156 EXPERIMENT STATION RECOKD. 



Histological relations of sugar-beet seedlings and Phoma betse, H. A. 

 Edson (U. S. Dept. Agr., Jour. Agr. Research, 5 {1915), Xo. 1, pp. 55-58, pis. 2). — 

 In a previous publication (E. S. R., 33, p. 246), the author pointed out the infec- 

 tion of practically all sugar-beet seed with the fungus P. beta: 



In the present publication an account is given of a study of the seedlings in 

 relation to the fungus. Damped-off and root-sick seedlings were selected at 

 different stages of the disease, and it was found that cells of badly diseased 

 but still living seedlings were often nearly filled with the fungus, which showed 

 a tendency to remain in the interior of the cell rather than in the middle lamella. 

 Occasionally the fungus was observed running between the cells, but the indi- 

 cations are that, while it dissolves the middle lamella, it does not feed upon it. 

 In heavily invaded cells the cell walls are consumed, the cytoplasm disappears, 

 jind the nuclei disintegrate. 



In case of less serious infection, where recovery is possible, the cell walls show 

 a gelatinized condition only in moderate degree and in an area confined to ix)ints 

 where the cells have been penetrated by the mycelium. 



Sugar beets attacked by the fungus frequently send out new side roots above 

 the invasion, and succeed in preventing the destruction of this new growth. In 

 such cases, the fungus is apparently established in a condition of reduced viru- 

 lence in the interior tissue of the beets. The invaded cells are not killed and 

 the adjacent ones appear perfectly normal in every respect. 



Attention is called to the difficulty of explaining how an organism capable of 

 such complete destruction has its action suddenly checked and confined to a 

 stiprophytic existence in the infected area. 



The diseases of the sweet potato and their control, J. J. Taubenhatjs and 

 T. F. Manns {Delaware .S/a. Bui. 109 {1915), pp. 3-55, pis. 26). — The authors 

 give an account of the following diseases of sweet potatoes, describe the organ- 

 isms which cause them, and give accounts of their distribution, the loss occa- 

 sioned by their presence, and means of control: Black rot {Sphwroncma fim- 

 briatum), vine wilt or yellows, also called stem rot {fusarium batatatis and 

 F. hypcroxysporum), soil rot {Acrocystis batatas), soil stain or scurf {Moni- 

 lochoctcs infuscans) dry rot {Diaporthc batatatis), foot rot {Phcnodomus des- 

 truens), white rust or leaf mold {Cystopvs ipomorw payidura^io'), Septoria leaf 

 spot {S. batatieola), soft rot and ring rot {Rhizopus nigricans), Trichoderma 

 rot {T. koningi), charcoal rot {Sclcrotium batatieola), and the Java black rot 

 {Diplodia tubericola) . 



The black rot is claimed to be carried with the seed to the seed bed, and 

 from there to the land. The stem wilt or yellows is also carried inside the seed, 

 and, it is claimed, may also persist for a long time in the land. Soil rot is said 

 to be a very severe disease when once introduced in the soil, but its presence in 

 Delaware is as yet limited to one section. Soil stain is a superficial disease 

 which affects only the market value of the roots and not their e<lible quality. 

 White rust is said to often cause premature dying of the foliage, but the leaf 

 spot, though prevalent in Delaware, is of little economic Importance. The soft 

 rot, ring rot. Trichoderma rot, and charcoal rot are storage troubles, some of 

 which are quite serious. 



For the prevention of these diseases, the authors give various suggestions, 

 which include seed treatment in which corrosive sublimate is said to give better 

 results than formaldehyde, although formaldehyde is recommended for the 

 disinfection of the seed-bed soil. For prevention of the storage troubles, proj^er 

 attention should be given to temperature, ventilation, etc. 



Apple collar rot, H. R. Fulton {Pennsylvania Sta. Rpt. 1912, pp. 2.'il-253). — 

 Collar rot of apple trees, which is described as to its general symptoms and 

 progress, was studied in Pennsylvania in 1910 and 1911. 



