Naïve ticks acquire the bacterium Borrelia burgdorferi by feeding on infected hosts, e.g. small rodents. In later stages, these ticks then transmit the Lyme borreliosis pathogen to other hosts, including dogs and man during the feeding process. The bacteria are maintained in the tissues of the hosts

Transmission

The spirochetes are transmitted by the tick bite of different Ixodes species. The pathogens are localized in the mid gut of their vector ticks, where they are capable to adhere to the gut wall supposedly through expression of the outer surface protein A (OspA). Attachment of the tick to temperate host skin and the influx of blood into the tick’s gut are expected to cause a change in the surface structure of Borrelia. An increased expression of OspC is considered to facilitate that the bacteria penetrate the tick gut wall and migrate via the hemolymph to the salivary gland. From there the pathogens can be transmitted with the saliva during feeding of the tick. Besides OspC, host plasminogen and its activators also play a role during transmission. The change within the surface structure of the spirochete and the subsequent migration to the salivary gland of the tick usually takes about 24 to 48 hours. Transovarial transmission does not occur or only occurs to a small percentage, being of no importance for the transmission in nature. Thus eggs and larvae are usually not infected with Borrelia. Feeding on an infected host will infect the larva. In general, between 10 – 25 % of the nymph population is infected. Another blood meal by the nymph can transmit the spirochetes to new mammalian or avian hosts; on the other hand it can cause an infection of still Borrelia-negative nymphs or a super-infection with additional spirochetes. In adult ticks a large proportion can be infected in form of single, double or even triple infection with a variety of Borrelia species.

Dissemination of Borrelia burgdorferi

B. burgdorferi enters the skin at the site of the tick bite. The infection may spread in lymph, producing regional adenopathy. From the site of entry the spirochetes spread to further distant tissues during the following weeks and months. The relative paucity of organisms in the involved tissue suggests that most manifestations of infection are due to host immune response rather than to the destructive properties of the organism.

Although a high proportion of dogs may be seropositive in endemic areas, relatively few report with clinical signs, like fever and lameness. Several mechanisms have been incriminated in causing joint damage in dogs. The production of the inflammatory mediator nitric oxide is up-regulated, as is interleukin 8, a cytokine that recruits neutrophils into infected synovial membranes. Neurological abnormalities occur in some cases of borreliosis, cutaneous and cardiac diseases are rare and were not experimentally confirmed in dogs.

Further information

• Shaw SE et al.: Tick-borne infectious diseases of dogs. Trends Parasitol 2002, 17:74-80 (Download)
• Straubinger RK: Transmission of the various Borrelia spp., current knowledge on pathophysiology etc. Proceedings of the 1st Int. CVBD Symposium, 2006, 6-7 (Download)