Multiple opioid system involvement in the mediation of parasitic-infection induced analgesia.

Although parasite modification of host behaviour is well established, little is known about the mechanisms underlying such effects. The present study examined the relationships between subclinical infection with the enteric sporozoan parasite, Eimeria vermiformis, nociceptive responses and endogenous opioid systems in male mice. Infected mice displayed significant analgesia which increased through the prepatent period [oocyst formation (pre-infective); days 1-7 post-infection (PI)], reached a maximum with the onset of patency (onset oocyst shedding and infectivity; days 7-8 PI) and declined during patency (oocyst shedding), with response latencies declining to basal levels with the cessation of oocyst production and infectivity (day 15 PI). The increasing nociception during the prepatent period (day 4 PI) was associated with kappa opioid mechanisms, being reduced by the kappa antagonist, nor-binaltorphimine, and insensitive to either the delta antagonist, ICI 174,864, or the general, predominantly mu antagonist, naloxone. Maximum analgesia (day 7 PI) associated with the onset of patency (infectivity) was sensitive to both the kappa and mu antagonists, but insensitive to the delta antagonist, while the declining analgesia during patency (day 10 PI) was reduced by the mu and delta antagonists, but was insensitive to the kappa antagonist. These results indicate that mu, delta and kappa opioid systems are involved in the mediation of subclinical parasitic infection-induced analgesia and likely other associated parasite-induced modifications of host behaviour.