Infection of Drosophila melanogaster by Tubulinosema kingi: Stage-specific susceptibility and within-host proliferation

EXPERIMENTAL EVOLUTION SHOWSDROSOPHILA MELANOGASTERRESISTANCE TO A MICROSPORIDIAN PATHOGEN HAS FITNESS COSTS

“…The additive genetic variation and the response to selection we observed to a microsporidian challenge was modest, more akin to the fungal and bacterial cases than the parasitoid. Unfortunately we know very little about the natural history of T. kingi that has chiefly been studied as an adventitious pathogen of laboratory Drosophila populations (Armstrong et al 1986; Armstrong and Bass 1989b; Futerman et al 2006; Vijendravarma et al 2008). Similarly, we know very little about the extent to which D. melanogaster is attacked by T. kingi or other species of Microsporidia in the field– a small‐scale field study our group conducted in Southern England (Futerman et al 2006) failed to find Microsporidia in the local wild species of Drosophila .…”

“…They observed 59 genes that were upregulated after microsporidian but not bacterial infection, although most of the genes were of unknown function and included no antimicrobial peptides nor components of the signaling cascades that regulate them. Note that this study involved feeding microsporidian spores to adult flies, whereas infection of larvae by eating medium contaminated by infected adult cadavers appears to be the more normal transmission route (Vijendravarma et al 2008). A proteomic study of Aedes mosquitoes attacked by the Microsporidian Vavraia culicis did find antimicrobial peptides to be upregulated, although could not exclude secondary infection by other micro‐organisms as a possible cause (Biron et al 2005).…”

“…Molecular and ultrastructural studies (Franzen et al 2006) showed it to belong to the genus Tubulinosema and although the original description (Kramer 1964) omits some details it is almost certainly conspecific with Tubulinosema kingi which was described from Drosophila . Aspects of the biology of T. kingi have been studied by Armstrong and colleagues (Armstrong 1976; Armstrong et al 1986; Armstrong and Bass 1989a,b), and more recently by Futerman et al (2006) and Vijendravarma et al (2008) using the same fly population as that employed here. Adult flies infected by T. kingi suffered a 35–55% reduction in early‐life fecundity, while development time and pupal mortality were also increased (Futerman et al 2006).…”

“…Adult flies infected by T. kingi suffered a 35–55% reduction in early‐life fecundity, while development time and pupal mortality were also increased (Futerman et al 2006). The larval stage is the only host life‐stage susceptible to the pathogen (Vijendravarma et al 2008) and transmission appeared chiefly through larval ingestion of spores derived from the cadavers of infected adults, with peri‐ovarial vertical transmission also occurring but at low frequency (Futerman et al 2006).…”

Fly culture collapse disorder: detection, prophylaxis and eradication of the microsporidian parasiteTubulinosema ratisbonensisinfectingDrosophila melanogaster

“…5 It appears that Drosophila larvae get infected by feeding on infected cadavers or possibly empty eggshells. 10,11 The exact route of infection in the digestive tract remains to be established.…”