This article was downloaded by: [Ams/Girona*barri Lib] On: 02 December 2014, At: 00:54 Publisher: Taylor & Francis Informa Ltd Registered in England and Wales Registered Number: 1072954 Registered office: Mortimer House, 37-41 Mortimer Street, London W1T 3JH, UK
Veterinary Quarterly Publication details, including instructions for authors and subscription information: http://www.tandfonline.com/loi/tveq20
Pathogenicity of two strains of Newcastle disease virus in the grey‐breasted helmet guinea fowl a
a
a
N.J. Agoha , S.O. Akpavie , O.A. Durojaiye & D.F. Adene
a
a
Faculty of Veterinary Medicine , University of Ibadan , Ibadan, Nigeria Published online: 01 Nov 2011.
To cite this article: N.J. Agoha , S.O. Akpavie , O.A. Durojaiye & D.F. Adene (1992) Pathogenicity of two strains of Newcastle disease virus in the grey‐breasted helmet guinea fowl, Veterinary Quarterly, 14:2, 51-53, DOI: 10.1080/01652176.1992.9694328 To link to this article: http://dx.doi.org/10.1080/01652176.1992.9694328
PLEASE SCROLL DOWN FOR ARTICLE Taylor & Francis makes every effort to ensure the accuracy of all the information (the “Content”) contained in the publications on our platform. However, Taylor & Francis, our agents, and our licensors make no representations or warranties whatsoever as to the accuracy, completeness, or suitability for any purpose of the Content. Any opinions and views expressed in this publication are the opinions and views of the authors, and are not the views of or endorsed by Taylor & Francis. The accuracy of the Content should not be relied upon and should be independently verified with primary sources of information. Taylor and Francis shall not be liable for any losses, actions, claims, proceedings, demands, costs, expenses, damages, and other liabilities whatsoever or howsoever caused arising directly or indirectly in connection with, in relation to or arising out of the use of the Content. This article may be used for research, teaching, and private study purposes. Any substantial or systematic reproduction, redistribution, reselling, loan, sub-licensing, systematic supply, or distribution in any form to anyone is expressly forbidden. Terms & Conditions of access and use can be found at http:// www.tandfonline.com/page/terms-and-conditions
PATHOGENICITY OF TWO STRAINS OF NEWCASTLE DISEASE VIRUS IN THE GREY-BREASTED HELMET GUINEA FOWL N. J. Agoha, S. 0. Akpavie, 0. A. Durojaiye, and D. F. Adenel Veterinary Quarterly 1992; 14: 51-3
Downloaded by [Ams/Girona*barri Lib] at 00:54 02 December 2014
SUMMARY
1. Eggs and guinea fowl keets
maternal antibodies to Newcastle disease virus, were infected with Hens strain (33/56) and Kumarov strain of Newcastle disease virus intramucularly (m) or intranasally (IN). Clinical signs were first noticed four days post infection (n) in
One hundred and fifty eggs from guinea fowl hens that had not been vaccinated with Newcastle vaccines were purchased from
the group infected al but five days PI in the group infected IN with Hens strain of Newcastle disease virus. These clinical signs were
similar in both groups and included anorexia, droopiness, huddling together, greenish diarrhoea and marked cachexia. Prominent nervous signs, including spasms of the head and neck, were observed in groups infected with Hens strain. The major gross lesions observed were emaciation with prominent keel bone, empty intestinal tract and distended gall bladder in most keets. The histological lesions were characterised by meningoencephalitis, necrosis and loss of lymphocytes from splenic and lymphoid aggregates. There was muscular degeneration and necrosis in the gizzard and mild pulmonary congestion and oedema in some keets. Neither gross or microscopic lesions were observed in keels that had received the Kumarov strain.
the National Veterinary Research Institute (NVRI), Vom, Nigeria. After hatching, the guinea fowl keets were transferred to poultry cages made of wood and chicken-wire mesh, covered with polythene and heated electrically. The keets were provided with water and fed ad libitum.
