Egg Drop Syndrome-76 (EDS-76) in Japanese Quails (Coturnix coturnix japonica): An Experimental Study Revealing Pathology, Effect on Egg Production/Quality and Immune Responses
Jag Mohan Kataria,
Egg Drop Syndrome-76 (EDS-76) is a recognized disease of chickens and Japanese Quails, which is of high economic importance due to its drastic negative effects on egg production in laying birds. The aim of the present study was to better understand the EDS-76 viral disease process in Japanese quails (Coturnix coturnix japonica), since very limited studies have been conducted in this species of birds. For this purpose, an experimental study was conducted with infection of EDS-76 virus in laying Japanese quails to reveal pathology, effect on egg production/quality and immune responses of this virus in these birds. By 7, 9 and 13-15 Days Post Infection (DPI), drop as well as aberrant egg production and lower mean egg quality were observed compared to control birds. Significant histopathological changes were observed in genitalia and spleen. Haemagglutination Inhibition (HI) and Enzyme Linked Immunosorbant Assay (ELISA) titres rose rapidly by 2nd week when it became maximum; thereafter declined and maintained at low levels up to 10 week post infection. The mean total protein values in infected quail gradually increased to 4.10±0.05/100 mL without any change in mean albumen value at 12 DPI. In conclusion, the course of the EDS-76 is significant not only in chickens but also in quails even though it occurs occasionally in quails. Explorative pathological, blood biochemical and immunological studies are suggested during EDS-76 viral disease course in quails. This would aid in formulating effective disease prevention and control measures for this economically important disease of poultry.
to cite this article:
Narayan Mohapatra, Jag Mohan Kataria, Sandip Chakraborty and Kuldeep Dhama, 2014. Egg Drop Syndrome-76 (EDS-76) in Japanese Quails (Coturnix coturnix japonica): An Experimental Study Revealing Pathology, Effect on Egg Production/Quality and Immune Responses. Pakistan Journal of Biological Sciences, 17: 821-828.
June 28, 2013; Accepted: August 26, 2013;
Published: January 29, 2014
Egg drop syndrome (EDS-76), reported by Van Eck et al.
(1976) and McFerran et al. (1978), is
a vertically transmitted and an economically important disease of laying hens
(Kumar et al., 2003; Kataria
et al., 2005; Ezeibe et al., 2008;
Dhama et al., 2011). Fragility of eggs together
with decreased rate of fertility and hatchability are the outcomes. The EDS-76
virus (EDSV) has been classified under group 3 of genus Aviadenoviridae. A large
variety of wild as well as domestic vertebrate animals are infected by medium-sized
Adenoviruses that are non-enveloped DNA viruses. In the mid 1970s Egg
Drop Syndrome (EDS) emerged throughout the world (Baxendale,
1978; Swain et al., 1997; McFerran
and Smyth, 2000; Kumar et al., 2003). Serological
evidence of EDS-76 virus infections in India has been found in chickens and
quail (Kataria et al., 1991; Das
and Pradhan, 1992; Das et al., 1995; Shaw
et al., 1995) and in some instances the causative EDS-76 virus has
been isolated and characterized biochemically and biologically (Swain
et al., 1993; Chandramohan, 1996; McFerran
and Adair, 2003; Woolcock, 2008). Many reports have
been published regarding the etiology and pathogenesis of experimentally reproduced
EDS-76 viz., (Taniguchi et al., 1981; Yamaguchi
et al., 1981a; Van Eck 1986; Kumar,
1990; Swain et al., 1993, Chandramohan,
1996) and systematic study of this condition in chicken has been done. The
disease occurs naturally in turkeys but the disease in ducks is more severe
(Bidin et al., 2007; Su et
al., 2011). The natural occurrence of this condition in Japanese quails
(Coturnix coturnix japonica) has also been reported by Dash
and Pradhan (1990) and Kataria et al. (1991)
and a virus serologically indistinguishable from that of the chicken has been
isolated for the first time. However, no systematic study of this disease condition
in Japanese quail has been done (McFerran and Adair, 2003).
