How do ticks become infected with encephalitis and borreliosis?

Understanding Tick-borne Diseases

What Are Ticks?

Life Cycle of Ticks

Ticks progress through four distinct stages: egg, larva, nymph, and adult. Each stage, except the egg, requires a blood meal to advance. After laying, eggs hatch into six-legged larvae that seek a small vertebrate host, such as a rodent or bird. The larva feeds for several days, then drops off to molt into an eight‑legged nymph. Nymphs locate a second host, often a larger mammal, feed, and detach to molt into adults. Adult females attach to a large host—typically a deer, livestock, or human—feed, mate, and engorge before laying thousands of eggs, completing the cycle.

Pathogen acquisition occurs primarily during the larval and nymphal blood meals. When a larva feeds on an infected reservoir, such as a field mouse carrying Borrelia burgdorferi or a small mammal harboring tick‑borne encephalitis virus, the microorganisms enter the tick’s midgut. The pathogen persists through molting (transstadial transmission), allowing the tick to retain infection into the nymphal and adult stages.

Transmission to a new host happens when an infected nymph or adult inserts its mouthparts and secretes saliva containing the pathogen. Salivary proteins facilitate pathogen migration from the midgut to the salivary glands, where they are expelled with the blood meal. The brief attachment period of larvae reduces transmission risk, whereas nymphs and adults, which feed longer, present the greatest threat for encephalitis virus and Borrelia transmission.

Key points of the tick life cycle relevant to disease spread:

Egg → larva (single‑host blood meal) → nymph (second host) → adult (third host).
Pathogen uptake occurs during larval or nymphal feeding on infected reservoirs.
Transstadial maintenance preserves infection through molting.
Salivary secretion during nymphal or adult feeding delivers pathogens to new hosts.

Habitats of Ticks

Ticks thrive in environments that support their life‑stage requirements and host availability. Moist leaf litter, dense vegetation, and shaded ground provide the humidity necessary for questing nymphs and adults, preventing desiccation. Forest edges, meadow‑forest ecotones, and tall grass fields maintain the microclimate ticks need while offering abundant wildlife such as rodents, birds, and deer that serve as blood meals.

Ground‑level habitats differ among species. Ixodes ricinus, the primary vector for European encephalitis and Lyme disease agents, prefers deciduous and mixed woodlands with leaf‑covered understories. Dermacentor variabilis, a North American carrier of similar pathogens, occupies open grasslands, scrub, and transitional zones where vegetation is sparse but host mammals are plentiful. Amblyomma americanum, associated with southern encephalitis‑like illnesses, occupies humid, wooded areas and coastal marshes where temperature and moisture remain high.

Seasonal changes modify habitat suitability. Spring and early summer bring increased humidity and rising host activity, prompting peak questing behavior. Summer drought reduces leaf litter moisture, forcing ticks to retreat to deeper soil layers or leaf piles. Autumn offers cooler temperatures and sustained humidity, extending the active period for late‑stage nymphs and adults.

Human exposure correlates with habitat overlap. Recreational trails traversing leaf litter, meadow borders, or brushy undergrowth increase the probability of contact with questing ticks. Managing vegetation height, removing excess leaf litter, and creating buffer zones of low‑growth grass can lower tick density in high‑use areas, thereby reducing the chance that ticks acquire and later transmit encephalitis‑causing viruses and Borrelia bacteria.

Pathogens Involved

Tick-borne Encephalitis Virus («TBEV»)

Tick‑borne encephalitis virus (TBEV) belongs to the Flaviviridae family and circulates primarily between ixodid ticks and small‑to‑medium mammals. Infected rodents, shrews, and birds serve as amplifying hosts; their viremia introduces the virus into feeding ticks. The virus persists in the tick midgut epithelium, spreads to the hemocoel, and colonizes salivary glands, where it becomes available for subsequent blood meals.

Ticks acquire TBEV through three main pathways:

Horizontal acquisition – ingestion of infected blood during a larval or nymphal feed on a viremic vertebrate.
Co‑feeding transmission – simultaneous feeding of infected and uninfected ticks on the same host, allowing virus passage without detectable host viremia.
Transstadial maintenance – retention of the virus as the tick molts from larva to nymph and from nymph to adult, preserving infectivity across life stages.