2. Antibody assay At 3 weeks of age, and at the time of infection the guinea fowl keets were assayed for antibodies using the haemagglutination inhibition (HI) test.
Seronegative keets were used in the experimental infection. Antibodies to Newcastle Disease Virus (NDV) Herts and NDV Kumarov were assayed at 4 days and 2 weeks PI.
3. Newcastle disease challenge virus The NDV for the challenge was Herts 33/56 obtained from NVRI, Vom, Nigeria. It was originally obtained from Central Veterinary Laboratory, Weybridge, United Kingdom. The Kumarov strain of NDV (NDV(K)) was also obtained from
INTRODUCTION There have been extensive studies on the pathology of Newcas-
NVRI, Vom.
tle disease in the domestic chicken and turkey but not in the
4. Experimental groups The seronegative keets were divided into five groups. Each
guinea fowl, and very few reports on viral or bacterial diseases of the guinea fowl are available. However, guinea fowls are
susceptible to diseases such as fowl typhoid and Newcastle disease (2). Johnson and Anderson (7) and Moore (8) reported outbreaks of fowl typhoid in guinea fowls in the United States of America. Adewuyi et al. (1) diagnosed infectious bursal disease
(IBD) in Market guinea fowls, and Durojaiye and Adene (5) diagnosed Newcastle disease and Egg-Drop Syndrome '76 in a small flock of guinea fowls kept intensively at the University of Ibadan. The guinea fowl is native to the savannah zone of West Africa and the bird is seen mostly in the wild. At present, there is an increasing tendency to domesticate and commercialise its production. Because of the possibility of commercial production
and the fact that Newcastle disease is perhaps one of the most endemic and fatal diseases of poultry in Nigeria, this study was undertaken to determine the pathogenecity and pathology of Newcastle disease in the guinea fowl. The Herts and Kumarov strains were used in this study because one is the vaccine strain commonly used and the other, a strain commonly encountered in field outbreaks of Newcastle disease in Nigeria. I
MATERIALS AND METHODS
Thirty-five 6-week-old guinea fowl keels, seronegative for
Faculty of Veterinary Medicine, University of lbadan, lbadan, Nigeria.
51
.
group was placed in a separate cage. Group I was made up of 10 guinea keets. Each keet was infected intramuscularly with 0.5 ml of a 1:10 dilution of NDV (Herts) viral suspension in allantoic fluid. Group II had five guinea keets and each was infected intranasally with the same dose and dilution of NDV (Herts) as Group I keets. Group III had five guinea keets. They were each infected INt with 0.5 ml of a 200 dose NDV (K) vial after reconstitution with 100 ml buffered normal saline. Group IV had five guinea keets, each
of which received the same dose of NDV (K) as Group III but IN.
Group V contained 10 guinea keets which were used as controls. All keets were killed at the end of the experiment and examined.
Pathology
Tissues were obtained from the brain, lungs, liver, spleen, kidney, bursa of Fabricius, pancreas, oesophagus, crop, proventriculus, gizzard, intestine, gall bladder and sciatic nerve. These
were fixed in 10% buffered formalin for at least 24 hours, processed routinely for histopathology and stained with haematoxylin and eosin.
THEVETERI NARYQUARTERLY, VOL
1
4
,
No
.
2, APR
I
L
,
1
992
RESULTS
Clinical signs Clinical signs were first observed four days Pi in Group I keets
The gall bladder was distended with bile in 11 (73.3%) keets while 6 (40%) showed mild pulmonary congestion. One keet showed mottling of the kidney.
infected INA while clinical signs were first observed five days PI in
the group infected IN. The clinical signs were similar in both
groups and include ruffled feathers, anorexia, depression, huddling together and greenish-white faeces. Nervous signs were first noticed five days PI in Group I keets and included spasms of the head and neck, torticollis in some keets and paralysis of the extremities followed by death. Death first occurred on the sixth day PI, and it occurred in both groups I and
II. All keets in both groups were dead by the eight day pi. In Group III, two keets showed mild anorexia, depression and ruffled feathers five days Pl. These signs lasted for three days and
the keets recovered fully. No clinical signs were observed in Group IV and V. The morbidity and mortality pattern in the experimental guinea keets is shown in Table 1.