In this study, results of experimental studies carried out in Japanese quails
following infection with EDS-76 virus of quail origin has been reported with
particular reference to pathological findings, changes in blood biochemical
parameters during the course of the disease and immunological studies, which
would help in better understanding of EDS-76 viral disease process in quails
and prevent and control the disease in a better way.
MATERIALS AND METHODS
Birds: One hundred and thirty five, 4 weeks old quail pullets seronegative
to EDS-76 virus were obtained from Experimental Quail Farm of Central Avian
Research Institute (CARI), Izatnagar. The birds were maintained in the Experimental
Shed of the Division of Avian Diseases, Indian Veterinary Research Institute
(IVRI) Izatnagar. The birds started laying at 6 weeks and at about 8 weeks the
production increased up to 50%. Before start of the experiment the birds were
serologically screened for Ranikhet Disease (RD), avian Infectious Bronchitis
(IB), Chicken Embryo Lethal Orphan (CELO) virus, Salmonella and Mycoplasma
and found negative to these avian pathogens.
Virus, antisera and conjugate: Virus and antisera of EDS-76 virus of
quail origin (QEDS-76-1/AD-1/91) was obtained from the Virus Laboratory of the
Division of Avian Diseases, Indian Veterinary Research Institute, Izatnagar
in the form of freeze dried allantoic fluid. The virus was inoculated in 12-14
days old embryonated duck eggs for reactivation before the experiment. The standard
serum against EDS-76 virus and its FITC conjugated globulin were also obtained
from the above laboratory.
Experimental design: A total of 80 birds were inoculated with EDS-76
virus (109.5 EID50/mL/2 birds) by naso-oral route and
rest 55 birds were treated as healthy. The infected and healthy birds were divided
into 3 separate groups, viz., Group 1: For clinico-pathological, immunological,
contact transmission and excretion studies-50 infected and 10 healthy birds
were kept together, Group 2: For egg production study-30 infected birds were
kept in colony cages and rest 30 healthy birds were kept in a separate cage
and for control Group 3:15 healthy birds were kept as control in a separate
shed. All the three groups of birds were reared under similar managemental conditions.
Egg production and egg quality studies: The eggs were collected from
infected and healthy birds of group 2 up to 21 days. The egg production rate
was noted. Randomly 10 eggs from control and 10 from infected birds were taken
for study of egg quality viz., shell texture, shell colour, shell thickness,
egg weight and Internal Quality Unit (IQU) determination. The IQU was used as
a measure of egg quality in relation to egg weight and was calculated as per
the formula of Kondaiah et al. (1981):
IQU = 100 Log (H + 4.18-0.898W 0.6674)
where, H is albumen height and W is weight of the egg in grams.
The statistical analysis of all the values was carried out by using Students
T test (Snedecor and Cochran, 1967).
Virus localization and histopathology: Three quails from the group-1
and one quail from group 3 were sacrificed at 3, 6, 9, 12, 15, 18, 21, 28, 35,
42 and 49 Days Post Infection (DPI) each. Serum was collected from each bird
and tested for antibodies against EDS-76 virus by Haemagglutination Inhibition
(HI) method (Swain et al., 1993). From the sacrificed
birds pieces of uterus, vagina, spleen and ovary were collected in 10% formalin
for histopathological examination and pieces of uterus, spleen, vagina and nasopharynx
were also kept at -20°C for detection of viral antigen by Fluorescence Antibody
Test (FAT). At 3, 4, 5 and 6 DPI, the buffy coat was separated from the blood
of the infected birds and stained with anti-EDS-76 virus FITC conjugated globulin
to demonstrate the presence of viral antigen in the circulating white blood
cells as per the method of Van Eck (1986).
Virus excretion and contact transmission: The virus excretion study
was performed by isolation of the EDS-76 virus from cloacal swabs collected
at every alternate day from infected and healthy birds up to 3 weeks post infection
(WPI). Contact transmission study was done on the basis of seroconversion in
contact healthy birds. The cloacal swabs were processed for virus isolation
in Chicken Embryo Liver (CEL) cell culture which was prepared by using method
of Adair et al. (1979).
