Epidemiology

About 2000 Eimeria spp. have been described so far in mammalian, avian, reptilian, and other vertebrates as well as in invertebrate hosts (Megía-Palma et al. 2015). Following the distribution of their host, Eimeria sp. are ubiquitously distributed all over the world. Besides wildlife species, Eimeria spp. infect all major livestock species such as ruminants, pig, chicken, and other poultry. In Table 3.2 the economically important pathogenic Eimeria spp. in avian and mammalian hosts are shown. In general, Eimeria species are homoxenous—i.e., they infect one defined host species. One explanation for the narrow host range of Eimeria compared to other apicomplexans such as Toxoplasma or Cryptosporidium may be their comparatively small repertoire of microneme proteins. As these proteins are essential for host cell recognition, a small number of specific microneme proteins may translate into a limited recognition of host cell types (Cowper et al. 2012). However, it has also been proposed that host specificity of Eimeria is rather an adaptive phenomenon than a co-phylogenetic determination (Kvičerová and Hypša 2013). Interestingly, a limited oligoxenous host range has been observed in some avian Eimeria spp. a characteristic that may contribute to parasite distribution by wildlife and livestock cross-infection (Vrba and Pakandl 2015). The usually observed homoxenous transmission limits the spread of the infection in an ecosystem or between different species within a mixed population. Nonetheless, since the infection dose is low—the ingestion of a single oocyst may establish an infection—the infection rate is commonly high in a given population of susceptible naïve hosts in a contaminated area or stable. However, the presence of pathogenic Eimeria spp. on a farm does not necessarily translate into clinical outbreaks in a herd or flock. Natural trickle infections—the repeated uptakes of low oocyst doses— are common in the field inducing protective immunity and endemic stability (Daugschies and Najdrowski 2005). The shift from a subclinical to a clinical infection is thought to be induced by additional factors such as malnutrition and/or concurrent diseases that undermine the animal health status. Except for porcine and some chicken-specific Eimeria spp., young animals are at highest risk to develop clinically relevant infections. This observation is rather due to the lack of immunity in younger and not to an age-specific resistance in older animals. Susceptibility to the infection is also genetically determined, as it has been shown to be dependent on the breed (Reeg et al. 2005; Passafaro et al. 2015). Accordingly, it has been reported that chicken breeds with an efficient innate immune response are less susceptible to Eimeria infections (Swaggerty et al. 2011). Eimeriosis is a herd or flock disease building up over several infection cycles within a group of animals. Spreading within a herd or flock may occur within several days—e.g., chicken—or weeks, e.g., cattle. On endemic farms, on-site prevalences of up to 100% have been observed in susceptible populations (Matjila and Penzhorn 2002). In the environment, unsporulated Eimeria oocysts develop quickly into the infective sporulated oocyst at favorable moisture and temperatures of about