How should Lyme disease contracted from a tick be treated?

Understanding Lyme Disease

What is Lyme Disease?

Lyme disease is an infectious illness caused by the spirochete Borrelia burgdorferi, transmitted to humans through the bite of infected Ixodes ticks. The bacterium colonizes the tick’s midgut and migrates to the salivary glands during feeding, entering the host’s skin within 24–48 hours of attachment.

The disease is most prevalent in temperate regions of North America and Europe, where tick habitats overlap with human activity. Seasonal peaks correspond to the nymphal stage of the tick, which is small enough to evade detection.

Clinical presentation progresses through stages:

Early localized infection (3–30 days): erythema migrans rash, flu‑like symptoms, fatigue.
Early disseminated infection (weeks to months): multiple rashes, facial nerve palsy, meningitis, carditis, migratory joint pain.
Late disseminated infection (months to years): arthritis, neuropathy, cognitive disturbances.

Diagnosis relies on a two‑tier serologic algorithm: an initial enzyme‑linked immunosorbent assay (ELISA) followed by a confirmatory Western blot if the first test is positive. Direct detection methods, such as polymerase chain reaction (PCR), are reserved for specific specimens.

Prevention focuses on avoiding tick exposure, promptly removing attached ticks, and applying repellents containing DEET or permethrin. Awareness of endemic areas and early recognition of the characteristic rash reduce the risk of progression.

How Lyme Disease is Contracted

Tick Identification

Accurate identification of the tick that transmitted the infection is essential for guiding clinical management of Lyme disease. Different tick species vary in their capacity to carry Borrelia burgdorferi and in the geographic areas where they are encountered; recognizing the species informs risk assessment and the urgency of treatment.

Key morphological characteristics distinguish the primary vectors:

Ixodes scapularis (eastern black‑legged tick) – reddish‑brown body, dark scutum, distinctive “hour‑glass” pattern on the ventral side, palps longer than the basis capituli.
Ixodes pacificus (western black‑legged tick) – similar coloration, but the scutum bears a darker central spot; the coxae are more rounded.
Dermacentor variabilis (American dog tick) – brown scutum with white‑gray festoons on the posterior edge, mouthparts visible from above.

Identification procedures:

Collect the tick with fine tweezers, avoiding crushing the body.
Place the specimen on a white background and examine under at least 10× magnification.
Compare observed features with a validated reference key or reputable online database.
Document the life stage (larva, nymph, adult) and engorgement level, as these influence transmission probability.

Clinical implications:

Nymphal Ixodes spp. are most frequently linked to human infection; prompt antibiotic therapy is recommended when a bite is confirmed.
Adult Ixodes spp. may transmit larger inocula; treatment decisions should consider the duration of attachment (>24 hours) and local infection rates.
Non‑Ixodes ticks generally present a lower risk for Lyme disease; however, they may transmit other pathogens, requiring alternative therapeutic considerations.

By integrating precise tick identification into patient assessment, clinicians can tailor antimicrobial regimens to the likelihood of B. burgdorferi exposure, minimize unnecessary treatment, and improve outcomes.

Transmission Process

Lyme disease is transmitted when an infected Ixodes tick attaches to human skin and feeds for a sufficient period. The bacterium Borrelia burgdorferi resides in the tick’s midgut and moves to the salivary glands during prolonged feeding. Saliva containing the pathogen is then injected into the host’s dermal tissue, establishing infection.

Key elements of the transmission process:

Tick attachment – larvae, nymphs, or adults attach to exposed skin, often in warm, moist areas.
Feeding duration – a minimum of 36–48 hours of blood intake is required for the bacterium to migrate to the salivary glands.
Pathogen transfer – saliva released during feeding introduces B. burgdorferi into the host’s bloodstream and skin.
Early infection sites – the spirochetes initially colonize the skin, producing the characteristic erythema migrans rash before disseminating systemically.

Symptoms of Lyme Disease

Early Stage Symptoms

Early-stage Lyme disease typically appears within 3–30 days after a tick bite. The hallmark sign is a circular skin lesion, often expanding outward from the bite site. This rash, known as erythema migrans, measures 5–70 mm in diameter, may have a central clearing, and is usually not painful or itchy.