Biochemical study: The serum samples collected from the sacrificed birds
at 3, 6, 9, 12, 15, 18 and 21, DPI were used for biochemical studies. The total
serum protein, albumen, calcium and inorganic phosphorus contents were estimated
by following directions mentioned in standard diagnostic kits (supplied by Span
Diagnostics, Udharia, Surat, Gujrat, India). The serum globulin concentration
was determined by subtracting the albumen quantity from total protein value.
All the values were subjected to statistical analysis using Students
Immunological studies: Detection of humoral immune response in infected,
in-contact and healthy birds against EDS-76 virus was done using haemagglutination
(HI) test, Agar Gel Precipitation Test (AGPT) (Swain, 1991)
and Enzyme Linked Immunosorbent Essay (ELISA) (Adair et
al., 1986). At weekly intervals, 10 birds from infected and 10 birds
from control group were bled and tested for serum antibodies against EDS-76
RESULTS AND DISCUSSION
Clinical sign and egg production study: Japanese quail layer birds,
following artificial infection of EDS-76 virus via oral route, experienced drop
in egg production with production of thin shelled eggs which was exhibited as
the only clinical sign. The drop in egg production in infected quails was from
70-63% at 7 Days Post Infection (DPI). The lowest egg production was of 40%
at 13 DPI. The birds remained apparently healthy during the entire observation
period. The egg production increased gradually thereafter and at 21 DPI became
53%. The total hen day production and pattern of egg drop is shown in Fig.
1. The infected birds started laying abnormal eggs at 9 DPI and this remained
upto 21 DPI. The number of abnormal eggs laid was maximum (42%) at 13 DPI. These
abnormal eggs were soft shelled, thin shelled, shell less and smaller in size
(Fig. 2). The number of abnormal eggs laid gradually decreased
but it remained up to 6% even after 21 DPI, when the aberrant eggs were excluded
from the total daily egg production, the lowest egg production was observed
at 13 DPI and the drop was at level of 47% which remained up to 20% at 21 DPI.
Internal egg quality was also affected. The effects on egg quality characters
viz., egg weight, IQU, shell thickness are depicted in Table 1.
The mean egg weight of the infected birds was significantly lower than those
of the control at 13-15 DPI (p<0.01) and gradually there was improvement
in egg weight after 19 DPI. The IQU of eggs laid were lower (57.16±0.54-58.16±0.44)
during 11-16 DPI. The IQU value of eggs laid by the infected quails was lowest
at 13 DPI (55.16±0.58) as compared to (61.42±0.26) in control
birds, which gradually increased and became par with control group after 19
||Effect of EDS-76 virus infection on egg production of quails
||Effect of EDS-76 virus infection on egg shell thickness of
|| Effect of experimental EDS-76 virus infection on egg quality
traits of Japanese quails
|Each value is the Mean±SE of ten observations, Significance
of difference from control values: *p<0.05, **p<0.01
Similarly, the mean shell thickness of eggs laid by the infected birds was
lowest (0.140±0.01 mm) at 10-13 DPI, which gradually increased and became
normal at 20 DPI onwards.
The pattern of egg drop and production of abnormal eggs was similar to the
findings reported in chicken (Yamaguchi et al.,
1981b; Brugh et al., 1984; Van
Eck 1986; Kumar, 1990; Swain
et al., 1993; Ezeibe et al., 2008).
The egg production recovered after 21 DPI but the laying of abnormal eggs (46%)
persisted till the end of the entire observation period.
Gross pathological changes: The gross changes in infected Japanese quails
were confined to uterus and spleen were similar in nature as reported earlier
in case of chicken (Van Eck 1986; Taniguchi
et al., 1981; Kumar, 1990; Swain,
1991). The uterine folds were swollen during 9-18 DPI. Exudate in the uterine
lumen was present during 12-15 DPI. At 2 and 6 DPI, the spleen was found to
be congested. Splenomegaly was present during 6-15 DPI. However, no gross abnormalities
were detected in vagina, ovary and any other organ.
