Between the 16th and 19th centuries malaria, known as the ague, or marsh fever, killed or contributed to the deaths of thousands of people in the marshland villages of coastal southern and eastern England where stagnant pools were a breeding haven for the British estuarine mosquito, Anopheles atroparvus. But why malaria had such an impact perplexes scientists.
The malaria parasites endemic in England were Plasmodium vivax and P malariae, not P falciparum, the tropical strain responsible for the life- threatening form of malaria. The obvious explanation is that the benign forms of malaria were indirectly responsible for deaths of people whose health was compromised by low standards of living. There is also a suspicion that there were more virulent strains of P vivax and P malariae in circulation, but there is little evidence to support this.
What is known is that over the 200 years running up to the mid-nineteenth century, death rates began to fall in the marsh parishes as malaria receded. When it did occur, the disease was less severe than it had been previously. Improved drainage of marshland, better ventilation in houses, and an increase in the size and health of animal herds which provided an alternative blood meal for mosquitoes, were all helpful factors, according to a 1994 paper in the journal Parassitologia CORR by Mary Dobson, senior research fellow at the Wellcome Unit for the History of Medicine in Oxford. Quinine was available to treat marsh fever when it did occurr.
By the 20th century, indigenous malaria had all but disappeared, but cases of "imported" malaria were still reported. An outbreak in Kent was blamed on soldiers returning from India and Greece with the disease who went to the coast to convalesce. Mosquitoes passed malaria on to locals. The last cases of indigenous malaria are attributed to two neighbouring Londoners in Stockwell who contracted the disease in the summer of 1953.
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