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Comparative Nephropathogenicity of Different Strains of Infectious Bronchitis Virus in Chickens
ENVIRONMENT AND HEALTH Comparative Nephropathogenicity of Different Strains of Infectious Bronchitis Virus in Chickens MANIK CHANDRA1 Nephrology Division, Box 133, Department of Medicine, School of Medicine, University ofVirgina, Charlottesville, Virginia 22908 (Received for publication July 2, 1986)
1987 Poultry Science 6 6 : 9 5 4 - 9 5 9 INTRODUCTION
In 1962, Cumming described infectious bronchitis (IB) virus from cases showing kidney lesions. Later, nephropathogenetic strains of IB virus were isolated by Rinaldi et al. (1966). Subsequently, several workers (Pohl, 1974; Siller and Cumming, 1974; Chandra, 1979; Chandra et al., 1981; Chong and Apostolov, 1982) have reported the histopathology of Australian T and H 52 strains of IB virus, and Siller (1981) reviewed the literature on renal pathology. The present paper compares the nephropathogenicity of Australian T, Holte, Gray, and M 41 strains of IB virus injected intravenously in 2-week-old White Leghorn chickens. MATERIALS AND METHODS
Viruses. Australian T, Holte, Gray, and M 41 strains were used. Source and characteristics of these viruses have been described previously (Cumming, 1962; Winterfield and Hitchner, 1962; Bracewell, 1973). The embryo passage levels of these viruses were unknown. Each virus was propagated in 10-day-old specificpathogen-free chicken embryos, and the chorioallantoic fluids were harvested 48 hr postinoculation (pi). Titration and testing for bacte-
'Present address, correspondence, and reprint requests: Manik Chandra, Division of Pathology, International Research and Development Corporation, Mattawan, MI 49071.
954
rial contamination were done before use. Chickens. One hundred, 2-week-old specificpathogen-free White Leghorn males were used. Serological surveys of the birds in the commercial hatchery were negative for Newcastle disease, infectious laryngotracheitis, IB virus, and mycoplasmas. Infection. The concentration of virus in each case was adjusted in nutrient broth to give 106 median effective inoculation dose per chick. Chickens were randomly divided into five groups of 20 each. Chickens in Groups 1 through 4 were injected intravenously with .1 ml of virus. The controls (Group 5) were given appropriate dilutions of uninfected allantoic fluid. Infected chickens were housed separately in cages and examined daily. Virus Neutralization and Virus Isolation. At 21 days pi, prior to sacrifice, blood samples were collected from 5 chickens of each group. The virus neutralization (VN) tests were done in 10-day-old embryonated chicken eggs using constant serum volumes with 10-fold virus dilutions (American Association of Avian Pathologists, 1980). Isolation attempts were made using kidney tissue obtained from five cases of each group by a previously described method (Chandra et al, 1980). Histopathology. Kidney tissues were fixed in 10% neutral buffered formalin. They were processed for paraffin wax embedding, sectioned, and stained with hemotoxylin and eosin and periodic acid-Schiff (PAS). Lesions were graded on a 0 to 4 + numerical scale.
Downloaded from http://ps.oxfordjournals.org/ at Purdue University Libraries ADMN on June 12, 2015
ABSTRACT Two-week-old White Leghorn chickens were injected intravenously with Australian T, Holte, Gray, and M 41 strains of infectious bronchitis virus. A total of 100, 90, 85, and 20% of the chickens infected with Australian T, Holte, Gray, and M 41, respectively, had variable degrees of nephritis. The Australian T strain induced the most rapid and the most severe kidney lesions followed by Holte, Gray, and M 41 in descending order. (Key words: chicken, interstitium, mononuclear cell, nephropathogenicity)
INFECTIOUS BRONCHITIS EFFECT ON KIDNEYS RESULTS
Clinical
Observations
15 to 21 days pi had trace, mild, and moderate kidney lesions, respectively. Immune Response and Virus Recovery. The VN titers ranged from log 10 3.42 to 4.75 for chickens infected with IB viruses and < 1 for the controls. The IB virus could be recovered from each kidney sample processed from infected chicken. Histopathological Observation. Mean score index for chickens infected with various strains of IB virus and that died or were sacrificed at different intervals are presented in Table 1 .The lesions are described in three phases. Acute Phase. Tubules showed variable degrees of degeneration and desquamation of epithelium (Figure 1). Mitotic figures were frequently seen in the plump epithelial cells. Single cell necrosis was fairly common. In many instances, tubular epithelium contained PAS-positive granules. At times these granules were intermingled with desquamated epithelium and were seen in the proximal and distal convoluted tubules, collecting ducts, and collecting tubules. Mononuclear cells and heterophils were seen around the tubules and glomeruli. These cells were also present in the submucosa of the ureters. In some cases sloughed ureteral epithelium
•*9Sr*U"; $ FIG. 1. Acute phase, 2 days postinfection of Australian T strain. Note tubular degeneration. Some of the tubules show desquamation of epithelium from basement membrane, others have one or more detached cells in their lumen. Hematoxylin and eosin stain. x200.