Adult female ticks can transmit TBEV to their progeny via transovarial passage, though the efficiency is lower than horizontal routes. After colonization of the salivary glands, the virus is expelled into the host’s skin during the next blood meal, initiating infection in humans or other mammals. The combination of co‑feeding, transstadial persistence, and occasional vertical transmission sustains TBEV circulation in natural foci and underlies the risk of encephalitis transmission by tick bites.

Borrelia burgdorferi («Lyme Disease Bacteria»)

Borrelia burgdorferi is a helical spirochete that causes Lyme disease in humans and mammals. The bacterium resides primarily in wild vertebrate reservoirs, especially small rodents such as the white‑footed mouse and certain bird species. When an unfed larval tick attaches to an infected reservoir, the spirochete enters the tick’s midgut during the blood meal.

After acquisition, B. burgdorferi persists through the larva‑to‑nymph molt (transstadial transmission).
The pathogen multiplies in the midgut, upregulating surface proteins that facilitate migration.
During the next feeding stage, usually as a nymph, the spirochete moves from the midgut to the salivary glands.
Salivary secretion introduces the bacteria into the new host’s skin, establishing infection.

Survival of B. burgdorferi within the tick depends on several variables: the density of competent reservoir hosts, the bacterial load carried by those hosts, the tick species’ feeding behavior, and ambient temperature and humidity that affect tick development rates. High reservoir host prevalence and favorable climate accelerate the proportion of infected nymphs, which are most responsible for human transmission.

The combined effect of reservoir competence, efficient transstadial persistence, and timely migration to salivary glands determines the overall risk of Lyme disease transmission by ticks.

Mechanisms of Pathogen Acquisition

From Vertebrate Hosts

Role of Reservoir Animals

Reservoir animals maintain the pathogens that infect ticks, ensuring continual circulation of both tick‑borne encephalitis viruses and Lyme disease spirochetes. Small mammals, particularly rodents such as the bank vole (Myodes glareolus) and the wood mouse (Apodemus sylvaticus), harbor high concentrations of Borrelia burgdorferi sensu lato. Their frequent grooming and limited mobility increase the likelihood that feeding larvae and nymphs acquire the bacteria during blood meals.

Birds contribute to the spread of encephalitis virus across larger distances. Species that migrate seasonally, like the common blackbird (Turdus merula) and several passerines, develop sufficient viremia to infect feeding ticks and subsequently transport infected ticks to new habitats. Ground‑feeding birds also support larval and nymphal stages, creating additional acquisition opportunities.

Larger mammals, especially ungulates such as roe deer (Capreolus capreolus) and red deer (Cervus elaphus), do not serve as competent reservoirs for Borrelia, but they provide abundant hosts for adult ticks, facilitating tick reproduction and population growth. Their presence indirectly amplifies infection risk by increasing tick density.

Key points summarizing reservoir contributions:

Rodents: primary source of Borrelia for immature ticks.
Migratory and resident birds: source of encephalitis virus and vector dispersal agents.
Deer and other large mammals: sustain adult tick populations, indirectly affecting pathogen prevalence.

Understanding these host–pathogen dynamics clarifies how ticks acquire infection and why control measures often target reservoir management alongside vector suppression.

Small Mammals

Small mammals, primarily rodents such as mice, voles, and chipmunks, maintain the enzootic cycles of tick‑borne encephalitis virus (TBEV) and Borrelia burgdorferi sensu lato. Infected individuals develop transient bacteremia or viremia, providing a source of pathogens for feeding ticks. When a larval or nymphal tick attaches to an infected host, it ingests the pathogen along with the blood meal. The pathogen then replicates within the tick’s midgut, migrates to the salivary glands, and becomes transmissible during the tick’s subsequent molt or feeding event.