Accompanying systemic manifestations include:

Fever, often low‑grade.
Headache, sometimes resembling migraine.
Fatigue that limits normal activity.
Muscular or joint aches, especially in the neck, shoulders, or knees.
Neck stiffness or mild meningitis‑like symptoms.
Cognitive disturbances such as difficulty concentrating or short‑term memory lapses.

These clinical features guide prompt antimicrobial therapy, which reduces the risk of disseminated infection and long‑term complications. Early recognition of the rash and associated symptoms enables clinicians to initiate oral doxycycline or amoxicillin within the first few weeks, optimizing treatment outcomes.

Later Stage Symptoms

Later‑stage Lyme disease, also called disseminated or chronic infection, typically emerges weeks to months after the initial tick bite when the spirochete Borrelia burgdorferi has spread to multiple organ systems. At this point, antimicrobial therapy must address systemic involvement and prevent irreversible damage.

Common manifestations in the later phase include:

Arthritis affecting large joints, especially the knee, with swelling and limited motion.
Neurological deficits such as peripheral neuropathy, facial nerve palsy, and meningitis‑like symptoms (headache, stiff neck, photophobia).
Cardiac involvement, most often atrioventricular block or myocarditis, leading to irregular heart rhythms.
Cognitive disturbances, including memory loss, difficulty concentrating, and mood changes.
Fatigue and musculoskeletal pain that persist despite initial treatment.

Recognition of these signs guides clinicians to extend antibiotic courses, select agents with central nervous system penetration when neurologic symptoms are present, and monitor cardiac function. Early identification of late manifestations improves prognosis and reduces the risk of permanent sequelae.

Diagnosis of Lyme Disease

Clinical Diagnosis

Clinical diagnosis of Lyme disease guides therapeutic decisions and prevents unnecessary antimicrobial exposure. Physicians rely on a combination of exposure history, symptom chronology, and objective findings to differentiate early infection from other tick‑borne conditions.

Typical early manifestations include:

Recent attachment of an Ixodes tick, usually within the past 30 days.
Expanding erythema migrans lesion measuring ≥5 cm, often with central clearing.
Flu‑like symptoms such as fever, headache, myalgia, or arthralgia.

When erythema migrans is absent, diagnostic criteria expand to include:

Multiple erythema migrans lesions.
Neurologic signs (e.g., facial palsy, meningitis) with supporting cerebrospinal fluid pleocytosis.
Cardiac involvement (atrioventricular block) confirmed by electrocardiography.
Arthritis of large joints, especially the knee, accompanied by synovial fluid analysis showing inflammatory changes.

Laboratory confirmation employs a two‑tiered serologic algorithm:

First tier: enzyme‑linked immunosorbent assay (ELISA) for IgM and IgG antibodies.
Second tier: Western blot interpretation according to CDC criteria; positive IgM required within 30 days of symptom onset, IgG after 30 days.

Accurate clinical identification determines the need for antibiotic regimens, ranging from doxycycline for early disease to intravenous ceftriaxone for disseminated neurologic or cardiac involvement. Misdiagnosis can delay appropriate therapy and increase the risk of chronic sequelae.

Laboratory Testing

ELISA Test

The ELISA (enzyme‑linked immunosorbent assay) is the first‑line serologic test used to detect antibodies against Borrelia burgdorferi, the bacterium that causes Lyme disease. Laboratories perform the assay by attaching specific bacterial antigens to a solid surface, adding the patient’s serum, and then applying an enzyme‑linked secondary antibody that produces a measurable color change when bound.

Key steps of the ELISA procedure:

Immobilize B. burgdorferi antigens on a microtiter plate.
Add patient serum; if antibodies are present, they bind to the antigens.
Introduce enzyme‑conjugated anti‑human IgM/IgG antibodies.
Add substrate; enzymatic reaction generates a color intensity proportional to antibody concentration.
Measure optical density with a spectrophotometer and compare to calibrated controls.

Antibody development follows a predictable timeline:

IgM antibodies become detectable 2–4 weeks after tick bite.
IgG antibodies appear 4–6 weeks post‑exposure.
Testing before this window frequently yields false‑negative results, especially in early localized disease.

Interpretation guidelines:

A positive ELISA result triggers a confirmatory Western blot to differentiate true infection from cross‑reactivity.
A negative ELISA generally excludes Lyme disease, except when testing occurs during the early window period; clinicians may repeat testing if symptoms persist.

