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Global Veterinaria 8 (1): 08-14, 2012
ISSN 1992-6197
© IDOSI Publications, 2012
Corresponding Author: Tesfaheywet Zeryehun, College of Veterinary Medicine, P.O. Box 301, Haramaya University,
Haramaya, Ethiopia. Tel: +0920556154.
8
Biochemical Changes in Specific-Pathogen-Free Chicks Infected with
Infectious Bursal Disease Virus of Malaysian Isolate
Tesfaheywet Zeryehun, M. Hair-Bejo and A. Rasedee
1 2 2
College of Veterinary Medicine, Haramaya University, Haramaya, Ethiopia
1
Faculty of Veterinary Medicine, Universiti Putra Malaysia 43400 UPM Serdang, Selangor, Malaysia
2
Abstract: A study was conducted to determine the biochemical changes following very virulent infectious
bursal disease virus (vvIBDV) infection of Malaysian isolate. One-hundred-ten, 32-day-old specific-pathogen-
free (SPF) chicks were divided into two groups namely, IBD (n=55) group inoculated with vvIBDV and
control (n=55) group which served as uninoculated control. The chicks in the IBD group were examined for
clinical signs and blood samples were collected for biochemical assay. Typical clinical signs of acute IBD
were noted as early as 2 day post-inoculation (pi) in the IBD group. The serum samples revealed significant
(p<0.05) reduction in total protein (TP), albumin (Alb) and albumin to globulin (A:G) ratio at days 5 and
7 pi leading to hypoalbunaemia meanwhile, significantly (P<0.05) increased aspartate aminotransferase (AST),
alanine transferase (ALT), lactate dehydrogenase (LDH), gluteral dehydrogenase (GLDH), alkaline phosphatase
(ALP) and creatine kinase (CK) at day 3 and/or 5 and 7 pi were observed. The concentrations of uric acid was
significantly (P<0.05) increased at days 5 and 7 pi, while the cholesterol level was significantly (P<0.05)
decreased at day 7 pi. Further, significant (P<0.05) hypocalcemia, hyponatermia, hyperchloremia and
hyperkalemia at days 5 and/or 7 pi in the IBD group were observed compared with the control group.
These changes correspond to the clinical signs observed, mainly the anorexia, diarrhoea and dehydration and
also reflected an insult to those organs that produce, metabolize or excrete them, among others liver and kidney.
By and large, the present study revealed the vvIBDV of Malaysian isolate produced biochemical changes
consistent with its pathogenicity and these changes could be used in the clinico-pathological study and further
understanding of pathogenesis of the disease.
Key words: Vvibdv Infection % SPF Chicks % Biochemical Changes % Clinico-Pathology
INTRODUCTION mortality, reduced weight gain and condemnation of
Infectious bursal disease (IBD) is a highlymuscle [1-4] and secondary losses due to
contagious, acute viral disease of poultry caused by IBDimmunosuppression [5, 6].
virus (IBDV). The causative agent is a bisegmented,Among the pathogenic strains, the vvIBDV causes
double stranded RNA virus that belongs to the genusan acute form of the disease characterized by severe
Avibirinavirus family Birnaviridae. Two distinctclinical signs and mortality in susceptible chicks.
serotypes of IBDV namely, serotypes 1 and 2 areBesides, it exhibits several pathological changes as part
identified. Serotype 1 is pathogenic to chicks andof the pathogenesis of the disease which could
classified as classical (c), variant (va) and very virulentessentially be explained in biochemical changes in
(vv) IBDV [1], while serotype 2 is not pathogenic torelation to the effect of the virus in several organs
chicks. among others, liver and kidney [6-8]. Few studies
Infectious bursal disease has worldwide distributionhave tried to determine those biochemical changes
and the effects of the disease are economically significant in IBDV infection [7, 9, 10] and found variable biochemical
to the commercial poultry industry [2] through theprofiles.
carcasses due to marked haemorrhage in the skeletal
Global Veterinaria, 8 (1): 08-14, 2012
9
In Malaysia although the disease has beenwire-floored isolation unit in a closed house that had been
previously known to occur, mortalities with clinical signs fumigated three times with 100% formaldehyde prior to
and pathological changes associated with acute IBD have rearing of the chickens. They were provided feed and
been confirmed for the first time during the middle of 1991water ad-libitum.