Histopathology: Significant histopathological changes were observed
in uterus, spleen, vagina and ovary. Early changes in uterus were detected at
3 DPI and characterized by oedema and congestion of the blood vessels which
progressed further at 6 DPI when there was mononuclear cells infiltration into
mucosa, focal hyperplasia of the surface epithelium and pyknosis of the nuclei
of glandular cells. At 9-12 DPI, extensive hyperplasia of uterine epithelium,
focal lymphoid cell infiltration into submucosa and muscular layer and atrophy
of the tubular glands was marked (Fig. 3a). The development
of lesions corresponded with the egg drop and egg shell abnormalities at 9-15
||Histopathological changes in the tissue sections of EDS-76
virus infected quail (a) Uterus showing oedema and depletion of glands in
submucosa at 9 DPI (H and Ex200), (b) Vagina showing lymphoid follicle and
mononuclear cell infiltration in submucosa at 21 DPI (H and Ex200), (c)
Ovary showing distorted follicles at 18 DPI (H and Ex50) and (d) Spleen
showing a number of secondary follicles in Periarteriolar Lymphoid Tissue
(PALT) around the central arteriole at 15 DPI (H and Ex200)
Intranuclear inclusion bodies in goblet cells and ciliated cells of uterine
epithelium and uterine glandular cells were present at 15-18 DPI. During this
time more empty spaces were seen in submucosa due to depletion of glands. The
condition gradually improved and by 28 DPI there was mild focal hyperplasia
of epithelium, mononuclear cells infiltration and presence of lymphoid follicles.
All these findings were similar to the observations made by earlier workers
(Taniguchi et al., 1981; Yamaguchi
et al., 1981b; Van Eck, 1986; Kumar,
1990; Swain et al., 1993) in case of experimentally
In vagina, the changes were observed during 9-28 DPI. At 9-12 DPI, mononuclear
cells infiltration was marked in submucosa but during 15-18 DPI it was also
noticed in the muscular layer. The lymphoid follicle formation in vaginal submucosa
was seen during 21-28 DPI (Fig. 3b). The changes were similar
to those observed by Kumar (1990). In ovary, the mononuclear
cells infiltration was observed as early as 6 DPI which persisted upto 12 DPI
during which the lymphoid follicles were present in ovarian tissue. During 9-18
DPI the number of developing primary ovarian follicles was few and during 15-18
DPI these follicles were distorted and collapsed (Fig. 3c).
Badstue and Smidt (1978) and Taniguchi
et al. (1981) also reported similar changes in ovary of chickens
infected with EDS-76 virus.
In spleen, the microscopic changes were first noticed after 3 DPI which consisted
of congestion, presence of disrupted follicles, large lymphoblasts in follicles
and karyorrhexis of macrophages in red pulp. At 6-9 DPI, these changes were
present along with focal areas of lysis of macrophages and presence of secondary
follicles in Peri-arteriolar Lymphoid Tissue (PALT). During 12-15 DPI these
secondary follicles were seen in PALT (Fig. 3d) which were
found to be devoid of reticular capsule and consisted of large number of mesenchymal
cells and macrophages by 5-18 DPI. In spleen the changes were same as the report
of Swain et al. (1993). No microscopic changes
were observed in any tissues of healthy birds throughout the observation period.
The changes in ovary were marked by infiltration of mononuclear cells and lymphoid
follicle formation during 6-12 DPI with presence of few and distorted follicles.
Localization of viral antigens: In FAT, granular fluorescence was detected
in the nuclei of uterine epithelium as early as 6 DPI. At 9 DPI, the number
of fluorescing cells increased and at 12 DPI the glandular cells showed fluorescence.
At 21 DPI, few epithelial cells were still showing fluorescence. In circulating
blood leukocytes, fluorescent antigen was detected at 4-6 DPI. In spleen, granular
fluorescence was seen in macrophages of red pulp as early as 3 DPI. At 6 DPI,
the intensity was maximum and more cells were involved. In vagina, fluorescence
was marked in epithelial cells only at 12 DPI, where as in nasopharynx it was
only observed at 3 DPI. Granular immunofluorescence was also demonstrated in
nuclei of epithelial cells which persisted till 21 DPI. No fluorescing antigen
could be detected in any of the three organs of the control birds. These findings
are in accordance with those observed in chickens infected with CEDS-76 virus
(Yamaguchi et al., 1981b; Van
Eck, 1986; Kumar, 1990).
