Malaria and Rome: A History of Malaria in Ancient Italy, Robert Sallares [reading a book TXT] 📗
- Author: Robert Sallares
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⁷⁶ Enwere et al. (1999), cf. Hovette et al. (1999) for recent research on the malaria–tuberculosis interaction.
⁷⁷ Baccelli (1881: 165–6).
⁷⁸ Whittle et al. (1984).
⁷⁹ Marchiafava and Bignami (1894: 120–1); Roy et al. (2000).
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leads to an increased prevalence and severity of malaria in semi-immune adults’.⁸⁰
Since the evidence of Galen and Asclepiades suggests that malaria was common in imperial Rome (see Ch. 8 below), the balance of probability in the light of modern medical research is that malaria dominated the mortality regime of the population in at least some districts of the city, just as it did in Grosseto, and in the surrounding countryside, even if a large majority of all deaths might have appeared to doctors in antiquity to be the result of other diseases. In the same way, when Corvisier observes that ‘fever’
(puretÎß) can only be directly connected to malaria in a small proportion of the cases in the Hippocratic Epidemics, this is only to be expected under the conditions of endemic malaria, and should not be taken to minimize its importance.⁸¹ The paradoxical yet logical conclusion of modern research is that ‘in very highly endemic centres the amount of sickness [sc. in adults] is greatly reduced in comparison with epidemic areas’, because acute illness is concentrated in infants and children.⁸² Nevertheless very highly endemic centres have higher overall mortality (including adult mortality) than areas where malaria has an epidemic character, never mind areas where it does not occur at all. Of course it is quite possible to have excess seasonal mortality patterns without the presence of malaria, but under those circumstances overall mortality for the whole population is lower, as the example of Florence shows.
5. 3 M
The effects of malaria in antiquity were probably, in their turn, exacerbated by the moderate degree of chronic malnutrition that was arguably endemic among the masses in most if not all ancient populations. If the recent trend towards increasing average height in the populations of modern developed countries is to be attributed to improved nutrition, as seems to be the case, then it is an inevitable conclusion that malnutrition was endemic in historical populations. Specifically in the case of ancient Rome, preliminary reports of research on the skeletal population from Vallerano near ⁸⁰ Whitworth et al. (2000).
⁸¹ Corvisier (1994: 305–8); contrast Grmek and Gourevitch (1998: 223–5), using the figurines from Smyrna in the Louvre as evidence for virulent P. falciparum malaria in the Hellenistic period.
⁸² Hackett (1937: 174).
Demography of malaria
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Rome, dating to the second century , have revealed a significant frequency of porotic hyperostosis attributed to iron-deficiency anaemia. Together with palaeodemographic evidence for low life expectancy (unreliable in detail, yet probably still reasonably accurate in respect of the overall impression given), and better-known literary evidence such as Soranus’ comments on the frequency of rickets in the city of Rome (caused by vitamin-D deficiency), it suggests a rather low standard of life in the suburbs of Rome itself with repeated infections and widespread chronic malnutrition, especially of infants and children. Such problems continued, inci-dentally, throughout the history of the city of Rome. The explanation of Soranus’ evidence was provided by Lapi in the eighteenth century. He admitted that rickets was common in Rome in his own time, even though he argued that Rome was healthier than its reputation suggested. Lapi states that rickets manifested itself in babies in Rome between the ages of nine months and two years. He attributed the prevalence of rickets in Rome to the custom of keeping infants inside rooms, with the unintended consequence that they were never exposed to ultraviolet radiation in sunlight, which converts the sterol 7-dehydrocholesterol in skin into cholecalci-ferol, vitamin D3.⁸³ We may infer that infants were kept indoors because of the widespread fear of ‘bad air’ among the Roman population. Evidently their diet did not include fish-liver oils, the most important potential dietary source of vitamin D, and was inadequate to compensate for the lack of exposure to sunlight, but an inadequate diet was not the only reason for rickets in the Roman population, both ancient and early modern.
Malnutrition of the host adversely affects the parasite as well as the host. At the most extreme level, it has been suggested that severe malaria is rare in children suffering from the worst forms of protein-energy malnutrition, but the most recent research indicates that protein-energy malnutrition is indeed associated with increased morbidity and mortality from malaria.⁸⁴ A considerable body of research has found that deficiencies of several different vitamins reduce the reproduction rate of malarial parasites, leading to lower parasite counts in the blood of patients. For example, a ⁸³ Ricci et al. (1995); Soranus, Gynaecology 2.43–4; Lapi (1749: 75): il tenere i bambini a marcire nelle camere lontanissimi dal sentire l’alito dell’aria esterna; Levi (1945: 34, 76) on the association of rickets, general malnutrition, malaria and trachoma in Lucania; Davidson et al. (1979: 121–4).
⁸⁴ Shankar (2000) gives a detailed survey of all facets of the malaria-nutrition problem.
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shortage of vitamin E, an antioxidant, predisposes erythrocytes to oxidant-induced premature lysis, rupturing the red blood cells before the parasites have completed their development inside.
Deficiency of vitamin C has been reported to have the same effect in experiments on monkeys. Other experiments have shown that a diet deficient in a nutrient essential for the malaria parasite, para-aminobenzoic acid, suppresses infections of rats with the malaria species Plasmodium berghei. Para-aminobenzoic acid is a precursor of the important coenzyme folic acid. It has been suggested that a diet of pure breast milk, which contains a very small proportion of this chemical, may increase resistance to malaria among very young human infants, although there is no experimental proof, and
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