SummaryTick-borne pathogens would appear to be vulnerable to vertebrate host immune responses during the protracted duration of feeding required by their vectors. However, tick salivary components deposited during feeding may inhibit hemostasis and induce immunosuppression. The mode of action and the nature of immunosuppressive salivary components remains poorly described. We determined that saliva from the main vector of the agent of Lyme disease, Ixodes dammini, profoundly inhibited splenic T cell proliferation in response to stimulation with concanavalin A or phytohemagglutin, in a dose-dependent manner. In addition, interleukin 2 secretion by the T cells was markedly diminished by saliva. Tick saliva also profoundly suppressed nitric oxide production by macrophages stimulated with lipopolysaccharide. Finally, we analyzed the molecular basis for the immunosuppressive effects of saliva and discovered that the molecule in saliva responsible for our observations was not PGE2, as hypothesized by others, but rather, was a protein of 5,000 tool wt or higher.
Keloids and hypertrophic scars represent exuberant forms of scar formation that frequently are pruritic, painful, and occasionally form strictures. As well, they may result in significant cosmetic disfigurement. Recent years have seen an increased understanding in the molecular and biological mechanisms of keloidal scar formation, allowing for the development of more specific therapeutic options for these lesions. Despite these developments, keloids and hypertrophic scars remain difficult to manage. Clinical, histopathological, and biochemical features of keloids and hypertrophic scars, as well as treatment guidelines, are discussed.
In areas where the agent of Lyme disease is intensely enzootic, the mouse reservoirs may be universally infected. Because a large proportion of the vector tick population appears to feed upon these hosts, the prevalence of infection in the vectors should approach 100%. However, infection in host-seeking nymphal ticks in nature rarely exceeds 40%. To help reconcile this apparent paradox, we examined whether estimates of prevalence might differ if we did not assume that infected ticks are randomly or uniformly distributed within a site. Nymphal Ixodes dammini were collected by dragging a series of 10-meter replicates within an intensely enzootic site. Estimates of the prevalence of spirochetal infection, based upon the monthly means of individual 10-meter collections, were then compared with estimates derived by pooling all samples. Host-seeking ticks tended to cluster. The Lyme disease spirochete was present in 15.6% of 469 pooled ticks. When the prevalence estimate was based solely on ticks in clusters that contained one or more infected ticks, however, at least 50% of the ticks were infected. We conclude that nymphal deer ticks infected by Lyme disease spirochetes tend to aggregate spatially in nature, and that prevalence estimates based upon a mean value for pools may be misleading.
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