The Hyper-Disease Hypothesis: Did Humans Bring About Doomsday for the Megafauna of the Pleistocene?

By Erika Lyon

It is a concern that we are entering Earth’s 6th mass extinction.  Mass extinctions occur when a large number of species die off in a short amount of time relative to background extinction rates (to read more about extinctions, click here).   Some of the major questions being asked include what are the mechanisms behind extinction events and could humans possibly cause a mass extinction?  One of the more recent extinctions in geologic time that may provide some insight into these questions is the Pleistocene megafaunal extinction that occurred in North America.  Three hypotheses have been made on the cause of the Pleistocene extinction, which include: 1) vegetation and climate change, 2) over-hunting by humans, and 3) the introduction of disease brought into North America by humans, the last of which is known as the hyper-disease hypothesis (MacPhee and Marx 1997; Lyons et al. 2004). 

The hyper-disease hypothesis emphasizes that human vectors carried pathogens from the Eastern hemisphere to the Western hemisphere and transmitted these pathogens to megafaunal species that were “naïve” (naïve means a species did not come into contact with a pathogen historically and therefore did not develop resistance to that pathogen).  MacPhee and Marx (1997) state that the hypothesis explained why the disappearance of animals corresponded to the arrival of early humans in North America and why there were differences in extinction rates between larger, slow reproducing species and smaller, fast reproducing species (K-selected and R-selected groups).

Fig1

Fig. 1: Estimated number of extinctions after the arrival of humans in the Western Hemisphere. Click to enlarge. Image by Linda Huff.

The hypothesis is based on certain criteria in order to hold: a pathogen must be able to sustain itself when there are no optimal hosts to infect, rate of infection must be high in all sexes and ages, it must be highly lethal, and it must be able to infect multiple species without causing significant decline in reservoir species (in this case, humans) (MacPhee and Marx 1997; Lyons et al. 2004).  So why would these diseases cause the extinction of larger mammals versus smaller ones?  The hypothesis assumes that although many organisms of all sizes may be susceptible to certain virulent strains, larger body size equates to slower recovery of populations from infection (i.e. large body sizes are linked to smaller populations and longer gestation times, which means low birth rates and, in pandemics, high mortality).  This would become problematic for the North American megafauna.

The occurrence of disease during the Pleistocene has been evident in the fossil record, and recent evidence of tuberculosis in mastodon bones may support the hyper-disease hypothesis (Rothschild and Laub 2006).  Rathschild and Laub (2006) suggested that a majority, if not all, American mastodon populations were afflicted with “white plague” tuberculosis (Rothschild and Laub 2006).  However, the disease was not considered lethal by itself.  In humans, tuberculosis is not always fatal, but stress can aggravate the disease.  In combination with changes in climate and vegetation, megafaunal extinctions might have been more likely to occur with the presence of the pathogen causing the outbreaks of tuberculosis (Rothschild and Laub 2006).

Fig. 2: Erosion on Mastodon tooth characteristic of tuberculosis (Rothschild and Laub 2006).

Fig. 2: Erosion on Mastodon tooth characteristic of tuberculosis (Rothschild and Laub 2006).

Evidence of introduced diseases wiping out entire populations is prevalent in modern history.  One example is that of the endemic island rat, Rattus macleari, a distinct species of rat that went extinct over the last century.  R. macleari inhabited Christmas Island, which was isolated until the mid-1800s.  These rats were “naïve” in that they had never come into contact with other diseases found commonly in other species of rats (Wyatt et al. 2008).

Then humans arrived and brought the black rat (Rattus rattus) with them.  Sadly, these black rats were infested with fleas.  (Let’s face it: rats + fleas = a really bad day for somebody).  The fleas were vectors for a pathogenic trypanosome organism, and soon after introduction, the island’s population of R. macleari went extinct (Wyatt et al. 2008).  So was disease the cause of it?  Something to consider is that black rat eats just about anything (Wyatt et al. 2008), so should we exclude the possibility of rat cannibalism?  Maybe not entirely, but the island also had endemic shrews that survived the introduction of the black rats. (Would these not be just as tasty as fellow rats?)  Also, prior to its introduction, no island rats had the disease, and after the introduction, it took just 9 years to wipe out R. macleari (Wyatt et al. 2008). 

Fig. 3: Christmas Island timeline for extinction of endemic rat (Wyatt et al. 2008).

Fig. 3: Christmas Island timeline for extinction of endemic rat (Wyatt et al. 2008).

So the extinction of the Christmas Island rats may support the hyper-disease hypothesis on a local scale, but does the hypothesis work on larger scales and on larger organisms?

