Introduction Human populations are becoming increasingly vulnerable to infection by tick-borne pathogens (Arboviruses, Babesia, Theileria, Bacteria). These infections are more intense and diverse now than they appeared to be during the mid 1900s. Our recent experience with Lyme disease, human babesiosis and human ehrlichiosis illustrates this pattern of emergent tick-borne infection.
This trend is driven by a proliferation of vector ticks in many parts of the world and wide-spread human encroachment into forested sites. The purpose of this review, therefore, is to identify the environmental determinants of tick-borne disease. In particular, we shall review concepts concerning the diverse modes of perpetuation of tick-borne agents and identify conditions leading toward human infection.
Although Lyme disease will be emphasized, this review will include other tick-borne pathogens that share similar ecological features.
Biology of Ticks Ticks are arthropods, as are insects, but are classified with the mites and spiders. They may readily be distinguished from insects by their characteristic flat, unsegmented bodies, absence of antennae and four pairs of legs in the nymphal and adult stages. All ticks share various structural features employed for finding and feeding on vertebrate hosts.
Their mouth parts include retractable chelicerae that penetrate the vertebrate skin and a multispined hypostome that affixes the feeding tick to its host. Olfactory setae, located on the anterior ends of their legs, serve to detect the presence of such animals. Hook like-structures at the ends of their legs enable ticks to attain contact with passing hosts. These features facilitate the parasitic mode of life.
The two major taxa of ticks, the Argasidae (soft ticks) and the Ixodidae (hard ticks), differ radically in structure, life-history and pathogen associations. The cuticle encasing the bodies of soft ticks is leathery while that of hard ticks is rigid. It becomes elastic, however, as a hard tick fills with blood.
Soft ticks are endemic to arid regions and are closely associated with the nests or burrows of birds or rodents. Such ticks feed frequently during each trophic stage and become attached to their hosts only briefly, generally for no more than an hour. Each of these feeding episodes provides a tick-borne pathogen with another opportunity to infect susceptible hosts.
Hard ticks, in contrast, feed for several days or more and do so only three times during their entire lifespan: once during each of the three trophic stages. Although pathogens of hard ticks have fewer transmission opportunities than do soft ticks, they maintain a diverse array of viral, bacterial, protozoan and metazoan pathogens.
Soft-ticks in contrast, transmit only relapsing fever spirochetes, a complex of pathogens that is restricted to a few particularly arid sites. The following discussion, therefore, will focus exclusively on hard ticks and their associated pathogens.
Ticks require vertebrate blood to grow and to reproduce. Molting follows each feeding episode by a subadult tick. The life cycle culminates after adult ticks feed and the female deposits a batch of eggs.
Ticks ingest enormous quantities of blood, hundreds of times their prior weight. A complex series of physiological events within the vertebrate host and vector tick facilitates this feeding process. The mouth parts of the tick penetrate the skin and secrete a cement-like substance that affixes it to the host.
During blood feeding, anti-hemostatic and anti-inflammatory components of the saliva are secreted into the host to prevent platelet activation and suppress the immune response of the host. The tick ingests a mixture of blood and tissue fluids from the skin of its host in a manner that is poorly understood.
The exoskeleton then becomes plastic and unfolds, accordion-like, to accommodate the final phase of blood feeding. Vast quantities of blood are ingested during the final 24 hours of feeding. The bloated tick then withdraws its feeding apparatus and proceeds to digest its meal of blood. Replete ticks either molt to the next developmental stage, if subadult, or, if adult, produce a clutch of eggs. Death follows oviposition.
Ticks may survive for months or even years between feeding episodes. They remain motionless in a dormant state until environmental conditions permit them to resume activity. Day-length and temperature serve as seasonal cues to initiate or suppress questing activity.
During their questing season, ticks generally ambush their hosts. They leave their sheltered habitats, ascend on vegetation to a height commensurate with the body-form of their host, and wait for any passing object. Those ticks that hunt more aggressively may actively pursue their hosts. Such ticks will move great distances in response to carbon-dioxide and other host-related stimuli to locate suitable hosts.