Clinical impact on treatment:

Positive confirmed serology supports initiation of doxycycline or ceftriaxone, depending on disease stage and symptom severity.
Serial ELISA testing is not recommended for monitoring therapeutic response; clinical assessment remains primary.

Overall, the ELISA assay provides rapid, quantitative evidence of exposure to B. burgdorferi, informing diagnostic confirmation and guiding appropriate antibiotic therapy.

Western Blot Test

The Western blot is employed to confirm the presence of antibodies against Borrelia burgdorferi after an initial screening test. Serum proteins are separated by electrophoresis, transferred to a membrane, and probed with patient antibodies. Detection of IgM and IgG bands indicates an immune response to the pathogen.

Interpretation follows established criteria:

IgM: presence of at least two of the 23‑kDa, 39‑kDa, and 41‑kDa bands.
IgG: presence of at least five of the 18‑kDa, 23‑kDa, 28‑kDa, 30‑kDa, 39‑kDa, 41‑kDa, 45‑kDa, 58‑kDa, 66‑kDa, or 93‑kDa bands.

IgM antibodies typically appear 2–4 weeks after the tick bite; IgG antibodies develop after 4–6 weeks. Testing performed earlier may yield false‑negative results, necessitating repeat analysis if clinical suspicion persists.

A positive Western blot substantiates the diagnosis and justifies initiation of an appropriate antibiotic course. A negative result, when paired with a compatible clinical picture, may prompt reconsideration of alternative diagnoses or delayed retesting to capture seroconversion.

Differentiating from Other Conditions

When evaluating a patient with a recent tick bite, confirming Lyme disease requires separating it from other illnesses that produce similar symptoms. Accurate differentiation guides appropriate antimicrobial therapy and prevents unnecessary treatment.

Key clinical clues that favor Lyme infection include:

Erythema migrans: expanding, usually annular rash appearing 3‑30 days after exposure; central clearing is common, but the lesion may be uniformly red.
Flu‑like presentation accompanied by facial nerve palsy or cardiac conduction abnormalities, which are relatively specific for Borrelia burgdorferi.
History of exposure in endemic regions during peak tick activity months.

Conditions that can mimic Lyme disease:

Anaplasmosis and ehrlichiosis: present with fever, headache, and leukopenia, but lack characteristic rash; PCR or serology for Anaplasma/Ehrlichia is diagnostic.
Babesiosis: produces hemolytic anemia and thrombocytopenia; peripheral blood smear reveals intra‑erythrocytic parasites.
Rocky Mountain spotted fever: rash typically starts on wrists and ankles and spreads centripetally; spotted fever rickettsial DNA detection confirms diagnosis.
Viral exanthems (e.g., parvovirus B19, Epstein‑Barr virus): produce rash and fatigue but do not yield serologic evidence of Borrelia infection.
Autoimmune disorders such as rheumatoid arthritis or systemic lupus erythematosus: generate joint pain and serologic abnormalities but lack acute tick exposure and rash.

Laboratory differentiation:

Two‑tier serology (ELISA followed by Western blot) remains the standard for Lyme; positive IgM/IgG bands correspond to disease stage.
PCR testing of synovial fluid or skin biopsy can identify Borrelia DNA when serology is equivocal.
Complete blood count, liver enzymes, and inflammatory markers help exclude hematologic or systemic infections.

Timely recognition of these distinguishing features ensures that antimicrobial regimens—doxycycline, amoxicillin, or cefuroxime—are prescribed only when Lyme disease is confirmed, while alternative diagnoses receive targeted therapy.

Treatment Approaches for Lyme Disease

Antibiotic Treatment Regimens

Early Stage Treatment

Early Lyme disease is best managed with a short course of oral antibiotics. Doxycycline (100 mg twice daily) for 10–21 days is the preferred agent for patients older than eight years who are not pregnant. For children under eight, or for pregnant or lactating women, amoxicillin (500 mg three times daily) or cefuroxime axetil (500 mg twice daily) for the same duration are recommended.

The chosen regimen should begin promptly after the characteristic rash or other early symptoms appear. Treatment aims to eradicate Borrelia burgdorferi before dissemination, reducing the risk of neurologic, cardiac, or arthritic complications. Patients must complete the full prescribed course even if symptoms improve rapidly.

