Trichinella spiralis: Genetics of worm expulsion in inbred and F1 mice infected with different worm doses

The nematode Trichinella spiralis is rejected from the intestine at a time that is characteristic for each inbred strain of mouse. Previous work (R. G. Bell et al. 1982a) had empirically identified strong, intermediate, and weak phenotypes (NFR, $\text{C}\text{H}\text{He}$, and $\text{C57}\text{10}$ mice, respectively) in mice infected with 400 muscle larvae. It is shown that this classification applies to another eight inbred strains: SWR, $\text{DBA}\text{2}$, $\text{DBA}\text{1}$, LP, $\text{Bub}\text{Bn}$—all intermediate, and $\text{NZB}\text{BIN}$, C57L, A, and Mus molossinus—all weak. This phenotypic classification consistently applies with infections of 400–800 muscle larvae. Below doses of 300 muscle larvae, the strain designation of phenotype does not consistently apply. By this it is meant that the relative rejection rate changes for certain strains so that eventually some strains that were strong (NFR) or intermediate (AKR) responders to 400 muscle larvae become weak responders to 50 muscle larvae. Other strains increase their relative rejection time (B10 · BR, B10 · Q) while many do not change (NFS, $\text{C}\text{3}\text{Heb}\text{Fe}$, $\text{DBA}\text{2}$, $\text{DBA}\text{1}$). The phenomenon is most apparent in inbred parental strains rather than in F₁ crosses, and it represents a phenotypic variation in rejection time that is dependent on dose. It is also demonstrated that time of rejection is directly proportional to dose in all inbred and F₁ mouse strains that we have examined. Analysis of F₁ crosses shows that most have the rejection time of the strongest responding parental line, suggesting simple genetic control of strong, intermediate, and weak responses. Two F₁ crosses invalidated this theory. The $\text{DBA}\text{1}\text{×}\text{C3}\text{H}\text{He}$ (intermediate × intermediate) showed a strong response. The additive effects of parental rejection phenotype indicated that these lines could not be genetically identical for intermediate responsiveness. Similarly, the NFR (strong) × B10 · BR (weak) F₁ showed intermediate rejection, indicating partial dominance of $\text{C}\text{57}\text{B}\text{1}\text{10}$ genes over the strong responder NFR strain. Neither the primary expulsion time phenotype, phenotypic variation to low doses, or the rejection characteristics of F₁ crosses could be ascribed to genes linked to the major histocompatibility complex.