Perpetuation of Infection Virtually all tick-borne microbes that cause human disease are zoonotic, in that they perpetuate mainly as parasites of certain non-human reservoirs. Each human infection, therefore, constitutes a diversion that reduces the force of transmission. Ticks that narrowly focus their feeding on a particular reservoir population most effectively amplify the natural cycle of transmission of the pathogen.
Vector ticks that feed most frequently on people would seem to contribute least to the enzootic cycle of transmission because their host-range is broad. Infections tend to perpetuate most readily in those ticks that seem innocuous because they rarely come in contact with ``dead-end'' human hosts.
This paradox, that is common to all zoonoses, is resolved in sites where species diversity is limited. In such sites, vectors that fail to discriminate between hosts may sustain enzootic transmission while allowing for episodes of human infection to occur.
Contribution of Vector Ticks The intensity of transmission of a tick-borne pathogen is determined, in part, by a series of vector-related physiological and ecological variables. The salient properties of the tick population include
(1) competence, (2) abundance, (3) site-fidelity, (4) longevity, (5) seasonality and (6) narrowness of host range.
The term ``vectorial capacity,'' which is based on a comprehensive synthesis of these six entomological properties, describes the number of new infections derived from each originally infected reservoir animal per unit of time.
The relative contribution of each of these variables to the force of transmission of a tick-borne pathogen remains poorly defined. These variables will be discussed, in turn, in the discussion that follows.
Vector competence describes the physiological suitability of a particular kind of arthropod as host for a microbe. This parameter is measured in the laboratory and estimates the proportion of ticks that acquire, maintain and transmit a pathogen between vertebrate hosts.
Vector ticks, therefore, must be able to ingest sufficient infectious organisms for the pathogen to become established, must maintain infection transtadially through the relevant molt and must deliver a sufficiently large innoculum to infect a particular vertebrate host. In addition to this horizontal mode of transmission, certain pathogens are maintained vertically, by inherited infection.
The various babesial infections of cattle, for example, illustrate this pattern of transmission by inheritance, while the rodent babesias rely exclusively on horizontal passage between the larval and nymphal stages of development.
Although Lyme disease spirochetes (Borrelia burgdorferi) mainly perpetuate in a similarly horizontal cycle, occasional episodes of inherited infection seem to occur. Transmission by co-feeding, that is, direct passage of a pathogen from the mouth parts of an infected tick to those of a non-infected tick, has been demonstrated in laboratory experiments but not in the field. These cycles defy generality.
Vector abundance constitutes an important variable in the force of microbial transmission. When vector ticks are sparsely distributed, individual reservoir hosts may not sustain the requisite number of vector contacts; only a few reservoir animals would acquire and subsequently pass-on the pathogen. They might only rarely acquire infection or acquire infection so late in the transmission season that they would infect few ticks. Intensity of transmission correlates directly with vector density relative to the density of reservoir hosts.
Because the environmental requirements of ticks tend to be highly specific, their distribution is discontinuous. Vector ticks, therefore, must be sessile enough to preclude dispersal from their point of origin. Although ticks generally remain close to their point of origin, some may migrate several hundred meters in response to such host-associated stimuli as carbon-dioxide.
Those that attach to vagile hosts, such as birds, may readily be carried away from a permissive habitat and be lost to the transmission cycle. In this manner, tick-borne infections simulate the classical Russian concept of the ``nidality of disease.''
The proportion of the tick population that survives long enough to become infectious also influences the force of transmission. Incidence of infection in the reservoir population, therefore, depends directly on interstadial survival of the vector tick. Indeed, the vast majority of ticks that feed as larvae fail to feed once again as nymphs.
In the northeastern U.S., for example, 3.5 times as many larval as nymphal deer ticks (Ixodes dammini) attach to white-footed mice (Peromyscus leucopus). Almost a third of these ticks appear to survive to feed again.
In addition to longevity, however, this estimate of survival assumes that each relevant developmental stage of the tick responds similarly to the array of available hosts. Trans-stadial survival has not been estimated directly, and the magnitude of its contribution to the force of transmission remains unknown.