Follow‑up evaluation within two to four weeks confirms clinical resolution. Persistent or worsening signs warrant re‑assessment, possible extension of therapy, or referral to an infectious‑disease specialist. Laboratory testing is not required for initiating therapy but may be useful for baseline documentation.

Disseminated Stage Treatment

Disseminated Lyme disease requires systemic antimicrobial therapy to eradicate Borrelia burgdorferi from multiple organ systems. Intravenous ceftriaxone (2 g daily) for 14–28 days is the standard regimen, supported by randomized trials showing superior efficacy for neurological and cardiac manifestations. Alternatives include intravenous cefotaxime (2 g every 8 hours) or oral doxycycline (100 mg twice daily) for 28 days when central nervous system involvement is absent or when intravenous access is problematic.

Adjunctive measures focus on symptom control and organ‑specific support:

Anti‑inflammatory agents for arthritic pain (e.g., NSAIDs, short‑course corticosteroids if severe).
Cardiac monitoring for atrioventricular block; temporary pacing may be required until antimicrobial effect restores conduction.
Neurocognitive rehabilitation for persistent encephalopathy; repeat lumbar puncture only if clinical deterioration occurs.

Follow‑up includes serologic testing at 6‑month intervals to confirm seroconversion, neurological examination, and assessment of joint swelling. Persistent symptoms after completion of therapy should prompt evaluation for co‑infection (e.g., Babesia, Anaplasma) and consideration of extended antimicrobial courses only within clinical trial protocols, as evidence for benefit remains limited.

Chronic Lyme Disease Treatment Controversies

Chronic Lyme disease treatment remains a contested area despite clear guidelines for acute infection. Divergent views stem from differences in diagnostic criteria, recommended duration of antibiotic therapy, and interpretation of clinical trial data.

Key points of disagreement include:

Diagnostic standards – The Infectious Diseases Society of America (IDSA) requires laboratory confirmation and objective signs, whereas the International Lyme and Associated Diseases Society (ILADS) accepts broader clinical presentations, often without serologic evidence.
Antibiotic duration – IDSA recommends a 2–4‑week course for most manifestations; ILADS advocates for extended or repeated courses lasting months, citing anecdotal improvement in persistent symptoms.
Evidence interpretation – Randomized trials funded by government agencies show limited benefit of long‑term antibiotics and highlight increased adverse events. Pro‑longed‑therapy proponents emphasize uncontrolled studies and patient‑reported outcomes that suggest symptom relief.
Insurance coverage – Payers generally follow IDSA guidelines, denying reimbursement for prolonged regimens, while patient advocacy groups pressure for broader coverage based on perceived clinical necessity.
Research gaps – Absence of universally accepted biomarkers for chronic infection fuels debate, prompting calls for large‑scale, double‑blind studies to resolve efficacy and safety questions.

The controversy influences clinical practice, leading some providers to adhere strictly to guideline‑based short courses, while others prescribe extended regimens under compassionate‑use provisions. Consensus remains elusive until robust, reproducible data clarify the underlying pathophysiology and therapeutic response of persistent Lyme‑related symptoms.

Managing Symptoms and Complications

Pain Management

Pain associated with Lyme disease frequently involves arthralgia, myalgia, and peripheral neuropathy. Effective relief requires early assessment, classification of pain type, and coordination with antimicrobial therapy.

First‑line pharmacologic relief relies on non‑steroidal anti‑inflammatory drugs (NSAIDs) such as ibuprofen or naproxen. NSAIDs reduce inflammation and provide moderate analgesia. Acetaminophen offers an alternative when gastrointestinal risk limits NSAID use.

Neuropathic components respond to agents that modulate neuronal excitability. Recommended options include:

Gabapentin or pregabalin, titrated to symptom control.
Duloxetine, a serotonin‑norepinephrine reuptake inhibitor, useful for mixed nociceptive‑neuropathic pain.
Low‑dose amitriptyline, when other agents are ineffective.

Opioid analgesics may be considered for severe, refractory pain, but only for short durations. Morphine, oxycodone, or hydromorphone require strict monitoring for tolerance, dependence, and interaction with doxycycline or other antibiotics.

Non‑pharmacologic measures complement drug therapy:

Physical therapy emphasizing range‑of‑motion exercises and gradual strengthening.
Heat or cold application to affected joints.
Transcutaneous electrical nerve stimulation (TENS) for localized discomfort.
Cognitive‑behavioral techniques to address pain‑related stress.

