ATEACHME27r 2 - PACX 2 
Lcx^ histologically and grossly to determine pathologic changes 
due to direct action of the toxin on the gut or on viscera 
attributable to toxin that esc^ied, and hence determine cause of 
death. Examine 7 day survivors for other effects, namely dis- 
figurement, profound neurological changes, or histological damage 
to the intestine itself. Antibody titers? 
(b) Repeat (a) with injection into the various levels of the gut in 
order to mimic possible colonization by toxinogenic clones, namely; 
i) uH»r gut 
ii) proximal ileum 
iii) distal ileum (site of uptake of 8^2 salts) 
iv) colcn 
(c) To mimic the continuous production of a toxin by a bacterial clone: 
Is the lethal dose much reduced by split doses? Inject sublethal 
doses into marked sites of the gut. Wait (2 days?) for histological 
damage to occur, and reinject the same doses into the same sites. 
(d) Perhaps to show that any potentiation by split doses is truly caused 
by a rise in permeability, repeat particular experiments in (c) 
using difhtheria toxin for the first injection and tetanus toxin 
for the second injection. Is there a change in the dose-lethality 
curve for tetanus toxin? 
Question 2 : To further determine how much of a toxin passes out of the gut 
under normal and ataiormal ccxiditions. 
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