Malaria and Rome: A History of Malaria in Ancient Italy (31 page)

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.

Demography of malaria

155

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 that in northern Italy
P. vivax
infections in autumn tended to produce acute attacks immediately after the normal incubation period. In other words there was no delay of the primary attack until the spring as in Holland, for example. Consequently the spring wave of
P. vivax
malaria in northern Mediterranean countries was probably mainly composed of relapses, not primary attacks. The hotter the year, the more likely it was that P. falciparum
would overshadow
P. vivax
and
P. malariae
in the late summer and autumn in Mediterranean countries. Sorgoni (1832) noted that pernicious symptoms were more frequent around Narni the greater the difference between the daytime and the night-time temperatures.

¹²² Maitland
et al
. (1997); contrast Covel and Nicol (1951) and Shute (1951).

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Demography of malaria

the case of simultaneous infections with the two different species, P. vivax often fares poorly.¹²³ It is difficult to generalize about the demographic consequences at the population level of the
P. vivax
–P. falciparum interaction because of the complicated results found in individuals. Nevertheless the fact remains that the evidence from more recent periods of European history discussed in this chapter suggests that being infected with
P. vivax
in the past was not necessarily any better in the long run than being infected with
P. falciparum
. As far as antiquity is concerned, Galen’s comments in the second century  indicate that
P. falciparum
infections tended to occur at an early age then (Ch. 8 below). This suggests a different epidemiology from that described recently in Vanuatu. This Pacific island group seems to lack the full range of genotypes of
P.

falciparum
found in Africa and Eurasia, as is suggested by a greatly reduced range of polymorphism in the merozoite surface protein genes.¹²⁴ Presumably a large proportion of the organism’s range of genetic polymorphism failed to make it across the ocean during the human population movements which colonized the Pacific islands.

Alternatively they might have been eliminated when the human population of Vanuatu passed through a severe bottleneck within the last two hundred years. Either way, the evolution of malaria in Vanuatu, an example of evolution in an isolated island population, is not directly relevant to the historical situation in Europe, although it is certainly of considerable intrinsic interest.

In passing, it should be noted that
P. vivax
probably already existed and operated in the way described by Dobson in Britain in classical antiquity. The disease of the marshes that severely affected the army of Septimius Severus in Scotland in  208 may well have been
P. vivax
malaria, as Bordier suggested a long time ago.¹²⁵ In the seventeenth century Doni expressed the opinion that quartan fever was unknown in Scotland, implying that he believed that tertian fever did occur there.¹²⁶ An inscription, now lost, from Risingham ¹²³ Mason and McKenzie (1999). Bruce
et al
. (2000) suggested that in tropical regions where malaria is continuously active there is density-dependent regulation of infections that transcends species as well as genotype, resulting in non-independent sequential episodes of infection with each species.

¹²⁴ Maitland
et al
. (2000).

¹²⁵ Bordier, cited by Fraccaro (1919: 86 n. 2), drew attention to Cassius Dio 77.13.2: ËpÏ

t0n Ëd3twn dein0ß ƒkakoınto (they were badly affected by the waters). Herodian 3.14.6–8

emphasized the marshiness of Britain in the early third century .

¹²⁶ Doni (1667: 7):
in Scotia quartanam febrim ignotam esse credi potest
. It will be remembered that the British mosquito vector
A. atroparvus
is a poor carrier of
P. malariae
(Shute (1951) ), although it could have been transmitted by
A. plumbeus
instead.

Demography of malaria

157

(Roman Habitancum), a Roman fort north of Hadrian’s Wall, has been frequently cited as a dedication to the goddess of tertian fever.

Unfortunately this reading of the text is a guess made in the early seventeenth century. It appears to be unreliable.¹²⁷ Dobson noted that the opium poppy was widely cultivated in East Anglia in the early modern period to provide opium, which was used to relieve the symptoms of
P. vivax
malaria. It did not create addiction under those circumstances. Archaeobotanical finds of opium poppy (
Papaver somniferum
) from Iron Age–Roman archaeological sites in East Anglia show that it was already being cultivated there by Roman times, probably for the same reason. Localized extreme variation in mortality patterns caused by malaria was probably already occurring in Roman Britain.¹²⁸