[11] and there was no attempt to date to investigate the
biochemical changes following infection of chicks withExperimental Design: One-hundred-ten, 32-day-old SPF
IBDV of local isolate. Therefore, it is the objective of this chicks were distributed into two groups, namely the IBD
paper to elucidate biochemical changes that areand control groups. The IBD group was inoculated
pertinent to vvIBDV infection of a Malaysian isolate inorally with 0.1 ml per chick with the virus titter
specific-pathogen-free (SPF) chicks. of 10 EID unit/mL. The control group remained
MATERIALS AND METHODS abnormalities for at least twice daily and were given feed
Virus Isolates: Malaysian isolate namely UPM0081 examinations from both groups. Sampling of chicks was
which is characterized as vvIBDV (Gen Bank, with anscheduled at 1 hour (h), 3h, 6h, 12h, 1 day (d), 3d, 5d, 7d,
accession number of AY791998 [12], was used in the10d and 14d post-inoculations (pi) from the control and
present study. the IBD group and equal number of 5 chicks each was
IBDV Inoculums: The vvIBDV isolate acquired from the group at days 3, 4 and 5 pi, the trial was terminated at day
bursa of fabricus (BF) of infected chickens during a 2004 7 pi.
IBD outbreaks in Selangor, Malaysia, [13] was kept
at-20°C (Senyo, Japan) as a stock virus. The isolate wasSerum Biochemistry Determination: Three mL of
then passaged 3 times in chorioallantoic membraneblood was collected from each chick via jugular
(CAM) of 10-day-old embryonated SPF chicken eggs prior vein or intra-cardiac route using a 23 G needle
to inoculation by the method described by Senne [14].and 3.0 ml syringe and were immediately placed
The harvested CAM was freezed and thawed three timesinto non-heparinized tubes. The blood samples were
and ground separately using sterile pestle and sands tocentrifuged at 3000 rpm for 15 min. and serum
make 1:2 (w/v) dilution of each in sterile phosphate obtained was stored at-20°C until analysis.
buffer saline (PBS) with pH 7.4. Processed samples Total protein (TP), albumin (ALB), globulin (Glb),
was centrifuged at 3000 rpm for 15 min at 4°Cglucose, cholesterol, aspartate transaminase (AST),
(MSE, Mistral 4L, Germany). The supernatant werealanine transaminase (ALT), lactate dehydrogenase
collected through filtration by 0.45 µm pore filter(LDH), glutamate dehydrogenase (GLDH),
syringe and treated with antibiotic-antimycotic solution(-glutamyltransferase (GGT), alkaline phosphatase (ALP)
(GIBCO Lab., USA) in 1:10 (v:v). The viral inoculums wereand creatine kinase (CK), sodium ion (Na ), chloride ion
kept at -20°C (Senyo, Japan) until used. (Cl ), potassium ion (K ) and calcium ion (Ca ) were
Virus Titration and Inoculation: The titration of the virusalbumin (Alb) from the total protein. These serum
was carried out in 10-day-old SPF embryonated chickbiochemistry components were measured by an automatic
eggs based on method described by Reed and Muenchanalyzer (Hitachi: 902, Japan) using standard reagents
[15]. Accordingly the titer of the virus was determined as(RoCHE, Switzerland).
10 EID50/mL. Each chick in the IBD group was
4.8
inoculated with 0.1 ml of vvIBDV inoculum, via the oralStatistical Analysis: Means were obtained and subjected
route using a 1.0 ml syringe. to statistical test of significance using one-way analysis
Experimental Chicks: Day-old embryonated chick eggssoftware version 15.0 (SPSS Inc. Chicago IL., USA) [16].
were obtained from specific pathogen free (SPF) singleValues were expressed as mean ± standard deviation (SD)
comb white Leghorn flocks, hatched and reared in anand statistical significance (P<0.05) among the means
experimental unit. The flock was reared on slatedwere determined using Duncan’s multiple range test.
