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THOMPSON YATES LABORATORIES REPORT 
The red points noticed at the post-mortem were due to marked dilatation of the 
capillaries in certain lobules, combined with compression of the adjacent hepatic cells. 
These lesions being seldom associated with focal necrosis were perhaps the result of 
passive congestion, though neither their microscopic appearances nor distribution were 
typical ; on the other hand, Longridge described marked localized dilatations of the 
hepatic capillaries in a case of focal necrosis, and Flexner produced dilatation and focal 
necrosis in the liver of rabbits by the inoculation of ricin in small quantities. 
The hepatic capillaries were blocked at intervals with dense clusters of micro- 
organisms, which from their morphology and staining reactions, and on account of 
the fact that B. coli was not isolated from the spleen, must be regarded as typhoid 
bacilli. As there was no relation between the focal lesions and the groups of typhoid 
bacilli, their presence in such numbers was probably due to post-mortem invasion and 
multiplication. 
Divergent views are held as to the composition of the necrotic areas, and the 
origin of the irregular nuclei. All writers agree that the hepatic cells necrose, but 
according to Orth and others the nuclei arise from lymphoid cells. Wagner holds 
that they are produced by the multiplication of hepatic cells. According to Reed 
they 'owe their origin, in small part, to the disintegration of the nuclei of the liver 
cell involved, and in greater part to the presence of polynuclear leucocytes.' Mallory 
maintains that invasion with polynuclear leucocytes is 'rare,' and also that the lesions 
are due to the 'obstruction of the liver capillaries by phagocytic cells derived in 
small part from the lining endothelium of the liver capillaries, but chiefly by embolism 
through the portal circulation of cells originating from the endothelium of the blood 
vessels of the intestines and spleen,' for the typhoid toxme produces a diffuse pro- 
liferation and desquamation of the endothelial cell which is, he believes, the 
' essential lesion of typhoid fever.' 
Polynuclear leucocytes were absent in my sections ; there was no evidence that 
large endothelial cells were associated with the formation of focal necrosis, perhaps 
because the tissues had been fixed and hardened in spirit. 
The exact causation of the lesion is also disputed. Observers agree that typhoid 
bacilli are not found in the necrotic area. Therefore, the lesions probably originate either 
by the action of the diffusable typho-toxin on groups of cells in which the resistance 
had been lowered for some reason or other, or in the manner which Mallory 
suggests. But if the embolism of phagocytic endothelial cells be the main cause of 
the focal lesion, why are they not confined to the portal zone of the hepatic lobule, 
and why, as Mallory himself asks, are phagocytic endothelial cells not present in 
the blood of typhoid patients ? Reed, however, produced focal lesions in the liver 
of rabbits by injecting pure cultures of typhoid bacilli into the mesenteric veins. 
Apparently no investigator has yet tested the effect of typho-toxin alone, though 
Welsh and Flexner have produced circumscribed necrosis in the liver of guinea 
