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1、Viral Agents Associated with Poult Enteritis and Mortality Syndrome: The Role of a SmallRound Virus and a Turkey CoronavirusAuthor(s): M. Yu, M. M. Ismail, M. A. Qureshi, R. N. Dearth, H. J. Barnes and Y. M. SaifSource: Avian Diseases, Vol. 44, No. 2 (Apr. - Jun., 2000), pp. 297-304Published by: Ame
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5、04, 2000 Viral Agents Associated with Poult Enteritis and Mortality Syndrome: The Role of a Small Round Virus and a Turkey Coronavirus M. Yu,A M. M. Ismail,A M. A. Qureshi,B R. N. Dearth,A H. J. Barnes,c and Y. M. SaifAD AFood Animal Health Research Program, Ohio Agricultural Research and Developmen
6、t Center, The Ohio State University, Wooster, OH 44691 BDepartment of Poultry Science CDepartment of Farm Animal Health and Resource Management, College of Veterinary Medicine, North Carolina State University, Raleigh, NC 27695 Received 30 June 1999 SUMMARY. Intestinal samples from turkey poults aff
7、ected with poult enteritis and mor- tality syndrome (PEMS) were examined for viruses by immune electron microscopy and double-stranded RNA virus genome electropherotyping. Turkey coronavirus (TCV), avian rotaviruses, reovirus, and a yet undefined small round virus (SRV) were detected. The SRV and TC
8、V were isolated and propagated in turkey embryos. Challenge of specific-pathogen- free turkey poults with SRV, TCV, or both resulted in mortality and clinical responses similar to those of natural PEMS. Our experiments indicate that SRV and TCV are possibly im- portant agents in the etiology of PEMS
9、 and the combination of these infections might result in outbreaks with high mortality. The severity of clinical signs and mortality of PEMS are postulated to be partly related to the virus agents involved in individual outbreaks. RESUMEN. Agentes virales asociados con el sindrome de mortalidad y en
10、teritis en pavos: Papel de un virus pequefio y redondo y un coronavirus de pavo. Se examinaron muestras intestinales de pavitos afectados con el sindrome de mortalidad y enteritis de pavitos para la presencia de virus mediante el microscopio electr6nico y mediante la electroferotipificaci6n. Se dete
11、ctaron coronavirus de pavos, rotavirus aviares, reovirus y un virus pequefio redondo todavia no definido. El virus pequefio redondo y el coronavirus de pavo fueron aislados y propagados en embriones de pavo. El desaflo de pavos libres de pat6genos especificos con el virus pequefio y redondo, con el
12、coronavirus del pavo 6 con los dos virus, result6 en mortalidad y repuestas clinicas similares a las del sindrome de mortalidad y enteritis del pavo. Los experimentos indican que el virus pequefio y redondo y el coronavirus del pavo son agentes importantes en la etiologia del sindrome de mortalidad
13、y enteritis de pavitos y que la combinaci6n de estas infecciones puede resultar en un brote de la enfermedad con alta mortalidad. Se cree que la severidad de los signos clinicos y la mortalidad del sindrome de mortalidad y enteritis del pavo estain parcialmente relacionados con los agentes virales i
14、nvolucrados en brotes individuales. Key words: poult enteritis and mortality syndrome, small round virus, turkey coronavirus Abbreviations: DPI = days postinoculation; EID50 = mean embryo infective dose; GI = gastrointestinal; IEM = immune electron microscopy; PEMS = poult enteritis and mortality sy
15、ndrome; PTA = phosphotungstic acid; SPF = specific-pathogen free; SRV = small round virus; TCV = turkey coronavirus Poult enteritis and mortality syndrome (PEMS) is a transmissible disease commonly af- fecting young turkeys between 1 and 4 wk of age. The disease is characterized by diarrhea, anorexi
16、a, growth depression, immune dysfunc- tion, and high mortality (1). PEMS has caused significant losses to turkey producers in North Carolina and several other southeastern states DCorresponding author. 297 This content downloaded from 195.78.109.12 on Sat, 21 Jun 2014 23:44:21 PMAll use subject to J