Downloaded by [Ams/Girona*barri Lib] at 00:54 02 December 2014
Table 1. Morbidity and mortality pattern in the experimental guinea keets.
No. of keets
Strain of virus used Route of
Group I
Group II
Group III
Group IV
Group V (control)
10
5
5
5
10
NDV (Herts)
NDV
NDV (K) NDV
(Herts)
IM
IN
IM
Histopathological lesions On microscopy, 10 (66.67%) keets showed pulmonary congestion and oedema which varied from mild to moderately severe. Twelve (80%) keets had brain lesions characterised by lymphocytic infiltration of the meninges, pericascular lymphocytic cuffs
and vasculitis (Fig. 1). There was vascular congestion in the cerebrum and marked spongiosis in the cerebellum of one keet (Fig. 2). The splenic lesion was characterised by necrosis and depletion of lymphocytes from the lymphoid follicles in six (40%) of the keets (Fig. 3). A few keets had liver lesions which were characterised by periportal necrosis with lymphocytic and
plasma cell infiltrates. The kidney lesion consisted of mild congestion with focal areas of lymphocytic infiltration into the
interstitium. The proventricular lesion was characterised by mild glandular degeneration with lymphocytic infiltration into the lamina propria. There was muscular degeneration and necrosis with lymphocytic and plasma cell infiltration in the gizzard.
(K) IN
infection
Morbidity (days pl)
ft
1
0
0
0
2
0
3
0 0
4
0 4
0 0 0
5
10
3
9 0
4
7 8
0
0
6
.
0
0 2
2 0 0
Mortality (days PH
0
3
0 0 0
4
0
0 0
5
0
0
1
2
6 7 8 9
0
1
9
0 0
3 1
0
o
Fig. 1. Cerebellum of a guinea keet showing severe vasculitis. Haemotoxylin and eosin staining. Magnification 750 x.
NDV = Newcastle disease virus IM = Intramusculair IN = Intransal
(K) = Kumarov PI = post infection
- PATHOLOGY
Gross lesions On post-mortem examination, lesions observed in Groups I and II keets included emaciation, with prominence of keel bones, and the pasting of the vent feathers with greenish-white faecal matter in some keets. Nine of the 15 keets (60%) had varying
quantities of feed in their crops. Four (26.6%) had catarrhal exudate in the duodenum. The intestine was virtually empty in 12 (80%) keets and the caecum was balloned in 7 (46.6%) keets.
52
Fig. 2.
Marked spongsiosis in the cerebellum of a guinea keet. Haemotoxylin and eosin staining. Magnification 465x.
THEVETERINARYQUARTERLY
,
VOL
1
4, No.
2
,
APR
I
L
,
1
992
naturally infected with NDV (2, 9) and turkeys experimentally infected with the Velogenic strain of NDV (3). The respiratory signs of dyspnoea, gasping, coughing, nasal discharge and rales often associated with Newcastle disease infection, especially in young chicks (9), were not observed.
The nervous signs such as the spasms of the head and neck, torticollis and paralysis of extremities described in chickens (9) and turkeys (3) were observed in this study. The predominance of nervous signs in this study may be associated with the fact that
the virus is essentially neurotropic, with minor effects in the digestive tract of guinea fowls. All keets that showed nervous signs died. The longer incubation period (four days as against five days) for keets infected Im and IN, respectively, may be attributed to the rapidity by which virus administered via the Im route enters the general circulation after rapid virus multiplication in tissues. The IN route of infection however exposes the virus to the natural defence mechanisms of
the respiratory tract and hence a reduction in the amount of
4,41
Antibody assay in guinea keets with NDV (Herts) and NDV (K)
virus available to produce disease. The gross pathological lesions observed were few and mild and included emaciation with prominent keel bone, mild congestion of the lungs, empty intestinal tract and distended gall bladder in some of the keets. In the chicken, however, gross lesions such as cloudy air sacs, congestion of the lungs, haemorrhages in the proventricular mucosa and/or hyperaemia of lymphoid aggregates have been described (2, 4, 6). Histologically, proventricular lesions such as congestion haemorrhage, cellular infiltration especially by mononuclear cells,
The results of the HI test using the beta procedure at four days PI was negative for all keets irrespective of virus strain and route of administration. However, two weeks pi the antibody in Groups
have been described for chickens (2, 4, 6), were not seen in this study. However, mild glandular degeneration with lymphocytic infiltration was observed in the proventriculus.