Virus excretion and contact transmission: EDS-76 virus, following naso-oral
infection, was re-isolated from cloacal swabs of experimental birds upto 6 DPI.
However, no virus was isolated from control birds. Transmission of the virus
to in-contact birds was evidenced by sero-conversion in healthy birds. The healthy
birds kept in contact with the infected layers developed HI-antibodies at 5
WPI. However, the antibody titre was very low and persisted only for a short
duration. Out of 10 birds only two birds showed HI-antibody titre of 21-22,
these birds were found positive by ELISA and AGPT. These findings are indicative
that the degree of contact transmission is fully dependent on the housing system
of the birds. This study suggest contagiousness of EDS-76 virus in quails as
agreed with the reports of Heffels et al. (1982)
and Swain et al. (1993).
Serology: The infected birds also developed antibodies as early as 1
WPI, which was successfully detected using HI, ELISA and AGPT (Adair
et al., 1986; Swain et al., 1993;
Piela and Yates, 1983; Bishop
and Cardozo, 1996). The result of humoral immune response of experimentally
infected birds is presented in Table 2. From the table it
is evident that the HI-antibody (mean HI titre 26.1) was detected
at 1 WPI which increased slightly to 27.2 at 2 WPI but gradually
declined and during 6-18 WPI the antibody titre was as low as 22-23.
||Humoral immune response and virus excretion pattern in Japanese
quails experimentally infected with EDS-76 virus
|Values in parentheses indicate the geometric mean of HI titres,
In AGPT column, Numerator: No. of sera samples found to be positive; --
Denominator: No. of sera samples tested, -: Negative, +: Positive
|| Effect of experimental EDS-76 virus infection on serum total
protein, albumin and globulin
|Each value is the Mean±SE of three observations, Significance
of difference from control values, *p<0.05, **p<0.01
||Effect of experimental EDS-76 virus infection on serum calcium
and inorganic phosphorus content of Japanese quails
|Each value is the Mean±SE of three observations
All the infected birds were positive by ELISA and highest mean ELISA titre
of 1120±160 was detected at 2 WPI. The ELISA titre raised parallel to
the HI-antibody and remained 10-12 times higher than the later during the observation
period. The precipitating antibodies to EDS-76 virus were first detected in
3 out of 10 birds in 1st week. At 2 WPI, all the birds developed precipitins.
The titre of precipitins was very low and only at 2 WPI all the birds were screened
positive by AGPT. The precipitins level also declined afterwards and after 8
WPI the birds were found negative for the presence of precipitins. The poor
immune response to EDS-76 virus in Japanese quails might be due to species factors
associated with it. Das and Pradhan (1992) also detected
low HI-antibody titre in the quails of old ages.
Biochemical studies: The mean values of total serum protein, calcium,
phosphorus, albumen and globulin are depicted in Table 3 and
4. The mean total protein values in infected quail gradually
increased and the highest value of 4.10±0.05/100 mL was observed at 12
DPI, thereafter the value declined gradually and remained higher than that of
the control birds. No change in the mean albumen value (1.56±0.06/100
mL) was observed at 12 DPI. The values of calcium and phosphorus of blood serum
of the infected birds was nearly the same as those of control. There are conflicting
reports available regarding the changes of these two minerals in the serum.
Van Eck and Vertommen, (1984) and Asi
et al. (1987) on one hand did not find any difference in these values,
where as Kumar (1990) reported significant increase in
serum phosphorus and calcium level, respectively. However, there is no significant
change in these values in the Japanese quails in the present report.
In conclusion, the course of EDS-76 disease was found equally significant both
in chickens and quails inspite of the fact that it occasionally occurs in quails.
The pathology and pathogenesis, changes in blood biochemical parameters during
disease course and immunological studies for EDS-76 virus need to be elaborately
explored in this species of birds. This will altogether help in understanding
the disease process in quails in a better way, which would aid in designing
effective vaccines and formulating appropriate disease prevention and control
measures for this economical important poultry disease.
Adair, B.M., D.J. Todd, J.B. McFerran and E.R. McKillop, 1986. Comparative serological studies with EDS-76 virus. Avian Pathol., 15: 677-686.
