Abstract
Based on an exhaustive review, a theory was proposed with an immunoendocrine perspective on the reactivation of dormant Toxocara canis larvae in pregnant bitches and their transmission to fetuses through the placenta, or milk and colostrum to puppies. A historical review was carried out on the reactivation of dormant larvae of T. canis in pregnant bitches which suggested that larval reactivation of T. canis is not solely the effect of a single hormone (prolactin) but is the result of a series of events triggered by progesterone, prolactin, and estrogens. In the first third of gestation, progesterone is capable of directly stimulating the reactivation of larvae through hormonal receptors, indirectly downregulating the granulomatous proinflammatory response around dormant T. canis larvae, and directing the response to a Th2 profile with increased levels of antibodies and blood eosinophils. After a time, when progesterone levels decrease, prolactin and estrogen maintain larval stimulation through hormonal receptors and downregulation of Th1 and the granulomatous proinflammatory response. Collectively, these hormones play major roles in the reactivation of T. canis larvae in pregnant bitches. The series of complex events that occur during larval reactivation is a clear example of transregulation, in which host hormones regulate the vital functions of the parasite to positively influence its establishment and/or proliferation. Understanding larval reactivation from an immunoendocrine perspective helps us to comprehensively understand the complex parasite-host relationship of T. canis.
Published Version
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