Downloaded by [Ams/Girona*barri Lib] at 00:54 02 December 2014
Fig. 3.
Necrosis and depletion of lymphocytes from the lymphoid follicles of a guinea keet's spleen. Haemotoxylin and eosin staining. Magnification 307,5x.
Maternal antibody assay Results of the antibody assay in the keets at three weeks of age showed that 7 out of 47 keets had antibodies in the 4-64 HI titre range. These keets were used for the experiment.
III and IV keets inoculated with NDV(K) showed HI titres (Table 2). Table 2. Antibody assay two weeks after infection with NDV(K).
hyperaemia and/or necrosis of lymphoid aggregates, which
The meningoencephalitis observed in this study has been described for chickens (2, 4, 6). The splenic lesions observed were those of necrosis and depletion of lymnphocytes in the splenic follicles, and were similar to those described for chickens
Bird no.
Route of infection
HI
Titre
259
IM
+
1024
281
IM
+
256
400 890 999
IM
+ + +
32
130 295
IN
419 540 880
IN
IM
IM
IN
IN IN
+ + + + +
Group mean
294
18
(2). Myocardial lesions such as degeneration and necrosis, which have been described for Newcastle disease infection in chickens (2), were not seen in the keets. However, similar lesions were seen in the gizzard. This study has established that the grey-breasted helmet guinea fowl is also susceptible to Newcastle disease, as is the domestic
32
chicken (2, 6) and turkey (3). Further work is in progress to
32
study the pathogenesis of Newcastle disease in the guinea fowl.
128 32 256 32
References
96
I. Adewuyi OA, Dojaiye OA, and Adene DF. Zentralbl Veterinar Med 1989b; 36: 43-8. Aitken I, Allan WH, Biggs RM, Gordon RF, and Jordan FTW. Newcastle disease: In Poultry Diseases. Ed RF Gordon. Balliere Tindal, London 1977: 81-94. 3. Sheikhly Al, Faud A, and Carlson HI. Pathology of Velogenic Newcastle disease virus infection in turkeys. Avian Dis 1975; 19: 397-407. 4. Brandly CA, Hanson RP. Newcastle disease: In Diseases of Poultry. Ed Biester HE and Schwarte LH. Iowa State University Press 5th. Ed 1967: 633. 5. Durojaiye OA, Adene DF. Newcastle disease and Egg Drop Syndrome '76 2,
in4 = Intramuscular IN = Intransal + = Positive HI = Haemagglutination inhibition
Controls The control group showed no clinical signs during the study period and neither gross nor microscopic lesions were observed
at post-mortem in this group. Antibodies to NDV were not detected in this group. DISCUSSION
The clinical signs observed in this study include anorexia, depression, ruffled feathers and greenish-white faeces. These
in guinea fowls Numida meleagris galeata Pallas. J Vet Med B 1988; 35: 1-3. 6.
Hanson RP. Newcastle disease. In Disease of Poultry Ed Biester HE and Schwarte LH. Iowa State University Press, 19878: 513. 7. Johnson EP, Anderson GW. An outbreak of fowl typhoid in guinea fowls. J Am Vet Med Assoc 1933; 82: 258-9. 8. Moore EN. Fowl typhoid diagnosed in guinea fowl. Poultry Sci 1946; 25: 387-8. 9.
Okaeme AN. Diseases of young helmet guine fowl under intensive management in Nigeria. Bull Anim Hlth Prod. Afr 1981; 29: 317-9.
clinical signs are similar to those observed in domestic chickens
53
THEVETER
I
NARYQUARTERLY, VOL
1
4
,
N o. 2
.