Key aspects of the transmission cycle involving small mammals:

Reservoir competence – Certain species exhibit high pathogen loads without severe disease, ensuring efficient acquisition by feeding ticks.
Life‑stage exposure – Larvae acquire infection during their first blood meal; nymphs can become infected when feeding on already infected hosts, while adult ticks may acquire the pathogen from the same host species during a second feeding.
Seasonal dynamics – Peak activity of rodent populations in spring and early summer coincides with the emergence of larval and nymphal ticks, amplifying transmission rates.
Habitat overlap – Forest edges, shrublands, and grasslands provide the microenvironment where small mammals and questing ticks intersect most frequently.

After infection, the tick retains the pathogen through molting (transstadial transmission). Horizontal transmission to new vertebrate hosts, including humans, occurs when infected nymphs or adults attach and feed. The persistence of small mammal reservoirs, combined with their high reproductive rates and frequent contact with questing ticks, sustains the continuous circulation of both encephalitic viruses and Borrelia spirochetes in natural settings.

Birds

Birds serve as natural hosts for both tick‑borne encephalitis viruses and Borrelia spirochetes. When an immature tick attaches to an infected bird, it ingests blood containing the pathogen and becomes a carrier. After molting, the tick can transmit the infection to new hosts, including mammals and humans.

Key mechanisms involving avian hosts:

Reservoir competence – Certain bird species maintain high levels of virus or spirochete in their bloodstream without severe illness, providing a reliable source for feeding ticks.
Feeding preference – Larval and nymphal ticks frequently feed on ground‑dwelling birds such as thrushes, robins, and blackbirds, increasing the probability of pathogen acquisition.
Migratory movement – Seasonal migrations transport infected ticks across large geographic areas, facilitating the spread of encephalitis and Lyme‑disease agents to new regions.
Co‑infection potential – Birds can harbor both pathogens simultaneously, allowing a single tick to acquire multiple agents during one blood meal.

The result is a continuous cycle: infected birds supply pathogens to feeding ticks; ticks mature and disperse; subsequent bites introduce the agents to other vertebrates. This cycle sustains the prevalence of tick‑borne encephalitis and Borrelia infections in endemic zones.

Blood Meal as a Transmission Vector

Ticks acquire pathogens primarily through the ingestion of infected host blood. When a tick attaches to a vertebrate that carries encephalitic viruses or Borrelia spirochetes, the pathogen enters the tick’s midgut along with the blood meal. The midgut epithelium provides the initial environment for pathogen survival and replication.

During subsequent molts, some pathogens migrate from the midgut to the salivary glands. This migration enables the tick to inoculate new hosts during later feedings, completing the transmission cycle. The process differs between viral and bacterial agents:

Encephalitic viruses replicate within midgut cells, then disseminate via the hemolymph to salivary glands.
Borrelia spirochetes detach from the blood clot, traverse the midgut barrier, and are transported to the salivary ducts by specific outer‑surface proteins.

Several factors modulate the efficiency of pathogen acquisition during a blood meal:

Host viremia or bacteremia levels at the time of feeding.
Tick species and developmental stage, which determine gut receptor compatibility.
Duration of attachment, influencing the volume of ingested blood and exposure time.
Environmental temperature, affecting pathogen replication rates inside the tick.

Understanding the blood meal as the central conduit for both encephalitic viruses and Borrelia bacteria clarifies how ticks become vectors of these diseases.

Transovarial Transmission

Mother Tick to Offspring

The female tick acquires pathogens while feeding on infected vertebrate hosts. After ingestion, the agents circulate in the hemolymph and reach the ovarian tissue. In the ovaries, the tick‑borne encephalitis virus replicates within follicular cells, while Borrelia burgdorferi adheres to the basal lamina and penetrates developing oocytes. This direct colonisation enables the pathogens to be incorporated into the eggs that the tick lays.

When the eggs hatch, the larvae already contain infectious particles or spirochetes. Consequently, newly emerged larvae can transmit the encephalitis virus or Lyme‑disease bacteria to a new host without an intervening blood meal. The efficiency of this vertical passage varies:

Tick‑borne encephalitis virus: transovarial transmission rates of 10‑30 % in Ixodes ricinus and I. persulcatus; virus persists through all developmental stages.
Borrelia burgdorferi: transovarial transmission is rare, typically <5 % in I. scapularis; bacterial presence is more dependent on subsequent feeding (transstadial maintenance).