It is difficult to find a modern proxy for disease to compare to past extinctions (Lyons et al. 2004). Not to mention we have no more mammoths or mastodons left to test this hypothesis on.  In fact, the only known proxy that exists today is West Nile Virus (WNV) in birds.  Lyons et al. (2004) used WNV as a model since the virus met the 4 criteria originally proposed by MacPhee and Marx (1997).  They found that size variations in study organisms (birds) did not lead to a significant difference in disease incidence.  Their results suggested that even though WNV was one of the few modern diseases that can be described as a hyper-disease, it was unlikely that a disease like WNV would only lead to the extinction of the megafauna and not small mammals.  Although their results did not support a hyper-disease as the cause of the Pleistocene megafaunal extinctions, they did not exclude the possibility that a hyper-disease might cause a future mass extinction.

Fig. 4: Percent of species pool plotted against body bin size. X axis is rescaled for mammals. The patterns of WSN infections versus Pleistocene mammalian extinctions are dissimilar, which contradict the hyper-disease hypothesis (Lyons et al. 2004).

Fig. 4: Percent of species pool plotted against body bin size. X axis is rescaled for mammals. The patterns of WSN infections versus Pleistocene mammalian extinctions are dissimilar, which contradict the hyper-disease hypothesis (Lyons et al. 2004).

Others have also argued that the hypothesis is implausible for the megafaunal extinctions since exchange of fauna occurred across the continents throughout the late Cenozoic.  This exchange would mean that the North American megafauna were not isolated and would not be “naïve” enough to be devastated by a hyper-virulent pathogen vectored by humans (Koch and Barnosky 2006).  The hypothesis also assumes rapid extinction, which is undermined by the fact that humans arrived in North America thousands of years before the Pleistocene extinction occurred (Koch and Barnosky 2006; Haile et al. 2009).

So while the debate continues about whether or not the hyper-disease hypothesis is valid in the cause of the Pleistocene extinction of megafauna, we are left to ponder whether future climate change will create novel environments that might allow a global scale pandemic to occur.  Recent emergent diseases have appeared that have become a major concern, such as the skin disease in frogs caused by Batrachochytrium dendrobatidis or Pseudogymnoascus destructans that causes white nose syndrome in bats.  The origin of many of these pathogens are still unknown and the diseases caused by them may push certain species to extinction.  It has been debated whether or not humans are spreading these pathogens.  Are humans potentially a Typhoid Mary?

REFERENCES

Haile, J., D.G. Froese, R.D.E. MacPhee, R.G. Roberts, L.J. Arnold, A.V. Reyes, M. Rasmussen, R. Nielsen, B.W. Brook, S. Robinson, M. Demuro, M. Thomas, P. Gilbert, K. Munch, J.J. Austin, A. Cooper, I. Barnes, P. Moller, and E. Willerslev. (2009). Ancient DNA reveals late survival of mammoth and horse in interior Alaska. PNAS 106(52):22352-22357.

Koch, P.L. and A.D. Barnosky. (2006). Late Quaternary Extinctions: State of the Debate. Annual Review of Ecology, Evolution, and Systematics 37:215-250.

Lyons, S.K., F.A. Smith, P.J. Wagner, E.P. White & J.H. Brown. (2004). Was a ‘hyperdisease’  responsible for the late Pleistocene megafaunal extinction? Ecology Letters 7:859-868.

MacPhee, R.D.E. & Marx, P.A. (1997). Humans, hyperdisease, and first-contact extinctions. In: Natural Change and Human Impact in Madagascar (eds Goodman, S.M. & Patterson, B.D.). Smithsonian Institution Press, Washington, DC, pp. 169–217.

Rothschild, B.M. and R. Laub. 2006. Hyperdisease in the late Pleistocene: validation of an early 20th century hypothesis. Naturwissenschaften 93:557-564.

Wyatt, K.B., P.F. Campos, M.T. P. Gilbert, S.O. Kolokotronis, W.H. Hynes, R. DeSalle, P. Daszak, R.D.E. MacPhee, A.D. Greenwood. (2008). Historical Mammal Extinction on Christmas Island (Indian Ocean) Correlates with Introduced Infectious Disease. PLoS       One 3(11):1-9.

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One thought on “The Hyper-Disease Hypothesis: Did Humans Bring About Doomsday for the Megafauna of the Pleistocene?

  1. Nice post! The mastodon-tuberculosis connection is really interesting. I wonder if that’s where humans were first exposed, or vice versa, or none of the above?

    To me, the most compelling argument against a hyper-disease is that we don’t have any good analogs for that now. The Lyons et al. (2004) study was so cool for that reason– it was a nice mechanistic test.

    Well done!

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