Where do encephalitis and borreliosis come from in ticks?

The Lifecycle of Ticks

Stages of Development

Ticks progress through four distinct developmental phases: egg, larva, nymph, and adult. Each phase determines the likelihood of acquiring and maintaining the agents that cause encephalitis and borreliosis.

Egg – Pathogens are rarely present; only transovarial transmission can introduce virus particles into offspring.
Larva – First blood meal on small vertebrates; larvae may ingest Borrelia spirochetes or tick‑borne encephalitis virus if the host is infected.
Nymph – Retains pathogens acquired as larvae (transstadial transmission). Nymphs often feed on larger hosts, increasing the chance of transferring infection to humans.
Adult – Continues to harbor pathogens from earlier stages; females can pass virus particles to eggs, while Borrelia persists through successive molts.

Tick‑borne encephalitis virus primarily relies on transovarial passage to appear in larvae, but it also survives across molts. Borrelia burgdorferi lacks transovarial transmission; it depends on acquisition during the larval blood meal and persists through nymph and adult stages. Both agents exploit the tick’s developmental continuity to maintain their life cycles and to reach vertebrate hosts.

Understanding these developmental steps clarifies how the disease‑causing agents originate within the vector and why certain life stages pose greater risk for human exposure.

Host-Seeking Behavior

Ticks acquire the agents of encephalitis and borreliosis during their quest for a suitable host. Questing ticks position themselves on vegetation at a height matching typical host passage, extending forelegs to detect heat, carbon dioxide, and volatile compounds. This sensory array enables discrimination among mammals, birds, and reptiles, directing attachment to species that harbor the relevant pathogens.

Key elements of the questing cycle include:

Elevation selection: Ticks climb blades or twigs to the stratum most frequented by target hosts.
Chemical sensing: Specialized Haller’s organs respond to host‑derived cues such as CO₂ plumes and skin odorants.
Thermal detection: Minute temperature gradients trigger leg extension and readiness to grasp.
Mechanical response: Physical contact with a passing animal initiates rapid attachment and insertion of the feeding apparatus.

Successful host engagement permits the transfer of encephalitis‑causing flaviviruses and Borrelia spirochetes from the tick’s salivary glands into the vertebrate bloodstream, completing the transmission cycle.

Encephalitis Virus in Ticks

Viral Reservoirs

Ticks acquire the agents of tick‑borne encephalitis and Lyme disease primarily from vertebrate hosts that maintain the pathogens in nature. The viral component, tick‑borne encephalitis virus (TBEV), persists in small mammals and certain bird species, while the spirochete causing Lyme disease, Borrelia burgdorferi sensu lato, is maintained by a broader range of mammals.

Key reservoir groups for TBEV include:

Rodents such as bank voles (Myodes glareolus) and wood mice (Apodemus sylvaticus).
Ground‑feeding birds, notably thrushes and blackbirds, which transport infected ticks over long distances.
Occasionally, larger mammals (e.g., hedgehogs) that support low‑level viral replication.

For Borrelia spp., primary reservoirs are:

White‑footed mice (Peromyscus leucopus) and other small rodents.
Shrew species that sustain spirochete populations.
Certain bird species that contribute to geographic spread.

Ticks become infected during larval or nymphal feeding on these hosts. The pathogen survives the molt (transstadial transmission) and can be passed to subsequent life stages. In some regions, adult females may transmit the virus or spirochetes to offspring (transovarial transmission), albeit at low efficiency for TBEV and negligible for Borrelia.

Reservoir composition varies with climate, habitat, and host density. In northern Europe, rodent‑dominated cycles dominate TBEV transmission, whereas in central and eastern Europe, mixed rodent‑bird cycles increase viral spread. Lyme disease reservoirs display similar regional shifts, with higher Borrelia diversity in forested habitats rich in small mammal populations.

Understanding these reservoirs clarifies the ecological origin of encephalitis‑causing viruses and Lyme‑causing spirochetes in ticks, informing surveillance and control strategies.

Transmission Mechanisms

Ticks acquire the agents of tick‑borne encephalitis and Lyme disease primarily from infected vertebrate reservoirs during blood meals. The virus that causes encephalitis (usually a flavivirus) and the spirochete responsible for borreliosis persist within the tick after the initial infection and are passed to subsequent life stages.