The seasonality of feeding activity of the vector tick relative to the density of the reservoir population may also affect transmission. In the case of the American vector of the agent of Lyme disease, seasonality is highly punctuated.
The nymphal stage of the tick feeds, each season, before the younger larval stage. This inverted pattern of feeding serves to intensify transmission of pathogens because the reservoir population receives its infectious innocula before the larval recipient stage of the tick commences feeding. Because European wood ticks (Ixodes ricinus) lack such a precisely punctuated developmental cycle, the cycle in Europe seems less efficient than in eastern North America.
The requirement for precision would be exacerbated in the event that reservoir hosts remain infectious only for a brief period of time. The pathogen must then become available to the vector population precisely when the appropriate stage of the vector quests for hosts. Seasonal events may profoundly affect transmission.
Narrowness of host range of the vector tick powerfully affects transmission because hard ticks feed only three times per generation. At least two of these feeding episodes must be directed toward the population of reservoir animals that enables vectors to successfully acquire and ultimately transmit the pathogen.
For example, only larval and nymphal stages of the deer tick feed on rodent reservoirs, while adults parasitize larger non-competent hosts such as deer. Diversion of either of the sub-adult stages to non-competent hosts, therefore, negates transmission for the other feeding episode.
Contribution of Reservoir Hosts Although vector ticks may acquire infection from an array of hosts existing in nature, only one generally serves as the main reservoir of the pathogen. ``Reservoir capacity'' expresses the relative number of infected ticks derived from each host species.
An effective reservoir host must be
(1) competent for the pathogen, (2) sufficiently abundant, (3) parasitized by numerous vector ticks, (4) parasitized by at least two developmental stages of the vector tick and (5) continuously resident in the enzootic site.
These biological properties, together, define the capacity of reservoir populations to perpetuate tick-borne pathogens.
Reservoir competence is a measure of the physiological ability of a vertebrate host to exchange a pathogen with vector ticks and generally is analyzed experimentally in the laboratory. A competent reservoir must readily acquire infection, sustain its development and ultimately present the pathogen to the vector. This parameter should be measured over a span of time that corresponds to that of the seasonal activity of the vector tick.
For the Lyme disease agent in North America, for example, reservoir hosts must become and remain infectious over the two month interval spanning the maximum feeding activity of nymphal and larval deer ticks. The white-footed mouse fulfills this criterion because it attains infectivity within 2 weeks of infection and remains infectious for life.
A competent reservoir, therefore, must remain infectious long enough to pass infection to the relevant stage of the tick.
Reservoir hosts should be sufficiently abundant in nature that vector ticks are likely to encounter them before encountering other less suitable but tick-attractive hosts. Although the force of transmission initially increases with reservoir density, greater host density might dilute the vector population such that individual hosts that become infected are unlikely to encounter and infect non-infected ticks.
The presence of tick-attractive but pathogen-incompetent hosts would divert vector ticks, a relationship known as ``zooprophylaxis.'' Transmission, therefore, tends to be most intense in ecological island sites where host diversity is restricted and particular reservoir hosts predominate.
A complex set of ecological and physiological properties of reservoir and vector populations determines the frequency of vector-host contact. Effective reservoirs, of course, must occupy the same habitats as do vector ticks. Ticks position themselves on the vegetation at an appropriate height above the ground, thereby insuring a degree of host specificity. The stature of particular hosts influences the probability of encountering a tick in nature.
In addition, reservoir hosts must forage at a time of day when ticks actively seek hosts. Ticks quest most effectively at night and during the morning and evening hours when the atmosphere is sufficiently humid.
Once a questing tick attains host-contact, it must successfully feed without invoking an inflammatory response. Poorly-adapted hosts develop an inflammatory response against tick bites after repeated exposure. Such resistant animals feed fewer ticks due to the direct effects of host immunity and irritation induced by tick bites which increases host grooming. The physiological and ecological variables that regulate host-tick contact remain poorly understood.