4.8 50
un-inoculated. The chicks were monitored for any clinical
and water ad-libitum. Blood was collected for biochemical
sampled. But because of the death of 6 chicks in the IBD
+
- + ++
measured. Globulin was determined by subtracting
of variance (ANOVA) for equal replication using SPSS
Global Veterinaria, 8 (1): 08-14, 2012
10
RESULTS control group. On the contrary, there was no significant
The chicks in the infectious bursa disease (IBD)between the control and the IBD groups throughout the
group showed signs of depression, weakness diarrhoeatrial. The albumin to globulin (A:G) ratio, was significantly
and vent picking at day 2 pi and became recumbent and(p<0.05) decreased in the IBD group at days 5 and 7 pi
mortality was recorded beginning on day 3 pi.with respect to the control group (Table 1).
Accordingly, 2, 3 and 1 chicks died at days 3, 4 and 5 pi.With regard to the serum enzymes analyzed in the
The concentration of protein (TP) and albumin (Alb) present study the glutamate dehydrogenase (GLDH) and
in both the IBD and control groups was fairly close toalanine phosphatise (ALP) concentration in the IBD
each other and showed no significant difference (p>0.05)group showed significant increase (P<0.05) at days 5 and
between the two groups during this time. Significantly 7 pi and day 7 pi respectively when compared with the
(p<0.05) decreased TP and Alb was recorded at days control group (Table 2). On the other hand, the aspartate
5 and 7 pi in the IBD group compared with the transferase (AST), alanine transferase (ALT),
difference (p>0.05) in the concentration of globulin (Glb)
Table 1: The TP, Ab, Glb in u/L, A:G ratio of the control and IBD groups throughout the trial period
TP (u/L) ALB (uL) GLB (u/L) A:G
Sampling ---------------------------------------- ------------------------------------------ ----------------------------------------- ----------------------------------
time (pi) Control IBD Control IBD Control IBD Control IBD
1 hr 23.74±2.04 23.12±2.22 9.80±0.70 10.00±1.39 13.94±2.43 13.12±2.50 0.73±0.18 0.79±0.24
3 hrs 23.74±1.82 24.72±1.97 10.02±1.49 10.40±1.92 13.72±2.21 14.32±0.94 0.75±0.18 0.73±0.15
6 hrs 23.04±2.05 25.84±1.88 9.42±1.40 11.44±1.72 13.62±1.08 14.40±1.02 0.69±0.10 0.79±0.13
12 hrs 22.56±1.81 25.70±1.61 9.42±2.11 12.04±1.57 13.14±0.93 13.66±1.20 0.72±0.19 0.89±0.15
Day 1 22.80±1.15 25.28±2.00 9.62±1.95 11.68±1.93 13.18±1.16 13.60±1.49 0.74±0.22 0.87±0.19
Day 3 24.26±1.96 25.52±0.33 10.08±1.15 11.96±0.83 14.18±2.72 13.56±0.55 0.75±0.26 0.88±0.10
Day 5 24.78±1.72 15.98±0.88 10.46±1.29 4.40±1.53 14.32±1.67 11.58±1.17 0.74±0.14 0.37±0.06
a a a
Day 7 23.14±2.06 15.70±2.22 9.26±0.70 3.48±1.07 13.88±1.49 12.22±2.23 0.78±0.05 0.28±0.11
a a a
statistically significant compared with the control group (p<0.05)
a
Table 2: The ALT, ALP and AST in u/L, of the control and IBD groups throughout the trial period
GLDH (u/L) ALP (u/L) CK (u/L)
---------------------------------------------- --------------------------------------------------- ------------------------------------------------
Sampling time Control IBD Control IBD Control IBD
