Mar. 3,1933 
Gray Mold of Castor Bean 
701 
a pore, 50 to no p by 6 to 10 p, usually 80 to 100 p by 8 p; ascospores 8, ellipsoidal, 
often sub-fusoid, hyaline, continuous, bi-guttulate, 9 to 12 /x by 4 to 5 /x; paraphyses 
abundant, filiform, septate, hyaline, 1.5 to 2 p in diameter. Conidial stage (Botrytis 
sp.) forming widespreading cobwebby or somewhat woolly mass, pale drab-gray to 
drab, dried specimens dark olive-gray; sterile hyphae procumbent, hyaline, many- 
septate, often vacuolate, frequently anastomosing; fertile hyphae long, slender, smooth, 
slightly constricted at the base, olivaceous when mature, dichotomously branched, 
terminal branching compact, apices non inflated, thin-walled, collapsing when the 
conidia fall; proliferation sometimes occurring; conidia borne on stengmata, globose, 
smooth, hyaline, 6 to 12 p, usually 7 to 10 p, compactly grouped; microconidia globose, 
hyaline, 2 to 3.5 p, borne apically on short, obclavate, single or clustered conidio- 
phores that develop on the sides of hyphae or on tips of special branches; appressoria 
rare, microscopic, 20 to 60 p across base. Sclerotia black, rough, elongate, irregular, 
1 to 25 mm. in length, usually 3 to 9 mm., suberumpent to superficial, often anasto¬ 
mosing, developing on axes ana peduncles of old castor bean inflorescences and on 
stalks. 
Parasitic on Ricinus communist usually on inflorescences, also on stems and leaves; 
type locality, Orlando, Fla.; distribtition Florida, Mississippi, Louisiana, Texas, and 
Cuba. Type specimens deposited with the Office of Pathological Collections, Bureau 
of Plant Industry, U. S. Department of Agriculture, Washington, D. C. 
ORIGIN OF THE PATHOGENE 
Early in the progress of the disease it was suspected that the patho- 
gene had been introduced with the seed. This was not proved abso¬ 
lutely for some time, but much evidence pointed in that direction. 
For example, the disease was found in nearly every field where Bombay 
seed had been planted, provided the climatic conditions were favorable 
for the development of the fungus. One such field was at Baton Rouge, 
La. A field planted to American-grown seed only a mile or two away 
was not attacked. Native castor beans had been grown for years in 
Florida without any report of it, and in 1918 they were not affected until 
late in the season. Much evidence was found in connection with seed 
produced in diseased fields in America. The fungus was capable of 
living over for a long period on the seed. On October 30, 1918, speci¬ 
mens were collected at Alvin, Tex. The fungus was readily isolated, 
and some of the material was laid away in a sealed envelope. Two 
months later the fungus was again isolated from this same material. 
On October 25, waste from a hulling plant at Plant City, Fla., including 
some light-weight beans, was collected. Two weeks at least must have 
elapsed since the beans were harvested. The material was placed in a 
sealed envelope. Six months later the fungus was isolated from this 
material. Plate 7, D, shows the development of the fungus on one of 
the castor beans in a poured plate of nutrient agar. Finally, sclerotia 
17 months old developed the apothecial stage. This shows that sclerotia 
carried with the seed are able to reproduce the disease even after a long 
period. 
In addition, many observations showed the close contact of the fungus 
with the developing seed pods in diseased spikes. A castor bean reaches 
full size long before it is matured. It is then soft and very succulent and 
the caruncle is prominent, as shown in Plate 7, A. In such condition 
it offers no resistance to the penetration of the fungus. Plate 7, B, 
shows a seed in its pod with the mold growing out of the caruncle and 
even the seed coat; C shows several such seed with the gray mold dis¬ 
tinctly visible; E shows several seed which had been attacked before 
maturity, with sclerotia attached to the seed coat and the remains of 
the pods. These specimens were collected under natural conditions in 
diseased castor bean fields. 
