has ever had: we can build the tools that allow us to fight back.

RESOURCES

Castle, Matt. The Unfortunate Sex Life of the Banana. Accessed at http://www.damninteresting.com/the-unfortunate-sex-life-of-the-banana/#continue

Quamman, David. Spillover: Animal Infections and the Next Human Pandemic. W.W. Norton & Company. 2012.

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