1 hr 24.00±3.35 21.00±2.11 199.90±25.40 210.00±24.59 223.26±28.23 221.40±27.77
3 hrs 22.20±1.68 22.80±1.99 210.80±28.36 200.00±29.51 205.34±22.11 210.88±33.07
6 hrs 23.40±2.40 24.00±3.23 180.10±29.76 191.50±36.67 212.62±28.22 200.94±36.02
12 hrs 20.40±3.37 22.00±3.33 200.10±37.23 202.70±30.88 201.86±19.31 212.94±29.30
Day 1 22.80±4.33 19.80±2.01 204.50±35.51 210.00±44.53 199.12±37.25 199.64±29.66
Day 3 22.20±3.34 20.40±1.89 208.80±39.27 220.20±37.65 201.62±42.88 195.68±17.22
Day 5 24.60±3.56 33.60±1.75 219.90±25.79 224.90±37.03 211.78±27.43 217.72±10.51
a
Day 7 23.40±3.60 36.00±1.93 222.60±30.37 263.20±21.00 201.78±18.13 198.46±18.16
a a
statistically significant compared with the control group (p<0.05)
a
Table 3: The GGT, LDH, ALT and AST in u/L, of the control and IBD groups throughout the trial
GGT (u/L) LDH (u/L) ALT (u/L) AST (u/L)
Sampling ------------------------------------- ------------------------------------------ ----------------------------------- ------------------------------------------
time (pi) Control IBD Control IBD Control IBD Control IBD
1 hr 21.40±1.95 21.40±1.82 168.54±45.68 169.50±38.51 3.80±0.52 4.10±1.10 189.36±14.54 185.26±25.61
3 hrs 22.60±3.05 23.00±0.71 173.32±33.19 180.19±24.85 4.02±0.76 4.58±1.20 191.34±13.19 185.98±11.90
6 hrs 23.20±0.84 25.00±1.81 179.90±28.18 188.06±33.40 3.80±0.71 3.82±0.84 182.28±13.93 188.76±3.70
12 hrs 24.20±0.84 25.20±1.30 188.09±24.03 199.05±37.56 3.01±0.78 2.96±0.57 186.64±13.84 190.52±12.45
Day 1 25.60±1.37 26.00±1.54 191.41±35.16 194.06±38.23 3.08±0.62 3.12±0.62 188.62±9.61 193.32±11.44
Day 3 25.80±1.19 42.00±1.22 184.01±25.16 240.65±25.04 3.42±1.37 5.18±0.98 183.58±11.06 300.82±7.04
a a a a
Day 5 26.60±1.14 37.40±4.20 189.00±30.01 265.30±28.03 3.56±0.38 6.78±0.86 183.22±18.75 353.22±17.24
a a a a
Day 7 26.80±1.39 46.20±5.20 198.80±28.18 370.37±23.33 3.94±0.64 13.68±1.87 180.28±12.40 405.22±20.20
a a a a
statistically significant compared with the control group (p<0.05)
a
Global Veterinaria, 8 (1): 08-14, 2012
11
Table 4: The concentration of creatine, uric acid, cholesterol and glucose in mmol/L of the control and IBD groups and throughout the trial
Creatine (mmol/L) Uric acid (mmol/L) Cholestrol (mmol/L) Glucose (mmol/L)
Sampling ------------------------------------- --------------------------------------------- ----------------------------------- -------------------------------------
time (pi) Control IBD Control IBD Control IBD Control IBD
1 hr 23.80±1.64 22.40±1.82 214.08±78.95 227.12±67.98 3.60±0.29 3.49±0.36 16.32±0.93 15.96±1.02
3 hrs 24.80±1.17 24.00±2.35 261.78±52.47 242.74±47.25 3.44±0.45 3.19±0.35 16.18±2.28 15.42±0.80
6 hrs 23.00±1.16 23.80±3.27 241.78±52.40 274.42±57.59 3.21±0.46 3.04±0.35 15.64±1.76 15.10±0.93
12 hrs 25.40±1.99 25.40±1.95 262.56±78.91 251.54±69.67 3.47±0.54 3.13±0.44 15.58±1.19 15.02±1.20
Day 1 26.40±2.70 22.60±1.52 212.50±64.09 225.10±73.84 3.19±0.59 3.03±0.22 15.76±1.63 14.58±0.63
Day 3 23.80±1.48 24.20±1.19 232.40±67.31 245.06±41.61 3.07±0.27 2.97±0.20 13.30±0.52 14.12±1.27
Day 5 24.20±1.39 28.40±2.71 216.80±79.21 352.60±80.54 3.11±0.49 1.41±0.32 13.76±1.51 13.94±1.05
