Acquired resistance to ticks. III. Cobra venom factor and the resistance response.
Guinea-pigs developed resistance to larvae of the ixodid tick, Dermacentor andersoni, after one infestation. Resistant hosts were characterized by allowing significantly fewer larvae to engorge than non-resistant hosts. Larvae engorging on non-resistant hosts had a mean weight six times that of larvae obtained from resistant hosts at the end of a 5-day infestation. This immunologically based resistance was previously shown to have a cell-mediated and a humoral component. In an attempt to ascertain the role of complement in the resistance response, cobra venom factor (CoF) was administered to guinea-pigs producing prolonged (85--95 per cent) depletion of complement titres. CoF was administered during an initial infestation with tick larvae to determine if complement depletion altered the acquisition of tick resistance. CoF was also administered to tick-resistant hosts in an attempt to determine if the expression of tick resistance and the development of the basophil-packed lesion, characteristic of the tick-attachment site in resistant hosts, could be altered by complement depletion. CoF did not alter the acquisition of resistance when complement levels were reduced during a primary infestation. However, complement depletion of an animal which had acquired tick resistance blocked the expression of that resistance during a challenge infestation. In addition to increased numbers and weights of larvae engorging on tick-resistant animals depleted of complement, the basophil packed lesion at the tick attachment site was greatly reduced. Complement plays an important role in the expression of tick resistance in guinea-pigs.
D000818:Animals; D003165:Complement System Proteins / Q000378:metabolism; D004546:Elapid Venoms / Q000494:pharmacology*; D006168:Guinea Pigs; D007814:Larva; D013984:Tick Infestations / Q000517:prevention & control*; D013987:Ticks / Q000033:anatomy & histology
D004546:Elapid Venoms; D003165:Complement System Proteins