Adair, B.M., J.B. McFerran, T.J. Connor, M.S. McNulty and E.R. McKillop, 1979. Biological and physical properties of a virus (strain 127) associated with the egg drop syndrome 1976. Avian Pathol., 8: 249-264.
Asi, Y., T. Asi, A. Gruel and A. Ozpinar, 1987. The relationship of serum calcium and phosphorus with low egg production and quality of layers with the egg drop syndrome and infectious bronchitis. Pendik Harayan Hastaliklari Merkez Arastirma Enustitusii Dergisi, 18: 52-59.
Badstue, P.B. and B. Smidt, 1978. Egg-drop syndrome 76 in Danish poultry. Nordisk Veterinaermedicin, 30: 498-505.
Baxendale, W., 1978. Egg drop syndrome 76. Vet. Rec., 102: 285-286.
Bidin, Z., I. Lojkic, M. Mikec and B. Pokric, 2007. Naturally occurring egg drop syndrome infection in turkeys. Acta Veterinaria Brno, 76: 415-421.
Bishop, S.C. and P. Cardozo, 1996. Egg drop syndrome 76 in Bolivia. Trop. Anim. Health Prod., 28: 199-206.
Brugh, M., C.W. Beard and P. Villegas, 1984. Experimental infection of laying chickens with adenovirus 127 and with a related virus isolated from ducks. Avian Dis., 28: 168-178.
Direct Link |
Chandramohan, A., 1996. Studies on egg drop syndrome. Ph.D. Thesis, Tamil Nadu Veterinary and Animal Sciences University, Chennai, India.
Das, B.B. and H.K. Pradhan, 1992. Outbreaks of egg drop syndrome due to EDS-76 virus in quail (Coturnix coturnix japonica). Vet. Rec., 131: 264-265.
Das, B.B., H.K. Mohapatra, H.K. Panda and B.C. Tripathy, 1995. Seroprevalence of EDS-76 in the state of Orissa. Indian Vet. J., 72: 463-465.
Dash, B.B. and H.K. Pradhan, 1990. Egg drop syndrome-76 (EDS-76) in quail: A preliminary report. Proceedings of 13th Annual Conference and National Symposium of Indian Poultry Science Association, December 20-22, 1990, Bombay, India, pp: 130-.
Dhama, K., R. Kumar, D. Kumar and S.D. Singh, 2011. Egg drop syndrome-76, an economically important disease of poultry. Poult. Fortune, 8: 23-29.
Ezeibe, M.C., O.N. Okoroafor, J.I. Eze and I.C. Eze, 2008. Seroprevalence of egg drop syndrome-76 virus as cause of poor egg productivity of poultry in Nsukka, South East Nigeria. Trop. Anim. Health Prod., 40: 137-140.
Heffels, U., S.E.D. Khalaf and E.F. Kaleta, 1982. Studies on the persistence and excretion of egg drop syndrome 1976 virus in chickens. Avian Pathol., 11: 441-452.
Kataria, J.M., C.M. Mohan, S. Dey, B.B. Dash and K. Dhama, 2005. Diagnosis and immunoprophylaxis of economically important poultry diseases: A review. Indian J. Anim. Sci., 75: 555-567.
Direct Link |
Kataria, J.M., P. Swain, B.B. Dash and K.C. Verma, 1991. Egg drop syndrome-76 (EDS-76) virus infection in Japanese quail. Proceedings of the Souvenir 12th Annual Conference of IAVMI and National Symposium on Important Infectious Diseases of Livestock and Poultry, September 12-14th, 1991, Tirupati, India, pp: 6-.
Kondaiah, N., B. Panda and R.A. Singhal, 1981. Internal quality units for quail eggs: A ready reckoner table. Indian Poult. Gazette, 65: 113-126.
Kumar, N.S., J.M. Kataria, M. Koti, K. Dhama and B.B. Dash, 2003. EDS: A review. Indian J. Comp. Microbiol. Immunol. Infect. Dis., 24: 1-14.
Kumar, R., 1990. Immunopathological studies on egg drop syndrome in poultry associated with adenovirus infections. Ph.D. Thesis, Deemed University, Indian Veterinary Research Institute, UP, India.