Downloaded from http://ps.oxfordjournals.org/ at Purdue University Libraries ADMN on June 12, 2015
Tracheal rales and gasping were detected 2 to 7 days pi in 30, 45, 55, and 100% of the chickens infected with Australian T, Holte, Gray, and M 41 strains, respectively. Generally speaking no respiratory signs were seen after 7 days pi. A total of 8, 2, 1, and 7 chickens infected with Australian T, Holte, Gray, and M 41 died within the 7 days pi. After 7 days pi, no mortality was recorded in the group infected with M 4 1 . Two chickens infected with the Australian T strain and 1 chicken infected with the Holte strain died between 8 to 14 days pi. The only mortality after 2 week pi was in 2 chickens infected with T strain found dead on the 19th day pi. Chickens that died after 1 week pi stood hunched, appeared depressed, and had ruffled feathers. Gross Lesions. Macroscopic renal lesions were seen only in dead or dying chickens. There was no definite pattern of kidney involvement, but generally all lobes of the kidney were enlarged and pale. Chickens that died within 7 days pi, between 8 to 14 days pi, and between
955
CHANDRA
956
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|l FIG. 2. Acute phase. 3 days postinfection of Australian T strain. Note massive mononuclear cell infiltration in the interstitium. Hematoxylin and eosin stain. X 100.
mixed with inflammatory cells was seen in the ureteral lumen. The interstitium showed variable degrees of heterophilic and lymphocytic infiltration (Figure 2). The Australian T straininfected chickens showed dilation of some distal convoluted tubules, collecting ducts, and collecting tubules. Subacute Phase. In addition to the tubular changes described in acute phase, some tubules showed very early changes of regeneration. Tubules were widely separated by severe interstitial inflammation. In some cases massive focal aggregates of inflammatory cells caused severe damage to the tubules (Figure 3). Presence of the inflammatory cells around the tubules and glomerular capsule was observed frequently (Figure 4). The inflammatory cells were predominantly lymphocytes, a few heterophils, and occasional plasma cells containing PAS-positive Russell bodies. At some locations, interstitial reticuloendothelial cells showed proliferation. At this stage, lesions were more pronounced in the medullary region than in the cortex. Chronic Phase. Mild tubular lesions were occasionally seen. In general, no mitotic figures were evident in the tubules and most tubules
had regenerated. Inflammatory reaction consisted of lymphocytes and plasma cells with Russell bodies still evident in some locations. Lesions were seen both in the cortex and medulla. DISCUSSION
The most severe respiratory signs were seen in chickens infected with the M 41 strain. The other described clinical signs were most severe in Australian T strain-infected chickens where 60% of animals died on study. Eighty-five percent of the chickens infected with the Australian T strain showed gross renal lesions versus 35, 20, and 5% infected with the Holte, Gray, and M 41 strains, respectively. Although kidney lesions were least severe in the chickens infected with the M 41 strain, high mortality in these chickens may have been due to respiratory failure. Unfortunately, pathology of respiratory organs was not done. All chickens with gross kidney lesions had variable degrees of microscopic renal lesions. Some of the chickens with no gross lesions also revealed the disease. The microscopic renal lesions were more severe in chickens infected with the T strain than with Holte or Gray strains (Table 1). The chick-
Downloaded from http://ps.oxfordjournals.org/ at Purdue University Libraries ADMN on June 12, 2015
A'M.