Reservoir hosts must have sufficient contact with pathogen-acquiring and infecting stages of the tick to perpetuate the pathogen. Entomological inoculation rate (EIR) describes the frequency of vector ticks delivering infection to the reservoir population. This variable depends on the frequency with which pathogen-infective stages of the tick feed on a particular reservoir population and the prevalence of infection in these ticks.
To complete transmission, reservoir hosts must be abundantly parasitized by the pathogen-receptive stage of the tick. Reservoir inoculation rate (RIR) describes the number of infections generated in the vector population per unit of time. Together, these variables describe the ability of particular kinds of hosts to receive (EIR) and deliver (RIR) infection to and from the vector population.
Reservoir hosts should remain within the enzootic site throughout the transmission season. Mobile hosts such as birds tend to be ineffective reservoirs because they may readily disperse the pathogen to an inappropriate site that lies outside of the focus of transmission.
Although migratory hosts may fail to maintain infection locally, they may passively transport ticks into new permissive sites. In this manner, excessively mobile hosts may reduce the force of transmission of a pathogen locally while accelerating the expansion of its range.
Risk of Infection The potential for tick-borne pathogens to infect human hosts depends on the questing density of infected ticks and the behavior of human hosts. Herein, we explore the conditions that may favor human infection.
The density of ticks largely correlates with that of their main vertebrate host(s). Definitive hosts, in particular, powerfully affect tick abundance because they comprise the main food-source for the reproductive stage of the tick. Successful feeding of the adult stage of the tick results in huge increments of increase: thousands of larvae may result.
In contrast, feeding success by subadult ticks merely promotes development. Adult deer ticks, for example, feed mainly on deer and proliferate solely where deer are abundant. This relationship was tested experimentally by depriving deer ticks of access to their cervid hosts.
Deer inhabiting an island site were virtually eliminated, which resulted in a diminished tick population. The density of larvae per mouse declined five fold during the year following the intervention, and that of nymphs somewhat more slowly, extending over several years.
This relationship, however, appears to be non-linear because incremental decreases in deer density may fail to reduce tick densities. Modest reductions in deer abundance may simply cause more ticks to feed on each remaining host. The quantitative relationships between tick and host density have not been defined precisely.
Seasonality in the questing density of ticks may profoundly affect the shape of the epidemic curve representing any pathogens that they transmit. In North America, human Lyme disease infections tend to occur most frequently during July because fewer people engage in risk-promoting activities during May and June, when deer tick densities are greatest.
Nymphal densities decline greatly by July and are virtually nonexistent in August. Fewer human infections occur during the fall and winter months, although adult ticks, which quest at that time of year, are far more frequently infected than are nymphal ticks. Few people, however, are exposed and those that enter forested sites then are fully clothed.
Then too, adult ticks are more readily discovered before they can feed long enough for transmission to occur. Risk of human infection is modified by a complex interaction of the stage-specific activity of vector ticks and human behavior.
Pathogen-infected vector ticks may be more abundant in certain sites than in others and infection far more prevalent than in the case of insect-borne disease. The Lyme disease spirochete, for example, infects 20-40% of deer tick nymphs and 40-70% of adults in the northeastern and northcentral U.S. but rarely infects ticks south of Maryland.
Likewise, human infections cluster in space and time mainly in the upper Midwest and Northeast, but also in several sites in California. Elsewhere, the scattered distribution of human cases suggests that infected ticks may be imported, perhaps carried by south-migrating birds.
Enzootic transmission implies that both vector and pathogen populations propagate locally. Larval ticks, for example, would outnumber nymphs where transmission is stable; a preponderance of nymphs would imply that the vector population is sustained by importation from some remote enzootic site.
In a stable zoonotic focus, the RIR (prevalence of infection in the reservoir and feeding density of vector ticks on those hosts) would be consistent with the EIR (stage-specific density of infected ticks). Stable transmission requires long-term constancy in the incidence of infection in both vector and reservoir populations.
Outbreaks of tick-borne disease may emerge when people encroach upon previously silent transmission foci. In this manner, focused contacts between reservoir hosts and vector ticks may be altered and redirected toward human hosts.
