|Livestock Research for Rural Development 29 (3) 2017||Guide for preparation of papers||LRRD Newsletter||
Citation of this paper
Avian leucosis (AL) is an oncogenic disease that affects poultry caused by avian leucosis virus (ALV), an RNA virus which belongs to the genus Alpharetrovirus. This disease is worldwide in distribution and has global significance. This study, conducted between February and June 2014 was therefore carried out to ascertain the seroprevalence of AL in chicken flocks in Nairobi and surrounding Counties. This was determined by random blood sampling from 385 birds comprising indigenous, broilers and commercial layer chicken. The blood samples collected were tested for AL p27 antigen using an enzyme linked immunosorbent assay (ELISA).
One hundred and five (58.33%) indigenous chicken (12 – 96 weeks old), nineteen (18.63%) commercial layer chicken (8 – 65 weeks old) and seven (6.8%) broilers (6 – 10 weeks old) were positive for avian leucosis virus (ALV) p27 antigen; yielding an overall seropositive rate of 34.03%. Among the sampled birds, Kajiado County had the highest seroprevalence rate of 77.78% (35/45), followed by Nairobi County 52.94% (27/51), Machakos County 45.35% (39/86) and Kiambu County 14.78% (30/203).
Hence therefore, this study concludes that AL is prevalent in chicken flocks in Nairobi and surrounding Counties, with over 30% of sampled birds testing positive on ELISA. Majority of seropositive birds were indigenous.
Key words: Elisa, oncogenic, p27 antigen, poultry
Avian leucosis is an inconspicuous, but important disease of chicken (Fadly 1990). Outbreaks of AL have been reported worldwide (Payne and Nair 2012) and are a major cause of serious economic losses to the poultry industry in terms of reduced growth, uneven flock growth rates, immunosuppression and predisposition to bacterial diseases (Bagust et al 2004). It is caused by ALV, an RNA virus which belongs to the genus Alpharetrovirus; of the subfamily Orthoretrovirinae; of the family Retroviridae. Avian leucosis viruses are classified into ten subgroups; A, B, C, D, E, F, G, H, I and J; and this is based on interactions between virus-specific cell receptors, viral envelope glycoprotein, virus neutralization test, and host range (Payne 1998; Cheng et al 2010).
Subgroups A, B, C, D and J are oncogenic and exogenous (transmitted as infectious virus particles) ALVs, while subgroup E is endogenous (vertically transmitted). The other four subgroups, namely, F, G, H and I, are endogenous ALVs and occur in quails, partridges and pheasants (Payne 1992).
Avian leucosis viruses are prevalent in several breeding flocks (Payne and Nair 2012) although subgroups A, B and J are the most common ALVs occurring in commercial poultry flocks worldwide (Gao et al 2014). Subgroups C and D have rarely been reported while subgroup E is the ubiquitous endogenous leucosis virus of low pathogenicity (Adkins et al 2001). Subgroup A and J have also been isolated from broiler hybrids (Liu et al 2011). Outbreaks of subgroup J have recently been reported to affect parent and commercial layer chicken, and indigenous Chinese chicken flocks (Gao et al 2014). Cases of subgroup J outbreaks among broiler breeding flocks have also been reported in several European countries (Payne, 1998), America, Asia (Sun and Cui 2007), Africa (Egypt) (Aly 2000) and Australia (Bagust et al 2004). The ALV p27 antigen has been detected among exotic commercial layers and broilers; and the indigenous chicken of Nigeria (Sani et al 2011; 2012). In Sudan, multiple ALV subgroups have been detected among broiler parent flocks (Latif and Khalafalla 2005).
In Kenya, there is no current documented evidence on the occurrence of the disease in the country, apart from antibodies which were detected in the wildfowl, domestic chicken and man (Morgan 1967). Hence such a wide knowledge gap and scanty information on prevalence of the disease among chickens is a hindrance to the implementation of effective disease control measures in the country. Results from this study will give insights into the prevalence of the disease within Nairobi and surrounding Counties. This information will help in instituting control measures, which are useful when making objective recommendations on disease control strategies to improve the health and productivity of chicken in the country.
