“Brown etch”, or ‘’rust mark” is a major issue for pumpkin growers. The problem affects butternut pumpkins (Cucurbita moschata) and, occasionally, related hybrids such as Kent. Brown etch regularly results in major losses; up to 50% of a crop may be affected. Paddocks may be abandoned due to the large percentage of affected fruit. Even where fruit appears clean at harvest, etch can develop during storage and transport. Etched fruit arriving at wholesale markets may be rejected outright or resorted and downgraded, further increasing costs to growers.

Brown etch has commonly been thought to be caused by disease. Initial laboratory work isolated a number of different pathogens from affected pumpkins. These included Stagonosporopsis cucurbitacearum (gummy stem blight/black rot) as well as Fusarium species, Colletotrichum and Rhizoctonia spp.. A high percentage of immature pumpkins scratch inoculated with S. cucurbitacearum developed etch-like symptoms. The pathogen could then be re-isolated from sections of etched skin, suggesting the Koch’s postulates had been satisfied. However, many of these pumpkins also developed symptoms of black rot, whereas this did not occur in naturally etched fruit. Moreover, many attempts to isolate this pathogen from etched fruit were unsuccessful. It was concluded that while S. cucurbitacearum can trigger etch it is not the sole cause of this disorder.

This was supported by RNA analysis of etched pumpkins. A number of genes involved in lignin synthesis were strongly upregulated in etched compared to non-etched sections of tissue, with borderline areas intermediate. Lignin is produced as a defence against stress – microbial or physical. Observation of this tissue with light and scanning electron microscopes revealed cellular disruption, including massive lignification of the cell walls. However, no fungal hyphae were found in these areas.

A large number of field trials were conducted with both commercial and experimental pumpkin crops. Treatments included foliar nutrients (potassium, silicon, calcium + boron), elicitors of plant resistance (Bacillus subtilis, chitosan), inoculation with disease (S. cucurbitacearum, Fusarium spp), fungicide programs, plastic mulch and different varieties. Temperature and relative humidity (RH) were recorded along with development of etch in the field.

None of the treatments consistently reduced or increased etch. However, a strong correlation was observed between wet conditions in the 14 days before harvest and high RH and etch development. Modelling suggests that 50 to 150 hours at >90%RH, with fruit wet 15 to 30% of the time, will result in 5 to 10% of the crop developing etch. Longer periods will further increase the number of etched fruit. For example, if fruit is wet >50% of the time, at least one in four pumpkins is likely to develop etch. A second model suggests that in the month before harvest, a continuous period of wetness for more than 24hrs is likely to result in >10% of the crop developing etch.

Postharvest trials demonstrated that etch continues to expand after harvest and can appear on initially clean fruit. The amount of etch occurring postharvest is strongly related to etch in the field: non-etched crops will not develop etch postharvest. In contrast, if etch is observed in the field then even clean fruit may develop symptoms, especially during the first week after harvest. High RH during storage increases etch, whereas low RH and cold temperatures can greatly reduce appearance of the disorder.

Brown etch is a superficial disorder and does not reduce the eating quality of the pumpkins. A retail study examined consumer willingness to purchase etched / non etched pumpkins displayed as cut, overwrapped halves. Discounting etched fruit by 50c/kg slightly increased sales compared to clean fruit. When the discount was reduced to 20c/kg or zero, sales were generally similar. This suggests that consumers are actually willing to purchase cut fruit when they can see the quality of the flesh, and may not even notice that the skin is discoloured.