The human body requires an adequate supply of ascorbic acid (L-xyloascorbic acid or vitamin C) to enable it to function normally, and a lack of the vitamin results in the emergence of the condition known as scurvy (scorbutus or avitaminosis C). Unlike plants, and the majority of animals thus far studied, humans are unable to produce ascorbic acid endogenously and, thus, are dependent upon dietary sources – mainly fruit and vegetables – for a supply of the vitamin. In the absence of vitamin C, formation of collagen, an essential glycoprotein component of connective tissue, is impaired, which is believed to be the main underlying biochemical lesion in scurvy (Counsell and Hornig 1981; Englard and Seifter 1986).

The earliest signs of scurvy (fatigue and lassitude) may emerge in humans some 12 weeks after removal of dietary vitamin C, and the more overt traditional signs (hemorrhagic spots under the skin [petechiae], softening of the gums, and defective wound healing) after some 17 to 26 weeks of deprivation.

In 1753, James Lind concluded his pioneer study of scurvy with a chronological Bibliotheca Scorbutica, which imparted a mild historical flavor to his text (Stewart and Guthrie 1953). But more than a century was to pass before the first sustained efforts to produce a history of the disease emerged. One of these was J. Maré’s 200-page article in the Dictionnaire Encyclopédique des Sciences Médicales in 1880, and the second was August Hirsch’s 60-page article in his Handbook of Geographical and Historical Pathology (1883–6).