The study was carried out within Nairobi and surrounding Counties, which included randomly selected areas of Kiambu, Machakos and Kajiado Counties. Nairobi County is the capital city of Kenya and occupies an area of approximately 696 square kilometres. It lies between 01° 17´S latitude and 36° 48´E longitude. Nairobi has two main agroecological zones; lower highland with an altitude of between 1820 m (metres) and 2070 m above sea level and the other upper midland with an altitude of between 1200 m and 1820 m above sea level. There are two rainfall seasons in these areas. The long rainfall season is in the months of April to June, while the short rainfall season is in the months of October to December. The estimated annual rainfall is a maximum of 765 mm (millimetres) and a minimum of 36 mm. Machakos County borders Nairobi to the East, Kiambu County is adjacent to the northern border of Nairobi County, while Kajiado County borders Nairobi to the South.
Minimum sample size for the study was calculated as described by Martin et al (1987);
Where n = minimum sample size, p = prevalence rate (0.5), q= (1-p), e= precision error rate (0.05), z= 1.96
The percentage prevalence caused by this disease in chicken was calculated by dividing the total number of chicken that were diagnosed with avian leucosis by the overall number of chicken that were sampled and multiplying the answer by 100. This was done as follows:
% prevalence of avian leucosis = Total number of chicken diagnosed with avian leucosis
& Total number of chicken sampled
Seroprevalence study involved surveillance using an antigen capture (ac) ELISA kit. Lists of the flock/ farm/ abattoir establishments in the randomly selected county wards within the study area were obtained from the local veterinary and/or agricultural offices. These chicken establishments were randomly selected; and a total of 385 blood samples randomly collected from 180 indigenous chicken (12 - 96 weeks old), 103 exotic broiler chicken (6 – 10 weeks old) and 102 exotic commercial layer chicken (8 – 65 weeks old) in the study area. A total of 51, 203, 45 and 86 birds were sampled from Nairobi, Kiambu, Kajiado and Machakos Counties respectively.
Of the 385 sera samples tested, 131 (34.02%) were positive to ALV p27 antigen. Nineteen (18.63%) of 102 commercial layers’ sera tested positive, while 7 (6.8%) of 103 broiler birds’ sera were positive to ALV p27 antigen. A total of 105 (58.33%) of 180 indigenous chicken sera were positive for the ALV p27 antigen. Of the 19 commercial layer sera that were positive to ALV p27 antigen; 11 (57.90%) were weakly positive with Elisa unit values (EUs) ranging from 10% to 25%, 4 (21.05%) sera samples were moderately positive with EUs ranging from 28% to 73%, while 4 (21.05%) sera samples were strongly positive with EUs ranging from 80% to 99% (Figure 1).
Among the 7 broiler chicken sera that were positive, 6 (85.71%) were weakly positive with EUs ranging from 10% to 23%, while 1 (14.29%) serum sample was moderately positive with an EU reading of 40%. Eighty eight (83.81%) of 105 indigenous chicken sera were weakly positive with EUs ranging from 10% to 25%, 15 (14.29%) serum samples were moderately positive with EUs ranging from 26% to 37%, while 2 (1.90%) sera samples were strongly positive with EU values of 91% and 93% (Figure 1).
Among the sampled birds, Kajiado County had the highest prevalence rate of 77.78% (35/45), followed by Nairobi County 52.94% (27/51), Machakos County 45.35% (39/86) and lastly Kiambu County 14.78% (30/203) (Figure 2)).
|Figure 1. Enzyme linked immunosorbent assay unit values in seropositive chicken in Nairobi and its surrounding Counties|
|Figure 2. A graph showing counties in Nairobi and its environs from where chicken diagnosed with avian leucosis originated in the period of February to June 2014|
Results of this study showed that indigenous chicken had AL prevalence of 58.33%, as reported in other parts of the world among these birds. Sani et al (2011) reported a high prevalence of 60% among Nigerian indigenous chicken while Mohammadi et al (2008) reported a prevalence rate of 76% in Iran.