The first outbreak of Rocky Mountain spotted fever erupted, for example, when pioneers cleared land in the Bitterroot Valley of Montana. The result was devastating, nearly preventing this fertile region from developing. Tick-borne encephalitis, likewise, became intensely prevalent when forestry workers and trappers relocated into undisturbed tracts of Siberian forest. Human disruption of enzootic cycles serves to produce sporadic outbreaks of tick-borne disease.
Environmental change may promote epidemics of tick-borne disease when particular hosts and ticks become extraordinary abundant. Reforestation of previously cultivated land in the eastern United States has permitted deer to proliferate, often in close proximity to residential communities. Lyme disease emerged as a significant health problem when deer and their associated tick ectoparasites increased in abundance and expanded in distribution.
The first outbreak of Crimean-Congo hemorrhagic fever occurred when population densities of hares and Hyalomma marginatum vectors exploded after hunting was prohibited and fields were abandoned. Massive outbreaks of human infection followed the resulting proliferation of these apparent reservoir hosts. Any disruption in the balance of vertebrate hosts may support an overabundance of vector ticks.
Example of Lyme Borreliosis Although Borrelia burgdorferi is the sole causative agent of human Lyme disease in North America, the etiologic agents in Europe and Asia are more diverse. They include the ``genospecies'' designated as Borrelia burgdorferi, B. afzelii and B. garinii.
These spirochetal agents of human disease are transmitted by members of the Ixodes ricinus complex, including I. dammini in eastern North America, I. pacificus in western North America, I. ricinus in Europe, I. persulcatus in eastern Europe and Asia.
People become infected mainly via the bites of nymphal ticks, although some infections may be derived from the adult stage of the tick. In certain communities, Lyme disease transmission may be particularly intense. Lyme disease spirochetes may infect as many as 40% of nymphal ticks and virtually all of the rodents.
Human seroprevalence may approach 25%, and 5% of residents may become infected each year. Currently, Lyme disease accounts for more than 90% of all reports of vector-borne disease in the United States.
In the northeastern United States, the Lyme disease spirochete perpetuates in a cycle involving vector deer ticks (I. dammini) and white-footed mouse reservoir hosts (Peromyscus leucpous). White-tailed deer (Odocoileus viginianus) are not directly involved in the transmission cycle, but play a vital role in maintaining tick densities because they serve as the preferred hosts of the adult stage of the vector tick.
Although various other vertebrate hosts may inhabit zoonotic sites and come in contact with vector ticks, white-footed mice provide the main source of spirochetal infection to the nymphal stage of the vector tick. These mice serve as effective reservoirs because they are locally abundant in zoonotic sites, are the main hosts for the larval and nymphal stages of the vector, are frequently infected in nature and readily infect vector ticks.
Estimates of reservoir capacity suggest that one white-footed mouse infects as many ticks as do 12 chipmunks or 221 meadow voles. Some kinds of passerine birds may also transmit infection to the vector population. The greater mobility of avian hosts diminishes their contribution to local transmission but aids in dispersing vector ticks and Lyme disease spirochetes to new sites.
The apparent diversity of vector ticks, spirochete variants and the vertebrate reservoir fauna of the western United States renders the epizootiology of these microbes more complex than in the Northeast. Although Ixodes pacificus serves as the principle vector to people in this region, relatively few harbor Lyme disease spirochetes. The diversity and abundance of non-competent hosts in western United States appear to contribute to low infection rates in I. pacificus.
I. neotomae, in contrast, narrowly focuses its feeding on wood rats and kangaroo rats and may effectively maintain Lyme disease spirochetes in an enzootic cycle involving these hosts. Lyme disease spirochetes may perpetuate in this I. neotomae-wood rat cycle and occasionally infect the I. pacificus population. It is not clear, however, whether wood rats and kangaroo rats represent the main source of spirochetal infection within the I. pacificus population.
The force of transmission of the agent of Lyme disease in western Europe tends to be weaker than in northeastern North America. European I. ricinus ticks transmit these microbes less efficiently than do their North America counterpart, I. dammini, because each trophic stage feeds most frequently on different kinds of hosts.