APR
I L
,
1
992
Veterinary Quarterly Publication details, including instructions for authors and subscription information: http://www.tandfonline.com/loi/tveq20
Pathogenicity of two strains of Newcastle disease virus in the grey‐breasted helmet guinea fowl a
a
a
N.J. Agoha , S.O. Akpavie , O.A. Durojaiye & D.F. Adene
a
a
Faculty of Veterinary Medicine , University of Ibadan , Ibadan, Nigeria Published online: 01 Nov 2011.
To cite this article: N.J. Agoha , S.O. Akpavie , O.A. Durojaiye & D.F. Adene (1992) Pathogenicity of two strains of Newcastle disease virus in the grey‐breasted helmet guinea fowl, Veterinary Quarterly, 14:2, 51-53, DOI: 10.1080/01652176.1992.9694328 To link to this article: http://dx.doi.org/10.1080/01652176.1992.9694328
PLEASE SCROLL DOWN FOR ARTICLE Taylor & Francis makes every effort to ensure the accuracy of all the information (the “Content”) contained in the publications on our platform. However, Taylor & Francis, our agents, and our licensors make no representations or warranties whatsoever as to the accuracy, completeness, or suitability for any purpose of the Content. Any opinions and views expressed in this publication are the opinions and views of the authors, and are not the views of or endorsed by Taylor & Francis. The accuracy of the Content should not be relied upon and should be independently verified with primary sources of information. Taylor and Francis shall not be liable for any losses, actions, claims, proceedings, demands, costs, expenses, damages, and other liabilities whatsoever or howsoever caused arising directly or indirectly in connection with, in relation to or arising out of the use of the Content. This article may be used for research, teaching, and private study purposes. Any substantial or systematic reproduction, redistribution, reselling, loan, sub-licensing, systematic supply, or distribution in any form to anyone is expressly forbidden. Terms & Conditions of access and use can be found at http:// www.tandfonline.com/page/terms-and-conditions
PATHOGENICITY OF TWO STRAINS OF NEWCASTLE DISEASE VIRUS IN THE GREY-BREASTED HELMET GUINEA FOWL N. J. Agoha, S. 0. Akpavie, 0. A. Durojaiye, and D. F. Adenel Veterinary Quarterly 1992; 14: 51-3
Downloaded by [Ams/Girona*barri Lib] at 00:54 02 December 2014
SUMMARY
1. Eggs and guinea fowl keets
maternal antibodies to Newcastle disease virus, were infected with Hens strain (33/56) and Kumarov strain of Newcastle disease virus intramucularly (m) or intranasally (IN). Clinical signs were first noticed four days post infection (n) in
One hundred and fifty eggs from guinea fowl hens that had not been vaccinated with Newcastle vaccines were purchased from
the group infected al but five days PI in the group infected IN with Hens strain of Newcastle disease virus. These clinical signs were
similar in both groups and included anorexia, droopiness, huddling together, greenish diarrhoea and marked cachexia. Prominent nervous signs, including spasms of the head and neck, were observed in groups infected with Hens strain. The major gross lesions observed were emaciation with prominent keel bone, empty intestinal tract and distended gall bladder in most keets. The histological lesions were characterised by meningoencephalitis, necrosis and loss of lymphocytes from splenic and lymphoid aggregates. There was muscular degeneration and necrosis in the gizzard and mild pulmonary congestion and oedema in some keets. Neither gross or microscopic lesions were observed in keels that had received the Kumarov strain.
the National Veterinary Research Institute (NVRI), Vom, Nigeria. After hatching, the guinea fowl keets were transferred to poultry cages made of wood and chicken-wire mesh, covered with polythene and heated electrically. The keets were provided with water and fed ad libitum.
2. Antibody assay At 3 weeks of age, and at the time of infection the guinea fowl keets were assayed for antibodies using the haemagglutination inhibition (HI) test.