Transstadial transmission – the pathogen remains viable as the tick molts from larva to nymph and from nymph to adult, ensuring continuity across the three feeding stages.
Salivary inoculation – during attachment, the tick injects saliva containing the infectious agent directly into the host’s dermal tissue, facilitating rapid transmission.
Co‑feeding transmission – adjacent, simultaneously feeding ticks can exchange pathogens without the host developing a systemic infection, a route documented for both agents.
Transovarial transmission – female ticks can incorporate the virus into eggs, producing infected larvae; this mechanism is more efficient for the encephalitis virus than for the Lyme spirochete.

The efficiency of each pathway varies. The encephalitis virus shows a higher propensity for vertical passage, whereas Borrelia burgdorferi relies heavily on the reservoir host‑tick cycle and co‑feeding. Understanding these mechanisms clarifies how ticks serve as vectors for both diseases.

Acquisition from Hosts

Ticks become vectors for tick‑borne encephalitis virus and Borrelia burgdorferi during successive blood meals. The pathogens reside in the bloodstream of infected vertebrate hosts, allowing the feeding tick to ingest them. Primary reservoir species differ between the two agents.

Tick‑borne encephalitis virus: small mammals such as bank voles (Myodes glareolus), field mice (Apodemus spp.) and, in some regions, birds provide the virus. Infected hosts develop transient viremia, which is sufficient for acquisition by feeding nymphs and adults.
Borrelia burgdorferi sensu lato: rodents (e.g., white‑footed mouse, Peromyscus leucopus), shrews, and certain bird species maintain spirochetes in their blood and skin. Larval ticks feeding on these hosts become infected, and the pathogen persists through molting to the nymphal stage.

After ingestion, the pathogen colonizes the tick midgut, migrates to the salivary glands during subsequent feeding, and is transmitted to a new host. The efficiency of acquisition depends on host infection prevalence, duration of viremia or spirochetemia, and the tick’s developmental stage at the time of feeding.

Transovarial Transmission

Transovarial transmission refers to the passage of pathogens from an infected female tick to her offspring through the egg. This mechanism enables the maintenance of certain disease agents within tick populations without the need for vertebrate hosts.

Evidence shows that Borrelia burgdorferi, the bacterium responsible for borreliosis, can be transmitted transovarially in some Ixodes species, although the efficiency varies among tick strains and environmental conditions. In contrast, viruses causing tick‑borne encephalitis, such as the tick‑borne encephalitis virus (TBEV), are consistently passed to progeny, ensuring the virus persists in tick colonies across generations.

Key implications of transovarial transmission for the origin of encephalitis‑ and borreliosis‑causing agents in ticks include:

Direct introduction of pathogens into the larval stage, eliminating the requirement for early blood meals to acquire infection.
Preservation of pathogen reservoirs during periods of low host availability, supporting year‑round disease risk.
Potential for vertical spread to geographically distant areas when infected nymphs or adults disperse and lay eggs in new habitats.

Understanding the dynamics of transovarial transmission informs vector control strategies, such as targeting gravid females or disrupting egg development, to reduce the baseline prevalence of these pathogens in tick populations.

Impact on Tick Biology

Encephalitis‑causing viruses and Borrelia bacteria alter tick physiology in several measurable ways. Infection triggers changes in salivary gland protein expression, enhancing the secretion of anticoagulants and immunomodulatory molecules that facilitate pathogen transmission. Simultaneously, pathogen presence modifies the expression of tick midgut receptors, increasing the efficiency of pathogen acquisition during blood meals.

Metabolic adjustments accompany infection. Ticks harboring viruses show elevated glycolytic activity, supporting the high energy demand of viral replication. Borrelia‑infected specimens display altered lipid metabolism, reflected in increased cholesterol ester storage, which may stabilize the spirochete’s outer membrane within the vector.

Reproductive parameters are also affected. Studies report a modest reduction in oviposition rates for virus‑positive females, while Borrelia infection can extend the duration of the gonotrophic cycle, delaying egg laying but not decreasing total fecundity. These shifts influence population dynamics, potentially favoring longer‑lived, pathogen‑carrying individuals.