17、STOR Terms and Conditions298 M. Yu et al. Fig. 1. Turkey coronavirus detected by immune electron microscopy in intestinal samples from poults affected by the poult enteritis and mortality syndrome. Bar = 100 nm. since its recognition in 1991 (2). Although ex- tensive research has been done, the etio
18、logy of the disease remains controversial. Coronavirus (6) and some other unidentified virus particles (4) as well as bacteria like Escherichia coli (3) have been implicated in the disease, but no eti- ologic relationship has been definitely estab- lished. In the present study, we detected several v
19、iruses in intestinal samples from PEMS-affect- ed poults, including a turkey coronavirus (TCV) and a small round virus (SRV). The pathogenicities of the TCV and SRV were stud- ied in experimental infection trials to elucidate their roles in the etiology of PEMS. MATERIALS AND METHODS Intestinal samp
20、les. Thirty-six samples of gastro- intestinal (GI) tracts from 1-to-4-wk-old poults af- fected by PEMS were submitted to our laboratory over a 1-yr period. The samples were collected from 36 turkey flocks in 22 turkey farms in the states of North Carolina and Indiana. Samples were received frozen an
21、d contained one to six whole GI tracts. Antisera. Convalescent sera were collected from poults that recovered from PEMS at about 2 wk after the onset of the disease and were submitted together with intestinal samples from the same flocks. The sera were inactivated at 56 C for 30 min and were then st
22、ored at -20 C until used. Poults and embryos. All specific-pathogen-free (SPF) turkey embryos and SPF poults originated from the SPF flock maintained by the Food Animal Health Research Program. The flock is free of all rec- ognized turkey pathogens, including all enteric virus- es. Immune electron m
23、icroscopy (IEM). The GI tracts were thawed and the contents were stripped and homogenized 1/10 (w/v) in 0.05 M Tris-HCI buffer, pH 7.5, and clarified by centrifugation at 3000 x g for 30 min at 4 C. The supernatants were then filtered through 0.45-pLm disposable syringe fil- ters (Corning Glass Work
24、, Corning, NY) and stored at -70 C until tested. Two hundred microliters of the above supernatants were incubated overnight at 4 C with 200 Al of con- valescent sera of the same flocks diluted 1/20 in 0.1 M sterile phosphate-buffered saline, pH 7.4. The di- lutions for the supernatants and convalesc
25、ent sera were chosen on the basis of preliminary trials. After incubation, the mixtures were ultracentrifuged for 15 min at 160,000 x g through a 50-?pl cushion of 30% sucrose with a Beckman tabletop airfuge?. Pellets were resuspended in 400 pl of sterile distilled water and ultracentrifuged again a
26、s previously described (without sucrose cushion). The pellets were finally resuspended in 25 Al of sterile distilled water. One drop of the resuspended solution was placed on a carbon-coated 300 mesh Formvarg copper grid and stained with a drop of phosphotungstic acid (PTA) solution (3% PTA, 0.4% su
27、crose, pH 7.0). The grids were examined for viruses at 80 kV with a transmis- sion electron microscope (Philips 201; Philips No- relco, Eindhoven, The Netherlands). Virus isolation and propagation. Samples con- taining coronavirus only as identified by IEM were This content downloaded from 195.78.10
28、9.12 on Sat, 21 Jun 2014 23:44:21 PMAll use subject to JSTOR Terms and ConditionsViruses associated with PEMS 299 Fig. 2. The small round virus detected by immune electron microscopy in intestinal samples from poults affected by the poult enteritis and mortality syndrome. Bar = 100 nm. used for viru
29、s propagation. About 0.2 ml of the GI tract content supernatant was inoculated into 22-day- old turkey embryos via the amniotic sac. After 3-4 days of incubation at 37 C, the intestines of the em- bryos were harvested, homogenized, and diluted 1/ 10 (w/v) in 0.05 M Tris-HCI buffer, pH 7.5. The homog
30、enates were clarified by centrifugation at 3000 x g for 30 min at 4 C. The supernatants were then examined by IEM as described above and used for subsequent passages in turkey embryos. For the SRV isolation and propagation, about 5 ml of the supernatant containing the SRV only as identified by IEM (
