Malaria and Rome: A History of Malaria in Ancient Italy by Robert Sallares (beach read .TXT) 📕

¹¹⁵ Dobson (1997: 320–7, 349); Smith (1956).

¹¹⁶ Snow (1990) described the mosquitoes of England. Shute (1951) described the laboratory culture of A. atroparvus. He noted that to breed it one only needs some grass with some soil attached to the roots in a basin of rainwater about two feet in diameter.

¹¹⁷ Cipolla (1992: 69); Garnham (1966: 139) stated that he had observed fatal cases of P. vivax malaria in young children.

¹¹⁸ Modebe and Jain (1999) described a recent case of severe complications caused by P. vivax malaria. Dobson (1989: 269) concluded that vivax malaria had less effect on colonists in the United States than it did in England because of a relative shortage of other diseases in North America, even though P. vivax malaria was probably imported from England (Kukla (1986) ).

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intermittent fevers, although he noted that ague was more dangerous to the elderly than to infants.¹¹⁹ There is no doubt that P. vivax was indeed responsible for the demographic patterns found in the English marshlands, because the parasites were found in the blood of the last few people to have indigenous English malaria, in the early years of the twentieth century. In addition, quinine, which would not have substantially helped sufferers from other diseases, relieved the symptoms.

Important research by Mary Dobson discovered that before the nineteenth century crude death rates were as low as 20–30 per 1,000 in many rural parishes of south-east England, but in the marshy areas of Kent and Essex crude death rates were over 50–60

per 1,000, sometimes as high as 80 per 1,000. It is very important to appreciate that the excess mortality produced by malaria is not a marginal phenomenon. The differences in overall mortality levels between the parishes most severely afflicted by P. vivax malaria and the healthiest parishes in the same area were quite literally of the order of 300–400%. Similarly, comparing fifteen marsh and fifteen non-marsh parishes between 1551 and 1837 in the same parts of England, Dobson found that crude burial rates in the marsh parishes exceeded 100 per 1,000 in about 11% of the years, while such high burial rates were only attained in non-marsh parishes about once every two centuries on average. These staggeringly high mortality rates occurred in the malarial districts at a time when the population of the rest of England was increasing and was quite healthy.

Life expectancy at birth was slashed in the malarial regions.

Dobson reported that in three North Shore malarial parishes in north Kent it was 33 years, compared to no less than 58 years in four parishes in the East Downs where P. vivax was not endemic, in the early nineteenth century.¹²⁰ The difference between the life ¹¹⁹ Meynell (1991: 122, 135).

¹²⁰ Dobson (1997) is fundamental on malaria in England, esp. pp. 133–49 and 172 on local variations in death rates. Many of the results of her long book are summarized in her (1980) and (1994) articles. See also Reiter (2000). One might also compare the situation around Valencia in Spain in the eighteenth century (Palmero (1994) ). Palmero and Vega (1988,: 351) translated and quoted the following comments of Francisco Llansol, written in 1797: ‘the dwellers of the Upper Riverside in certain towns like, for example, Cárcer Valley, Castellón, Alberique and so on, are likely to have poor health. They are pale yellow-skinned, there are many women with swollen bodies, and people living in these areas, in general, are likely to have a short life . . . when people die, they are mostly between forty and fifty years of age’.

Jagailloux (1986: 262) regarded the debilitating effects of P. vivax malaria as an important factor in mortality in Egypt.

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expectancy of 33 in malarial parishes in England and the life expectancy at birth of 20 in Grosseto only a few years later represents the difference between P. vivax and the more virulent P. falciparum (see also discussion below). However, P. vivax was also very common in Mediterranean countries in antiquity and will have made its mark on mortality patterns there as well. Where both species of malaria coexist in an endemic form, as in western central Italy in the past, P. falciparum often tends to outcompete P. vivax because of its higher rate of reproduction, especially in very hot years when environmental conditions are most favourable for it.¹²¹

Some recent research in Vanuatu in the Pacific has generated the hypothesis that prior infections with P. vivax may confer some immunity to subsequent infections with P. falciparum. The modern experience that P. vivax is a relatively mild disease is then invoked to suggest that cross-immunity could give rise to a low incidence of severe malaria even under holoendemic epidemiological conditions. It is not clear if these results can be generalized. The artificial infection experiments at Horton Hospital in England yielded different results, suggesting that P. vivax is unable to prevent subsequent infections with P. falciparum, although P. falciparum does inhibit P. vivax.¹²² In any case this particular idea does not seem relevant to European historical populations, such as Grosseto and Croton (see below), where both P. vivax and P. falciparum were undoubtedly present yet the demographic effects of malaria as a whole on the human population were very severe. Mathematical modelling of the interaction of P. falciparum and P. vivax in the human bloodstream yields complicated results depending on the relative timing of the various infections. An existing P. vivax infection can reduce the parasite load in the blood of a subsequent P. falciparum infection by as much as 50%, but on the other hand, a subsequent P. vivax infection or even relapse can actually exacerbate an earlier low-level, asymptomatic, P. falciparum infection. In ¹²¹ Gill (1938: 36–9) noted