Seronegative keets were used in the experimental infection. Antibodies to Newcastle Disease Virus (NDV) Herts and NDV Kumarov were assayed at 4 days and 2 weeks PI.
3. Newcastle disease challenge virus The NDV for the challenge was Herts 33/56 obtained from NVRI, Vom, Nigeria. It was originally obtained from Central Veterinary Laboratory, Weybridge, United Kingdom. The Kumarov strain of NDV (NDV(K)) was also obtained from
INTRODUCTION There have been extensive studies on the pathology of Newcas-
NVRI, Vom.
tle disease in the domestic chicken and turkey but not in the
4. Experimental groups The seronegative keets were divided into five groups. Each
guinea fowl, and very few reports on viral or bacterial diseases of the guinea fowl are available. However, guinea fowls are
susceptible to diseases such as fowl typhoid and Newcastle disease (2). Johnson and Anderson (7) and Moore (8) reported outbreaks of fowl typhoid in guinea fowls in the United States of America. Adewuyi et al. (1) diagnosed infectious bursal disease
(IBD) in Market guinea fowls, and Durojaiye and Adene (5) diagnosed Newcastle disease and Egg-Drop Syndrome '76 in a small flock of guinea fowls kept intensively at the University of Ibadan. The guinea fowl is native to the savannah zone of West Africa and the bird is seen mostly in the wild. At present, there is an increasing tendency to domesticate and commercialise its production. Because of the possibility of commercial production
and the fact that Newcastle disease is perhaps one of the most endemic and fatal diseases of poultry in Nigeria, this study was undertaken to determine the pathogenecity and pathology of Newcastle disease in the guinea fowl. The Herts and Kumarov strains were used in this study because one is the vaccine strain commonly used and the other, a strain commonly encountered in field outbreaks of Newcastle disease in Nigeria. I
MATERIALS AND METHODS
Thirty-five 6-week-old guinea fowl keels, seronegative for
Faculty of Veterinary Medicine, University of lbadan, lbadan, Nigeria.
51
.
group was placed in a separate cage. Group I was made up of 10 guinea keets. Each keet was infected intramuscularly with 0.5 ml of a 1:10 dilution of NDV (Herts) viral suspension in allantoic fluid. Group II had five guinea keets and each was infected intranasally with the same dose and dilution of NDV (Herts) as Group I keets. Group III had five guinea keets. They were each infected INt with 0.5 ml of a 200 dose NDV (K) vial after reconstitution with 100 ml buffered normal saline. Group IV had five guinea keets, each
of which received the same dose of NDV (K) as Group III but IN.
Group V contained 10 guinea keets which were used as controls. All keets were killed at the end of the experiment and examined.
Pathology
Tissues were obtained from the brain, lungs, liver, spleen, kidney, bursa of Fabricius, pancreas, oesophagus, crop, proventriculus, gizzard, intestine, gall bladder and sciatic nerve. These
were fixed in 10% buffered formalin for at least 24 hours, processed routinely for histopathology and stained with haematoxylin and eosin.
THEVETERI NARYQUARTERLY, VOL
1
4
,
No
.
2, APR
I
L
,
1
992
RESULTS
Clinical signs Clinical signs were first observed four days Pi in Group I keets
The gall bladder was distended with bile in 11 (73.3%) keets while 6 (40%) showed mild pulmonary congestion. One keet showed mottling of the kidney.
infected INA while clinical signs were first observed five days PI in
the group infected IN. The clinical signs were similar in both
groups and include ruffled feathers, anorexia, depression, huddling together and greenish-white faeces. Nervous signs were first noticed five days PI in Group I keets and included spasms of the head and neck, torticollis in some keets and paralysis of the extremities followed by death. Death first occurred on the sixth day PI, and it occurred in both groups I and
II. All keets in both groups were dead by the eight day pi. In Group III, two keets showed mild anorexia, depression and ruffled feathers five days Pl. These signs lasted for three days and
the keets recovered fully. No clinical signs were observed in Group IV and V. The morbidity and mortality pattern in the experimental guinea keets is shown in Table 1.