Factors influencing maternal transmission include:

Pathogen load in the engorged female.
Tick species and genetic strain.
Environmental temperature affecting viral replication.
Timing of infection relative to oviposition.

Detection of infected offspring employs quantitative PCR for viral RNA and culture or PCR for Borrelia DNA in larval homogenates. Monitoring maternal transmission provides insight into early‑stage infection risk for humans and wildlife, highlighting the importance of controlling adult tick populations to reduce pathogen spillover.

Significance in Disease Cycle

Ticks act as the primary vector that links wildlife reservoirs to humans and domestic animals for both tick‑borne encephalitis viruses and Borrelia spirochetes. Their blood‑feeding behavior creates a conduit through which pathogens move from infected rodents, birds, or small mammals into naïve hosts.

Acquisition occurs when a larval or nymphal tick attaches to a reservoir animal carrying the pathogen. The blood meal introduces the virus or bacterium into the tick’s midgut. After engorgement, the pathogen survives the molting process (trans‑stadial transmission), allowing the same individual to remain infectious as it progresses from larva to nymph to adult. In addition, co‑feeding on adjacent, uninfected hosts enables virus transfer without systemic infection of the host, reinforcing the pathogen’s persistence within the tick population.

Maintenance of the disease cycle relies on the tick’s capacity to harbor the pathogen for months to years. The pathogen resides in the salivary glands, midgut, and, for some viruses, the ovaries, facilitating vertical transmission to offspring (trans‑ovarial transmission). This internal reservoir reduces dependence on external host availability and stabilizes endemic foci.

Transmission to new hosts occurs during subsequent feedings. Salivary secretions released at the feeding site contain the pathogen, which is deposited directly into the host’s skin. The brief attachment period required for virus or spirochete inoculation increases the likelihood of human exposure in endemic regions.

Key aspects of significance in the disease cycle

Bridge between reservoirs and humans – ticks translate wildlife infection into human cases.
Trans‑stadial continuity – infection persists across developmental stages, extending the infectious period.
Co‑feeding amplification – simultaneous feeding on multiple hosts spreads pathogen without systemic infection of the host.
Potential trans‑ovarial passage – vertical inheritance sustains pathogen presence even when reservoir density declines.
Efficient inoculation mechanism – salivary delivery ensures rapid pathogen transfer during brief attachment.

These mechanisms collectively ensure the continuity, amplification, and geographic spread of encephalitic viruses and borrelial bacteria within natural and peri‑urban ecosystems.

Co-feeding Transmission

Uninfected Tick Acquiring Pathogens from Infected Tick

Ticks acquire viral and bacterial agents from already infected conspecifics primarily through three biologically distinct pathways.

Co‑feeding transmission occurs when an uninfected nymph or larva attaches to the same host skin area as an infected tick within a short time window. Salivary secretions from the infected tick release virus particles (e.g., tick‑borne encephalitis virus) and spirochetes (Borrelia spp.) into the local dermal interstitium. The neighboring uninfected tick ingests these pathogens while feeding, bypassing the host’s systemic infection.

Transstadial passage enables a tick that has become infected during one developmental stage (larva or nymph) to retain the pathogen through molting to the next stage (nymph or adult). When the same species later feeds on a naïve host, it can transmit the pathogen acquired earlier from an infected sibling.

Transovarial transmission allows infected adult females to deposit pathogen‑laden eggs. The resulting larvae hatch already carrying the agent and can subsequently infect vertebrate hosts or other ticks during co‑feeding events.

Sexual transfer of pathogens has been documented in some tick species. Mating between an infected male and an uninfected female can result in the movement of spirochetes or viruses to the female’s reproductive tract, subsequently contaminating her offspring.

Environmental acquisition is limited but possible when ticks ingest pathogen‑containing blood remnants or tissue fluid present on the host’s skin surface after the infected tick has detached.

Collectively, these mechanisms explain how a pathogen‑free tick becomes a vector capable of transmitting encephalitis‑causing viruses and borreliosis‑inducing spirochetes to new hosts.

