Re. Doerfler et al., HYPOTHERMIA, HYPOGLYCEMIA, AND HYPOTHYROIDISM ASSOCIATED WITH POULT ENTERITIS AND MORTALITY SYNDROME, Poultry science, 77(8), 1998, pp. 1103-1109
A metabolic dysfunction contributes to the poor performance and mortal
ity associated with Poult Enteritis and Mortality Syndrome (PEMS). Wit
hin 2 d after contact-exposed poults were removed from the presence of
PEMS-infected poults and returned to their respective treatment rooms
to infect experimental poults, the experimental poults began to huddl
e together and show signs of the disease. When separated from the hudd
le, body temperatures of exposure poults were depressed significantly.
Body temperatures decreased progressively through 8 d after exposure
with a maximum depression of 2 C and returned to a normal level at 18
d after PEMS exposure. Similar decreasing patterns in serum glucose, i
norganic phosphorus, triiodothyronine, and thyroxine were observed, wi
th maximum decreases in these serum constituents being found between 8
and 13 d after PEMS exposure. There were significant correlations amo
ng decreasing body temperatures, decreasing serum constituents, and mo
rtality in the PEMS-exposed poults. Daily mortality rates associated w
ith PEMS began at 6 d and peaked at 9 d after PEMS exposure. Mortality
rates decreased from 9 to 15 d after experimental PEMS exposure. Depr
essions in serum constituents, body temperature, and increased mortali
ty rates did not coincide with decreased feed intake associated with P
EMS. Therefore, it was concluded that the agent(s) causing PEMS may ha
ve a direct effect on energy metabolism in afflicted poults.