Although there is no direct evidence available, owing to the shortage of written sources for Roman Britain, the balance of probability is that the constant movements of soldiers, merchants, slaves, and administrators between Britain and other parts of the Roman Empire introduced malaria to Roman Britain, if it was not already present. As was seen earlier, the evidence of Gregory of Tours shows that malaria was frequent and familiar in France in the sixth century  (Ch. 4. 1 above). Moreover Pliny mentions tertian fever in the territory of the Tungri in Belgium and Holland in the first century .¹²⁹
P. vivax
malaria was present in these areas by then, only a short distance from Britain. Alcuin in the late eighth century  is a specific case of an individual who travelled from Britain to Rome, became infected with ‘Roman fever’, and brought the parasites back to northern Europe with him. He contracted malaria during his visit to Rome in 798 and was severely affected by it thereafter. Alcuin presumably had mixed infections, ¹²⁷ The text
Deae Tertianae sacrum Ael(ia)
(
CIL
7.999) was accepted by Weinstock in Pauly-Wissowa
RE
s.v.
Tertiana
(vol. v A.1 (1934), column 822), Schaffner in Cancik and Schneider (1998), s.v.
Febris
, and Burke (1996: col. 455, p. 2269). However, it was rejected in favour of the alternative reading (
Deae Dianae sacrum Aelia Timo posuit votum solvens laeta libens merito
) found in the manuscript tradition by Collingwood and Wright (1995: 397 no. 1209), who rejected the lectio difficilior. The inscription
CIL
12.3129 is a dedication to quartan fever in the third century  from Nemausus in Gallia Narbonensis (
quartanae votum reddet libens merito Byrria Sev-erilla
).

¹²⁸ Dobson (1997: 304–6); Pryor (1991: 130); Cameron (1993: 10, 54–5) described malaria as common in Anglo-Saxon England; the
lencten-ádl
of Old English texts probably signified spring relapses of
P. vivax
malaria, according to Bonser (1963: 403–5); Darby (1983: 52, 95, 107, 112, 146, 150–2, 176) on malaria in the East Anglian fens and its disappearance in the nineteenth century; Nicholls (2000).

¹²⁹ Pliny,
NH
31.8.12.

158

Demography of malaria

since he emphasizes that he had quotidian fevers. The timing of one episode of fever, after Easter 801, sounds like a typical spring relapse of vivax malaria, but it is possible that he contracted falciparum malaria as well in Rome.¹³⁰ There were undoubtedly other such individuals, since Bede and Paulus Diaconus both commented on the popularity among the Anglo-Saxons of pilgrimages to Rome in the early medieval period.¹³¹ More than one Anglo-Saxon king died in Rome. Bede related the story of the miracle of a young boy who was cured of a long-running intermittent fever by standing on the tomb of St. Oswald, king of Northumbria (633–642), at Bardney Abbey in Lincolnshire. This text constitutes some direct evidence for malaria in England
c
. 700 (at that time in the same monastery a little boy was severely affected by a prolonged fever. One day he was awaiting the hour of the attack,when one of the brothers entered and said to him: ‘my son, shall I teach you how to cure yourself from the trouble of this debilitating disease? Get up, enter the church, and go to Oswald’s tomb, remain there, stay quiet and remain by the tomb. Make sure that you don’t leave the church, or move from the spot, until the hour when your fever is scheduled to leave you. Then I will enter the church, and lead you away.’ The boy followed the brother’s instructions. While he sat by the tomb of the saint the disease never dared to touch him; indeed it was so terrified that it flew away, and did not dare to touch him on the second day, or the third day, or ever again.’)¹³²

¹³⁰
e.g.
febrium flagellatione . . . remanet cotidianus labor eiusdem castigationis
;
tamen febrium castigatio cotidianis diebus nos non reliquit
(By the lashing of fevers . . . the daily labour of the very same chastisement continues; the daily chastisement of fevers does not leave me.) Alcuin,
Epistolae 218, 221, ed. Duemmler (1895),
Monumenta Germaniae Historica. Epistolae
, iv. 362, 365, cf.
Epistolae
146,
febris et infirmitas me fatigatum habet
(fever and weakness keep me tired), and 149 (
febric-itantem
); Gaskoin (1904: 99, 110, and 124). Peter of Blois is another example of a person who returned to northern Europe after contracting malaria in Italy. He developed semitertian fever in Sicily in  1169, was treated at Salerno, and then returned home with a detailed knowledge of malaria to the Loire valley region of France, where in a letter to his friend Peter medicus
written
c.
1170–5 he described another case of semitertian fever in the knight Geldewin, which may also have been imported—Peter of Blois,
Letter
43, discussed by Holmes and Weedon (1962).