31、filtered through 0.45-pLm filter membrane earlier) was further filtered through 0.22- pLm, 0.05-pLm Millipore filter membranes. The final filtrate was used for experimental infection or was inoculated into 22-day-old SPF turkey embryos via the amniotic sac. Intestines of turkey embryos were collecte
32、d and processed by following the same steps as for TCV propagation. Both SRV and TCV were titrated in turkey em- bryos by a modification of a procedure described pre- viously (22). Turkey embryo intestinal homogenates containing SRV or TCV were diluted serially (10- 10-7) in 0.05 M Tris-HCI buffer,
33、pH 7.5. Each di- lution was inoculated to six SPF turkey embryos via the amniotic sac (0.2 ml/each). Embryos were con- sidered infected when the intestines were enlarged at 3-4 days postinoculation (DPI). The mean embryo infective dose (EID,0) was estimated by the method of Reed and Muench (13). Vir
34、us RNA extraction and electropherotyp- ing. Double-stranded viral RNA extraction and polyacrylamide gel electrophoresis were done accord- ing to the procedure described by Theil et al. (20, 21). In brief, double-stranded RNA was extracted from 1-2 g of intestinal contents and was then sub- jected to
35、 electrophoresis in 7.5% polyacrylamide gel slabs with a vertical gel slab (Hoefer SE 600; Phar- macia Biotech, Piscataway, NJ). The gels were stained with silver nitrate and photographed. Experimental infections. All SPF poults used in the different experimental groups were raised in wire cages ins
36、ide high-security isolation rooms pro- vided with HEPA-filtered intake and exhaust air. All the poults were provided with the same feed and wa- ter ad libitum. Different experimental groups were placed in separate rooms. Trial 1. Twenty-one 7-day-old SPF turkey poults were inoculated orally with 0.1
37、 ml each of the 0.05- pLm filtrate described above. The titer of the SRV in the filtrate was not determined. The poults were wing-banded and placed together with another 14 poults that served as contact-exposed poults. Another 21 poults were not inoculated and served as unex- posed controls. Poults
38、were observed daily for dinical This content downloaded from 195.78.109.12 on Sat, 21 Jun 2014 23:44:21 PMAll use subject to JSTOR Terms and Conditions300 M. Yu et al. signs. All poults were removed from the cages and weighed individually at 3, 4, 5, 7, 11, and 21 DPI. Two to six poults from each tr
39、eatment were euthan- atized at 3, 4, 5, 7, 11, and 21 DPI and examined for pathologic lesions. Intestinal samples were col- lected and examined for viruses by IEM. Trial 2. Eighty-three 5-day-old SPF turkey poults were randomly separated into two groups. One group consisted of 56 poults, 27 of which
40、 were orally in- oculated with 0.2 ml each of turkey embryo intestinal homogenate containing 103 EID,0 SRV. The inocu- lated poults were wing-banded and placed together with the remaining 29 poults that served as contact- exposed poults. The other group of 27 poults was kept as noninoculated control
41、. Poults were observed daily for clinical signs. Droppings were collected at 3, 4, 5, 6, and 7 DPI and used for IEM examination. Three to five poults from each group were necropsied at 3, 4, 5, 7, 14, and 21 DPI for examinations. The poults necropsied at 7, 14, and 21 DPI were weighed before euthana
42、sia. Trial 3. Thirty-six SPF poults were separated into four groups. Four 11-day-old poults in group I were inoculated orally with 0.2 ml each of turkey embryo intestinal homogenate containing 103 EID,0 SRV. Four 11-day-old poults in group II were inoculated orally with 0.2 ml each of turkey embryo
43、intestinal homogenate containing 102 EID50 TCV. Four 8-day- old poults in group III were inoculated orally with 0.2 ml each of turkey embryo intestinal homogenate containing 103 EID50 SRV, and the same poults were given 0.2 ml turkey embryo intestinal homogenate containing 102 EID50 TCV at 11 days o