Prevalence among the exotic commercial layers was 18.63% similar to 18.33% reported by Sani et al (2012) in commercial layers in Zaria and its environs in Nigeria. A prevalence of 6.8% in broiler chicken was found in this study which is slightly higher than 4.7% and 1.25% in Nigeria reported by Sani et al (2011) and Olabode et al (2009) respectively; and 3.33% in Iran by Mohammadi et al (2008). The high prevalence rate in indigenous chicken compared to other chicken can be attributed to the free range management system which exposes them more, to infectious agents than other chicken raised under the intensive system of management (Bebora et al 2005).
Age is also a factor that contributed to higher prevalence rates among indigenous chicken (12 - 96 weeks old) compared to both commercial layers (8 - 65 weeks) and broilers (6 – 10 weeks); and commercial layers compared to broilers. Higher prevalence rate could probably been due to longer exposure to the virus by older birds, which allows ample time for viral multiplication and establishment in the birds. These findings agree with Wu et al (2010) who reported higher ALV detection rates in old chicken. Kenyan indigenous chicken could be potential reservoirs and sources of contamination of the environment and spread of ALV and need to be targeted in control of the disease.
Avian leucosis infection in broilers could probably be due to vertical transmission, unlike indigenous and commercial layers whose infection could mainly be both vertical and horizontal transmission, and this could be attributed to age and life span of these birds.
Among ALV positive EU values of birds; broilers had 85.71% weak and 14.29% moderate; commercial layers had 57.90% weak and 21.05% moderate; and indigenous had 83.81% weak and 14.29% moderately positive birds. This is comparable to Sani et al (2011) who reported 92.86% weak and 7.14% moderate in broilers; and weak positives in commercial layers (Sani et al 2012).
In this study, higher levels (strongly positive) of p27 antigen levels were found in both commercial layers (80% to 99%) and indigenous chicken (91% to 93%) unlike reports by Sani et al (2011, 2012). However, Emikpe et al (2007) found 18.75% of sera from indigenous chicken in Nigeria being strongly positive to ALV p27 antigen. Higher than 25% EU levels found among the commercial layers and indigenous chicken in this study, could be an indication of repeated exposure to ALVs. This repeated exposure can either be through contact exposure with congenitally infected hatch mates or a contaminated environment/ formites (Aden, 1983). Wide range of antigen titre levels got from this study (10% - 99%), may also suggest differences in exposure time spans and exposure dose of the ALVs (Emikpe et al 22007).
The study showed that:
The authors declare that they have no competing interests.
The authors would like to thank the Department of Veterinary Pathology, Microbiology, and Parasitology; Department of Public Health, Pharmacology and Toxicology; Faculty of Veterinary Medicine, University of Nairobi; Director of Veterinary Services, Kenya, Dr. Kisa Juma Ngeiywa; and technical staff at VPMP and PHPT. Special gratitude goes to Mr. Kennedy Onguny for financial facilitation of the project. We thank Affini-Tech Limited, USA for donating the ELISA kit used in this study; and Prof. Philip Kitala, Prof. George Gitau, Dr. Jared Serem and Mrs. Dorcas Nduati for their statistical advice and assistance. Many thanks to the livestock production and veterinary officers, local guides and poultry farmers in the various sub - Counties and County wards visited for their cooperation and making it easy to access farms for sample collection.
Aden D F 1983 Serological survey of Marek’s disease in exotic and local chicken in Nigeria, Tropical Veterinarian, 1:138-140.
Adkins H B, Blacklow S C and Young J A 2001 Two functionally distinct forms of a retroviral receptor explain the nonreciprocal receptor interference among subgroups B, D and E avian leukosis viruses. Journal of Virology, 75: 3520–3526.
Aly M M 2000 Isolation of a subgroup J-like avian leukosis virus associated with myeloid leukosis in meat-type chicken in Egypt. Proceedings of International Symposium on ALV-J and Other Avian Retroviruse, Rauischholzhauzen, Germany, pp 165-176.
Bagust T J, Fenton S P and Reddy M R 2004 Detection of subgroup J avian leukosis virus infection in Australian meat-type chicken, Australian Veterinary Journal, 82:701–706.
