English 'sweate' (Sudor Anglicus) and Hantavirus pulmonary syndrome, The

British Journal of Biomedical Science, 2001 by Bridson, Eric

Particular Hantaviruses (19 species have been identified so far) have long associations with particular rodent hosts. With the exception of southern California, Hantavirus-infected rats have been found in major cities throughout the USA. Transmission of the virus is horizontal, although human-to-human transmission of Hantaviruses has not been documented in the USA. However, two reports from Argentina indicate that the HPS virus can be transmitted between humans. 15,16

Climate and epidemic cycles

It seems probable that three factors control the epidemic cycles of the 'sweate': the prevailing climate; the size of the rodent population; and the level of immunity in the human population.

Prevailing climate

Ice-core evidence from the Greenland Ice Sheet Project suggests that falling temperatures persisted throughout the 15th century, and did not rise until the second quarter of the 16th century.17 The sustained drop in temperature was accompanied by a considerable rise in rainfall, bringing periodic flooding to many parts of the country. Evidence of the change in climate was that viniculture almost ceased in Britain from 1400 onwards.

Size of the rodent population

The rodent virus-host population expanded in the spring and summer, when sufficient rain provided ample food. This could have happened in the years 1485, 1508, 1517, 1528 and 1551, when conditions may have been particularly favourable. Such rises in rodent populations would have led to rodent invasion of houses and dwellings, increasing the indoor viral load from their excreta. Figure 3 shows the epidemic cycle plotted over the five epidemics. It suggests a natural 10-11 year cycle (coinciding with the minimum age in the 100 HPS cases in the survey carried out in the USA") that has been distorted by the fact that two potential epidemics did not take place.

Level of immunity in the human population

This must have had a major influence on the epidemic. Highly lethal diseases are not successful pathogens; rapid slaughter of the host cannot ensure longevity of the organism. Highly lethal viruses usually have specific hosts in which they can exist in a reasonable association (e.g. Lassa fever and monkeys). When the organism changes host, it often demonstrates an enhanced lethality. In adapting to survive in the new host, the virus could expose lethal factors that have the effect of restricting the rate of species-hopping. The new host has defences but humoral and cellular immunity takes time to be activated fully. Viral load, virulence and host factors determine whether recovery or death is the result of infection. The approximately ten-year gap between epidemics may be dictated also by the critical numbers of non-immune adolescents entering the population between epidemics.

However, none of these three factors fully explain the sudden appearance of the 'sweate' or its equally baffling disappearance.

Conclusions

The possible cause of the English sweating sickness may have been identified with the discovery of HPS in 1993. The appearance of the disease, and this putative virus cause, may have been associated with the increased fur trade with north-eastern Europe, and the introduction of infected rodent hosts into England. The major spread of the `sweate,' as described in contemporary accounts, would seem to be human-tohuman infection, yet modern-day evidence for HPS transmission by this route remains very scanty.