Hard tick factors implicated in pathogen transmission

Abstract

Ticks are the most common arthropod vector, after mosquitoes, and are capable of transmitting the greatest variety of pathogens. For both humans and animals, the worldwide emergence or re-emergence of tick-borne disease is becoming increasingly problematic. Despite being such an important issue, our knowledge of pathogen transmission by ticks is incomplete. Several recent studies, reviewed here, have reported that the expression of some tick factors can be modulated in response to pathogen infection, and that some of these factors can impact on the pathogenic life cycle. Delineating the specific tick factors required for tick-borne pathogen transmission should lead to new strategies in the disruption of pathogen life cycles to combat emerging tick-borne disease.

Figure 1. Possible TBP transmission route from an infected host to a new host, via hard ticks.

Note that pathogen multiplication can occur in both the tick midgut or salivary glands, depending on the pathogen. Arrows indicate migrating pathogen pathways. A: Acquisition of TBP by a nymphal stage tick during blood feeding. B: TBP development within the tick; preservation in the tick gut (B1); dissemination into the hemolymph and migration to the salivary glands, which can occur either immediately after acquisition (B2) or after the stimulus of a new blood meal (C); dissemination into the hemolymph and migration to the ovaries (B3), which may or may not occur, and which can lead to transovarial transmission and infection of the succeeding generation. C: TBP transmission from the subsequent adult tick stage to a new vertebrate host during blood feeding; BV: blood vessel; CU: cutis; EP: epidermis; FL: feeding lesion; MG: midgut; MH: mouthparts (chelicera and hypostome); OV: ovaries; P: palp; TBP: tick-borne pathogens; SG: salivary glands. Small blue ovals represent TBP.