Bebora L C , Mbuthia P G, Macharia J M, Mwaniki G, Njagi L W and Nyaga P N 2005 Appraisal of Indigenous chicken’s potential in egg production. The Kenya Veterinarian, 29: 10-13.
Cheng Z, Liu J, Cui Z and Zhang L 2010 Tumors associated with avian leukosis virus subgroup J in layer hens of during 2007 to 2009 in China. Journal of Veterinary Medical Science , 72:1027–1033.
Emikpe B O, Oladele O A, Oluwayelu D O, Adene D F, Ohore O G and Bolarinwa A B 2007 Detection of avian leukosis virus P27 antigen in Nigeria indigenous chicken. Journal of Animal and Veterinary Advances, 6: 36-38.
Gao Q, Yun B, Wang Q, Jiang L, Zhu H, Gao Y and Gao, Y 2014 Development and Application of a Multiplex PCR Method for Rapid Differential Detection of Subgroup A, B and J Avian Leukosis Viruses. Journal of Clinical Microbiology, 52: 37-44.
Fadly A M 1990 Leukosis and sarcomas. In: Purchase HG, Arp LH, Domermuth CH, Pearson JE (eds), Isolation and Identification of Avian Pathogens, 3rd ed. Kendall/Hunt Publishing Dubuque, I. A. pp. 135-142.
Latif M M and Khalafalla A I 2005 Detection by PCR of multiple subgroups of avian leukosis virus in broilers in the Sudan. Journal of Animal and Veterinary Advances, 4: 407-413.
Liu S, Wang B, Zhang Z, Wang J, Sun S and Cui Z 2011 The separation of subgroup A and J ALV in soft tissue sarcomas of “817” broiler hybrids. Chinese Journal of Animal and Veterinary Sciences, 3:012.
Martin S W, Meek A H and Willeberg P 1987 Veterinary Epidemiology. Principles and Methods. Iowa State University Press, Ames, p. 32.
Mohammadi A, Masoudian K and Bozorgchami B 2008 Detection of avian leukosis virus (ALV) in albumen of Shiraz commercial and local layer flocks using ELISA and RT-PCR. Iranian Journal of Veterinary Research, 9:24.
Morgan H R 1967 Antibodies for Rous sarcoma virus (Bryan) in fowl, animal, and human populations of East Africa. II. Antibodies in domestic chicken, wildfowl, primates, and man in Kenya, and antibodies for Burkitt lymphoma cells in man. Journal of the National Cancer Institute, 39: 1229-1234.
Olabode H O K, Jwander L D, Moses G D, Ighodalo E and Egbaidomeh S A 2009 Prevalance of avian leukosis and mareks disease in Ilorin, Kwara state, Nigeria. Nigerian Veterinary Journal, 30: 64-68.
Payne L N and Nair V 2012 The long view: 40 years of avian leukosis research. Avian Pathology, 41: 11-19.
Payne L N 1992 Biology of avian retroviruses. The retroviridae, 1: (299-404).
Payne L N 1998 Retrovirus-induced disease in poultry. Poultry Science, 77:1204-1212.
Sani N A, Oladele S B, Raji M A and Ibrahim N D G 2012 Seroprevalence of avian leukosis virus antigen using ELISA technique in commercial exotic-layer chicken in Zaria and its environs. African Journal of Microbiology Research, 6: 4438-4442.
Sani N A, Oladele S B, Raji M A and Ibrahim N D G 2011 Seroprevalence of avian leukosis virus antigen using ELISA technique in exotic broilers and Nigerian local chicken in Zaria, Nigeria. Veterinary World, 4: 345-348.
Sun S and Cui Z 2007 Epidemiological and pathological studies of subgroup J avian leukosis virus infections in Chinese local “yellow” chicken. Avian Pathology, 36:221–226.
Wu X, Qian K, Qin A, Shen H, Wang P, Jin W and Eltahir Y M 2010 Recombinant avian leukosis viruses of subgroup J isolated from field infected commercial layer chicken with hemangioma and myeloid leukosis possess an insertion in the E element . Veterinary Research Communications, 34: 619–632.
Received 16 July 2016; Accepted 3 November 2016; Published 1 March 2017
Go to top