Behavioral changes emerge under pathogen pressure. Infected ticks exhibit heightened questing activity at lower temperatures, expanding the temporal window for host contact. This adaptation aligns with the seasonal prevalence of both encephalitis viruses and Borrelia species, improving transmission opportunities.

Collectively, these physiological, metabolic, reproductive, and behavioral modifications illustrate how the presence of encephalitis agents and Lyme disease spirochetes reshapes tick biology, reinforcing the vector’s capacity to maintain and spread the pathogens.

Borrelia Bacteria in Ticks

Bacterial Reservoirs

Ticks acquire the agents of encephalitis and borreliosis while feeding on vertebrate hosts that serve as bacterial reservoirs. Small mammals host the spirochete responsible for borreliosis; the white‑footed mouse (Peromyscus leucopus) and the bank vole (Myodes glareolus) maintain high infection prevalence and transmit the pathogen to feeding larvae and nymphs. Numerous bird species, especially passerines, also harbor Borrelia, facilitating geographic spread through migration. Larger mammals, such as roe deer (Capreolus capreolus) and red deer (Cervus elaphus), do not sustain the bacterium but support tick population growth, indirectly increasing infection risk.

Reservoirs for the encephalitis‑causing agent, although viral, overlap with bacterial hosts. Rodents (field mice, voles) and certain bird species retain the virus in their bloodstream, providing a source for tick acquisition. The co‑occurrence of bacterial and viral pathogens in the same reservoir species creates opportunities for simultaneous transmission to ticks.

Key reservoir characteristics:

High infection prevalence in host population
Ability to sustain pathogen without severe disease
Frequent exposure to tick larvae and nymphs
Mobility that enables pathogen dispersal across habitats

Understanding these reservoir dynamics clarifies how ticks become vectors for both encephalitis and borreliosis, highlighting the ecological link between host communities and disease emergence.

Transmission Mechanisms

Ticks acquire pathogens while feeding on infected vertebrate reservoirs. The virus that causes tick‑borne encephalitis (TBEV) is taken up from small mammals such as rodents, while Borrelia burgdorferi, the agent of borreliosis, is acquired from the same or larger mammals, especially deer and rodents. After ingestion, pathogens persist through the tick’s developmental stages—a process known as transstadial transmission. In the case of TBEV, a fraction of infected females also pass the virus to their offspring via transovarial transmission, allowing larvae to emerge already infected.

During subsequent blood meals, pathogens migrate to the salivary glands. Saliva‑assisted transmission facilitates entry into the host by suppressing local immune responses and enhancing pathogen entry. Additional mechanisms include:

Co‑feeding transmission: adjacent, non‑systemically infected ticks acquire the pathogen from a shared feeding site without the host developing a systemic infection.
Sequential feeding: a tick that previously fed on an infected host can transmit the pathogen during a later feed on a naïve host.
Environmental persistence: although ticks are the primary vectors, contaminated habitats support reservoir host populations that maintain pathogen cycles.

These mechanisms collectively enable ticks to serve as efficient vectors for both encephalitis‑causing viruses and borreliosis‑causing spirochetes.

Acquisition from Hosts

Ticks become vectors for tick‑borne encephalitis viruses and Borrelia spirochetes through blood meals taken from infected vertebrate reservoirs. During the larval stage, a tick attaches to a host that carries the pathogen in its bloodstream or tissues; the pathogen enters the tick’s midgut and persists through molting (transstadial transmission). The infected nymph or adult then transmits the pathogen to subsequent hosts during later feedings.

Primary reservoirs for encephalitis viruses include:

Small mammals such as rodents (e.g., bank voles, wood mice) that sustain high viremia.
Ground‑feeding birds that circulate the virus during migration periods.

Key reservoirs for Borrelia burgdorferi sensu lato, the agent of Lyme disease, comprise:

Rodent species (e.g., white‑footed mouse, bank vole) that harbor spirochetes in skin and blood.
Certain bird species that transport infected ticks across regions.
Larger mammals (e.g., deer) that support tick populations but typically do not infect ticks directly; they provide feeding opportunities that facilitate pathogen spread.

Co‑feeding on the same host permits pathogen exchange between ticks without systemic infection of the host, reinforcing transmission cycles. Consequently, the geographic distribution of encephalitis and borreliosis reflects the range of competent reservoir hosts and the habitats that support tick development.

