Host nutritional stress increases parasite establishment and transmission potential: experimental evidence from the Hymenolepis diminuta–Tribolium confusum model

Host nutritional status is a critical but underexplored determinant of parasite establishment and transmission dynamics. This study experimentally investigated the effect of nutritional stress (starvation) on the establishment of Hymenolepis diminuta in the intermediate host Tribolium confusum, and evaluated the infectivity of cysticercoid developmental stages in the definitive host Mus musculus. A total of 200 adult beetles were randomly assigned to starved (14 days of food deprivation prior to exposure) and fed control groups and exposed to gravid proglottids of H. diminuta. Infection outcomes were assessed across five post-infection dissection intervals. Recovered cysticercoids were subsequently used to infect Swiss albino mice.Starvation significantly increased infection prevalence (90.2% vs. 57%; p < 0.001) and mean parasite burden (5.18 ± 1.1 vs. 1.14 ± 1.27 cysticercoids per beetle). A binomial generalized linear model (GLM) confirmed that starvation increased the odds of infection approximately 6.8-fold (OR ≈ 6.8, 95% CI: 2.5–18.4; p < 0.001), while negative binomial regression demonstrated a more than fourfold increase in parasite burden (IRR ≈ 4.5, 95% CI: 3.2–6.3; p < 0.001). Post-infection interval had no significant effect on infection outcomes (p > 0.05), indicating that establishment is primarily determined at the point of ingestion. Infected beetles exhibited behavioural alterations, including reduced tunnelling and increased surface activity, from 11–15 days post-infection. Both mature and immature cysticercoids established infections in Mus musculus, with proglottid detachment observed at 15–16 days post-infection.These findings demonstrate that host nutritional stress is a key driver of parasite establishment and transmission potential in the H. diminuta–T. confusum system, likely mediated through increased feeding intensity and altered host physiological and immune responses. The results advance ecological immunology frameworks linking host condition to infection susceptibility and highlight the epidemiological significance of stored-product pests as vectors in zoonotic helminth transmission.