Role of Host Immunity

Host immunity directly influences the probability that a feeding tick acquires encephalitis‑causing viruses and Borrelia spirochetes. When a vertebrate host mounts a robust antibody response, circulating virus particles and spirochetes are cleared from the blood, reducing the pathogen load available to the tick’s mouthparts. Consequently, ticks feeding on immune‑competent animals ingest fewer infectious units than those attached to immunosuppressed or naïve hosts.

During the blood meal, tick saliva delivers anti‑inflammatory and anti‑coagulant compounds that suppress local immune reactions. This immunomodulation creates a microenvironment where residual pathogens can survive long enough to be taken up by the tick. Pathogens have evolved specific strategies to exploit this window:

Viral envelope proteins resist complement activation, allowing tick‑borne flaviviruses to persist in the blood despite host defenses.
Borrelia surface lipoproteins bind host factor H, inhibiting the alternative complement pathway and facilitating acquisition by the tick.

After ingestion, the pathogen must traverse the tick gut barrier and colonize salivary glands. Host‑derived immune factors, such as IgG and complement fragments, can be retained within the tick’s midgut lumen. These molecules may either neutralize the pathogen or, paradoxically, assist its passage by forming immune complexes that are taken up by gut epithelial cells. Experimental evidence shows that ticks feeding on animals deficient in complement C3 exhibit higher rates of pathogen colonization, indicating that host complement activity can limit tick infection.

The efficiency of subsequent transmission to a new host correlates with the initial immune status of the first host. Ticks that acquire pathogens from immunologically naïve reservoirs often harbor higher pathogen burdens, resulting in more effective inoculation during the next feeding cycle. Conversely, ticks that fed on hosts with strong humoral immunity tend to carry lower pathogen loads, decreasing transmission likelihood.

In summary, host immune competence shapes every stage of pathogen uptake by ticks: it reduces the initial pathogen concentration in the blood, influences the survival of ingested organisms within the tick gut, and determines the ultimate infectious dose delivered to subsequent hosts.

Factors Influencing Infection Rates

Environmental Conditions

Temperature and Humidity

Temperature determines the speed of tick development and the replication rate of pathogens within the vector. When ambient temperature rises above 10 °C, larval and nymphal stages complete molting faster, shortening the period between blood meals. Warmer conditions also accelerate replication of tick-borne encephalitis virus, increasing viral load before the next host encounter.

Humidity governs tick survival during questing. Relative humidity above 80 % prevents desiccation, allowing ticks to remain active on vegetation for extended periods. In dry environments (relative humidity below 50 %), ticks withdraw into the leaf litter, reducing host contact and consequently lowering transmission opportunities for both encephalitis virus and Borrelia burgdorferi.

The interaction of temperature and humidity creates optimal windows for pathogen acquisition:

Temperature 10–20 °C, humidity >80 %: high questing activity, elevated infection risk.
Temperature 20–25 °C, humidity 70–80 %: rapid pathogen replication, sustained host seeking.
Temperature >30 °C, humidity <60 %: increased mortality, reduced transmission potential.

Seasonal shifts that raise temperature and maintain high humidity correlate with spikes in human cases of encephalitis and Lyme disease. Monitoring these climatic parameters improves prediction of periods when ticks are most likely to acquire and transmit infectious agents.

Vegetation Type

Vegetation type determines the microhabitat where ticks encounter reservoir hosts and influences the likelihood that they acquire viral or bacterial agents. Dense understory, leaf litter, and moist ground cover create stable microclimates that support larval and nymphal development, while also harboring small mammals and birds that serve as carriers of encephalitis viruses and Borrelia spirochetes.

Specific plant communities affect host density and tick survival:

Deciduous woodlands – abundant leaf litter and diverse mammalian fauna; highest infection prevalence in nymphs.
Mixed forests – intermediate leaf litter depth; moderate host diversity; infection rates lower than pure deciduous stands.
Shrublands – limited litter, higher exposure to temperature fluctuations; reduced tick survival, but occasional high infection pockets where rodents concentrate.
Grasslands and meadows – sparse litter, open canopy; lower tick density, yet elevated risk where edge habitats intersect with forest fragments.

Vegetation structure also modulates humidity, a critical factor for tick questing activity. Areas with persistent moisture retain questing ticks longer, increasing contact frequency with infected hosts. Conversely, dry, sun‑exposed vegetation accelerates desiccation, reducing tick longevity and pathogen transmission opportunities.