Larvae tend to parasitize rodents, and nymphs to feed on medium-sized mammals, birds and lizards. Adults feed mainly on deer or sheep. So few of these rodents are parasitized by nymphs that the EIR may be limited.
Nevertheless, certain kinds of rodents harbor sufficient infectious nymphs to ensure perpetuation of the pathogen. Edible door mice (Glis glis) and black-striped mice (Apodemus agarius) serve as particularly efficient reservoirs because they are frequently infested by both the infectious and pathogen-acquiring stages of the wood tick.
Norway rats (Rattus norvegicus), too, may support transmission of the Lyme disease agent in particular urban sites. Because shrews and voles are far more abundant than mice in Sweden, these small mammals may perpetuate the life cycle in certain Scandinavian sites. The relative importance of each kind of vertebrate host as a reservoir of infection differs according to local conditions.
In eastern Asia, Lyme disease spirochetes appear to circulate in a cycle involving the taiga tick (I. persulcatus) and rodents of the genera Clethrionomys and Apodemus. To date, solely B. garinii and B. afzelii have been isolated from tick vectors and rodent hosts inhabiting these regions.
The bank vole (Clethrionomys glareolus) predominates in western Russia, whereas C. rufocanus, C. rutilus and Apodemus peninsulae dominate further to the east. Although numerous Borrelia isolates have been derived from these hosts, their relative contribution to infecting the tick population by xenodiagnosis remains uncertain.
Co-Infecting Pathogens Although public attention has focused on Lyme disease, Ixodes ticks may transmit numerous other agents of human disease.
Human babesiosis, a malaria-like illness, is caused by the protozoan parasites Babesia microti in North America and Babesia divergens in Europe. Signs of this illness become evident mainly among elderly or immunocompromised subjects and may be fatal if not treated promptly.
Viruses of the tick-borne encephalitis complex induce a potentially fatal form of encephalitis endemic to Europe and Asia. More recently, a new member of this viral complex was discovered in North America; transmission was attributed to deer ticks.
Finally, two closely-related pathogens (Ehrlichia phagocytophila and E. equi in eastern and western North America respectively) were recently implicated as agents of human disease. These rickettsial pathogens infect leukocytes, and human cases may also terminate fatally. The diverse array of pathogens transmitted by Ixodes ticks, thereby, severely burdens human health.
In the northeastern United States, the agents of Lyme disease, human babesiosis and human granulocytic ehrlichiosis perpetuate mainly in a cycle involving white-footed mice. Vector ticks, thereby, tend to acquire more than one of these microbes from reservoir rodents. This implies that individual human hosts tend to be vulnerable to co-infection.
Serological surveys indicate that 10 to 60% of Lyme disease patients had been co-infected by B. microti. Interestingly, these pathogens tend to synergize in human hosts such that the resulting illness is more severe than would be anticipated as the sum of symptoms produced by each pathogen. More symptoms are experienced, and the duration of illness is prolonged.
The particularly severe manifestations of Ixodes-borne disease that occur in certain enzootic sites may reflect a peculiar combination of coinfecting pathogens.
Anti-Vector Interventions Once established, local transmission cycles of tick-borne zoonoses tend to persist in the face of public health interventions. Various interventions, however, have been devised, and certain of them appear promising. The following discussion describes selected strategies designed to reduce the public health burden presented by vector ticks.
Individual residents of enzootic sites may practice preventive measures that effectively reduce their risk of infection by tick-borne pathogens. They should:
(1) avoid tick infested habitats whenever feasible; (2) wear light-colored trousers with cuffs that are tucked into their socks; (3) apply tick repellent containing DEET to exposed parts of their skin and permethrin to their clothing; (4) periodically examine the surface of their clothing and skin and remove any ticks that have attached using fine tipped forceps.
Prompt removal of attached ticks generally aborts transmission because transmission of many of these infections tends to require extended periods of host attachment. The arboviral agents may constitute an exception. Although the efficacy of these measures has not systematically been evaluated, they appear to provide an important degree of protection against tick-borne disease.