a
Day 7 27.60±2.66 29.80±2.88 246.42±67.31 412.84±105.56 3.97±0.12 1.60±0.02 13.14±1.78 12.96±0.63
a a
statistically significant compared with the control group (p<0.05)
a
Table 5: The concentration of Ca , Na , CL and K in mmol/L the IBD and control groups through out the trial
++ + - +
Ca (mmol/L) Na (mmol/L) CL (mmol/L) K (mmol/L)
++ + - +
Sampling ------------------------------------- -------------------------------------------- ---------------------------------------- ----------------------------------
time (pi) Control IBD Control IBD Control IBD Control IBD
1 hr 1.79±0.24 1.72±0.19 133.12±4.13 138.86±4.92 99.96±6.38 100.92±2.07 3.88±0.89 3.98±1.13
3 hrs 1.80±0.29 1.69±0.13 139.78±8.50 137.14±1.68 100.52±2.35 101.20±3.29 3.16±0.54 3.46±0.49
6 hrs 1.67±0.11 1.55±0.10 134.46±0.82 134.92±0.99 100.72±1.37 101.26±0.88 3.86±0.46 3.64±0.19
12 hrs 1.73±0.12 1.69±0.18 136.42±0.87 137.04±0.70 101.82±0.89 100.16±2.00 3.92±0.18 3.86±0.44
Day 1 1.80±0.22 1.77±0.14 136.86±0.95 136.36±1.15 102.14±0.90 100.80±1.75 3.74±0.39 3.36±0.42
Day 3 1.68±0.26 1.80±0.20 136.18±1.16 136.62±2.08 102.16±1.50 103.10±2.53 3.12±0.57 3.14±0.42
Day 5 1.76±0.31 0.67±0.29 138.02±0.91 69.60±6.02 103.02±3.32 154.60±14.28 3.21±0.42 3.98±0.41
a a a
Day 7 1.83±0.19 0.59±0.06 139.94±2.89 79.80±6.02 103.54±2.14 152.88±18.90 3.54±0.30 4.98±0.58
a a a a
statistically significant compared with the control group (p<0.05)
a
(-glutamyl transferase (GGT) and lactate dehydogenasethe calcium (Ca ) and sodium (Na ) concentration was
(LDH) concentrations in the IBD group, all have shown a reduced in the IBD groups at days 5 and 7 pi, while the
significant (P<0.05) increase at days 3, 5 and 7 pi whenconcentration of chloride (CL ) and potassium (K ) were
compared with the control group, while there was nosignificantly (P<0.05) increased at days 5 and 7 pi and day
significant (P>0.05) difference between the control and the 7 pi, respectively, when compared with the control group
IBD groups in the concentration of these enzymes during(Table 5).
the early phase of the disease from 1 hr to day 1 pi
(Table 3). There was no significant difference (p>0.05) in DISCUSSION
the concentration of creatine kinase (CK) throughout the
trial. The results of this study on serum chemistry
From the metabolites analyzed, only cholesterol andconfirmed the biochemical evidence of liver and kidney
uric acid showed significant changes in the IBD groupdamage of chickens infected with infectious bursal
when compared with the control group. In this regard,disease virus. Moreover, these biochemical changes
the cholesterol concentration was significantly (p>0.05)agreed with the typical clinical signs such as anorexia,
decreased at days 5 and 7 pi the IBD group. On thedehydration and diarrhoea as well as the pathological
contrary, the uric acid concentration of the IBD groupchanges such as hemorrhagic, necrotic and oedematous
showed a paramount change at the later stage of thelesions in quite a number of organs, observed in acute
disease where it was significantly (p<0.05) increased atIBDV infection [13, 17, 18].
