A description of village chicken production systems and prevalence of gastrointestinal parasites

Get Complete Project Material File(s) Now! »

Chapter 2: Literature review

Introduction

It is estimated that up to 70% of poultry products in the developing world are produced by resource-limited farmers and in family-managed poultry systems, of which 80% are found in rural areas under scavenging system (GuÈye, 1998; Branckaert et al., 2000). The scavenging production system predisposes the chickens to diseases and parasites especially helminthes (Swatson et al., 2003; Acamovic et al., 2005; Mungube et al., 2008). Various drugs for controlling parasites and treating diseases of chickens have been effectively developed and applied globally (Maphosa et al., 2004). However, rural farmers often does not use commercial drugs due to poor access, driven by geographic distance between suppliers and rural communities, limited veterinary extension services and the costly prices of these veterinary drugs (Mwale & Masika, 2009; Nyoni & Masika, 2012). Continued and improper use of veterinary drugs is also discouraged because of the residual effects of drugs in meat products and parasite developing resistance to drugs. Genetic control strategies are a more sustainable disease management strategy particularly for smallholder farmers that have limited resources (Lamont, 1998). Characterisation of parasitic pathogens as well as the host response to infection are crucial to the development of alternative control strategies, such as breeding of resistant host of development of protective vaccines. This study aims at characterising village chicken production systems and the role that village chickens play in communities. This chapter also includes a review on literature with regards to opportunities and challenges of applying genomics and transcriptomics in studying genetic diversity in village chicken populations.

Village chicken production systems

The distribution and characteristics of village chickens

There are approximately 21 billion poultry existing worldwide (FAOSTAT, 2014). Some 1.8 billion chickens are found on the African continent with a total of 200 million found in South Africa (FAOSTAT, 2014), kept by commercial and smallholder farmers. Although other poultry species which include ducks, turkeys, guinea fowl, quail and pigeons are important, village chickens are the most important and major poultry species bred for food security (Acamovic et al., 2005). Village chickens are commonly reared in the rural communities of South Africa under extensive systems of production (Swatson et al., 2001; van Marle-Köster et al., 2008; Mtileni et al., 2009; Mukaratirwa & Khumalo, 2010; Nyoni & Masika, 2012). Previous genetic diversity studies on South African village chickens suggested that village chicken populations hold valuable genetic diversity (van Marle-Köster et al., 2008; Mtileni et al., 2011b; Khanyile et al., 2015) that have been developed over many years, and survived successfully under extreme and unusual environmental conditions. These studies revealed a high level of genetic variation within and among the village chicken populations and identified maternal origins of South African chicken populations. Furthermore, the studies indicated that village chickens contribute genetic variation that is distinct from diversity exhibited by commercial and specialized chicken populations. Mtileni et al. (2011a) reported that the South African conserved and field chicken populations share some ancestral maternal lineages, which suggests that these populations could be from the same maternal lineages.

Characteristics of village chicken production systems

Village chickens are also known as rural, backyard, indigenous, scavenging, traditional, local, native or family chickens (Sonaiya, 2000; Permin et al., 2002; McAinsh et al., 2004; Oka et al., 2007; Moreki, 2010). These chickens are often left to scavenge for their feed and water around the homestead and in the fields after crop harvests for an average of 5 to 11.0 h per day between 5am-6pm (Maphosa et al., 2004). Some village chickens are then confined at night or left to sleep on trees or bushes (Maphosa et al., 2004). In some production systems, the chickens are occasionally supplied with feed supplements (Maphosa et al., 2004; Moreki, 2010) that ranges from yellow maize, kitchen wastes, cracked grains, maize bran, sunflower cake, grower’s mash for chicks and/or wheat (Muchadeyi et al., 2004; Nyoni & Masika, 2012). This production system is characterized by substandard management, lack of adequate nutrition, low production performance, slow growth rate, late sexual maturity (Gondwe & Wolly, 2007; Phiri et al., 2007; Mapiye et al., 2008; Nyoni & Masika, 2012) and to high mortality (Mungube et al., 2008). Their mean annual egg production is estimated at around 60 small eggs (Sørensen, 2010). The low productivity of indigenous chickens expressed in terms of egg production, egg size, growth and survivability of chicks kept under traditional production system could be attributed to incidence of diseases and predation, lack of genetic improvement and management factors (Sonaiya, 2000; Mengesha et al., 2008). In the village chicken production system chickens are exposed to the extreme environmental conditions that negatively influence production. The environmental conditions play a selective role (natural selection) in the village chicken population by eliminating animals that cannot utilize poor quality feeds and those that are susceptible to diseases (Ekue et al., 2006; Mtileni et al., 2009). Genotypes that are adapted to the environment and are able to make use of the available feed and those that can resist disease will be able to survive in such extreme environments.
It is proposed reported that there is constant disease pressure on scavenging chickens, due to the different ages mixed in a flock and possible disease transfer from wild birds as well as other poultry species that use the same land (Acamovic et al., 2005). Parasitism ranks high among factors that threaten village chicken production (Muchadeyi et al., 2007). As chickens get exposed to parasites during scavenging, parasitic infections are ubiquitous and high infection loads have been reported resulting in clinical disease (Oniye et al., 2000). Due to minimum intervention provided by resource-limited farmers, relatively high mortality are experienced.
Village chickens are mainly used for household consumption (Sonaiya et al., 1999; Nyoni & Masika, 2012) and plays a role in traditional ceremonies and festivals (Mtileni et al., 2009). Chicken meat and eggs provide animal protein to man and can give extra cash income when sold at the market (Kalita et al., 2004; McAinsh et al., 2004; Njenga, 2005; Nyoni & Masika, 2012). Cocks are also used as alarm clocks in the villages (Kusina & Kusina, 1999). Another important role of village chickens is the provision of manure (Nyoni & Masika, 2012). Fifteen adult chickens produce about 1.0-1.2kg of manure per day (Aini, 1990). Manure from chickens is applied in vegetable gardens, and is regarded to be of high value for vegetables in comparison to other manure obtained from goats or cattle (Maphosa et al., 2004; Muchadeyi et al., 2004). Chickens are also useful in the control of weeds when they graze young grass and other vegetation. Chickens are therefore an important component in integrated farming systems (Barua & Yoshimura, 1997; Birech, 2002).

