I often hear from the public that ticks are present because of deer. That would suggest that high deer numbers would lead to high tick numbers and high levels of tick related diseases (http://www.skinnymoose.com/professorsblog/2013/08/21/comments-and-responses-regarding-ticks-being-proactive-for-your-own-health/) in humans. So, if deer numbers are reduced the number of ticks will also be reduced. However, the initial statement and subsequent logic is incorrect. Let me start by explaining the life cycle of the blacklegged tick (Ixodes scapularis). The black-legged tick undergoes two metamorphic stages (larvae and nymph). At each stage a blood meal is required. Also, as an adult the tick needs blood for reproduction. However, over 100 vertebrates in North America can serve as hosts for the black-legged tick.
Let us start as an adult. An adult tick spends the winter in a dormant phase with a full belly of blood. In the spring, she lays her eggs which hatch into larvae by mid-summer. Larvae ticks patiently wait (called questing) for a vertebrate host to pass by and then attach and consume the first blood meal. Because of their small size larvae ticks have been shown to primarily quest near the ground. Hence, in the summer, the larvae attach primarily to shrews and mice. The life cycle from egg to adult takes two years to complete. The following fall, adult ticks will attach to larger vertebrates including deer for another blood meal and to mate.
Once the adult tick consumes blood from the deer and mates, they drop off. Over a 4 week period, one deer can supply blood for over 2 million fertilized tick eggs. Researches have concluded that all you need is a few deer to support high tick numbers. More important to the presence of an abundant tick population is an abundant small mammal (shrews and mice) population which provides the initial blood meal for the larvae. Also, mice, shrews, and chipmunks are inefficient groomers which allows many larvae ticks to survive. Researchers have demonstrated that over 90% of nymphal ticks get their initial blood meal from mice, shrews, and chipmunks.
However, the situation is more complex. The infective agent of Lyme Disease, Borrelia burgdorferi, does not pass vertically (from mother to young) between blacklegged ticks. Of the 2 million baby ticks that will hatch, none will be infected – they will be ‘clean’. The larval ticks must pick up the B. burgdorferi spirochete from – you guessed it, a shrew, mouse, or chipmunk. So, mammals actually make ticks sick which then make mammals (us) sick. This phenomenon is called ‘reciprocal infectivity’ and is the reason that B. burgdorferi prevelance is high in tick and host populations.
Although deer are involved in the tick life cycle and transmission of some tick borne illnesses, they play a very small role. In fact, researchers believe that deer and humans are dead end hosts – once infected the infection goes nowhere. The infection does not go back into ticks. Infected ticks bite mice, shrews, and chipmunks, which make the ticks carriers, the ticks then bite us and make us sick, and we don’t make anyone sick.
So, don’t blame the deer, blame the small mammals.
Further support can be found at http://www.thewildlifenews.com/2014/05/11/lyme-disease-rages-in-northeast/ where the authors discuss promoting meso-carnivores that prey on rodents and suggest that removal of white-tailed deer is an ineffective way to reduce tick numbers.