The Anthracnose Disease of the Raspberry 171 



infection are found only on the tips of the shoots. During the early 

 development of the disease the epidermal and the outer cortical cells col- 

 lapse. At this early stage the fungus has never been noticed in these cells, 

 but since the hyphae are very slender and the dead host tissue becomes so 

 deeply stained the mycelium would be difficult to detect. The paren- 

 chyma below this collapsed region is evidently affected with a toxin or 

 enzyme either produced by the fungus or resulting from the death of the 

 host tissue. The cells in this region divide very rapidly in a tangential 

 plane. This hyperplasia of the parenchyma cells causes the young lesion 

 to be slightly raised at first on the surface of the cane, but with further 

 development of the pathogene this tissue collapses and the lesion becomes 

 sunken. A thin stroma then fills the cavity and a very small trace of the 

 cortex remains or frequently its destruction is complete. During this 

 time the organism continues its invasion of the parenchymatous cells 

 between the vascular bundles. A hyperplasia of the phloem next occurs, 

 but no further pathological condition arises within this tissue in case of 

 late infection. On the other hand, with early and severe infection the 

 phloem cells collapse and the fungus destroys the cambium and extends 

 to the xylem. 



Normally a ring of fibers is formed in the cortex, which are not in a 

 continuous sheet but appear in groups associated with the phloem. If 

 the pathogene reaches these before they mature, the fibers become abnor- 

 mal or are completely suppressed. After their development, however, 

 they are very resistant to the attacks of the fungus. 



The xylem tissue is the least affected by the anthracnose disease, but 

 if infection takes place when the vascular bundles are small the xylem 

 ceases its normal development. It is difficult to determine whether this 

 tissue is invaded by the pathogene, since only the outer edge shows the 

 necrotic condition which might be indicative of the presence of the fungus. 

 Frequently it is impossible to determine the position of the cambium, 

 as the diseased phloem and xylem lose their distinctive characteristics and 

 become fused. Although hypoplasia is exhibited in the xylem beneath 

 the infection, it is offset by an excessive development of that tissue on 

 either side of the diseased spot. This is likewise true of the phloem. 



Because of the increased development of the vascular bundles on either 

 side of the lesion, and the hypoplasia and destruction of the tissue within 

 the lesion, an uneven growth of the cane results. Longitudinal fissures 

 appear in the diseased area and later extend into the xylem and in some 

 cases into the pith. This splitting of the cane is caused by the strain 

 placed on the diseased tissue due to the continued tangential and radial 

 growth of the surrounding normal tissues. It is delayed, however, to 

 some extent by the development of a group of parenchyma cells which 



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