*••
INFECTIOUS BRONCHITIS EFFECT ON KIDNEYS
_ ' *
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d* f
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£;T«.y r * !• FIG. 3. Subacute phase, 12 days postinfection of Australian T strain. Local mononuclear cell infiltration was damaging the tubules. Hematoxylin and eosin stain. X400.
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FIG. 4. Subacute phase, 10 days postinfection of Holte strain. Note mononuclear cell infiltration around the tubules and glomerular capsule. Hematoxylin and eosin stain. X400.
Downloaded from http://ps.oxfordjournals.org/ at Purdue University Libraries ADMN on June 12, 2015
*
958
CHANDRA TABLE 1. Comparison of microscopic renal lesions in infectious bronchitis virus-induced nephritis Mean score index 1
Days postinfection
Control
Australian T
Holte
Gray
M 41
1-7 (acute phase) 8 - 1 4 (subacute phase) 1 5 - 2 1 (chronic phase)
0 0 0
2.75 2.83 2.00
2.63 1.53 1.67
2.00 0.97 0.55
0.18 0.03 0
0
2.55
2.20
1.60
0.05
1-21 1
Number chickens with lesions times mean score with this value divided by the number of chickens examined.
ACKNOWLEDGMENTS
The author thanks Paul Tucek for his criticism and Neeru Chandra for typing the manuscript.
REFERENCES American Association of Avian Pathologists, 1980. Pages 70-72 in: Isolation and Identification of Avian Pathogens. S. B. Hichner, C. H. Domermuth, H. G. Purchase, and J. E. Williams, ed. Creative Printing Co. Inc., Endwell, NY. Bracewell, C. D., 1973. Antigenic relationship between strains of infectious bronchitis virus as shown by the plaque reduction test in chicken kidney cells. In: Proc. 5th World Congr. Vet. Poult. Assoc, Munich, Germany. Chandra, M., 1979. Studies on the prevalence and pathology of the nephritis-nephrosis syndrome in domestic fowl in Punjab. M.V.Sc. thesis, Punjab Agric. Univ., Ludhiana, Punjab, India. Chandra, M., G. Singh, and B. Singh, 1980. Isolation of infectious bronchitis, infectious bursal disease and avian adeno viruses from chickens with nephritis-nephrosis syndrome. Zentrabl. Veterinaermed. 16B:193212. Chandra, M., B. Singh, and G. Singh, 1981. Pathology of experimental nephrosis-nephritis in chickens induced by infectious bronchitis virus. Ind. J. Exp. Biol. 19:508-510. Chandra, M., T. Tyson, O. J. Fletcher, and W. K. Bolton, 1986. Nephropathogenicity of infectious bronchitis virus in normal and bursectomized chickens. J. Am. Vet. Med. Assoc. 189:362. (Abstr.) Chong, K. T., and K. Apostolov, 1982. The pathogenesis of nephritis in chickens induced by infectious bronchitis virus. J. Comp. Pathol. 92:199-211. Cumming, R. B., 1962. The etiology of uraemia of chickens. Aust. Vet. J. 38:554. (Abstr.) Jungherr, E., T. W. Chomiak, and R. E. Luginbuhl, 1956. Dosage response of tracheal mucosa to infectious bronchitis virus. Pages 24-28 in: Proc. 28th Annu. Mtg. Northeastern Congr. Laboratory Workers Pullorum Dis. Control. Macdonald, J. W., C. J. Randall, and D. A. McMartin, 1980. An inverse age resistance of chicken kidneys to
Downloaded from http://ps.oxfordjournals.org/ at Purdue University Libraries ADMN on June 12, 2015
ens infected with M 41 strain did not show any nephritic lesions after 1 week pi. The basic observation of interstitial nephritis is in agreement with the previous reports on the T and H 52 strains (Pohl, 1974; Macdonald et al., 1980; Chandra et al., 1980, 1981; Winterfield and Albassam, 1984). However, severe suppurative or granulomatous lesions or lymphoid follicles with germinal centers earlier reported with the Australian T strain (Pohl, 1974; Chong and Apostolov, 1982) were not evident in the present study. This variation in the lesions may be due to differences in the passage levels, virulence of the virus, or duration of the experiment. The respiratory route of IB virus infection does not lend selective susceptibility to the kidney but also results in severe respiratory disease (Jungherr et al., 1956; Winterfield and Fadly, 1971). Chandra et al. (1981) utilized intraperitoneal route while studying the pathogenesis of IB virus variant in chickens. Recently, in a separate study the Australian T strain was inoculated through the occular route in 4-week-old syngeneic SC chickens (Chandra et al., 1986). The present study was conducted using the intravenous route to investigate the differences in the onset and severity of renal lesions as compared to the other route described. Nephritic lesions observed in the present study were more severe than those described previously in chickens infected occularly or intraperitoneally (Chandra et al., 1981). This may be due to the variations in the route of infection, age of chickens and/or strain of chickens. From this study, it is apparent that the Australian T strain induces more frequent and more severe nephritic lesions followed by Holte, Gray, M 41 strains in descending order (Table 1).
