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    Lastly, the RDT is not specifically designed for cattle, thus has the potential to detect T. congolense or T. vivax infection in any susceptible species. Therefore, if the RDT shows satisfactory accuracy in field tests, this versatility implies that the test could also be used as an epidemiological tool.Funding statement and conflict of interestAcknowledgementsWe are grateful to the Global Alliance for Veterinary Medicines (GALVmed) for making available sera collected in the course of the various projects they sponsored. Our thanks go to the following people: Z. Benglay, L. Lomille, H. Vitouley, Y. Memel, H. Sakande (CIRDES); C. Cordell and H. Erasmus (ClinVet); Edith Authié (ex-ILRI), for providing sera from cattle infected with T. congolense and T. vivax; N. Matsinhe and G. M. Pascoal (CB-UEM) for technical assistance.IntroductionMany studies have shown that maternal AP20187 are the primary means of protection against infection in very young chickens (Jungherr and Terrell, 1948; Kowalczyk et al., 1985; Mockett et al., 1987; Heller et al., 1990; Mondal and Naqi, 2001; Akhter, 2003; Hamal et al., 2006; Gharaibeh et al., 2008). Transferring maternally derived antibodies from an immune individual to a non-immune individual via egg yolk confers passive immunity in the recipient (Brambell, 1970). There are three principal classes of homologous antibodies, IgM, IgG (IgY) and IgA to the corresponding mammalian isotypes, and in birds, IgY is found predominantly in the egg yolks rather than the egg white (Leslie and Clem, 1969; Kincade and Cooper, 1973; Dahan et al., 1983; Sharma, 1997; Härtle et al., 2014).The number of poultry farms with outdoor access, based on consumer demand (Gauly et al., 2002) and the European regulations for laying hens (Anonymous, 1999), has increased. Thus, the roundworm Ascaridia galli, is becoming one of the most abundant gastrointestinal nematodes (Permin et al., 1999; Chadfield et al., 2001; Idi et al., 2004; Pleidrup et al., 2014; Wongrak et al., 2014). A. galli has direct adverse effects on chicken performance (Ramadan and Abou Znada, 1991; Daş et al., 2010; Das et al., 2012), and can lead to economic losses (Gauly et al., 2005; Daş et al., 2010; Andersen et al., 2013) and increase the susceptibility of chickens to secondary infections (Dahl et al., 2002; Permin et al., 2006). Disinfection and pharmaceuticals are expensive (Gauly et al., 2001). A. galli has been controlled mainly by synthetic anthelmintics (Tarbiat et al., 2016). Financial costs, potential anthelmintic underdosing (Bettridge et al., 2014), future anthelmintic resistance (Johnston et al., 2012) and potential anthelmintic residues in food products (Bovenhuis et al., 2002) have led to the need to develop an inexpensive and environmentally friendly method of protecting offspring against A. galli. Parasite collagen-based cuticles with carbohydrate-rich surface-coated bodies (Fetterer and Rhoads, 1993), as well as the ability to change antigenic surfaces by moulting several times throughout the development cycle (Blaxter et al., 1992), play a dominant role in how parasitic worms evade by the host innate immune system (De Veer et al., 2007). There are few studies describing naturally acquired immunity against A. galli (Bovenhuis et al., 2002).Chickens experimentally infected with A. galli eggs develop both cellular and humoral immunity by secreting Th2-type cytokines and IgY, respectively (Degen et al., 2005; Marcos-Atxutegi et al., 2009; Schwarz et al., 2011). Maternal IgY antibodies can be transferred to progeny via the egg yolk (Marcos-Atxutegi et al., 2009); ovarian follicles, yolk sac membranes, and oviduct secretions are the main transfer paths (Kramer and Cho, 1970; Rose et al., 1974; Dohms et al., 1978; Loeken and Roth, 1983; Sharma, 1997; Grindstaff et al., 2003; West et al., 2004). A. galli infection can induce an humoral immune response in the host (Edgar, 1971), but this response may not be protective (Andersen et al., 2013; Norup et al., 2013). As far as we know, no studies have been conducted to identify passive immunity to A. galli in chickens. Thus, the aim of this study was to investigate whether maternal antibody positive (mab+) chicks are better able to resist A. galli infection than maternal antibody negative (mab−) chicks.