History of Avian Medicine in the United States. X. Control of Coccidiosis

Introduced and Native Congeners Use Different Resource Allocation Strategies to Maintain Performance during Infection

“…Prior to the experiment, birds were medicated with sulfadimethoxine, an anticoccidial and antibiotic drug, used as directed by the manufacturer for poultry, dissolved at a concentration of ∼0.05% in the drinking water and provided continuously except where noted below. Infections are not cleared by sulfadimethoxine (Brawner et al 2000); rather, the drug inhibits the first, asexual stage of coccidia replication in the host (Reid 1990). As such, sulfadimethoxine blocks the costs associated with acute infection and any further increases in burden as a result of parasite exposure during captivity.…”

The long view: a selective review of 40 years of coccidiosis research

“…The success of monensin, comprehensively reviewed by Chapman et al (2010), was almost instantaneous and prompted the discovery of other ionophores within Eli Lilly and Company and elsewhere, and, perversely, probably contributed to the longer-term demise of coccidiosis research within the commercial sector because a ''blockbuster'' anticoccidial drug became the ''norm'' and nothing less than another de novo blockbuster was likely to be considered a viable proposition. Three further new anticoccidial drugs were introduced in the 1970s*namely, Robenidine, Statyl and Lasalocid (the latter being an ionophore)*and the reader is referred to the timeline in the review by Reid (1990) for the history of the control of coccidiosis. The last new anticoccidial drug (of any class) was introduced in 1989 and, where research impinges on the identification of new chemotherapeutic leads, a critical early question is still ''How might the performance of any new compound compare with that of the ionophores?…”

Use of live vaccines for coccidiosis control in replacement layer pullets

“…Unlike many pathogens, the severity of coccidiosis in immunologically naïve birds is directly related to the number of infective stages that are ingested; oocysts ingested in the thousands produce overt clinical signs in immunologically naïve birds, whereas oocysts ingested in the hundreds may produce only subclinical infections [20]. The relationship between number of oocysts ingested and the resulting severity of infection occurs because Eimeria species produce self-limiting infections with a genetically predetermined number of asexual, pathogenic cycles.…”

“…even in the latter case where no disease is evident, coccidiasis has been shown to have an overall energy cost to the growing chicken [23]. Clinical coccidiosis can be displayed in birds housed in close confinement because oocysts may be concentrated in a small area; conversely, subclinical coccidiosis is usually associated with free-range-managed flocks because oocysts may be spread out, decreasing the potential of the definitive host to ingest large numbers of infective oocysts [20]. each oocyst ingested has the potential to give rise to hundreds of thousands of oocysts within the feces after endogenous development; nevertheless, reproductive potential varies depending on the species, quantity of oocysts in the inoculum, level of immunity, and environmental conditions [24,25].…”

“…Repeated reinfections can occur through ingestion of oocysts shed into the environment in the feces ("cycling") [26]. if cycling is prevented, then upon cessation of the asexual phase, multiplication and oocyst production will cease and the bird is no longer infected or affected by the parasite [20]. Additionally, infection with Eimeria may suppress host immune responses to pathogenic antigens, making the host vulnerable to other diseases as well as infection with other strains and species of Eimeria [26].…”