Glucose and electrolyte supplementation of drinking water improve the immune responses of poults with inanition.

Enteric disorders predispose poultry to malnutrition. The objectives of this paper were 1) to simulate the inanition of poult enteritis mortality syndrome by restricting feed intake and 2) to develop a drinking water supplement that supports the immune functions of poults with inanition. Poults were restricted to 14 g of feed/d for 7 d beginning at 14 d of age then fed ad libitum until 36 d (recovery). The control was fed ad libitum. During the feed-restriction period, duplicate groups of 6 poults received 1 of 5 drinking water treatments: 1) restricted feed, unsupplemented water; 2) restricted feed + electrolytes (RE); 3) RE + glucose + citric acid (REGC); 4) REGC + betaine (REGCB); or 5) REGCB + zinc-methionine (REGCBZ). Immunological functions were assessed by inoculating poults with SRBC and B. abortus (BA) antigen at 15, 22, and 29 d of age. Antibody (Ab) titers were determined 7 d later for primary, secondary, and recovery responses. The primary and secondary total Ab titers to SRBC for restricted feed were 4.71 and 6.16 log3, which where lower (P < 0.05) than for controls (8.00 and 9.66 log3) and the other treatments. The recovery Ab titer for controls was 10.7, significantly higher than restricted feed (8.71) and RE (8.10) groups but not different from other treatments. The primary total Ab responses to BA were significantly lower in the restricted feed and RE groups as compared with the control and other treatments. Although feed restriction of poults to maintenance reduces the humoral immune responses, these responses can be significantly improved by drinking water containing electrolytes and especially sources of energy such as glucose and citric acid.

Isolation of a reovirus from poult enteritis and mortality syndrome and its pathogenicity in turkey poults.

Poult enteritis and mortality syndrome (PEMS) is an acute, infectious intestinal disease of turkey poults, characterized by high mortality and 100% morbidity, that decimated the turkey industry in the mid-1990s. The etiology of PEMS is not completely understood. This report describes the testing of various filtrates of fecal material from control and PEMS-affected poults by oral inoculation into poults under experimental conditions, the subsequent isolation of a reovirus, ARV-CU98, from one of the PEMS fecal filtrates, and in vivo and in vitro studies conducted to determine the pathogenicity of ARV-CU98 in turkey poults. In order to identify a filtrate fraction of fecal material containing a putative etiologic agent, poults were challenged in two independent experiments with 220- and 100-nm filtrates of fecal material from PEMS-negative and PEMS-positive poults. The 100-nm filtrate was chosen for further evaluation because poults inoculated with this filtrate exhibited mortality and significantly lower (P < or = 0.05) body weight and relative bursa weight, three clinical signs associated with PEMS. These results were confirmed in a third experiment with 100-nm fecal filtrates from a separate batch of PEMS fecal material. In Experiment 3, body weight and relative bursa and thymus weights were significantly lower (P < or = 0.05) in poults inoculated with 100-nm filtrate of PEMS fecal material as compared with poults inoculated with 100-nm filtrate of control fecal material. Subsequently, a virus was isolated from the 100-nm PEMS fecal filtrate and propagated in liver cells. This virus was identified as a reovirus on the basis of cross-reaction with antisera against avian reovirus (FDO strain) as well as by electrophoretic analysis and was designated ARV-CU98. When inoculated orally into poults reared under controlled environmental conditions in isolators, ARV-CU98 was associated with a higher incidence of thymic hemorrhaging and gaseous intestines. In addition, relative bursa and liver weights were significantly lower (P < or = 0.05) in virus-inoculated poults as compared with controls. Virus was successfully reisolated from virus-challenged poults but not from control birds. Furthermore, viral antigen was detected by immunofluorescence in liver sections from virus-challenged poults at 3 and 6 days postinfection and virus was isolated from liver at 6 days postinfection, suggesting that ARV-CU98 replicates in the liver. In addition to a decrease in liver weight, there was a functional degeneration as indicated by altered plasma alanine aminotransferase and aspartate aminotransferase activities in virus poults as compared with controls. Although this reovirus does not induce fulminating PEMS, our results demonstrated that ARV-CU98 does cause some of the clinical signs in PEMS, including intestinal alterations and significantly lower relative bursa and liver weights. ARV-CU98 may contribute directly to PEMS by affecting the intestine, bursa, and liver and may contribute indirectly by increasing susceptibility to opportunistic pathogens that facilitate development of clinical PEMS.