reduction in the number of apertures that were penetrated by methyl- 

 ene blue. Very little decay developed in the naturally inoculated 

 fruit used in 1941 (see table 7) despite the presence of numerous open 

 lenticels and washing injuries. 



A histological study of the lenticels of apples immersed in methylene 

 blue corroborated the results obtained by Clements (4) that closure 

 generally is due to the formation of a continuous layer of cuticle or to 

 a combination of cuticularized and suberized cells (fig. 2, A). Len- 

 ticels rarely were closed by the formation of a layer of cork (fig. 2, B). 

 In open lenticels frequently only a small fissure extended through the 

 layer of modified cells in the lenticel basin (fig. 2, C). 



Lenticels in apples washed the day after harvest did not differ 

 histologically from those in unwashed fruit or in fruit washed after 

 various holding periods. The layer of cuticle on parts of the fruit 

 that developed washing injury was somewhat thinner than on those 

 that were resistant to this damage. If the thickness of the cuticle is 

 related to washing injury, it is not surprising that less injury and 

 fewer open lenticels were found in the fruit delayed in the warehouse 

 prior to washing than in apples washed immediately. 



The cuticle was not significantly thicker on unwashed apples than 

 on those cleaned in a dual-process wash consisting of sodium silicate 

 (80 pounds to 100 gallons) at 110° F. and 1.5-percent hydrochloric 

 acid at 100°. 



Miscellaneous Infection Courts 



When the so-called lenticel infections that developed in the fruit of 

 the 1939 season were studied microscopically, it was found that pene- 

 tration of true lenticels (those having a radial arrangement of the sub- 

 epidermal cells) had occurred in only 63 percent of the 216 lesions 

 examined. Approximately 23 percent of the invasions were through 

 apertures not having the origin of true lenticels, and the remaining 14 

 percent apparently represented penetration of the unbroken epider- 

 mis. Some of the nonlenticular openings appeared to be minute 

 washing injuries, but others were small punctures that apparently were 

 caused by the fruit striking sharp granular material, possibly orchard 

 sand in the bottom of field boxes. Many of the lenticel infections 

 were found in bruised areas, and, as Baker and Heald (2) concluded, 

 it is probable that localized pressure may have ruptured the layer of 

 modified cells in the lenticel basin and thus increased susceptibility. 



The relative importance of various infection courts in the initiation 

 of blue mold decay in Delicious apples is shown in table 3. When a 

 relatively severe dual-process washing treatment was used, most of 

 the infection occurred at lenticels and washing injuries. With milder 

 treatments washing injuries were relatively unimportant, but lenticels 

 continued to predominate as places of invasion. Mechanical injuries 

 were the most common avenues of infection in unwashed apples, but 

 stem and calyx infections were rare in both washed and unwashed 

 fruit. It appears from this study that acid and dual-process washing 

 treatments predispose lenticels to penetration by blue mold; silicate 

 solutions, however, appear to have little effect on lenticel suscepti- 

 bility. 



In the naturally contaminated apples used in 1941 (see table 7) 

 very little lenticel infection occurred and about 73 percent of the blue 

 mold decay originated at mechanical injuries. This fact, together 

 with the evidence that many lenticel infections occur in bruised areas 