Understanding the distribution of these plant communities enables precise mapping of disease risk zones. Targeted habitat management—such as reducing leaf litter depth in high‑risk woodland patches or creating buffer zones between forest edges and recreational areas—can lower the probability that ticks acquire and subsequently transmit encephalitis viruses and Borrelia bacteria.

Host Availability

Density of Reservoir Hosts

The abundance of reservoir hosts directly determines the probability that questing ticks encounter infected blood meals. High host density increases the number of feeding events per tick generation, thereby elevating the proportion of ticks acquiring pathogens such as tick‑borne encephalitis virus and Borrelia burgdorferi. Conversely, low host density reduces feeding opportunities, limiting pathogen circulation within tick populations.

Key mechanisms linking host density to tick infection rates include:

Greater host numbers raise the likelihood of co‑feeding transmission, where infected and uninfected ticks feed in close proximity on the same host.
Elevated host turnover accelerates the replacement of naïve individuals, sustaining a constant supply of susceptible blood sources.
Dense host assemblages often contain multiple competent species, expanding the reservoir community and diversifying pathogen strains available to ticks.

Spatial heterogeneity in host distribution creates focal hotspots of infection. Areas with clustered populations of rodents, shrews, or certain birds exhibit markedly higher infection prevalence in attached ticks compared with uniform or sparse habitats. Management actions that reduce reservoir host density—through habitat modification, targeted culling, or vaccination—consistently lower the infection burden in tick vectors, thereby decreasing the risk of human exposure to encephalitis and Lyme disease agents.

Movement Patterns of Hosts

Host mobility determines the geographic distribution of pathogens that ticks can acquire. Migratory birds transport infected ticks across continents, introducing encephalitic viruses and Borrelia into new ecosystems. When birds stop to feed, they deposit larvae that have fed on infected hosts, creating focal points of pathogen emergence far from the original reservoir.

Small mammals such as rodents exhibit limited home ranges but high population turnover. Their frequent movement within leaf litter and burrow systems increases contact rates with questing nymphs, facilitating efficient transmission of both viral and bacterial agents. Seasonal peaks in rodent activity coincide with tick larval emergence, aligning host availability with vector development.

Large ungulates, particularly deer, move over extensive territories during rut and foraging. Their movements expand the spatial reach of adult ticks, which attach for extended periods. As deer traverse areas inhabited by infected small mammals, adult ticks acquire pathogens indirectly through co‑feeding with infected nymphs on the same host.

Key mechanisms linking host movement to tick infection:

Spatial overlap: Areas where migratory birds, rodents, and ungulates intersect create multi‑host zones that support pathogen circulation.
Temporal synchrony: Seasonal peaks in host activity align with tick life‑stage emergence, maximizing feeding opportunities.
Habitat connectivity: Corridors such as hedgerows and riparian strips enable hosts to move between fragmented patches, spreading infected ticks.
Host density fluctuations: Population booms in rodents elevate the probability that questing larvae encounter infected individuals, boosting pathogen prevalence in subsequent tick generations.

Understanding these movement patterns informs surveillance strategies and habitat management aimed at reducing the spread of encephalitic viruses and Borrelia through tick vectors.

Tick Population Dynamics

Tick Species Susceptibility

Ticks vary in their capacity to acquire and transmit both tick‑borne encephalitis viruses and Borrelia spirochetes. Vector competence depends on species‑specific physiological traits, geographic range, and host preferences.

The principal vectors of tick‑borne encephalitis virus are members of the genus Ixodes. Ixodes ricinus dominates in Europe, efficiently acquiring the virus from small mammals and birds and maintaining it through transstadial transmission. In eastern Asia, Ixodes persulcatus fulfills a comparable role, often overlapping with I. ricinus in the far east. In North America, Ixodes scapularis and Ixodes pacificus are competent for the related Powassan virus, a flavivirus that produces encephalitis.

Borrelia species responsible for Lyme disease are transmitted primarily by Ixodes ticks as well. I. ricinus and I. scapularis exhibit high infection rates with Borrelia burgdorferi sensu lato complex, supporting both acquisition from infected rodents and subsequent transmission to new hosts. I. persulcatus carries Borrelia garinii and B. afzelii, prevalent in Siberia and parts of China.