Challenges to village chicken production systems

There are a number of factors affecting village chicken production. Poor nutrition due to lack of supplementation is a major challenge to scavenging chickens. Chickens are left to scavenge to meet their nutritional needs (Muchadeyi et al., 2004; Mwale & Masika, 2011). In event of supplementation, it is often thrown onto the ground further exposing chickens to internal parasites (Nyoni & Masika, 2012). Supplementary feed are mainly based on the farmers’ judgment (Mapiye et al., 2008; Nyoni & Masika, 2012) and not the nutritional requirements of chickens and tent to vary from household to household. In a 2012 study, supplementary feed was reported to range from as little as one handful (approximately 100 g) of yellow maize grain to about five handfuls (approximately 500 g) per day (Nyoni & Masika, 2012).  Parasitism ranks high amongst the factors affecting the health of village chickens, due to existence of conditions such as inadequate hygiene and rainfall, humidity, ambient temperature and compromised biosecurity (Smyth, 1976; Swatson et al., 2003). The prevalence of gastrointestinal parasites in village fowls have been studied in different countries (Njunga, 2003; Bowdridge, 2009; Kaufmann, 2011) and to a lesser extent in South Africa (Mwale & Masika, 2011). Different species of endo-parasites have been identified such as A. galli and H. gallinarum (Ssenyonga, 1982; Poulsen et al., 2000; Permin et al., 2002; Muhairwa et al., 2007). Poultry endo-parasites of economic importance include Eimeria species and helminthes (Norton & Ruff, 2003). Ascaridia galli, Capillaria spp. and H. gallinarum are the most commonly encountered helminthic species (Permin et al., 1999; Irungu et al., 2004b; Kaufmann & Gauly, 2009). Heavy A. galli infections may obstruct the small intestine and cause mortality (Ramadan & Znada, 1991) and have been associated with reductions in egg production in laying hens and in overall growth in chickens (Soulsby, 1982; Ramadan & Znada, 1991). Parasites can lead to secondary infections (Okulewicz & Złotorzycka, 1985; Chadfield et al., 2001; Dahl et al., 2002; Permin et al., 2006) and transmit diseases like histomoniasis, cestodosis and ascariodiosis (Soulsby, 1982; Fatihu et al., 1990). Ascaridia galli may also play a role in transmission of Salmonella infections (Chadfield et al., 2001; Eigaard et al., 2006).

