MODIFICATION OF RUNT DISEASE 



357 



ascitic fluid and moderately enlarged livers with sharply defined 

 yellow patches along the free margins of the lobes, a fmding also 

 mentioned by Siskind and Thomas (1959). Histological 

 examination of the liver shows these areas to consist of coagulative 

 necrosis associated with a varying amount of widespread patchy 

 cellular infiltrations, most notable in the periportal areas and 



15 



14 



13 



12 



I I 



10 



5 9 



S8 



if) 7 



X 



^6 



UJ 



Q 5 



4 - 



l40animols receiving at least 

 5,000,000 DBA splee n cells l/V 



median time of deoth-l4dys 



3.7% 



of group 



d 3 



2 



8 10 12 14 16 18 20 22 24 26 28 30 32 34 36 Survivors 

 DAYS 



Fig, 2. Time of death of 140 newborn C57BL/6 runts injected 



with 5 milHon or more DBA/i spleen cells intravenously at 



birth. Only 3 • 7 per cent of the animals survived. The median 



age at death of the remaining animals was 14 days. 



including both lymphoid cells and polymorphonuclear leucocytes 

 (Fig. 4). Since the haemopoietic elements present in the liver at 

 birth do not normally disappear for some days thereafter, the 

 interpretation of the origin of such cells in very young animals 

 may be particularly difficult. 



The spleen is usually firmer than normal and somewhat 

 enlarged, although this change is also more marked in animals 

 which have lived longer, presumably with a less acute form of the 



