Eimeria Falciformis BayerHaberkorn1970 and Novel Wild Derived Isolates from House Mice: Differences in Parasite Lifecycle, Pathogenicity and Host Immune Reactions

Species of Eimeria (Apicomplexa:Coccidia) differ in the timing of lifecycle progression and resulting infections vary in host immune reactions and pathology they induce. Eimeria infections in house mice are used as models for basic immunology and the most commonly used isolates have been passaged in laboratory mice for over 50 years. We questioned in how far such isolates are still representative for infections in natural systems. In the current study, we address this question by comparing the “laboratory isolate” E. falciformis BayerHaberkorn1970 with a novel, wild derived isolate E. falciformis Brandenburg88, and contrast this with another novel wild derived isolate, E. ferrisi Brandenburg64. We compare parasite lifecycle progression. We relate this to immune cell infiltration at the site of infection (in the caecum) and cytokine gene expression in the spleen as a measure of host immune response. We assess host weight loss as a measure of pathogenicity. A species-specific slower parasite lifecyle progression and higher pathogenicity are observed for E. falciformis vs. E. ferrisi. Host cytokines, in contrast, are expressed at significantly higher level in the spleen of mice infected with the E. falciformis laboratory isolate than in both wild derived isolates, irrespective of the species. Differences in histopathology are observable between all three isolates: The E. falciformis BayerHaberkorn1970 laboratory isolate induces the strongest inflammation and cellular infiltration (with lymphocytes, plasma cells and eosinophilic granulocytes) followed by the wild derived E. falciformis Brandenburg88 isolate. E. ferrisi Brandenburg64 is inducing milder histological changes than both E. falciformis isolates. It can be speculated that the serial passaging of E. falciformis BayerHaberkorn1970 has resulted in evolutionary divergence rendering this isolate more virulent in NMRI mice. Caution is needed when findings from experimental infection with laboratory strains should be integrated with observations in natural systems. Highlights E. ferrisi has a shorter pre-patency than wild-derived and laboratory isolates of E. falciformis. E. ferrisi is less virulent than both E. falciformis isolates and the timing of maximal oocyst shedding relative to host weight loss differs. The laboratory strain of E. falciformis induces stronger cytokine expression in the spleen than both wild derived strains of E. falciformis and E. ferrisi. The laboratory strain of E. falciformis induces stronger tissue infiltration of immune cells than the wild-derived strain. E. ferrisi infections are associated with the lowest infiltration.