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Significance

The Dutch scientist J. van Breda de Haan first described black shank on cigar wrapper tobacco in Java (Indonesia) in 1896, two years after arriving in Sumatra as the chief of the laboratory for Deli tobacco. Since tobacco was introduced to Northern Sumatra in the 1860s by the Dutch, it is likely that black shank had been occurring for years prior to the report in 1896. The native hosts of P. nicotianae in Sumatra are unknown, but it also is likely that the pathogen was surviving (causing disease?) on other plants prior to encountering its new tobacco host. Van Breda de Haan also reported P. nicotianae from Amaranthus in Sumatra, and other researchers have reported that tobacco isolates attack multiple plants. However, tobacco appears to be the only economically important host for tobacco isolates of this species.

The disease was observed in the western hemisphere in Florida and Georgia around 1915, but it is thought that it took multiple introductions before it became established in the United States and Puerto Rico by 1925. The disease is now present in all tobacco-producing continents and in most major production areas with the notable exception of Brazil. In the 1930s and 1940s, the pathogen was introduced and became established in the major tobacco growing areas of North Carolina and Kentucky, and is now in all tobacco producing states of the US. Losses to the disease were often so high that tobacco could no longer be grown on a farm. This was the case until resistant varieties were introduced in the 1950s. A single source of partial resistance was used for many years in the management of this disease and is still the basis for resistance worldwide. Today, single-gene resistance also is widely deployed, but races of the pathogen have quickly appeared where single-gene resistance has been used. Chemical control was based on soil fumigants until the 1980s, when the fungicide metalaxyl was labeled for use on tobacco.

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