Depriving ticks of access to their main vertebrate hosts may effectively reduce the density of ticks. This intervention strategy, however, is practical solely in sites that such hosts would not rapidly re-invade.
Deer inhabiting a study site on Great Island, MA were virtually eliminated, which resulted in decreased abundance of deer ticks. Host reduction proved to be effective largely because the relative isolation of the site restricted the movements of deer. Similar efforts on the mainland proved to be impractical and excessively costly.
Thousands of small rodents, for example, were destroyed in Montana in order to suppress the density of American wood ticks (Dermacentor andersoni), the vectors of the agent of Rocky Mountain spotted fever. Any gains were transient, however, because wood ticks from nearby undisturbed sites rapidly re-invaded the intervention site.
Anti-tick measures based on the removal of their vertebrate hosts require that the site be isolated in order to limit immigration from adjacent sites.
Although broad-scale applications of acaricides may destroy numerous ticks, environmental damage tends to result. Acaricidal applications focused around residential sites may alleviate the immediate tick burden. Residual pesticides such as carbaryl, chlorpyrophos and diazinon temporarily render such sites virtually tick-free.
Less toxic materials, containing pyrethroids, may also reduce tick density. These products, however, lack long-term residual activity and require at least monthly application to maintain satisfactory freedom from ticks.
Regardless of the kind of acaricidal compound that is applied, pesticide resistance should always be anticipated. Intensive and extensive applications of killing chemicals can only be temporary. Loss of acaricide susceptibility renders acaricidal interventions inherently unsustainable.
Innovative strategies have been developed for delivering acaricides directly to the hosts of vector ticks. Various self-medicating devices for destroying ticks on deer or other ungulates are in various stages of development and evaluation. In general, such devices deliver acaricide from a dispenser that the animal contacts when feeding on a bait contained within.
Another host-targeted strategy distributes grain impregnated with systemic acaricides, such as ivermectin. When deer are the targets of such interventions, they must be habituated to the bait-station, and this requires delivery of large quantities of grain, frequently a maize-molasses mixture. This has the undesirable side effect of promoting the density of various rodents as well as the targeted deer, themselves.
A cotton-baited acaricidal formulation has been implemented to target rodent hosts such as the white-footed mouse in eastern North America. This method is designed to reduce the force of transmission of Ixodes-borne pathogens by eliminating those ticks that feed on the rodent reservoirs.
Host-targeted acaricidal formulations are attractive because they limit any environmental damage that might be induced by these biologically active chemicals.
Ticks are vulnerable to destruction by various parasitic or predatory organisms. Although certain Dermacentor and Amblyomma ticks secrete a pheromone that deters attack by ants, Ixodes lack such protection against predation. To the extent that fire ants are important predators of these ticks, their presence might benefit public health.
A chalcid wasp (Hunterella hookeri) frequently parasitizes larval Ixodes ticks in northeastern North America and Europe and destroys them in their nymphal stage. Although these wasps infect as many as a third of the nymphal deer ticks in eastern North America where Lyme disease is enzootic, none infect spirochete- or B. microti-infected ticks.
Efforts to use these wasps to reduce risk of Lyme disease, therefore, would fail. Certainly, tick densities seem unaffected in the face of this natural burden. The applicability of bio-control efforts against vector ticks remains speculative.
The density of vector ticks may be reduced by removing understory vegetation and leaf litter, either mechanically, chemically or by fire. Where few buildings are present, the undergrowth or ground-cover that shelters ticks is most readily destroyed by burning. In a Massachusetts site, burning and mowing reduced deer tick densities by as much as 80%. Similar efforts in Tennessee greatly reduced the density of Lone Star ticks.
Safety considerations, however, limit the wide-scale application of this measure. Limited areas such as along a road, may be mowed, and this would seem to protect people from contact with ticks. The efficacy of this measure, however, remains ill-defined.
Routine herbicidal applications are poorly tolerated by many people and may excessively harm the environment. While vegetation management provides effective protection against ticks, it must be reapplied on a yearly basis.
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