McFerran, J.B. and B.M. Adair, 2003. Egg Drop Syndrome. In: Diseases of Poultry, Saif, Y.M., H.J. Barnes, J.R. Glisson, A.M. Fadly, L.R. McDougald and D.E. Swayne (Eds.). Iowa State Press, Ames, Iowa, pp: 227 - 237.
McFerran, J.B. and J.A. Smyth, 2000. Avian adenoviruses. Rev. Sci. Tech., 19: 589-601.
McFerran, J.B., R.M. McCracken, E.R. McKillop, M.S. McNulty and D.S. Collins, 1978. Studies on a depressed egg production syndrome in Northern Ireland. Avian Pathol., 7: 35-47.
Piela, T.H. and V.J. Yates, 1983. Comparison of enzyme-linked immunosorbent assay with hemagglutination-inhibition and immunodiffusion tests for detection of antibodies to a hemagglutinating duck adenovirus in chickens. Avian Dis., 27: 724-730.
Direct Link |
Shaw, A.M., R. Govindarajan, A. Chandramohan and A. Albert, 1995. Sero-epidemiology and egg drop syndrome 76 virus in Tamil Nadu. Indian Vet. J., 72: 793-797.
Snedecor, G.W. and W.G. Cochran, 1967. Statistical Methods. 6th Edn., Iowa State University Press, Ames, Iowa, USA., Pages: 593.
Su, J., S. Li, X. Hu, X. Yu and Y. Wang et al., 2011. Duck egg-drop syndrome caused by byd virus, a new tembusu-related flavivirus. PloS ONE, Vol. 6 10.1371/journal.pone.0018106
Swain, P, J.M. Kataria and K.C. Verma, 1993. Biological characterisation of an Indian isolate of egg drop syndrome-76 virus. Res. Vet. Sci., 55: 396-397.
Swain, P., 1991. Studies on a field isolate of egg drop syndrome-76 virus and to study its immunogenicity. Master's Thesis, Deemed University, Indian Veterinary Research Institute, UP, India.
Swain, P., J.M. Kataria, K. Dhama and K.C. Verma, 1997. Purification of egg drop syndrome-76 virus by velocity density gradient centrifugation. A comparative study. Acta Virol., 41: 303-304.
Taniguchi, T., S. Tamaguchi, M. Maeda, H. Kawamura and T. Horiuchi, 1981. Pathological changes in laying hens inoculated with the JPA-1 strain of egg drop syndrome-1976 virus. Nat. Inst. Anim. Health Q., 21: 83-93.
Van Eck, J.H., 1986. Egg drop syndrome-1976 in fowl: Aspects of manifestation, pathogenesis, histopathology, patho-physiology, immunology, epizootiology and incidence in the Netherlands. Ph.D. Thesis, Utrecht University, Netherland.
Van Eck, J.H., F.G. Davelaar, T.A. Heuvel-Plesman, N. van Kol, B. Kouwenhoven and F.H. Guldie, 1976. Dropped egg production, soft shelled and Shell-less eggs associated with appearance of precipitins to adenovirus in flocks of laying fowls. Avian Pathol., 5: 261-272.
PubMed | Direct Link |
Van Eck, J.H.H. and M. Vertommen, 1984. Biochemical changes in blood and uterine fluid of fowl following experimental EDS'76 virus infection. Vet. Q., 6: 127-134.
Woolcock, P.R., 2008. Viral Infections of Waterfowl. In: Diseases of Poultry, Saif, Y.M. (Ed.). 12th Edn., Blackwell Publishing, Ames, USA., pp: 414-425.
Yamaguchi, S., T. Imada, H. Kawamura, T. Taniguchi and M. Kawakami, 1981. Pathogenicity and distribution of egg-drop syndrome-1976 virus (JPA-1) in inoculated laying hens. Avian Dis., 25: 642-649.
Yamaguchi, S., T. Imada, H. Kawamura, T. Taniguchi, H. Saio and K. Shimamatsu, 1981. Outbreaks of egg-drop syndrome-1976 in Japan and its etiological agen. Avian Dis., 25: 628-641.
Direct Link |