44、f age. The remaining poults in each of the above groups were not inoculated and served as contact-exposed poults. Poults in group IV were not inoculated and served as a control group. The poults were observed daily for clinical signs. Three poults (one inoculated and two contacts) from each group we
45、re weighed and then euthanatized and examined for lesions at 2 and 4 DPI. All remaining poults were weighed and eu- thanatized at 7 DPI. Intestines were collected for IEM examinations. Statistical analysis. Statistical comparisons of body weights between control poults and challenged poults were per
46、formed with the two-sample t-test. The P-value was for two-tailed t-tests. RESULTS Virus detection. The TCV (Fig. 1), SRV (Fig. 2), rotavirus, and reovirus were detected either alone or incombination with other virus- es (Table 1). Rotaviruses were the most fre- quently detected viruses, followed by
47、 the SRV. Coronavirus was detected in 8 of 36 samples, and reovirus was detected in 5 of 36 samples. Table 1. Viruses detected by immune electron microscopy, double-stranded RNA genome electro- pherotyping, or both in the gastrointestinal tracts of poults affected by the poult enteritis and mortalit
48、y syndrome. No. positive/ no. sampled Positive Virus examinedA percentage SRV 16/36 44% TCV 8/36 22% RotavirusesB 26/36 72% ReovirusB 5/36 14% SRV + rotaviruses 8/36 25% SRV + TCV 3/36 8% SRV + TCV + rotaviruses 2/36 6% ASamples originated from 36 flocks on 22 turkey farms and each sample consisted
49、of contents from one to six gastrointestinal tracts. BRotaviruses were detected by either IEM or elec- tropherotyping or both. Reovirus was detected by electropherotyping. The SRV and rotaviruses in combination were detected in 8 of 36 samples. The SRV and TCV in combination were detected in 3 of 36
50、 samples. A combination of TCV, SRV, and ro- taviruses was detected in 2 of 36 samples. Avian rotavirus serogroups A, D, and F (17) and reo- virus were detected by electropherotyping. Group D rotavirus was detected more frequent- ly than the other serogroups (data not shown). Virus isolation and pro
51、pagation. The TCV was isolated and passaged serially in tur- key embryos via the amniotic cavity. The TCV had all the typical morphologic features of co- ronaviruses. Embryos inoculated with TCV showed distinct intestinal lesions. The whole GI tract was distended and contained greenish contents. The
52、 embryos were usually stunted. The SRV replicated in turkey embryos in- oculated via the amniotic sac. The SRV was 30-32 nm in diameter and had no distinguish- ing surface features. Turkey embryos inoculated with SRV had distended intestines, and the giz- zards were usually enlarged. The titer of SR
53、V in the embryonic intestinal homogenate reached as high as 107 EID50/ml. Experimental infections. Trial 1. Inocu- lated and contact-exposed poults showed severe diarrhea with frothy watery droppings starting at 3 DPI and lasting for about 5 days. The morbidity was 100% and there was no mortal- ity.
54、 The ceca were severely dilated and filled This content downloaded from 195.78.109.12 on Sat, 21 Jun 2014 23:44:21 PMAll use subject to JSTOR Terms and ConditionsViruses associated with PEMS 301 Table 2. Mean body weights of 7-day-old SPF poults in trial 1 challenged with the small round virus origi
55、nated from field outbreaks. Mean body weight (g) ? SD Treatment 3 DPI 4 DPI 5 DPI 7 DPI 11 DPI 21 DPI Control 126.0 ? 4.6 147.6 _ 10.5 165.1 + 10.3 187.7 ? 12.8 285.7 ? 30.1 530.4 ? 30.4 Inoculated 119.8 ? 4.6 131.1 _ 12.3* 133.9 + 9.8* 156.5 ? 13.7* 232.6 ? 20.4* 407.7 ? 29.8* Contact 130.6 ? 15.4
56、136.4 + 6.6 139.8 + 6.7* 150.9 ? 18.2* 209.6 ? 24.1* 425.7 ? 46.7* * = significantly different from controls (P 0.05). with yellow-to-brown frothy contents. The poults were severely stunted and depressed, be- ginning as early as 4 DPI in inoculated poults and 5 DPI in contact-exposed poults. The bod
57、y weights of these poults remained significantly depressed compared with the controls through- out the 21-day experimental period (Table 2). Some poults had pinpoint hemorrhages in the thymus that were not seen in the control poults. The SRV was detected by IEM in in- testinal contents of challenged