INFECTIOUS BRONCHITIS EFFECT ON KIDNEYS infectious bronchitis virus. Avian Pathol. 9:245-259. Pohl, R., 1974. The histopathogenesis of the nephrosis-nephritis syndrome. Avian Pathol. 3:1-13. Rinaldi, A., A. Crespi, G. Cervio, and G. Mandelli, 1966. Isolamento di un ceppo nephropatogeno del virus della bronchite infettiva del pallo. Selezion Vetenaire. 7:284-289. Siller, W. G., 1981. Renal pathology of the fowl-a review. Avian Pathol. 10:187-262. Siller, W. G., and R. B. Cumming, 1974. The histopathology of an interstitial nephritis in the fowl produced
959
experimentally with infectious bronchitis virus. J. Pathol. 114:163-173. Winterfield, R. W., and M. A. Albassam, 1984. Nephropathogenicity of infectious bronchitis virus. Poultry Sci. 63:2358-2363. Winterfield, R. W., and A. M. Fadly, 1971. Criteria for examining the immune response to infectious bronchitis virus. Avian Dis. 15:56-67. Winterfield, R. W., and S. B. Hitchner, 1962. Etiology of an infectious nephritis-nephrosis syndrome of chickens. Am. J. Vet. Res. 23:1273-1279.
Downloaded from http://ps.oxfordjournals.org/ at Purdue University Libraries ADMN on June 12, 2015
1987 Poultry Science 6 6 : 9 5 4 - 9 5 9 INTRODUCTION
In 1962, Cumming described infectious bronchitis (IB) virus from cases showing kidney lesions. Later, nephropathogenetic strains of IB virus were isolated by Rinaldi et al. (1966). Subsequently, several workers (Pohl, 1974; Siller and Cumming, 1974; Chandra, 1979; Chandra et al., 1981; Chong and Apostolov, 1982) have reported the histopathology of Australian T and H 52 strains of IB virus, and Siller (1981) reviewed the literature on renal pathology. The present paper compares the nephropathogenicity of Australian T, Holte, Gray, and M 41 strains of IB virus injected intravenously in 2-week-old White Leghorn chickens. MATERIALS AND METHODS
Viruses. Australian T, Holte, Gray, and M 41 strains were used. Source and characteristics of these viruses have been described previously (Cumming, 1962; Winterfield and Hitchner, 1962; Bracewell, 1973). The embryo passage levels of these viruses were unknown. Each virus was propagated in 10-day-old specificpathogen-free chicken embryos, and the chorioallantoic fluids were harvested 48 hr postinoculation (pi). Titration and testing for bacte-
'Present address, correspondence, and reprint requests: Manik Chandra, Division of Pathology, International Research and Development Corporation, Mattawan, MI 49071.
954
rial contamination were done before use. Chickens. One hundred, 2-week-old specificpathogen-free White Leghorn males were used. Serological surveys of the birds in the commercial hatchery were negative for Newcastle disease, infectious laryngotracheitis, IB virus, and mycoplasmas. Infection. The concentration of virus in each case was adjusted in nutrient broth to give 106 median effective inoculation dose per chick. Chickens were randomly divided into five groups of 20 each. Chickens in Groups 1 through 4 were injected intravenously with .1 ml of virus. The controls (Group 5) were given appropriate dilutions of uninfected allantoic fluid. Infected chickens were housed separately in cages and examined daily. Virus Neutralization and Virus Isolation. At 21 days pi, prior to sacrifice, blood samples were collected from 5 chickens of each group. The virus neutralization (VN) tests were done in 10-day-old embryonated chicken eggs using constant serum volumes with 10-fold virus dilutions (American Association of Avian Pathologists, 1980). Isolation attempts were made using kidney tissue obtained from five cases of each group by a previously described method (Chandra et al, 1980). Histopathology. Kidney tissues were fixed in 10% neutral buffered formalin. They were processed for paraffin wax embedding, sectioned, and stained with hemotoxylin and eosin and periodic acid-Schiff (PAS). Lesions were graded on a 0 to 4 + numerical scale.
