Dissecting the Hyperdisease Hypothesis

I decided to do a post on the disease hypothesis after Josh from http://no-mammoths.blogspot.co.uk/ suggested an interesting paper by Rothschild and Laub (2006). Here is the link to his post on this topic specifically. The hyperdisease hypothesis proposes that humans and their domesticates introduced novel hyperdisease to vulnerable populations of Pleistocene megafauna who had never encountered such diseases before and whose bodies were therefore unable to cope. Since migrations of animals from Europe to North America were not uncommon before the period we are studying, it is more likely that humans and their domesticates were the disease vectors (Lyons et al (2004).

Tuberculosis and the American Mastodon 
Rothschild and Laub (2006) have suggested that new evidence for the hyperdisease theory has surfaced in the form of bone alterations from infectious tuberculosis found in just over half of 113 mastodon skeletons in the Western Hemisphere. Since not all animals infected with tuberculosis develop this bone alteration, it must follow that probably almost all of the mastodon population must have been infected with tuberculosis. The disease thus qualifies as a pandemic in the sense that it had an extremely high infection rate. Besides, it has a persistent presence in the fossil record from around 34,000 – 10,000 years BP, establishing that it must have been present in the late Pleistocene period. 

However, there is a difference between infection and mortality – the disease was not necessarily fatal. Rothschild and Laub (2006) hypothesize that this disease may have weakened mastodons in the face of climate change and human impacts in the late Pleistocene, further stressing their populations. While the disease could have remained latent, the environmental stresses of that period could have resulted in a loss of latency, increasing mortality. However, it is unlikely that the hyperdisease could have been a major factor in the extinction event. 

The Modern Day West Nile Virus: A Proxy for the Mystery Hyperdisease?

I also found another paper by Lyons et al (2004) which proposes some criteria for the hyperdisease theory to be plausible. 

1. It must be able to survive in a carrier state in a ‘reservoir’ species when there are no susceptible hosts to infect.
2. It must have a very high infection rate.
3. It must be extremely deadly with a 50-75% mortality rate
4. It must be able to infect multiple host species without infecting humans

Lyons et al (2004) use the West Nile Virus in birds, a disease which has seen recent introduction and spread in North America’s bird population, as a proxy to test this hypothesis as it appears to fulfil all of the above criteria of a hyperdisease.

One of the unique features of the late Pleistocene megafauna extinction event was its size-selectivity – smaller and medium-sized animals were largely unaffected. Thus Lyons et al (2004) have tried to test if West Nile virus causes such size-selective infections in birds. It can be shown that it does not, as infection rate increases positively with body size (Fig. 1) and infection occurs across a range of body sizes. This contrasts with the pattern shown by late Pleistocene mammal extinctions. The x-axis of the graph shows the size category of the bird species infected by the West Nile virus and those of the mammals which went extinct during the late Pleistocene. It has been re-scaled for mammals since they contain a much larger range of body masses. Each filled square shows the percentage of species pool in each size category infected by the virus or that went extinct. 

Fig 1 (Lyons et al 2004)

Some have argued that large body size makes species inherently vulnerable to extinction because of life history factors, e.g. low reproduction rates which make it harder for populations to recover from mortality caused by disease. However, Lyons et al (2004) counter-argue that if this is true, then larger species should have high extinction rates relative to smaller species over evolutionary time, which is not the case. 

The Verdict?

I find the hyperdisease hypothesis unconvincing so far and I think it is only considered seriously as a factor in the extinction event because of the general lack of evidence surrounding even the exhaustively-researched hypotheses of climate change and human hunting (e.g. lack of kill sites). However, the even more severe lack of evidence in the hyperdisease hypothesis is even more disturbing. The only known modern disease which fulfils the 4 criteria of a hyperdisease capable of wiping out megafauna during Pleistocene times, the West Nile virus, itself cannot be shown to cause the size-selective extinction pattern in modern day bird populations in North America. Besides, the paper by Rothschild and Laub (2006) only shows a pandemic-scale disease in one type of animal, the American mastodon. It is difficult to find equivalent disease explanations for all other megafauna species killed during the late Pleistocene (mammoth, for example, were not affected by this disease and were close cousins of the mastodon). Therefore, I conclude that hyperdisease is an unlikely explanation for the megafauna extinction event we are studying here.

References

Lyons, S. K. et al (2004) ‘Was a hyperdisease responsible for the late Pleistocene megafaunal extinction?’, Ecology Letters, 7, pp. 859-868

Rothschild, B. M. and Laub, R. (2006) ‘Hyperdisease in the late Pleistocene: validation of an early 20th century hypothesis’, Naturwissenschaften, 93, 11, pp. 557-564