The present study histologically analyzed the salivary glands of Rhipicephalus sanguineus females fed for 2, 4, and 6 days in hosts which had been previously immunized with glandular extracts obtained from females from this same species in different periods of feeding, having as main objective verify the action of these extracts in the secretor cycle of these glands. For this, glandular extract of females fed for 2 days (SGE2), glandular extract of females fed for 4 days (SGE4), and glandular extract of females fed for 6 days (SGE6) extracts were obtained from salivary glands of R. sanguineus females fed for 2, 4, and 6 days respectively. Then, New Zealand White naive rabbits were inoculated either with extracts (test group = TG), or with a mixture of phosphate buffer and Freund's complete adjuvant (control group 2 = CG2). Each inoculated rabbit (TG and CG2) and non-inoculated (control group 1 = CG1) was posteriorly infested with 15 couples of fasting R. sanguineus from which the salivary glands had been collected from females fed for 2, 4, and 6 days. The results revealed that the resistance the hosts had acquired by the immunization with the extracts affected differently the secretory activity of the glandular cells. It was verified that the resistance to SGE2 and SGE4 extracts acted in the cells of acini II and III, being c1 and c5 from II and d from III inactivated due to the action of SGE2 and c1 and c4 from II and f from III inactivated by the action of SGE4. As for the resistance to SGE6 the effect was only on cells of acini II (c1, c3 e c4), which were also inactivated. In addition, the hosts' resistance to SGE2-SGE6 extracts made the degenerative process earlier in comparison to CG1. On the other hand, the resistance to the extracts did not influence the characteristics of the degenerative process normally found in salivary glands. The assynchronism of the degenerative process was maintained-acini III were always the most affected and I the less affected. The structural cell alterations, such as cytoplasmic vacuolation, nuclear alterations and formation of apoptotic bodies which characterize the occurrence of atypical apoptosis were also maintained in the glands of individuals from TG making it clear that the immunization of the hosts with glandular extracts SGE2-SGE6 had influenced the glandular physiology of R. sanguineus, which is an important piece of information in the search for a way to control these ectoparasites.

This study analyzed the histopathology of rabbit skin, previously immunized with SGE2, SGE4, and SGE6 gland extracts prepared from salivary glands of Rhipicephalus sanguineus female with 2, 4, and 6 days of feeding, at the region of the R. sanguineus female feeding lesion 2, 4, and 6 days after tick attachment. In this work, infestation-naïve New Zealand White rabbits were inoculated either with the extracts (test group (TG)) or with phosphate buffer and complete Freund's adjuvant mixture (control group 2 (CG2)). Each extract-inoculated- (TG and CG2) and non-inoculated (CG1) rabbit was subsequently infested with R. sanguineus. Skin biopsies were collected from the rabbit at the tick feeding lesion at 2, 4, and 6 days of feeding. Results revealed that rabbit immunization with gland extracts induced acquisition of resistance against this species. It should be stated that the SGE4 extract was the most effective in developing an immune-inflammatory response against ectoparasites, being this process characterized by the presence of an early and intense inflammatory cell infiltrate. On the other hand, SGE6 extract caused a later appearance of resistance with less infiltrate occurrence and intense edema at the feeding lesion site. As to the inflammatory process deriving from SGE2 extract inoculation, it was the less intense. It was concluded that immunization with different extracts from R. sanguineus female salivary glands did not change microscope features of the inflammatory process, although an earlier or more intense and later response, which was also dependent on the inoculate extract, was noticed.