Downloaded from http://ps.oxfordjournals.org/ at Purdue University Libraries ADMN on June 12, 2015
ABSTRACT Two-week-old White Leghorn chickens were injected intravenously with Australian T, Holte, Gray, and M 41 strains of infectious bronchitis virus. A total of 100, 90, 85, and 20% of the chickens infected with Australian T, Holte, Gray, and M 41, respectively, had variable degrees of nephritis. The Australian T strain induced the most rapid and the most severe kidney lesions followed by Holte, Gray, and M 41 in descending order. (Key words: chicken, interstitium, mononuclear cell, nephropathogenicity)
INFECTIOUS BRONCHITIS EFFECT ON KIDNEYS RESULTS
Clinical
Observations
15 to 21 days pi had trace, mild, and moderate kidney lesions, respectively. Immune Response and Virus Recovery. The VN titers ranged from log 10 3.42 to 4.75 for chickens infected with IB viruses and < 1 for the controls. The IB virus could be recovered from each kidney sample processed from infected chicken. Histopathological Observation. Mean score index for chickens infected with various strains of IB virus and that died or were sacrificed at different intervals are presented in Table 1 .The lesions are described in three phases. Acute Phase. Tubules showed variable degrees of degeneration and desquamation of epithelium (Figure 1). Mitotic figures were frequently seen in the plump epithelial cells. Single cell necrosis was fairly common. In many instances, tubular epithelium contained PAS-positive granules. At times these granules were intermingled with desquamated epithelium and were seen in the proximal and distal convoluted tubules, collecting ducts, and collecting tubules. Mononuclear cells and heterophils were seen around the tubules and glomeruli. These cells were also present in the submucosa of the ureters. In some cases sloughed ureteral epithelium
•*9Sr*U"; $ FIG. 1. Acute phase, 2 days postinfection of Australian T strain. Note tubular degeneration. Some of the tubules show desquamation of epithelium from basement membrane, others have one or more detached cells in their lumen. Hematoxylin and eosin stain. x200.
Downloaded from http://ps.oxfordjournals.org/ at Purdue University Libraries ADMN on June 12, 2015
Tracheal rales and gasping were detected 2 to 7 days pi in 30, 45, 55, and 100% of the chickens infected with Australian T, Holte, Gray, and M 41 strains, respectively. Generally speaking no respiratory signs were seen after 7 days pi. A total of 8, 2, 1, and 7 chickens infected with Australian T, Holte, Gray, and M 41 died within the 7 days pi. After 7 days pi, no mortality was recorded in the group infected with M 4 1 . Two chickens infected with the Australian T strain and 1 chicken infected with the Holte strain died between 8 to 14 days pi. The only mortality after 2 week pi was in 2 chickens infected with T strain found dead on the 19th day pi. Chickens that died after 1 week pi stood hunched, appeared depressed, and had ruffled feathers. Gross Lesions. Macroscopic renal lesions were seen only in dead or dying chickens. There was no definite pattern of kidney involvement, but generally all lobes of the kidney were enlarged and pale. Chickens that died within 7 days pi, between 8 to 14 days pi, and between
955
CHANDRA
956
"%r>. • > , - '
•'.«,*-«
".. '-3 -
*->i '^"-C^^^s,
'-^»'»; , "
. *X.'