days 5 and 7 pi when compared with the control group. A significant reduction in the total protein and
In the present study, the glucose and creatinealbumin at days 5 and 7 pi were noticed in the present
concentration didn’t show a significant change betweenstudy. These could be related to decrease synthesis by
the two groups throughout the trial (Table 4). the impaired liver or loss of proteins through damaged
All the electrolytes in the present study showedkidney which has been reported previously [7, 8].
significant differences (p<0.05) between the IBD andBecause liver is the main site for the synthesis of protein,
control groups towards the end of the trial. Accordingly,impaired liver morphology could lead to hypoprotenemia,
++ +
- +
Global Veterinaria, 8 (1): 08-14, 2012
12
while damaged kidney would lead to loss of smallinfection. Besides the absence of changes in creatinine
molecular size and osmotic sensitivity protein (albumin)kinase (CK), a muscle specific enzyme [30], in the present
leading to hypoalbuminaemia [19]. The anorexia in the IBDstudy exclude muscle damage. These changes in serum
infected chicks is another possible cause of theenzymes fairly elaborate the hypoprotenemia and
hypoprotenemia. The exhaustion of proteins in thehypoalbunemia due to liver and kidney pathology
process of recruiting the body need for proteins for tissuediscussed above.
repair, white blood cell and antibody production,The increased in uric acid (hyperurecemia) and
maintenance of plasma osmolality as well as enzymecreatinine at days 5 and 7 pi might be explained by the
production [20] should also be considered becauseprevailing dehydration [23] and impaired kidney function
vvIBDV potentially causes aplastic bone marrow andin the chicks suffering from IBD. The serum uric acid
lymphoid necrosis in the bursa of fabricus. The diarrhoeaconcentration is an indicator of renal function in chickens,
in the present study could also contribute for thebecause uric acid is the major nitrogenous end product of
hypoprotenemia. chickens and is excreted into the urine through the renal
The reduced A:G ratio at days 5 and 7 pi in the IBDtubules [31]. In a clinical chemistry observation study
group is most likely due to decreased albumin in the facecarried out by Ley et al. [7], it was observed that several
of unchanged globulin. Similarly, a decreased in A:G ratio chickens at 3 days pi had serum uric acid concentration
was previously reported in IBDV infection [10]. The A:G higher than the control groups. Moreover, deposition of
ratio has been used extensively in analysis of sera as anurate crystalloids in the tubules of kidney following IBDV
indicator of infection and antibody response [21].infection was associated with the severe dehydration in
This dysproteinaemia has a bigger diagnostic valueacute form of the disease [32]. Ley et al. [33] have
than the determination only of total protein [22].observed immune complex involvement in the
The significant reduction in A:G ratio in IBDV infectionpathogenesis of IBDV infection and suggested an
has also been attributed to hypo-albuminaemia andimmune-mediated glomerulonephrities compatible with
hyper-gamma-globulinaemia [23]. Nevertheless, in theimmune-complexemia [7].
present study, there was no change in the globulin levelThe increase in cholesterol concentration might be
in the present study. This finding was in full agreementrelated to liver damage, because most of the cholesterol is
with Afaleq [9]. On the other hand increased inmetabolized in liver [34]. The mobilisation of lipids due to
gamma-globulin [7, 24] and total globulin [10] followingphysiological stress is expected to raise cholesterol
IBDV infection has been described. These discrepanciesconcentrations [35], lipid metabolism might have been
could be related to the age, strain of the virus and immune impaired due to the damage to the liver. The decreased
status in the affected chicks. Moreover, the true serumcholesterol could also be related to anorexia and diarrhoea
gamma-globulin concentration might have been maskedcausing reduced availability and absorption of fatty acid.