Co-feeding Transmission

Co‑feeding transmission occurs when infected and uninfected ticks feed in close proximity on the same host without the host’s systemic infection. The pathogen moves directly between the feeding sites through the host’s skin, allowing the virus that causes tick‑borne encephalitis (TBE) and the bacterium responsible for Lyme disease to spread even when the host’s blood does not contain detectable levels of the agent.

During a co‑feeding event, an infected nymph or larva releases virus or spirochetes into the skin tissue. Adjacent ticks, typically larvae, acquire the pathogen through the localized blood pool that forms at the feeding lesion. This process bypasses the need for a viremic host and can maintain pathogen circulation in environments where reservoir competence is low.

Key characteristics of co‑feeding transmission:

Requires simultaneous attachment of multiple ticks on a single host.
Operates efficiently at low ambient temperatures, which favor TBE virus replication in the tick.
Supports maintenance of infection cycles in habitats with sparse rodent populations.
Enhances the probability of pathogen persistence during early spring and autumn, when systemic host infection rates are minimal.

Experimental studies have demonstrated that removal of systemic host infection does not prevent pathogen spread if co‑feeding ticks remain present. Field observations correlate high co‑feeding rates with increased incidence of TBE in regions where rodent density fluctuates seasonally. For Lyme disease, co‑feeding contributes to the early establishment of Borrelia in larval ticks before they acquire infection from systemic hosts.

Control measures that target co‑feeding include reducing tick density on wildlife hosts, applying acaricides to key host species, and managing habitat to limit host–tick contact during peak co‑feeding periods. Understanding this transmission route clarifies how both encephalitic viruses and borrelial bacteria persist in tick populations and informs strategies to interrupt their life cycles.

Impact on Tick Biology

Encephalitic and borrelial agents alter tick physiology at multiple levels. Infection triggers modulation of salivary gland proteins, enhancing blood‑meal acquisition and prolonging attachment time. Pathogen presence suppresses expression of antimicrobial peptides, reducing innate immune activity and allowing persistent colonization. Reproductive output shifts, with infected females often producing fewer eggs, while surviving larvae display increased questing activity to compensate for population loss.

Microbial interactions reshape the tick’s internal ecosystem. Borrelia spp. compete with resident symbionts for nutrients, leading to reduced diversity of gut microbiota. Encephalitis‑associated viruses promote changes in lipid metabolism that affect energy reserves, influencing overwintering survival. These physiological adjustments affect vector competence, as altered gut barrier integrity facilitates pathogen transmission during subsequent feedings.

Key biological impacts include:

Enhanced salivary secretion composition, improving pathogen delivery.
Down‑regulated immune effectors, permitting long‑term infection.
Modified reproductive metrics, influencing population dynamics.
Restructured microbiome, affecting nutrient processing and immunity.
Adjusted metabolic pathways, altering energy storage and survival rates.

Co-infection and Public Health Implications

Simultaneous Pathogen Presence

Ticks acquire pathogens during blood meals from vertebrate hosts that harbor infectious agents. A single tick may ingest both a flavivirus responsible for tick‑borne encephalitis (TBE) and spirochetes of the Borrelia burgdorferi complex, leading to simultaneous pathogen presence. This co‑acquisition occurs when a host, such as a small mammal or bird, is concurrently infected with TBE virus and Borrelia, or when the tick feeds on different hosts during successive life stages that each carry one of the agents.

Key mechanisms enabling dual infection include:

Transstadial persistence: Once a larva acquires either pathogen, it retains the infection through molting to the nymph and adult stages.
Co‑feeding transmission: Adjacent, unfed ticks can acquire pathogens from the same host without the host developing systemic infection, facilitating simultaneous colonization.
Vertical transmission: Limited evidence suggests occasional maternal passage of TBE virus, augmenting the pool of infected vectors.

Epidemiological surveys across Europe and Asia report co‑infection rates ranging from 1 % to 10 % in questing nymphs, with higher frequencies in regions where both diseases are endemic. Laboratory analyses consistently detect viral RNA and Borrelia DNA within the same tick specimen, confirming biological overlap rather than incidental contamination.