**-• V;**'-
fe ' ' • ; ' ,•• •ft; •I'
.yf'
*IF
, ;. ^'J< :
••'•
•'. -
'• ;;•
V-^S' ^"'
: f
''
'* **
v,*
|l FIG. 2. Acute phase. 3 days postinfection of Australian T strain. Note massive mononuclear cell infiltration in the interstitium. Hematoxylin and eosin stain. X 100.
mixed with inflammatory cells was seen in the ureteral lumen. The interstitium showed variable degrees of heterophilic and lymphocytic infiltration (Figure 2). The Australian T straininfected chickens showed dilation of some distal convoluted tubules, collecting ducts, and collecting tubules. Subacute Phase. In addition to the tubular changes described in acute phase, some tubules showed very early changes of regeneration. Tubules were widely separated by severe interstitial inflammation. In some cases massive focal aggregates of inflammatory cells caused severe damage to the tubules (Figure 3). Presence of the inflammatory cells around the tubules and glomerular capsule was observed frequently (Figure 4). The inflammatory cells were predominantly lymphocytes, a few heterophils, and occasional plasma cells containing PAS-positive Russell bodies. At some locations, interstitial reticuloendothelial cells showed proliferation. At this stage, lesions were more pronounced in the medullary region than in the cortex. Chronic Phase. Mild tubular lesions were occasionally seen. In general, no mitotic figures were evident in the tubules and most tubules
had regenerated. Inflammatory reaction consisted of lymphocytes and plasma cells with Russell bodies still evident in some locations. Lesions were seen both in the cortex and medulla. DISCUSSION
The most severe respiratory signs were seen in chickens infected with the M 41 strain. The other described clinical signs were most severe in Australian T strain-infected chickens where 60% of animals died on study. Eighty-five percent of the chickens infected with the Australian T strain showed gross renal lesions versus 35, 20, and 5% infected with the Holte, Gray, and M 41 strains, respectively. Although kidney lesions were least severe in the chickens infected with the M 41 strain, high mortality in these chickens may have been due to respiratory failure. Unfortunately, pathology of respiratory organs was not done. All chickens with gross kidney lesions had variable degrees of microscopic renal lesions. Some of the chickens with no gross lesions also revealed the disease. The microscopic renal lesions were more severe in chickens infected with the T strain than with Holte or Gray strains (Table 1). The chick-
Downloaded from http://ps.oxfordjournals.org/ at Purdue University Libraries ADMN on June 12, 2015
A'M.
*••
INFECTIOUS BRONCHITIS EFFECT ON KIDNEYS
_ ' *
-;
R
957
d* f
-i
£;T«.y r * !• FIG. 3. Subacute phase, 12 days postinfection of Australian T strain. Local mononuclear cell infiltration was damaging the tubules. Hematoxylin and eosin stain. X400.
i
•"I
* Wi
fJi
»
*
J? #•;
jut
FIG. 4. Subacute phase, 10 days postinfection of Holte strain. Note mononuclear cell infiltration around the tubules and glomerular capsule. Hematoxylin and eosin stain. X400.
Downloaded from http://ps.oxfordjournals.org/ at Purdue University Libraries ADMN on June 12, 2015
*
958
CHANDRA TABLE 1. Comparison of microscopic renal lesions in infectious bronchitis virus-induced nephritis Mean score index 1
Days postinfection
Control
Australian T
Holte
Gray
M 41
1-7 (acute phase) 8 - 1 4 (subacute phase) 1 5 - 2 1 (chronic phase)
0 0 0
2.75 2.83 2.00
2.63 1.53 1.67
2.00 0.97 0.55
0.18 0.03 0
0
2.55
2.20
1.60
0.05
1-21 1
Number chickens with lesions times mean score with this value divided by the number of chickens examined.
ACKNOWLEDGMENTS
The author thanks Paul Tucek for his criticism and Neeru Chandra for typing the manuscript.
