244 SECTIONAL ADDRESSES. 
Miss Allen 2! published a very careful and detailed cytological study of the 
infection of susceptible and immune wheats by forms III. and XIX. of 
P. graminis tritict. Mindum wheat is immune to form III. and Kanred 
to form XIX., so the behaviour of these two wheats was compared with 
that of other susceptible varieties. When Mindum is infected with the 
uredospores of form III. an appressorium is formed over the guard cells 
and entry occurs in the normal way through the stoma. Usually the first 
haustorium from the infection hypha develops in a mesophyll cell and its 
formation is the signal for a violent reaction on the part of this cell. The 
host-cell contents, including the cytoplasm, nucleus and plastids, flow 
rapidly towards the haustorium and become massed around it, forming 
apparently a sheath to the haustorium. Of the haustorium and host-cell 
cytoplasm Miss Allen states ‘each seems to be toxic to the other ; at least, 
both die very soon.’ The haustorium and its cytoplasmic sheath appear 
to be partially digested. The infection hypha is not killed by this reaction 
to the first formed haustorium, but only checked ; it may develop a few 
other haustoria in other host cells which are similarly killed; finally the 
limited resources of the hypha are exhausted and it succumbs. 
From a single infection only a small number of cells, about five or six, 
are killed by being entered directly by the fungus. The ‘ fleck’ visible to 
the naked eye which is the sign of an attack successfully repelled consists 
of a much larger number of dead or damaged cells. This is explained by 
the fact that the violent primary effect due to entry is followed by a mild 
secondary effect on the cells surrounding the area of cells killed by entry. 
These neighbouring cells in a region 3-4 cells deep become plasmolysed 
and shrunken, and some of them show marked swelling of the walls. 
Although in the cereal rusts we have the most complex reaction to 
attack by aninvading organism which has been observed in plants, we find 
very few phenomena analogous with the response to infectious disease of 
higher animals. When the susceptible forms are attacked we find no 
spontaneous cure, no recovery of the attacked cells. We have no evidence 
in the resistant forms of the productions of antibodies in either the suscep- 
tible or resistant forms; the death of the haustoria may be simply due to 
the death of the host cells in which they lie. It is true that we have a 
digestion of the haustorium, but this ‘ phagocytosis ’—since the digestion 
of the haustorium is associated with the digestion of the host-cell con- 
tents and takes place after the death of that host cell—may be nothing 
more than an effect of autolysis.22 Again, no general bodily reaction 
of the plant is apparent, each infection is highly localised, and each group of 
host cells fights a solitary battle independent of its neighbours. No analy- 
sis of plant resistance on the lines found so successful in animal disease 
can be achieved at present, nor is it likely in the future in view of the 
21 R. F. Allen ; ‘Cytological Studies of Infection of Baart, Kanred and Mindum 
Wheats by Puccinia graminis tritici.’ J. Agric. Res., XXVI., 571, 1923. 
22 It is true that in such peculiar symbiotic relationships as those of the orchid 
fungus and endotrophic mycorhiza—cases which donot fall into the category of ordinary 
disease—we do find digestion of invading fungal hyphe by living active host cells. 
Such cells are, however, far from acquiring any resistance by such phagocytosis, for it 
has been observed both in orchids and in mycorhiza that host cells which have success- 
fully coped with one attack by the process of digestion may be invaded again (vide 
Rivett, Annals of Bot., XX XVIII., 1924). 