Clinical implications stem from the possibility of concurrent human exposure. Bite victims may develop encephalitic symptoms and Lyme borreliosis concurrently, complicating diagnosis and therapy. Diagnostic protocols therefore recommend testing for both agents when patients present with neurologic signs accompanied by erythema migrans or other Lyme‑related manifestations.

Preventive measures focus on reducing tick exposure and employing broad‑spectrum acaricides, as single‑pathogen interventions cannot address the combined risk. Public health monitoring programs that track co‑infection prevalence improve risk assessments and guide resource allocation for vaccination against tick‑borne encephalitis and early treatment of Lyme disease.

Disease Manifestations in Humans

Tick‑borne encephalitis and Lyme borreliosis are transmitted by ixodid ticks that feed on infected vertebrate hosts. Human infection results from the inoculation of virus‑laden saliva (for encephalitis) or spirochetes of the Borrelia burgdorferi complex (for borreliosis). The clinical picture differs between the two agents but both can produce acute and chronic disease.

Tick‑borne encephalitis
- Sudden onset fever, headache, malaise.
- Meningitic signs: neck stiffness, photophobia.
- Encephalitic involvement: altered consciousness, seizures, focal neurological deficits.
- Myelitis or combined meningo‑encephalomyelitis in severe cases.
- Persistent sequelae: cognitive impairment, gait disturbance, hearing loss, tremor.
Lyme borreliosis
- Early localized stage: expanding erythema migrans, flu‑like symptoms.
- Early disseminated stage: cranial nerve palsy (especially facial), meningitis, radiculopathy, atrioventricular block, migratory musculoskeletal pain.
- Late stage: chronic arthritis of large joints, neuroborreliosis with peripheral neuropathy, encephalopathy, memory problems.

Both infections may progress from a brief febrile illness to organ‑specific damage if untreated. Prompt recognition of the characteristic manifestations guides antimicrobial or antiviral therapy, reduces the risk of long‑term disability, and limits the public health impact of tick‑borne disease.

Prevention and Control

Tick Surveillance

Tick surveillance provides systematic data on the prevalence of pathogens that cause tick‑borne encephalitis and Lyme disease. Surveillance programs collect ticks from vegetation, hosts, or drag‑sampling across defined regions, preserving specimens for laboratory analysis. Molecular assays such as PCR identify viral RNA and Borrelia DNA, while serological tests detect antigenic markers. Results are entered into geo‑referenced databases, enabling real‑time mapping of infection hotspots.

Surveillance outcomes guide public‑health interventions. High infection rates trigger targeted acaricide applications, public‑awareness campaigns, and vaccination efforts where applicable. Longitudinal data reveal temporal trends, informing risk assessments for emerging strains or expanding tick ranges due to climate change.

Effective tick surveillance relies on coordinated networks of entomologists, veterinarians, and epidemiologists. Standardized protocols ensure comparability across jurisdictions. Data sharing platforms disseminate findings to clinicians, researchers, and policymakers, supporting evidence‑based decision‑making and resource allocation.

Personal Protective Measures

Ticks transmit the virus responsible for tick‑borne encephalitis and the bacterium that causes Lyme disease. Personal protection reduces exposure and prevents infection.

Wear long sleeves, long trousers, and closed shoes; tuck trousers into socks to create a barrier.
Apply repellents containing DEET (20‑30 %), picaridin (20 %), or IR3535 to skin and clothing; reapply according to product instructions.
Treat outdoor clothing with permethrin (0.5 % concentration) and allow it to dry before wearing.
Conduct systematic tick checks every two hours while in endemic areas; inspect scalp, behind ears, underarms, and groin.
Remove attached ticks promptly with fine‑pointed tweezers; grasp close to the skin, pull upward with steady pressure, and disinfect the bite site.
Avoid high‑risk habitats such as dense underbrush, tall grass, and leaf litter; stay on cleared paths when possible.
Consider vaccination against tick‑borne encephalitis for individuals with frequent exposure; follow the recommended schedule for primary and booster doses.
Carry a small first‑aid kit containing antiseptic wipes, gloves, and a tick‑removal tool for immediate response.

Consistent application of these measures minimizes the likelihood of acquiring tick‑borne encephalitis and Lyme disease.