REFERENCES American Association of Avian Pathologists, 1980. Pages 70-72 in: Isolation and Identification of Avian Pathogens. S. B. Hichner, C. H. Domermuth, H. G. Purchase, and J. E. Williams, ed. Creative Printing Co. Inc., Endwell, NY. Bracewell, C. D., 1973. Antigenic relationship between strains of infectious bronchitis virus as shown by the plaque reduction test in chicken kidney cells. In: Proc. 5th World Congr. Vet. Poult. Assoc, Munich, Germany. Chandra, M., 1979. Studies on the prevalence and pathology of the nephritis-nephrosis syndrome in domestic fowl in Punjab. M.V.Sc. thesis, Punjab Agric. Univ., Ludhiana, Punjab, India. Chandra, M., G. Singh, and B. Singh, 1980. Isolation of infectious bronchitis, infectious bursal disease and avian adeno viruses from chickens with nephritis-nephrosis syndrome. Zentrabl. Veterinaermed. 16B:193212. Chandra, M., B. Singh, and G. Singh, 1981. Pathology of experimental nephrosis-nephritis in chickens induced by infectious bronchitis virus. Ind. J. Exp. Biol. 19:508-510. Chandra, M., T. Tyson, O. J. Fletcher, and W. K. Bolton, 1986. Nephropathogenicity of infectious bronchitis virus in normal and bursectomized chickens. J. Am. Vet. Med. Assoc. 189:362. (Abstr.) Chong, K. T., and K. Apostolov, 1982. The pathogenesis of nephritis in chickens induced by infectious bronchitis virus. J. Comp. Pathol. 92:199-211. Cumming, R. B., 1962. The etiology of uraemia of chickens. Aust. Vet. J. 38:554. (Abstr.) Jungherr, E., T. W. Chomiak, and R. E. Luginbuhl, 1956. Dosage response of tracheal mucosa to infectious bronchitis virus. Pages 24-28 in: Proc. 28th Annu. Mtg. Northeastern Congr. Laboratory Workers Pullorum Dis. Control. Macdonald, J. W., C. J. Randall, and D. A. McMartin, 1980. An inverse age resistance of chicken kidneys to
Downloaded from http://ps.oxfordjournals.org/ at Purdue University Libraries ADMN on June 12, 2015
ens infected with M 41 strain did not show any nephritic lesions after 1 week pi. The basic observation of interstitial nephritis is in agreement with the previous reports on the T and H 52 strains (Pohl, 1974; Macdonald et al., 1980; Chandra et al., 1980, 1981; Winterfield and Albassam, 1984). However, severe suppurative or granulomatous lesions or lymphoid follicles with germinal centers earlier reported with the Australian T strain (Pohl, 1974; Chong and Apostolov, 1982) were not evident in the present study. This variation in the lesions may be due to differences in the passage levels, virulence of the virus, or duration of the experiment. The respiratory route of IB virus infection does not lend selective susceptibility to the kidney but also results in severe respiratory disease (Jungherr et al., 1956; Winterfield and Fadly, 1971). Chandra et al. (1981) utilized intraperitoneal route while studying the pathogenesis of IB virus variant in chickens. Recently, in a separate study the Australian T strain was inoculated through the occular route in 4-week-old syngeneic SC chickens (Chandra et al., 1986). The present study was conducted using the intravenous route to investigate the differences in the onset and severity of renal lesions as compared to the other route described. Nephritic lesions observed in the present study were more severe than those described previously in chickens infected occularly or intraperitoneally (Chandra et al., 1981). This may be due to the variations in the route of infection, age of chickens and/or strain of chickens. From this study, it is apparent that the Australian T strain induces more frequent and more severe nephritic lesions followed by Holte, Gray, M 41 strains in descending order (Table 1).
INFECTIOUS BRONCHITIS EFFECT ON KIDNEYS infectious bronchitis virus. Avian Pathol. 9:245-259. Pohl, R., 1974. The histopathogenesis of the nephrosis-nephritis syndrome. Avian Pathol. 3:1-13. Rinaldi, A., A. Crespi, G. Cervio, and G. Mandelli, 1966. Isolamento di un ceppo nephropatogeno del virus della bronchite infettiva del pallo. Selezion Vetenaire. 7:284-289. Siller, W. G., 1981. Renal pathology of the fowl-a review. Avian Pathol. 10:187-262. Siller, W. G., and R. B. Cumming, 1974. The histopathology of an interstitial nephritis in the fowl produced
959
experimentally with infectious bronchitis virus. J. Pathol. 114:163-173. Winterfield, R. W., and M. A. Albassam, 1984. Nephropathogenicity of infectious bronchitis virus. Poultry Sci. 63:2358-2363. Winterfield, R. W., and A. M. Fadly, 1971. Criteria for examining the immune response to infectious bronchitis virus. Avian Dis. 15:56-67. Winterfield, R. W., and S. B. Hitchner, 1962. Etiology of an infectious nephritis-nephrosis syndrome of chickens. Am. J. Vet. Res. 23:1273-1279.
Downloaded from http://ps.oxfordjournals.org/ at Purdue University Libraries ADMN on June 12, 2015