by neutralization of the antibody by the virus [25] henceFurther, given the strong correlation between lipid and
less participation of the gamma-globulin fraction inalbumin, the hypoalbuminaemia might have resulted in
determining the total globulin concentration. low level of albumin bound lipids in the vvIBDV
The elevation in serum concentration of AST, ALT, infected chicks leading to low level of serum
GLDH and, LDH, GGT and ALP at day 3 pi and/or days 5 cholesterol [36]. This finding was contrary to a previous
and 7 pi in the IBD group suggested pathologicalreport [10]; however, who have reported an increased in
involvement of liver and kidney which are commoncholesterol concentration. This discrepancy could be
sequels in IBDV infection especially following secondary related to the strain of the virus and the extent of liver
viremia [7, 8, 13, 26, 27, 28,]. These hepatocellular anddamage.
kidney injuries are postulated to result from hypoxic state The decreased Ca (hypocalcemia) in the serum
caused by aplastic bone marrow following IBDV infection could be related to a decrease in intestinal absorption
[8]. GLDH is situated in the mitochondrion of theof dietary calcium due to anorexia and diarrhoea.
hepatocytes and its elevation in the serum is associatedThe dehydration and anorexia in IBDV infection are also
with severe necrosis of the hepatocytes [23]. Ley et al. [7] stressors that are supposed to induce corticosteroid
have reported increased LDH and AST that correspondssecretion [9] which in turn leads to reduced serum calcium
with pathological changes in kidney and liver. Though[37]. Moreover, hypoalbuminaemia is said to reduce the
elevation of LDH could also imply damage to the musclequantity of bound calcium and result in a decreased total
[29] there was no report of muscle damage in IBDVserum calcium concentration [37, 38].
++
Global Veterinaria, 8 (1): 08-14, 2012
13
Similarly, the decreased sodium Na concentration6. Lukert, P.D. and Y.M. Saif, 1997. Infectious bursal
+
(hyponatermia) in the IBD group could be related to thedisease. In Diseases of poultry, Eds., B.W. Calnek,
dehydration, anorexia and decreased water intake [39] that H.J. Barnes, C.W. Beard, L.R. McDougald and
were evident in the present study starting at day 2 pi.Y.M. Saif, 10th ed. Iowa State University Press,
The diarrhoea is another possible cause to be consideredAmes, pp: 271-738.
because excess water loss can cause reduction in the7. Ley, D.H., R. Yamamoto and A.A. Bickford, 1983.
Na level [38]. On the other hand, the increasedThe pathogenesis of infectious disease:
chloride CL (hyperchloridemia), decreased potassiumserologic, histopathologic and clinical chemical
-
K(hypokalemia) could be associated with the diarrhoeaobservations. Avian Disease, 27: 1060-1085.
+
[23]. Hypokalemia could result from kidney damage [37]8. Nunoya, T.Y.O., M. Hiraga and T. Saito, 1992.
which is a common pathology in IBDV infection. Occurrence of acute infectious bursal disease with
In conclusion, the result in this study presentedhigh mortality in Japan and pathogenicity of
biochemical changes in vvIBDV infection which werefield isolates in specific-pathogen-free chicks.
consistent with the pathogenicity of IBDV infection. Avian Disease, 36: 597-609.
By and large, these biochemical changes in vvIBDV9. Afaleq, A.I., 1998. Biochemical and hormonal
infection are mostly related to damage to the liver andchanges associated with experimental infection of
kidney following the localization of the virus in thesechicks with infectious bursal disease virus. Journal of
organs during secondary viremia along the course of theVeterinary Medicine, 45: 513-517.
disease and they can be used to assess the damage and10. Panigraphy, B., L.D. Rowel and D.E. Corrier, 1986.
its extent in these organs prior to necropsy or death.Hematological values and changes in blood
Furthermore, these parameters are essential inchemistry in chicks with infectious bursal disease.
clinco-pathological assessment of the disease and alsoResearch in Veterinary Science, 40: 86-88.
potentially contribute to the understanding of the11. Longnathan, P., S.H. Sharifah, V. Arunasalam and
pathogenesis of IBD. A.H. Mahani, 1992. Outbreak of infectious bursal
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