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. 2019 Dec 11;77(8):1103–1109. doi: 10.1093/ps/77.8.1103

Hypothermia, hypoglycemia, and hypothyrosis associated with poult enteritis and mortality syndrome

RE Doerfler 1, FW Edens 1, CR Parkhurst 1, GB Havenstein 1, MA Qureshi 1
PMCID: PMC7107120  PMID: 9706073

Abstract

A metabolic dysfunction contributes to the poor performance and mortality associated with Poult Enteritis and Mortality Syndrome (PEMS). Within 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 huddle together and show signs of the disease. When separated from the huddle, 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, inorganic phosphorus, triiodothyronine, and thyroxine were observed, with maximum decreases in these serum constituents being found between 8 and 13 d after PEMS exposure. There were significant correlations among decreasing body temperatures, decreasing serum constituents, and mortality in the PEMS-exposed poults. Daily mortality rates associated with 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. Depressions in serum constituents, body temperature, and increased mortality rates did not coincide with decreased feed intake associated with PEMS. Therefore, it was concluded that the agent(s) causing PEMS may have a direct effect on energy metabolism in afflicted poults.

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