Pain management must be synchronized with the antimicrobial regimen that eradicates Borrelia burgdorferi. Regular evaluation of pain intensity, functional status, and adverse effects guides adjustments. Discontinuation of analgesics occurs as infection resolves and inflammatory markers normalize.

Neurological Symptoms Management

Neurological involvement in Lyme disease may present as meningitis, cranial nerve palsy (most often facial), radiculitis, or encephalopathy. Prompt antimicrobial therapy reduces the risk of persistent deficits.

First‑line antibiotics for neuroborreliosis are administered intravenously for 14–28 days. Recommended regimens include ceftriaxone 2 g daily or cefotaxime 2 g every 8 hours; oral doxycycline 100 mg twice daily is an alternative when intravenous access is unavailable and the patient can tolerate oral medication. Dosage adjustments are required for renal or hepatic impairment.

Adjunctive measures focus on symptom relief:

Analgesics for headache and myalgia; NSAIDs are first choice, opioids reserved for severe pain.
Neuropathic agents (gabapentin, pregabalin, duloxetine) for radicular pain and dysesthesias.
Short courses of corticosteroids may be considered for severe facial nerve edema, but routine use is discouraged.
Physical therapy to maintain muscle tone and prevent joint contractures during facial palsy recovery.
Cognitive rehabilitation for attention and memory disturbances, incorporating graded exercises and compensatory strategies.

Follow‑up includes serial neurological examinations and, when indicated, repeat lumbar puncture to assess cerebrospinal fluid normalization. Persistent or worsening symptoms after completion of antibiotics warrant imaging (MRI with contrast) to exclude alternative pathology and may justify extended antimicrobial therapy under specialist supervision.

Joint Problems Management

Lyme infection transmitted by ticks frequently leads to inflammatory joint disease, most often affecting the knees. Prompt antimicrobial therapy reduces bacterial load and limits joint damage. Recommended regimens include doxycycline for 21 days or, when contraindicated, cefuroxime axetil or amoxicillin for the same duration.

After completing antibiotics, joint-specific management focuses on symptom control and functional recovery:

Non‑steroidal anti‑inflammatory drugs (NSAIDs) for pain and swelling; dosage adjusted for renal and gastrointestinal risk.
Short courses of oral corticosteroids when NSAIDs fail to provide relief; limit duration to avoid immunosuppression.
Intra‑articular glucocorticoid injection for persistent effusion; repeat only after reassessment.
Structured physical therapy emphasizing range‑of‑motion exercises, strengthening of peri‑articular musculature, and gait training.
Orthotic support or bracing when instability or malalignment contributes to discomfort.

Monitoring includes periodic joint examination, ultrasound or MRI if effusion persists, and serologic testing to confirm eradication of Borrelia. Referral to rheumatology is warranted for:

Arthritis lasting more than three months despite adequate antibiotics.
Recurrent joint inflammation with negative serology, suggesting post‑infectious autoimmune response.
Development of systemic manifestations such as uveitis or carditis.

Effective joint management combines eradication of the pathogen with targeted anti‑inflammatory measures and rehabilitative therapy to restore mobility and prevent chronic sequelae.

Prevention and Prognosis

Preventing Tick Bites

Personal Protective Measures

Personal protective measures reduce the likelihood of tick exposure and consequently lower the incidence of Lyme disease, which is essential for effective disease management.

Key actions include:

Wearing long sleeves and trousers; tuck shirts into pants and pants into socks to create a barrier against crawling ticks.
Applying EPA‑registered repellents containing DEET, picaridin, or IR3535 to skin and clothing; reapply according to product instructions.
Treating outdoor garments with permethrin; avoid direct skin contact with the chemical.
Conducting thorough body checks after outdoor activities; focus on ears, scalp, armpits, groin, and behind knees.
Removing attached ticks promptly with fine‑tipped tweezers; grasp close to the skin, pull straight upward, and cleanse the area with alcohol.

Additional practices reinforce protection:

Maintaining low, trimmed grass and removing leaf litter in yards to diminish tick habitat.
Using acaricide treatments on property per local health department guidelines.
Avoiding known high‑risk areas, such as dense underbrush, during peak tick activity seasons.