58、 poults at 3, 4, 5, and 7 DPI, and no SRV was detected after 11 DPI. Trial 2. Inoculated and contact-exposed poults had severe watery foamy diarrhea, an- orexia, and depression starting at 3 DPI and lasting up to 7 DPI. Morbidity was 100%, whereas mortality was 5.6% (3/54; one inocu- lated poult die
59、d at 6 DPI and two contact-ex- posed poults died at 4 DPI). The ceca were severely dilated with yellow foamy fluids. Other parts of the intestines were also filled with watery foamy contents. Some spleens were enlarged. Some poults had pin- point hemorrhages in the thymus. The inocu- lated and conta
60、ct-exposed poults showed sig- nificantly reduced weight gain at 7 DPI com- pared with control poults, but their body weight was similar to that of control poults by 14 and 21 DPI (Table 3). The SRV was de- tected by IEM in droppings between 3 and 7 DPI but not by 11 DPI. Trial 3. The poults in the S
61、RV-challenged group had symptoms and lesions similar to those of the poults trial 2. The poults in the TCV-challenged group had severe enteritis with yellowish loose droppings and were more de- pressed and stunted than poults in the SRV- challenged group. The intestines from the TCV-exposed poults w
62、ere flaccid, thin-walled, and filled with loose contents, and the disease was acute, with symptoms appearing as early as 2 DPI and lasting for about 4 days. Poults in the group challenged with SRV plus TCV had more severe symptoms than poults in the groups challenged with SRV or TCV alone. The thymu
63、s of some poults in all the chal- lenged groups had pinpoint hemorrhages. The mortality was as follows: SRV group, 11%; TCV group, 11%; SRV plus TCV group, 22%. The body weights of poults in all the chal- lenged groups were significantly depressed by 7 DPI, whereas the TCV-alone and SRV plus TCV-cha
64、llenged groups showed growth depres- sion as early as 4 DPI (Table 4). The mean weight gains from 2 to 7 DPI in all the three challenged groups were much lower than those in the control group. The TCV plus SRV-chal- lenged group was the lowest, followed by the TCV-only group and the SRV-only group.
65、The TCV was detected by IEM at 2 and 4 DPI. DISCUSSION We have detected and isolated TCV and SRV from field samples of PEMS-affected poults. We have also demonstrated that both TCV and SRV were pathogenic and contagious and they initiated diseases similar to PEMS in SPF poults. Poults challenged wit
66、h SRV showed severe diarrhea, growth depression, and varied mor- tality in trials 1, 2, and 3. The mortality rates in trials 1, 2, and 3 were 0, 5.6%, and 11%, respectively. The growth depression in trials 1, 2, and 3 was inconsistent. In trial 1, significant growth depression occurred from 4 DPI th
67、rough 21 DPI. In trial 2, the growth depres- sion was significant only at 7 DPI, and the poults had body weight comparable to controls at 14 and 21 DPI. In trial 3, the growth de- pression was significant in all experimental groups at 7 DPI. The variations might be be- cause of the difference in vir
68、us origin and dos- This content downloaded from 195.78.109.12 on Sat, 21 Jun 2014 23:44:21 PMAll use subject to JSTOR Terms and Conditions302 M. Yu et al. Table 3. Mean body weights of 7-day-old SPF poults from trial 2 challenged with turkey embryo-prop- agated small round virus. Mean body weights (
69、g) ? SD Treatment 7 DPI 14 DPI 21 DPI Control 164.8 + 36.0 263.0 ? 22.1 422.8 ? 27.9 Contact 119.2 + 27.1* 272.8 ? 24.2 443.0 ? 18.9 Inoculated 142.3 + 10.7* 282.4 ? 32.7 483.5 ? 45.1 * = significantly different from controls (P 0.05). age. The SRV induced a disease similar to the mild form of PEMS
70、in turkey poults. Conceiv- ably, under field conditions, the SRV infection in a flock of poults could cause significant con- sequences. The TCV alone was able to cause severe en- teritis, significant growth depression, and mor- tality in turkey poults. Although the prevalence of TCV as detected by I
71、EM in this study was low, this might be because of the low sensitivity of IEM. Moreover, because the disease caused by TCV was very acute, the TCV could be de- tected by IEM only during a limited period af- ter infection. Poults challenged with SRV plus TCV showed the most severe clinical responses