Downloaded by [Ams/Girona*barri Lib] at 00:54 02 December 2014
Table 1. Morbidity and mortality pattern in the experimental guinea keets.
No. of keets
Strain of virus used Route of
Group I
Group II
Group III
Group IV
Group V (control)
10
5
5
5
10
NDV (Herts)
NDV
NDV (K) NDV
(Herts)
IM
IN
IM
Histopathological lesions On microscopy, 10 (66.67%) keets showed pulmonary congestion and oedema which varied from mild to moderately severe. Twelve (80%) keets had brain lesions characterised by lymphocytic infiltration of the meninges, pericascular lymphocytic cuffs
and vasculitis (Fig. 1). There was vascular congestion in the cerebrum and marked spongiosis in the cerebellum of one keet (Fig. 2). The splenic lesion was characterised by necrosis and depletion of lymphocytes from the lymphoid follicles in six (40%) of the keets (Fig. 3). A few keets had liver lesions which were characterised by periportal necrosis with lymphocytic and
plasma cell infiltrates. The kidney lesion consisted of mild congestion with focal areas of lymphocytic infiltration into the
interstitium. The proventricular lesion was characterised by mild glandular degeneration with lymphocytic infiltration into the lamina propria. There was muscular degeneration and necrosis with lymphocytic and plasma cell infiltration in the gizzard.
(K) IN
infection
Morbidity (days pl)
ft
1
0
0
0
2
0
3
0 0
4
0 4
0 0 0
5
10
3
9 0
4
7 8
0
0
6
.
0
0 2
2 0 0
Mortality (days PH
0
3
0 0 0
4
0
0 0
5
0
0
1
2
6 7 8 9
0
1
9
0 0
3 1
0
o
Fig. 1. Cerebellum of a guinea keet showing severe vasculitis. Haemotoxylin and eosin staining. Magnification 750 x.
NDV = Newcastle disease virus IM = Intramusculair IN = Intransal
(K) = Kumarov PI = post infection
- PATHOLOGY
Gross lesions On post-mortem examination, lesions observed in Groups I and II keets included emaciation, with prominence of keel bones, and the pasting of the vent feathers with greenish-white faecal matter in some keets. Nine of the 15 keets (60%) had varying
quantities of feed in their crops. Four (26.6%) had catarrhal exudate in the duodenum. The intestine was virtually empty in 12 (80%) keets and the caecum was balloned in 7 (46.6%) keets.
52
Fig. 2.
Marked spongsiosis in the cerebellum of a guinea keet. Haemotoxylin and eosin staining. Magnification 465x.
THEVETERINARYQUARTERLY
,
VOL
1
4, No.
2
,
APR
I
L
,
1
992
naturally infected with NDV (2, 9) and turkeys experimentally infected with the Velogenic strain of NDV (3). The respiratory signs of dyspnoea, gasping, coughing, nasal discharge and rales often associated with Newcastle disease infection, especially in young chicks (9), were not observed.
The nervous signs such as the spasms of the head and neck, torticollis and paralysis of extremities described in chickens (9) and turkeys (3) were observed in this study. The predominance of nervous signs in this study may be associated with the fact that
the virus is essentially neurotropic, with minor effects in the digestive tract of guinea fowls. All keets that showed nervous signs died. The longer incubation period (four days as against five days) for keets infected Im and IN, respectively, may be attributed to the rapidity by which virus administered via the Im route enters the general circulation after rapid virus multiplication in tissues. The IN route of infection however exposes the virus to the natural defence mechanisms of
the respiratory tract and hence a reduction in the amount of
4,41
Antibody assay in guinea keets with NDV (Herts) and NDV (K)
virus available to produce disease. The gross pathological lesions observed were few and mild and included emaciation with prominent keel bone, mild congestion of the lungs, empty intestinal tract and distended gall bladder in some of the keets. In the chicken, however, gross lesions such as cloudy air sacs, congestion of the lungs, haemorrhages in the proventricular mucosa and/or hyperaemia of lymphoid aggregates have been described (2, 4, 6). Histologically, proventricular lesions such as congestion haemorrhage, cellular infiltration especially by mononuclear cells,
The results of the HI test using the beta procedure at four days PI was negative for all keets irrespective of virus strain and route of administration. However, two weeks pi the antibody in Groups
have been described for chickens (2, 4, 6), were not seen in this study. However, mild glandular degeneration with lymphocytic infiltration was observed in the proventriculus.
