Fowl Typhoid and Fowl Cholera 
41 
leucocytes indicating infection or concentration of the toxin at this point and 
constituting inflammation or nephritis. As a summary, it may be said that 
acute parenchymatous nephritis is present. 
The Liver. An examination under a lower magnification, of a prepared 
section of the liver, shows active congestion which is most marked at the 
aiteiioles of the periphery of the liver lobule. Passive congestion, as affect¬ 
ing the central vein and its tributaries, is present and is caused by a 
damming back of the venous blood. An examination under a higher magnifi¬ 
cation shows the hepatic cells to appear swollen because they have taken up 
fluids. This absorbed water causes a coagulation of the cell proteids, hence 
a swollen, granular appearance of the cell, which may make the nucleus less 
distinct, is present. In some areas a digestion of the nuclei, and to some 
extent the cytoplasm, has caused a disintegration of the cells, and conse¬ 
quently a point of beginning necrosis. These conditions are brought about 
by the toxins of the E. sanguinaria. Blood reaching the periphery of the 
lobule first would give to this part the most toxins, with a result that these 
focal centers of necrosis are, for the most part, located in the periphery of 
the lobules of the liver. Areas are invaded by leucocytes due to the con¬ 
centration of toxins or foci of infection of the E. sanguinaria. In these areas 
(see Figure 26) may be seen cells in a state of cloudy swelling or necrosis, 
leucocytes, other cells probably epithelioid replacing the hepatic cells and 
congestion of the blood vessels—both arteries and veins. 
As a summary, it may be said that acute parenchymatous hepatitis is 
present. 
The Spleen.—A microscopic study of prepared sections of the spleen 
shows similar conditions to those described in the liver, including both active 
and passive congestion. Acute spleenitis, then, may be present. 
Tlie Heart. Congestion may be present. In some cases the muscle 
fibers have partially or completely lost their cross striation. 
In conclusion we may say as Delafield and Prudden (5) say of human 
typhoid, so in fowl typhoid, toxemia may be manifested by disturbances 
in the circulatory, respiratory, and heat regulating mechanism, and in gen¬ 
eral metabolism, as well as by manifest lesions, such as albuminous (cloudy 
swelling) or other degenerations of parenchyma cells throughout the body, 
and alterations leading to leucocytosis. 
The spread of the disease in a flock is very rapid, and is usually recog¬ 
nized by the owner only after a number of birds have died. The symptoms 
on the onset are undecided, and not likely to be recognized by the casual 
observer. The affected birds become dull, droopy, and tend to segregate 
themselves from the rest of the flock. There is a sulphur colored discharge 
from the bowel, an elevation of temperature, and usually the birds become 
acutely thirsty, but lack appetite. As the disease advances, the symptoms 
become more marked, and mortality ensues. There is a dribbling of saliva 
from the mouth; many birds become too weak to walk; others walk with a 
staggery gait; some sit with the heads resting on the ground, eyes closed, 
and in a condition of partial coma. The temperature may rise to 113 degrees, 
the normal temperature being about 107.5 degrees. Sometimes the disease is 
confused by the owner with limberneek. Before death, complete prostration 
usually occurs, the diarrhea being profuse and watery, and the bird becomes 
more or less anemic according to the duration of the disease. Prior to death, 
there is usually a well-defined drop in temperature. Occasionally the birds 
die in convulsions. The disease may assume a very acute form, with a quick 
death; it may present the normal features of the disease, with death and 
recovery as the termination, or it may assume a long drawn out form which 