READ  Studies focused on HR Practices linked to business success

Parasite infection in village chickens

Classification of A. galli parasite and A. galli infections in village chickens

Ascaridia galli (Schrank, 1788, Freeborn, 1923 (synonyms A. lineata Schneider, 1866; A. perspicillus Rudol- phi, 1803) is a common parasitic nematode found in domestic and a number of wild fowl and shows a worldwide distribution (Permin et al., 1999; Magwisha et al., 2002; Marín-Gómez & Benavides-Montaño, 2007; Luna-Olivares et al., 2012). This parasite is classified under the group of ascarid worms (phylum Nematoda; Class Secernentia; order Ascaridida; family Ascaridiidae). The A. galli populations in Denmark and Sweden are reported to be sub-structured according to farms and geographical areas, with the genetic differentiation of populations contained within individual hens (Gasbarre et al., 2001). A previous study that sequenced A. galli, A. columbae and Ascaridia spp. (GHL-2012) reported this species share an identical arrangement of mitochondria (mt) genes that differ significantly from other nematodes (Alvarez et al., 2008). A separate study that looked at the phylogenetic relationships of these two species, observed A. galli and A. columbae grouping separately from other nematodes (Mair et al., 2004). A study by Li et al. (2011b) investigated phylogenetic relationships of nematodes classified in the Ascaridoidea using a total evidence parsimony analysis of a combination of morphology and one mitochondrial and two nuclear genes. Findings from this study indicated that Ascaris lumbricoides and Ascaris suum are sister taxa that share a most recent common ancestor with Parascaris equorum, which is a large ascarid affecting horses (Li et al. (2011b).
Ascaridia galli is prevalent in chickens, turkey, geese, guinea fowl and a number of wild birds but chickens are the primary host. Of all the nematodes of poultry, A. galli is known to be the largest (51-116 mm) and most pathogenic (Kates & Colglazier, 1970; Kawai & Akira, 2001; Lacy & Stow, 2011) and its predilection site being the small intestine (Soulsby, 1982). Reports from Denmark and other European countries showed that the majority of chickens kept in freerange systems are infected with A. galli (Permin et al., 1999; Jansson et al., 2010; Kaufmann, 2011). Infection with A. galli may directly contribute to economic losses due to weight loss, reduced growth rates and decreased egg production (Permin & Ranvig, 2001; Permin et al., 2006). Mortality has also been observed in severe cases (Permin et al., 2006). In addition, A galli damages the intestinal mucosa, which results in blood loss and compromised immunity leading to secondary infections (Permin et al., 1999). High infection loads of this parasite result in the blockage of the small intestines, which at to mortality (Ramadan & Znada, 1991; Permin et al., 2006). Symptoms of heavily infected chickens include droopiness of wings, bleaching of the head, ruffled feathers, emaciation and diarrhea that might be accompanied by anemia and intestinal obstruction in very heavy infections (Ackert & Herrick, 1928)

The life cycle of A. galli

The life cycle of A. galli is illustrated in Figure 1.1. Eggs are passed with the faeces of the host, where they develop outside the host animal. These reach the infective stage (L3) after 10 to 20 days (depending on temperature and relative humidity), (Ackert, 1931; Riedel, 1947; Reid & Carmon, 1958; Reid, 1960). For the eggs to proceed into the infective stage, a minimum of five days at 32-34°C is required when the eggs are incubated in water (Reid, 1960). The eggs may not survive after 22 hours at temperatures between -12°C to -8°C, (Ackert, 1931), but can however, survive a winter with moderate frost (Cruthers et al., 1974). Temperatures above 43°C are lethal for eggs at all stages (Ackert, 1931; Reid, 1960). In deep litter systems, eggs probably can remain infective for years depending on the temperature, humidity, pH and ammonium concentration (Hansen et al., 1953; Koutz, 1953; Reid, 1960; Cruthers et al., 1974; Matter & Oester, 1989).
The life cycle of A. galli is completed when the infective eggs (a) are ingested by new hosts through contaminated feed or water. The eggs containing the infective L3-larvae stage are mechanically transported to the duodenum (b). The larvae are protected by the three layers covering the eggs until they reach the duodenum or jejunum, where they hatch within 24 hours (Tugwell & Ackert, 1952; Soulsby, 1982; Kaufmann, 1996; Idi, 2004). The larvae will embed themselves into the mucosal layer of the intestine (c) (Herd & McNaught, 1975; Luna-Olivares et al., 2012). During hatching the mature coiled larvae protrude the anterior end of the egg through an opening in the shell moving out to the lumen of the intestine (d) (Ackert, 1931; (Ferdushy et al., 2013). The larvae then enter the histotropic phase where they embed themselves into the mucosal layer of the intestine (e) (Permin & Hansen, 1998). Thereafter, the larvae will mature in the lumen and be passed with the faeces of the host (f) (Anderson, 1992; Chadfield et al., 2001; Idi, 2004).

Acknowledgements 
Abstract 
Thesis outputs 
List of tables 
List of figures
List of abbreviations
Chapter 1 General introduction 
1.1. Background
1.2. Problem statement and justification
1.3. Aim and objectives
1.4. Thesis organization
Chapter 2 Literature review 
2.1. Introduction
2.2. Village chicken production systems
2.3. Parasite infection in village chickens
2.4. Disease and parasite control strategies in chickens
2.5. Transcriptome analysis technologies
2.6. Conclusion
2.7. References
Chapter 3:A description of village chicken production systems and prevalence of gastrointestinal parasites in low input chicken farming systems of Limpopo and KwaZulu-Natal provinces of South Africa 
Abstract
3.1. Introduction
3.2. Materials and methods
3.3. Results
3.4. Discussions
3.5. Conclusion
Chapter 4:Population genetic structure of Ascaridia galli from extensively raised chickens of South Africa inferred using cytochrome c oxidase subunit 1 gene 
4.1. Background
4.2. Methods
4.3. Results and discussion
Chapter 5:Transcriptome analysis of the small intestine of village chickens from Ascaridia galli infected environment 
Abstract
5.1. Introduction
5.2. Materials and Methods
5.3. Results
5.4. Discussion
5.5. Conclusion
Chapter 6  Critical review and discussion 
6.1. Critical review and discussion
6.2. Future studies
6.3. Conclusions
6.4. References
Chapter 7 Addendum 
GET THE COMPLETE PROJECT

Related Posts