180 
Saprogenesis. As the pathogene is continuously associated with 
its living host, it may be regarded as having no saprogenic phase in any of 
its life-cycles. However, as a matter of fact, there is often little living 
host-tissue in the galls during the period of the maturing of the ascospores. 
Secondary Cycles are initiated by the conidia, produced on the galls, 
during the next growing-season after that in which the primary infections 
were initiated. ‘These secondary cycles require slightly less than two full 
years for their completion and, like the primary, end with the production 
of ascospores. ‘The pathogene structures, developed during the secondary 
cycles, and the host reactions are like those of the primary cycles. 
Mycelium spreading from the primary (or secondary) galls into adja- 
cent healthy tissues often give rise to secondary galls. This is regarded by 
some as secondary infection (Stewart, Amer. Jour. Bot. 1:114). 
Pathological Histology. The effect of this pathogene on the host is one 
of stimulated overgrowth of the invaded tissues. Cut with a knife or scal- 
pel (not a razor) across one of the galls provided for this purpose. Trim 
the surface smooth and with hand-lens, MAKE OUT:— 
20. The anatomical distortions that have occurred in the elements 
of the vascular cylinder and bark, comparing constantly with the struc- 
tures in the normal portion of the twig. Make a diagrammatic DRAWING 
of the entire cross-section showing normal and pathological anatomy. 
Label corresponding tissues in each. 
Study under the microscope the prepared sections through young one- 
year old galls. OBSERVE :— 
21. The character of the host-tissué on which lies the stroma 
of the fungus; size, shape, contents of cells and tissue-relations. 
22. The mycelium in the tissues; inter- or intracellular? 
23. The mycelial strands and fans in some places; their pseudo- 
parenchymatous character. What is their relation to the stroma? 
24. The depth toward the pith to which the pathological effects 
are evident. 
25. The broadening of the rays in the diseased region; due to 
hyperplasia or hypertrophy? 
26. The isolation of the cambium at the outer ends of the xylem- 
wedges; wanting in the abnormally broad rays. 
27. The inhibition of xylem-elements and the abnormal develop- 
ment of parenchyma in the xylem-wedges. The enlargement of the gall 
ne second year is largely due to a marked hypertrophy of these parenchy- 
mal cells. 
28. The isolated groups of summer-wood vessels in the xylem- 
parenchyma just inside the cambium. 
29. The isolated xylem-elements in the diseased bark. These 
result from the misplaced and broken segments of the cambium opposite 
the broad rays. 
30. The proportional increase in thickness of bark and wood 
in the diseased region. The outer bark sluffs off before conidial formation. 
Make a full-page DRAWING, detailing cells in the different regions, to 
bring out the histological changes above emphasized. 
REPORT 
__ 1. Prepare a diagram showing the two types of life-cycles in 
Plowrightia morbosa (Schw.) Sacc. and their relation to each other. 