Consistent implementation of these measures minimizes tick bites, thereby decreasing the probability of infection and supporting overall therapeutic strategies for Lyme disease.

Tick Removal Techniques

Prompt removal of an attached tick reduces the risk of transmitting the spirochete that causes Lyme disease. The process must be swift, precise, and sterile.

Use fine‑tipped tweezers or a dedicated tick‑removal tool.
Grasp the tick as close to the skin surface as possible, holding the mouthparts, not the body.
Apply steady, gentle traction upward; avoid squeezing the abdomen.
Release the tick without twisting or jerking.
Disinfect the bite area with an alcohol swab or iodine solution.

Alternative methods:

Tick‑removal hook (e.g., “Tick Twister”) slides beneath the mouthparts, allowing upward motion without crushing the tick.
Small, flat, blunt instrument (credit‑card edge) can be wedged under the tick to lift it, provided the mouthparts remain intact.

After extraction:

Place the tick in a sealed container for identification if symptoms develop.
Clean the wound with soap and water, then apply an antiseptic.
Observe the site for erythema or expanding rash for up to 30 days; seek medical evaluation if such signs appear.

When the tick is embedded deeply, the mouthparts are not visible, or the patient cannot apply adequate force, refer to a healthcare professional for removal under magnification.

Long-Term Outlook and Follow-up Care

Post-Treatment Lyme Disease Syndrome («PTLDS»)

Post‑Treatment Lyme Disease Syndrome (PTLDS) refers to a constellation of persistent symptoms that develop in a minority of patients after completing an appropriate antibiotic regimen for early or disseminated Lyme infection. The syndrome typically emerges within six months of therapy and may last months to years.

Diagnostic criteria require:

Documented Lyme disease with a positive two‑tier serology or a recognized tick exposure and clinical manifestation;
Completion of a standard antibiotic course (doxycycline, amoxicillin, or cefuroxime for 10–21 days, or intravenous ceftriaxone for 14–28 days in neurologic or cardiac disease);
New or ongoing fatigue, musculoskeletal pain, or neurocognitive difficulties that cannot be attributed to another condition;
Absence of objective evidence of active infection (negative cultures, PCR, or repeat serology showing no escalation).

Epidemiology estimates PTLDS prevalence between 10 % and 20 % of treated patients, with higher rates observed after late disseminated disease.

Management focuses on symptom alleviation and functional restoration:

Graded exercise programs tailored to individual tolerance;
Cognitive‑behavioral strategies for memory and concentration deficits;
Analgesic regimens (acetaminophen, NSAIDs) for musculoskeletal pain;
Sleep hygiene measures to address fatigue;
Multidisciplinary coordination among primary care, infectious disease, neurology, and physical therapy specialists.

Repeated or prolonged courses of antibiotics have not demonstrated benefit and carry risks of adverse events; they are not recommended for PTLDS. Ongoing research investigates immunologic dysregulation, persistent antigenic debris, and host‑genetic factors as potential mechanisms, aiming to identify targeted therapeutics.

Clinical follow‑up should include periodic assessment of symptom severity, functional status, and psychosocial impact, with adjustments to supportive interventions as needed.

Importance of Early Intervention

Early treatment after a tick bite dramatically lowers the probability that Borrelia burgdorferi spreads beyond the skin. When antibiotics are administered within the first few weeks, the infection rarely progresses to involve joints, heart tissue, or the nervous system.

Prompt therapy yields measurable clinical advantages. Cure rates exceed 90 % when doxycycline, amoxicillin, or cefuroxime is started during the erythema migrans stage, whereas delayed initiation reduces success to 70–80 % and often requires longer courses. Early intervention also shortens symptom duration and minimizes the risk of post‑treatment Lyme disease syndrome.

Recognition of the initial rash or recent exposure guides therapy before serologic tests become reliable. Because antibody production may lag, clinicians rely on epidemiologic context and physical findings to justify immediate antibiotic use.

Potential outcomes of postponed treatment

Disseminated rash or multiple skin lesions
Arthritis affecting large joints
Carditis with conduction abnormalities
Neurological manifestations such as facial palsy or meningitis
Increased likelihood of persistent fatigue and cognitive complaints

Timely antibiotic administration therefore constitutes the most effective measure for preventing systemic complications and ensuring rapid recovery.