Malaria and Rome: A History of Malaria in Ancient Italy, Robert Sallares [reading a book TXT] 📗

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that other major parasitic diseases such as visceral leishmaniasis and trypanosomiasis also co-evolved with humans in Africa. P.

falciparum is one of mankind’s oldest, deadliest, and most persistent foes. This conclusion has considerable implications for the question of the size of host population required by P. falciparum. Evidently it was able to survive for very long periods during which all humans and their hominid ancestors were hunter-gatherers, long before the invention of agriculture, periods when human population sizes were very small. One thinks for example of the figure of 10,000 frequently given by molecular biologists as the effective population size (i.e. the size of the adult breeding population) of the populations (not necessarily the same population) to which belonged ‘mitochondrial Eve’, the last common female ancestor of all currently existing human mitochondrial DNA genotypes (assuming a rarity of recombination), and her male counterpart, the ‘Adam’

currently being revealed by studies of DNA sequences from the Y chromosome. P. falciparum is an extremely ancient human pathogen which was able to survive in small human populations in Africa, the cradle of human evolution.

In contrast, P. vivax and P. malariae are closely related to malaria parasites of monkeys in south-east Asia,outside the cradle of human evolution.⁶ P. vivax, for example, closely resembles P. cynomolgi, a parasite of Macaca monkeys in south-east Asia, in respect of both morphology and DNA sequences. P. vivax and P. malariae were not originally human diseases. They probably first encountered the evolving hominids when Homo erectus spread out from Africa across Asia, probably between one and two million years ago. The ago, even though they accept that the divergence between P. falciparum and P. reichenowi occurred several million years ago. Their controversial theory about P. falciparum cannot be discussed in detail here, but it is probably incorrect or, at best, an exaggeration (their views on the evolution of P. vivax and P. malariae are completely untenable). It does appear that different results are obtained from different parts of the genome, a problem frequently observed in research on molecular evolution (Gillespie (1991: 41) ). Other regions of the P. falciparum genome currently being studied by other scientists are yielding results incompatible with those obtained by Ayala and Rich (e.g. Verra and Hughes (2000) ). I hope that it will be possible within the next few years to obtain direct evidence from ancient DNA permitting an evaluation of the theory of Ayala and Rich concerning a recent cenancestor of P. falciparum.

⁶ Of course the distribution both of species of nonhuman malaria and of other primates might have been different in earlier geological epochs. Skinner et al. (1995) suggested that periodic episodes of linear enamel hypoplasia in fossil teeth of Dryopithecus apes from Can Llobateres in northeastern Spain, dating to the Miocene period about 9.5 million years ago, might have been caused by malaria.

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Evolution of malaria

question of the origin of P. vivax malaria in humans is tied to the question of the FY*O allele in the Duffy blood group locus, which prevents P. vivax parasites from adhering to and entering erythrocytes in nearly all members of sub-Saharan African populations. It is not known whether this allele spread in response to an existing parasite burden and drove P. vivax out of sub-Saharan Africa (its niche being taken by P. ovale), or whether an already high prevalence of this allele (perhaps in response to another pathogen) prevented P. vivax from ever establishing itself in Africa in the first place. In the last few years the Duffy negative allele has also appeared in Papua New Guinea, where P. vivax is endemic. This is an example of evolution in action in human populations today in response to malaria.⁷

Since P. falciparum was present in the heartland of human evolution in East Africa, presumably it would have been carried out of Africa by every successive wave of hominids and humans, from Homo erectus onwards. Whether it would have prospered outside Africa would have depended on the climate and on whether in new environments it encountered species of mosquito able to transmit it. These two factors are the last two pillars of the theory of the late spread of malaria into Mediterranean countries. Zulueta has quite correctly argued that the climate of Ice Age Europe was too cold both for the completion of the developmental cycle of P. falciparum itself within the mosquito and for the principal mosquito vector species in Italy, Anopheles labranchiae and A. sacharovi (= elutus).

He then reckoned that it would have taken thousands of years for conditions to become favourable enough for P. falciparum and its vectors to spread into southern Europe. However, this argument was based on old and out-of-date literature about the Holocene climate. It ignores the mass of evidence which is now available for what climatologists call the mid-Holocene climatic optimum, a period after the end of the last Ice Age and encompassing the Neolithic period until c.3000 , when, owing to periodic shifts in the earth’s position relative to the sun, the northern hemisphere received considerably more insolation than it does today. This resulted in the climate of many parts of the northern hemisphere being up to 2°C hotter than in subsequent millennia. Such temperatures are only now being approached again with the recent ⁷ Livingstone (1984); Zimmerman et al. (1999); Hamblin and Di Rienzo (2000).

Evolution of malaria

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trend towards anthropogenic global warming.⁸ The effects of these climate changes in Italy have recently attracted attention because of their relevance to the preservation of the famous ‘Iceman’ discovered in the Alps (as it turned out, just on the Italian side of the border with Austria). Fortunately for modern archaeologists,