Other tick genera display limited but noteworthy susceptibility:

Dermacentor reticulatus – occasional detection of TBEV in Central and Eastern Europe; low efficiency for Borrelia transmission.
Dermacentor andersoni – documented TBEV infection in western North America; rare Borrelia carriage.
Haemaphysalis longicornis – emerging vector in East Asia; sporadic TBEV isolates; not a primary Borrelia vector.
Amblyomma americanum – primarily associated with other pathogens; experimental infection shows poor replication of TBEV and Borrelia.

Susceptibility is influenced by tick immune responses, midgut barrier integrity, and salivary gland factors that facilitate pathogen survival and dissemination. Species that retain pathogens across developmental stages (larva → nymph → adult) and feed on multiple host species present the greatest epidemiological risk for encephalitis and borreliosis transmission.

Population Density

Population density directly shapes the epidemiology of tick‑borne encephalitis and Lyme disease. High human settlement density concentrates potential hosts—people, domestic animals, and peridomestic wildlife—within limited habitats, increasing the probability that questing ticks encounter an infected blood meal. Dense residential clusters often coexist with fragmented green spaces where small mammals, especially rodents, thrive; these mammals serve as primary reservoirs for both the encephalitis virus and Borrelia burgdorferi. Consequently, tick infection prevalence rises in areas where host density is amplified by urban sprawl.

Conversely, low‑density rural zones may support larger, contiguous habitats that host diverse wildlife assemblages. While overall tick abundance can be higher in such environments, the dilution effect—greater species diversity diluting pathogen transmission—may reduce infection rates among ticks. However, when livestock or hunting activities concentrate hosts in specific locales, localized spikes in pathogen prevalence can occur despite overall low human density.

Key mechanisms linking population density to pathogen acquisition in ticks include:

Increased host‑tick contact frequency due to proximity of humans and animals.
Elevated reservoir host abundance in fragmented habitats, boosting pathogen circulation.
Reduced predator presence in urbanized areas, allowing rodent populations to expand.
Management practices (e.g., pet grooming, acaricide use) that vary with settlement density, influencing tick survival and infection risk.

Understanding these density‑driven dynamics informs targeted interventions, such as habitat modification in densely populated districts and wildlife management in sparsely populated regions, to limit the acquisition of encephalitis‑causing viruses and Borrelia organisms by ticks.

Impact of Infection on Ticks

Pathogen Persistence within the Tick

Salivary Gland Tropism

Ticks acquire tick‑borne encephalitis viruses and Borrelia spirochetes during blood meals on infected vertebrates. After ingestion, pathogens traverse the midgut epithelium, enter the haemocoel, and migrate toward the salivary glands. Salivary gland tropism describes the selective colonisation and replication of these agents within the glandular tissue, a prerequisite for efficient transmission to a new host.

Encephalitis viruses exploit receptor‑mediated endocytosis in acinar cells, replicate within the cytoplasm, and are secreted with saliva during subsequent feeding. Viral replication peaks shortly before the tick detaches, synchronising pathogen load with salivation. Borrelia spp. adhere to the basal lamina of the glands via outer‑surface proteins (e.g., OspC, Vlp), resist complement‑mediated killing, and multiply in the lumen of the ducts. The bacteria accumulate in the salivary canal, ensuring their presence in the inoculum.

Key factors governing salivary gland tropism include:

Expression of pathogen‑specific adhesins that bind tick salivary proteins.
Modulation of tick immune pathways (e.g., suppression of antimicrobial peptides) that creates a permissive environment.
Hormonal cues from the feeding process that trigger glandular expansion and increased secretory activity.

The result is a concentrated pathogen reservoir in the saliva, enabling rapid deposition onto the host skin surface when the tick resumes feeding. This mechanism underlies the high transmission efficiency of both encephalitic viruses and Lyme‑disease spirochetes.

Midgut Colonization

Ticks acquire the agents of tick‑borne encephalitis and borreliosis during a blood meal from an infected vertebrate. Pathogens are deposited into the lumen of the midgut, where they must survive digestive enzymes, adhere to the epithelial surface, and establish a replicative niche.

