In 1615, a burning fever swept through Leicester. There is little information about this ailment, other than that its appearance coincided with a contagious sickness and the Hot Ague (fever) elsewhere in England and Europe. Unidentified fevers erupted in 1638, 1660 and 1661. Smallpox was prevalent in 1634-5 and goal fever was recorded in Oxford in 1577, York in 1581, Exeter in 1586, Lincoln in 1590 and Hereford in 1636. Small, generally local, outbreaks of Malaria occasionally caused alarm in the marshes of East Anglia. Typhus also appeared periodically, and it has been suggested that influenza, in various forms may have been responsible for the non-specific epidemics. Examination of the aetiology, epidemiology and the signs and symptoms of Haemophilus Influenza and adenoviruses or adenoassociated viruses⁶ reveal a strong correlation between Dr Caius's reports and these diseases. Although modern medicine may offer a range of what is uncertain is the actual epidemiology of the plague, feasible diagnosis, particularly in respect to transmission during the sixteenth Century. How did the disease pass between small communities and households, and what was the mode of transmission over long distances - between countries, counties and towns?

The role of fleas in the transmission of the bubonic plague is fairly certain. However, what is uncertain is the actual relationship between flea, rat and man. Once the diseased rat flea, Xenopsylla cheopis, has left the rat and infected man, can that flea pass from man to man without the intervention of the rat? English epidemiologists, basing their arguments on modern plagues in South Asia, generally claim not. However, French epidemiologists, basing their claims on the results of modern plagues in North Africa and India, propose that the human flea, Pulex irritans, can transmit the disease as it moves between human hosts. The wisdom of concluding that the human flea has played a major role in the transmission of the plague in England has been questioned. There is evidence to support the view that the concentrations of plague mortality in towns were often in isolated pockets, often on the outskirts, not in the centre; suggesting rats, not humans were the vectors of transmission. Furthermore, despite the frequency of multiple cases of plague within single households, it has not been demonstrated that mortality rates were related to the size of the household, as may be expected if the human flea was the culprit.7 It may be prudent to surmise that both forms of transmission were evident, however, not necessarily in equal weighting, or operating together.

A further controversy concerns the exact method by which the plague arrived in England. It certainly arrived via the ports, carried on merchant and Naval ships. However, were the infected fleas carried by the rats in the grain or bales of cloth and cotton, or on the backs of the crew, passengers or returning soldiers? Furthermore, how did the disease spread from the ports to the town and country? Via wild rodents in the countryside, by the rats and fleas in transported freight, or by the fleas on their human hosts?

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