Lyme Disease

It has gained particular attention as the most important vector of Lyme disease. It is the common understanding today, in contrast to older literature, that the deer tick must feed 24 hours to transmit Lyme disease.
While the tick is widespread, the incidence of Lyme disease remains isolated to areas of the Northeast and Upper Midwest¹.

Lyme disease was first recognized as a distinct clinical illness in 1975, when 51 residents from Old Lyme, Lyme and East Haddam, Connecticut were diagnosed as having a unique form of oligoarticular arthritis. Since its description, Lyme disease has emerged as one of the most significant threats to public health in the northeastern United States.

In 1982, Dr. Burgdorfer isolated a treponema-like spirochete from the midgut of adult Ixodes scapularis and suggested that this organism may be involved in the etiology of Lyme disease. Shortly thereafter, other researchers isolated spirochetes from the blood of Lyme disease patients and from adult I. scapularis. The following year the I. scapularis spirochete was recognized as a new species and named Borrelia burgdorferi.

The Lyme disease spirochete, B. burgdorferi, is transmitted from the tick to the host via salivation, regurgitation, both processes combined or through destruction of the tick due to host grooming. Although B. burgdorferi is found primarily in the lumen of the tick's digestive tract, the spirochete also disseminates through the tick's hemolymph and enters the salivary glands. The spirochete is most likely transmitted through the saliva, as these ticks salivate excessively during feeding.

Typically, immature I. scapularis acquires B. burgdorferi during its initial bloodmeal from infected reservoir hosts, primarily from white-footed mice. After molting, the subsequent life stage is transstadially infected.

Transstadially infected nymphs and adults can then transmit the spirochete to non-infected hosts. Nymphal deer ticks have had a single previous blood meal (in the larval stage) and subsequently approximately 25% of the nymphs can be found infected. On the other hand, adult deer ticks have had the benefit of two previous blood feedings (as larvae and nymphs) and therefore have a natural infection rate of nearly 50%.

Because nymphal feeding precedes larval feeding in a given year, the enzootic transmission of B. burgdorferi is highly efficient. Thus, the majority of mice become infected with Lyme disease spirochetes in the spring before serving as hosts to the larvae of a different population later that summer. Spirochetes overwinter in the fed larvae, in the unfed nymphs or in the host animal.

Human Babesiosis

Transmission of Babesia microti in humans takes place primarily through direct tick-host contact, although transfusion-acquired human babesiosis cases have been documented on several occasions.

Ixodes scapularis becomes infected with B. microti most likely while feeding on infective reservoir hosts. In the northeastern United States, this enzootic cycle is maintained principally between immature I. scapularis and their primary animal host, the white-footed mouse (P. leucopus). Larvae acquire the infection when feeding on B. microti-infected mice. Engorged larvae then overwinter and pass the parasites transstadially to the subsequent nymphal stage the following spring.

Research indicates that B. microti can survive in salivary glands of ticks for 9-10 months. Nymphs infected from the larval stage are able to transmit the infection to susceptible animals upon feeding.

In areas where B. microti is present, infection rates within tick populations typically range between 5 and 40%. Adults primarily feed on white-tailed deer (O. virginanus), which is not a competent reservoir for B. microti. In addition, attempts to demonstrate B. microti infection in adult Ixodes ticks have failed.

Apparently, B. microti parasites acquired by larval I. scapularis do not survive into the adult stage and only about 25% of the adults that derived the infection as nymphs become infectious. Transovarial transmission of the infection in I. scapularis has not been documented. Therefore, it appears that the role of adult I. scapularis in the transmission of B. microti infection is minimal.The development of B. microti within I. scapularis has been well documented. It has been reported that after larval ticks acquire B. microti, parasites enter the gut lumen from hemolyzed erythrocytes and undergo a complex differentiation, including gametogenesis and fertilization. When an infected tick attaches to a host, sporozoites are readily shed into the saliva and injected into the animal during the feeding process.

The prevalence of Ba. microti and Bo. burgdorferi in I. scapularis populations has been determined in some endemic areas. In Massachusetts, approximately 24% of nymphs and 47% of adults were infected with Bo. burgdorferi while only 11% of nymphs and 14% of adults were infected with B. microti. They suggested that spirochetal infection are more abundant than babesial infection in those ticks examined.

Concurrent infection by both pathogens in nymphal I. scapularis ticks has also been described. This is consistent with the findings that P. leucopus are sometimes simultaneously infected with both pathogens and immature I. scapularis ticks abundantly feed on this rodent species.

Human Ehrlichiosis

Human granulocytic ehrlichiosis (HGE) was first recognized as a clinical illness in 1994. The etiological agent of HGE is still unknown; however, evidence suggest that a single Ehrlichia species closely related to E. equi is the causative agent.

HGE has been diagnosed in human patients in Arkansas, California, Connecticut, Florida, Maryland, Massachusetts, Minnesota, New Jersey, New York, Rhode Island, Pennsylvania and Wisconsin.

There is evidence that the western blacklegged tick Ixodes pacificus (a closelsy related species to Ixodes scapularis) transmits E. equi to horses in California. Elsewhere in the United States, I. scapularis has been implicated as the vector of HGE.

Ixodes scapularis collected in Wisconsin in 1982 and 1991 were infected with HGE. Also, an engorged tick was removed from a patient with HGE in the same area, and HGE DNA was amplified from the salivary glands. Similarly, PCR-amplified DNA of HGE was detected in 50% of I. scapularis collected in Connecticut. The demonstration that blood from a high proportion of deer in Wisconsin contained HGE suggest that deer might be an important reservoir.

However, studies also suggest that meadow voles, Microtus pennsylvanicus

Tick-borne Encephalitis

A tick-borne encephalitis-like virus was first discovered in 1997 from Ixodes scapularis collected from Lyme disease endemic sites in coastal New England (Telford et al. 1997). Telford et al. reported a 0.43% infection rate in adult I. scapularis, a rate similar to those reported for enzootic Central European encephalitis in Europe. This virus, provisionally referred to as deer tick virus (DTV), was isolated and identified via reverse transcriptase PCR and direct sequencing of the products.

DTV is similar to, but distinct from, Powassan virus and may represent a new subtype of Powassan virus. Powassan virus primarily cycles between woodchucks, Marmota monax, and the tick Ixodes cookei. Interestingly, it has been demonstrated that I. scapularis is a competent laboratory vector of I. cookei-derived Powassan virus.

The public health significance of DTV remains unknown. To date, there have been no known human cases of tick-borne encephalitis in the United States. Historically, these viruses can be virulent, some resulting in encephalitis with a case fatality rate of nearly 40% in other parts of the world. Powassan virus usually causes severe encephalitis.
On the other hand, Central European encephalitis derived from tick bites typically produces a mild or silent infection.