72、and the mortality was the highest. Because the mor- tality in PEMS is usually high, it is highly pos- sible that most PEMS outbreaks are caused by concomitant or sequential infections of two or more viruses such as SRV and TCV. SRV and TCV may be important agents in the etiology of PEMS. Barnes and
73、Guy (1) speculated that TCV or some other viruses may be primarily responsible for initiating the en- teritis, growth depression, and increased suscep- tibility to bacterial infections, which might ac- count for the mortality. Our experiments indi- cate that SRV and TCV not only initiate en- teritis
74、 and growth depression but also cause mortality. We conclude that a combined infec- tion of SRV and TCV could be responsible for the outbreaks of the severe forms of PEMS, whereas an infection by SRV or TCV alone can initiate different milder forms of PEMS. Rotaviruses, especially serogroup D, were
75、the most frequently detected viruses. This finding was consistent with a previous report (18). In experimentally infected turkeys, turkey rotavi- ruses did not cause mortality. Under field con- ditions, clinical signs caused by rotavirus infec- tion varied in severity, with diarrhea and wet litter a
76、s the predominant signs (9). In our study, rotaviruses were frequently found in combina- tion with other viruses, such as SRV and TCV. Rotaviruses had been detected in combination with other viruses in diarrheic turkey poults in earlier studies (15,18). Their pathogenicity in combination with SRV, T
77、CV, or both in the etiology of PEMS needs to be evaluated. Reovirus was the least detected virus in this study. Reovirus has been found in feces of healthy turkey poults in other studies in our laboratory (unpubl. data). Because reovirus can be commonly found in the digestive and respi- ratory tract
78、s of clinically normal chickens and turkeys (16), it is unlikely to play an important role in the etiology of PEMS. Table 4. Mean body weights, mean body weight gains, and mortality in SPF poults from trial 3 challenged with the SRV, the TCV, and the SRV plus the TCV. Mean body Mean body weights (g)
79、 ? SD weight gain (g) from 2 Treatment 2 DPI 4 DPI 7 DPI to 7 DPI Mortality Control 143.3 ? 33.1 188.7 ? 27.3 283.3 ? 9.61 140.0 0% (0/9) TCV 97.3 ? 33.1 108.7 ? 36.2* 161.5 ? 19.1* 64.2 11% (1/9) SRV 146.3 ? 21.9 194.0 ? 52.3 253.2 + 21.8* 106.9 11% (1/9) SRV + TCV 117.7 ? 41.0 137.3 + 14.0* 136.3
80、? 38.0* 18.6 22% (2/9) * = significantly different from controls (P 0.05). This content downloaded from 195.78.109.12 on Sat, 21 Jun 2014 23:44:21 PMAll use subject to JSTOR Terms and ConditionsViruses associated with PEMS 303 The SRV or TCV infection caused hemor- rhagic lesions in the thymus, whic
81、h raised the question of a possible effect on the turkey im- mune system. In another study (12), SRV and TCV were thought to predispose the poults to infection by other opportunistic agents, such as E. coli. This may happen via either a per- manent or transitory blockage or dysfunction of the immune
82、 system. The PEMS poults have been shown to exhibit immune dysfunction at both cellular and humoral levels (8,10,11). SRV seems to be an agent that can potentially affect the immune system. The small round structured viruses include calicivirus, astrovirus, and enterovirus. Few studies have been rep
83、orted about astrovirus (14) and enteroviruslike viruses associated with poult diarrhea (5,7,19). The SRV described in this report does not have the distinguishing surface features of the astroviruses, though the size is similar. The enteroviruslike virus was reported to be 18-24 nm in size, much sma
84、ller than the SRV. The size of known caliciviruses is between 30 and 40 nm, and some strains have distin- guishing surface features such as circular oval surface hollow and scalloped feathery outer edge. Characterization of the SRV is in progress in our laboratory. REFERENCES 1. Barnes, H. J., and J
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