688 



causing the disease. Beijerinck^ appeared first among those who hold this 

 opinion. In 1898 he described a "contagium vivum fliddum" as the cause. 



Hunger says further-, "I consider the virus of the mosaic disease to 

 be a toxin which is akvays produced in the tobacco plant during the metabo- 

 lism of the cells but, in normal cases, exercises no effect, while it accumu- 

 lates when the metabolism is too strongly increased and then causes disturb- 

 ances such as the mosaic form of variegated leaves." I assume that the 

 toxin of the mosaic disease, which is produced primarily by external stimuli, 

 is capable, when penetrating into normal cells, of exercising a physiological 

 contact effect with the result that the same toxin is formed there secondar- 

 ily. In other words the toxin of the mosaic disease possesses the pecidiarify 

 of acting as a physiologico-autocatalytic agent. In this way the virus can be 

 make its way independently throughout the tobacco plant and, reaching the 

 paths leading to the meristem, can exert its influence there on the young 

 structures. This explains the capacity of the diseased substance for in- 

 crease. "This capacity does not depend on the active reproductivity of the 

 virus itself but simplv arises from the passive reproductive power of the 

 living cell substances." 



In contrast to the theory of poison we represent a second theory and 

 call attention to the experiments of Pantanelli and others who have proved 

 a change in the amount and action of the enzymes. HeintzeP says (1899, 

 p. 45), "The enzyme which causes the mosaic disease may, therefore, be 

 considered an oxydase." Accordingly, the cause of the mosaic disease 

 would be present also in a healthy plant and would have an abnormal action 

 only under special circumstances. Woods* expresses exactly the same 

 theory since he thinks only certain conditions are concerned under which 

 the oxidizing enzymes become eft'ective — "either become more active, or are 

 produced in abnormally large quantities." The condition of matters at 

 present is still uncertain and forbids a closer examination of the relations. 

 For the theory which we advance and have described in the first section of 

 this chapter, the question is less important, whether an increase of the 

 oxydases actually takes place, or whether a decrease of the reducing sub- 

 stances, always accompanying the oxydases, whereby the same amount of 

 oxydase has an increased activity. Hunger has actually proved that the 

 leaf with the mosaic disease contains less reducing and tannic substances 

 than do healthy tobacco leaves'*. A scantier sugar content has been proved 

 in the diseased leaf, corresponding to a lack of chlorophyll; besides this, 



1 Beijerinck. M. W., Over een coTitas:ium vivum fluiflum als oorzaak van de 

 Vlekziekte dor tabaksbladen. Koninkl. Akad. van "Wetenschappcn te Amsterdam. 

 Nov. 1898. tJber ein Contagium vivum fliiidum als Ursache der Fleckenkrankheit 

 der Tabaksblfltter. Centralbl. f. Bakeriologic 1899, Part II, No. 2, p. 27. 



2 Loc. cit., p. 296. 



3 Heintzel, Kurt, Kontapriose Pflanzenkrankheit ohne Mikroben, mit beson- 

 derer Berlicksichtig-unp: der Mnsaikkrankheit der Tabaksblatter. Inaug. -Dissert. 

 Erlangren 1900; cit. bv Hun.srer, loc. cit., p. 269. 



4 Woods, A. F., The destruction of chlorophyll by oxidizing- enzymes. Centralbl. 

 f. Bakt. 1899. Part II. Vol. V, No. 22, p. 745. 



■^ Hunger, F. W. T.. Bemerkungen zur "Wood'schen Theorie tiber die Mosaik- 

 krankheit des Tabaks. Bull. d. I'Inst. Bot. de Buitenzorg 1903, No. XVII. 



