30 



PLASMODIOPHOHALES 



cells, numerous parallelisms were drawn between 

 cancer and club root of crucifers. The superficial re- 

 semblance of the tumors on cruciferous roots to can- 

 cerous outgrowths in animals as well as the similarity 

 of the amoeboid stages c P. Brassicae to the cellu- 

 lar inclusions (Plimmer bodies, etc.) in cancer cells 

 led some workers to the belief that fungi, particu- 

 larly tlie myxomycetes and Plasmodiophora, may be 

 associated with, or the cause of cancer in animals. 

 Numerous experiments were accordingly performed 

 in which infected cruciferous tissues were implanted 

 in various kinds of animals. While these studies 

 failed to throw light on tlie cause of cancer, they 

 nonetheless focused attention on club root from the 

 purely pathological viewpoint and are of consider- 

 able liistorical interest. 



In 1898 and 1899 Behla pointed out the similarity 

 of club root and potato wart to cancer and discussed 

 the possible relation of Plasmodiophora and Sijn- 

 chytrhnn to this disease in animals. After having in- 

 fected animals with these fungi and noted the simi- 

 larity of their developmental stages to certain inclu- 

 sions in carcinoma cells, he concluded in 1903 that 

 cancer is caused by a chytridiaceous organism. In 

 1900 and 1903 Podwyssotzki reported that he had 

 succeeded in producing tumors in guinea pigs and 

 dogs by subcutaneous and intraperitoneal implanta- 

 tions of infected crucifer tissues. These tumors were 

 about the size of a walnut and resembled large-celled 

 sarcoma, endothelioma, or granuloma. They were 

 mesodermic in origin and had arisen through pro- 

 nounced hypertropiiy and repeated division of the 

 connective tissue cells and endothelium of the peri- 

 vascular fissures. Leucocyte infiltration was quite 

 evident at first but disappeared after 8 to 12 days. 

 Podwyssotzki found furtlier that P. Brassicae pro- 

 duced many other changes in animal cells which 

 were similar to those induced in cells of crucifers. 



Further attempts to draw analogies between the 

 inclusions of cancerous cells and those produced by 

 P. Brassicae in animal cells were made by Feinberg 

 ('02) and Gaylord ('04). The latter succeeded in 

 infecting animals locally with P. Brassicae, and 

 from his observations on tlie tumors produced he 

 pointed out in detail the parallel cellular symptoms 

 of club root and cancer. Gaylord concluded that can- 

 cer is caused by an amoeboid organism the develop- 

 mental stages of wiiich are very similar to P. Brassi- 

 cae. In 190.5, however, I.owenthal refuted all pre- 

 vious reports that the club root organism produces 

 typical cancerous tumors in animals. He implanted 

 infected crucifer tissues in the stomach, liver, and 

 kidney of dogs and in the skin of white rats, but 

 failed to get tumors or any other specific reactions in 

 the animals. In the same year Prowazek (0.5) made 

 an extensive comparison of P. Brassicae and the in- 

 clusions of carcinoma cells, particularly the Plimmer 

 bodies, and concluded that except for superficial 

 similarities they have very little in common funda- 

 mentally, ^lore recently Levine and I.evine ('22) 

 have made a comparison of the tumors of P. Bras- 



Fiir. 74. Simultaneous nuclear division (meiotic?) in a 

 large, somewhat vacuolate plasmodium. Note large starch 

 grains lying in clear regions. Xawaschin, I.e. 



Fig. 75. First meiotic division with centrosome-like bod- 

 ies and astral rays apart from nuclei in the cytoplasm. 

 Terby, I.e. 



Fig. 7(). Second meiotic division showing four chromo- 

 somes. Terby, I.e. 



Fig. 77. Second meiotic division showing centrosome-like 

 bodies. Terby, I.e. 



Fig. 78. Vacuolate stage of plasmodium prior to cleav- 

 age. Lutman, I.e. 



Fig. 79. Cleavage furrow at edge of plasmodium. Lut- 

 man, I.e. 



Fig. 80. Nuclear division in a large cleavage segment. 

 Milovidov, I.e. 



Fig. 81, 8-2, 83. Mitosis and cell division in smaller cleav- 

 age segments. Lutman, I.e. 



Fig. 84. Fully formed resting spores witli chromatin 

 around inner periplierv of nucleus. Cook and Schwartz, 

 I.e. 



Fig. 8.5. Mature resting spore with fat droplets. Lutman, 

 I.e. 



Fig. 86. Resting spores with chondriosomes. Milovidov, 

 I.e. 



Fig. 87. Variations In size and shape of resting spores. 

 Milovidov, I.e. 



Fig. 88. Fusion of incipient resting spores. Prowazek, 

 '0,5. 



Fig. 89. Binucleate resting spore. Prowazek, I.e. 



Fig. 90. Division of one gametic nucleus. Prowazek, I.e. 



Fig. 91, 9-3. Formation of "reduction bodies." Prowazek, 

 I.e. 



Fig. 93. Karyogamv. Prowazek, I.e. 



Fig. 94. Centrosome separating from nuclear membrane 

 to become the blephoroplast. Terby, I.e. 



Fig. 95. Resting spore with blephoroplast. Terby, I.e. 



Fig. 96. Binucleate resting spore. Terby, I.e. 



Fig. 97. Host cell filled with resting spores. Woronin, I.e. 



P. J>iphnifherae 



Fig. 98. Infected plant of Diplanthera U'rif/htii with 

 hvpertrophled bead-like intcrnodes. Ferdinandsen and 

 Winge, "14. 



Fig. 99. Cleaving plasmodium which fills enlarged host 

 cell and envelops host nucleus. Drawn from photograph. 

 Ferdinandsen and Winge, I.e. 



Fig. 100. Host cell filled with resting spores. Drawn from 

 photograph. Cook, '33. 



Fig. 101. Normal and collapsed resting spores. Drawn 

 from photograph. Ferdinandsen and Winge, I.e. 



/'. Flcl-rej)(ntis 



Fig. 102. Gall on branch of FIciis repen.-:. Drawn from 

 l)hotograph. Cook, I.e. 



P. II(ilujihil<(e 



Fig. 103. Hypertro])hied petiole of IlalophUii ovnVis. 

 Ferdinandsen and Winge, '13. 



Fig. 104, 105. Normal and collapsed resting spores. 

 Ferdinandsen and Winge, I.e. 



P. Iiirtaifldtit 



Fig. 106. Plasmodium t-nvcloping enlarged host mu'leus. 

 Feldmann, '40. 



Fig. 107. Cleavage into resting spores. Feldman, I.e. 

 Fig. 108. Resting spores. Feldman, I.e. 