Colonization proceeds through defined steps. First, the pathogen contacts the peritrophic matrix that lines the midgut lumen. Successful agents either degrade this barrier enzymatically or traverse it by exploiting transient pores. Second, surface adhesins on the pathogen bind specific receptors on midgut epithelial cells, anchoring the organism and preventing washout. Third, the pathogen evades or suppresses the tick’s innate immune responses, including antimicrobial peptides and phagocytic hemocytes, allowing proliferation within the epithelial layer. Finally, the organism migrates to the basal lamina, positioning itself for subsequent transmission to the salivary glands.

Specific mechanisms differ between the viral and bacterial agents. Tick‑borne encephalitis virus utilizes envelope proteins that interact with glycosaminoglycans on epithelial cells, facilitating entry and replication in midgut cells. Borrelia species express outer‑surface proteins (e.g., OspA, OspC) that recognize the tick’s midgut receptor TROSPA, enabling stable attachment and growth. Both agents modulate the expression of tick immune genes to reduce antimicrobial peptide production.

Factors influencing midgut colonization include:

Composition of the resident microbiota, which can outcompete or inhibit invading pathogens.
Integrity and thickness of the peritrophic matrix, altered by blood‑meal volume and host‑derived enzymes.
Levels of tick‑derived antimicrobial peptides such as defensins and lysozymes.
Genetic variation in tick receptors that bind pathogen adhesins.

Understanding these processes clarifies how the midgut serves as the initial reservoir that transforms a blood‑feeding arthropod into a competent vector for encephalitic viruses and Lyme‑disease spirochetes.

Tick Survival and Reproduction

No Significant Detrimental Effects

Ticks acquire encephalitic viruses and Borrelia bacteria primarily through blood meals from infected vertebrate hosts. The pathogen uptake occurs in the midgut, followed by migration to the salivary glands where transmission to subsequent hosts becomes possible. Throughout this cycle, ticks show minimal physiological disruption. Evidence indicates that infection does not impair feeding behavior, molting success, or survival rates.

Key observations supporting the lack of major adverse effects:

Feeding efficiency remains comparable between infected and uninfected individuals; engorgement volumes and attachment durations show no statistically significant differences.
Developmental milestones, including larval-to-nymph and nymph-to-adult molts, occur on schedule, suggesting that pathogen presence does not interfere with hormonal regulation or cuticle formation.
Longevity studies reveal equivalent life spans under controlled conditions, implying that metabolic burden imposed by the pathogens is negligible for the arthropod host.
Reproductive output of adult females, measured by egg batch size and hatchability, does not decline in the presence of encephalitic viruses or Borrelia spirochetes.

These findings reflect a co‑evolutionary balance wherein the pathogens exploit the tick as a vector without compromising the arthropod’s fitness. Consequently, the tick population maintains its capacity to disseminate disease agents despite harboring infectious agents.

Enhanced Transmission Opportunities

Ticks acquire and subsequently disseminate pathogens that cause encephalitis and borreliosis through several mechanisms that increase transmission opportunities. High host density in fragmented habitats forces ticks to aggregate on a limited number of mammals and birds, raising the probability that an uninfected tick will feed on an infected host. Co‑feeding, where multiple ticks attach to the same host simultaneously, enables virus or spirochete transfer without systemic infection of the host, effectively bypassing immune barriers. Overlapping activity periods of larval, nymphal, and adult stages extend the window for pathogen exchange, especially when environmental temperatures accelerate development and prolong questing seasons.

Additional factors amplify exposure risk:

Migratory birds transport infected nymphs across regions, introducing pathogens into naïve tick populations.
Climate‑driven shifts in vegetation alter microclimates, creating favorable conditions for tick survival and increasing questing height, which improves contact with larger hosts.
Anthropogenic land use, such as pasture expansion, concentrates livestock and deer, concentrating tick feeding events and facilitating pathogen circulation.

These dynamics collectively create a network of enhanced transmission pathways, ensuring that ticks frequently encounter infected hosts and that pathogens are efficiently passed to subsequent generations of vectors.