Downloaded by [Ams/Girona*barri Lib] at 00:54 02 December 2014
Fig. 3.
Necrosis and depletion of lymphocytes from the lymphoid follicles of a guinea keet's spleen. Haemotoxylin and eosin staining. Magnification 307,5x.
Maternal antibody assay Results of the antibody assay in the keets at three weeks of age showed that 7 out of 47 keets had antibodies in the 4-64 HI titre range. These keets were used for the experiment.
III and IV keets inoculated with NDV(K) showed HI titres (Table 2). Table 2. Antibody assay two weeks after infection with NDV(K).
hyperaemia and/or necrosis of lymphoid aggregates, which
The meningoencephalitis observed in this study has been described for chickens (2, 4, 6). The splenic lesions observed were those of necrosis and depletion of lymnphocytes in the splenic follicles, and were similar to those described for chickens
Bird no.
Route of infection
HI
Titre
259
IM
+
1024
281
IM
+
256
400 890 999
IM
+ + +
32
130 295
IN
419 540 880
IN
IM
IM
IN
IN IN
+ + + + +
Group mean
294
18
(2). Myocardial lesions such as degeneration and necrosis, which have been described for Newcastle disease infection in chickens (2), were not seen in the keets. However, similar lesions were seen in the gizzard. This study has established that the grey-breasted helmet guinea fowl is also susceptible to Newcastle disease, as is the domestic
32
chicken (2, 6) and turkey (3). Further work is in progress to
32
study the pathogenesis of Newcastle disease in the guinea fowl.
128 32 256 32
References
96
I. Adewuyi OA, Dojaiye OA, and Adene DF. Zentralbl Veterinar Med 1989b; 36: 43-8. Aitken I, Allan WH, Biggs RM, Gordon RF, and Jordan FTW. Newcastle disease: In Poultry Diseases. Ed RF Gordon. Balliere Tindal, London 1977: 81-94. 3. Sheikhly Al, Faud A, and Carlson HI. Pathology of Velogenic Newcastle disease virus infection in turkeys. Avian Dis 1975; 19: 397-407. 4. Brandly CA, Hanson RP. Newcastle disease: In Diseases of Poultry. Ed Biester HE and Schwarte LH. Iowa State University Press 5th. Ed 1967: 633. 5. Durojaiye OA, Adene DF. Newcastle disease and Egg Drop Syndrome '76 2,
in4 = Intramuscular IN = Intransal + = Positive HI = Haemagglutination inhibition
Controls The control group showed no clinical signs during the study period and neither gross nor microscopic lesions were observed
at post-mortem in this group. Antibodies to NDV were not detected in this group. DISCUSSION
The clinical signs observed in this study include anorexia, depression, ruffled feathers and greenish-white faeces. These
in guinea fowls Numida meleagris galeata Pallas. J Vet Med B 1988; 35: 1-3. 6.
Hanson RP. Newcastle disease. In Disease of Poultry Ed Biester HE and Schwarte LH. Iowa State University Press, 19878: 513. 7. Johnson EP, Anderson GW. An outbreak of fowl typhoid in guinea fowls. J Am Vet Med Assoc 1933; 82: 258-9. 8. Moore EN. Fowl typhoid diagnosed in guinea fowl. Poultry Sci 1946; 25: 387-8. 9.
Okaeme AN. Diseases of young helmet guine fowl under intensive management in Nigeria. Bull Anim Hlth Prod. Afr 1981; 29: 317-9.
clinical signs are similar to those observed in domestic chickens
53
THEVETER
I
NARYQUARTERLY, VOL
1
4
,
N o. 2
.
APR
I L
,
1
992
