What symptoms are characteristic of tick‑borne encephalitis in humans?

Understanding Tick-Borne Encephalitis

Tick‑borne encephalitis (TBE) is a viral infection transmitted by Ixodes ticks, affecting the central nervous system. After an incubation period of 7‑14 days, the disease typically progresses through two clinical phases.

The initial phase presents with nonspecific, flu‑like symptoms: fever, headache, myalgia, and malaise. This stage often resolves spontaneously within several days, giving way to a second phase in which neurological involvement becomes evident.

Neurological manifestations include:

High‑grade fever persisting beyond the first phase
Severe headache, often resistant to analgesics
Nuchal rigidity and photophobia indicating meningeal irritation
Altered mental status ranging from confusion to coma
Focal neurological deficits such as ataxia, dysarthria, or paresis
Seizures, particularly in severe cases
Cranial nerve palsies, most commonly facial nerve involvement

Recovery may be incomplete; residual deficits such as cognitive impairment, motor weakness, or persistent tremor occur in a substantial proportion of patients. Early recognition of these characteristic signs facilitates timely supportive care and improves long‑term outcomes.

Phases of Tick-Borne Encephalitis Symptoms

First Phase Symptoms («Prodromal Stage»)

Onset of Fever

Fever commonly appears early in the clinical course of tick‑borne encephalitis, typically emerging 3–7 days after the initial tick bite. The temperature rise is often abrupt, reaching 38–40 °C, and may be accompanied by chills and sweating. In many cases, the febrile phase persists for 2–4 days before neurological signs develop.

Key aspects of the febrile onset include:

Sudden elevation of core body temperature above 38 °C.
Duration of the fever lasting 48–96 hours in the majority of patients.
Absence of a rash, distinguishing it from other tick‑transmitted infections such as Lyme disease.
Possible association with mild headache, malaise, and myalgia, which may precede central nervous system involvement.

Recognition of this early febrile pattern aids timely diagnosis and facilitates monitoring for subsequent encephalitic manifestations.

General Malaise

General malaise, described as a diffuse feeling of discomfort, fatigue, and reduced energy, frequently appears early in the clinical course of tick‑borne encephalitis. Patients often report an inability to perform routine activities despite the absence of focal neurological deficits.

The symptom typically emerges within the first week after infection and may persist for several days. It commonly co‑occurs with:

Low‑grade fever
Headache of moderate intensity
Myalgia affecting large muscle groups
Nausea or loss of appetite

The presence of malaise, especially when combined with fever and headache, alerts clinicians to the possibility of a viral encephalitic process transmitted by ticks. Its nonspecific nature requires careful exclusion of other febrile illnesses such as influenza, Lyme disease, and early bacterial infections.

Management focuses on symptomatic relief. Adequate hydration, antipyretics, and rest are recommended while awaiting serological confirmation. Monitoring for progression to overt neurological involvement—meningitis, ataxia, or focal deficits—remains essential, as early detection influences prognosis.

Headache and Muscle Aches

Headache is a frequent early manifestation of tick‑borne encephalitis, often described as moderate to severe and persistent. The pain may be localized to the frontal or occipital region and can precede neurological signs by several days. In many cases, headache intensity increases as the infection progresses, prompting medical evaluation.

Muscle aches accompany the headache in a substantial proportion of patients. The myalgia is usually diffuse, affecting the limbs and trunk, and may be accompanied by mild weakness. Muscle tenderness can be pronounced, contributing to discomfort and reduced mobility. Both headache and muscle aches are considered initial systemic symptoms that signal the onset of the disease and warrant prompt diagnostic testing.

Nausea and Vomiting

Nausea and vomiting frequently appear during the early phase of tick‑borne encephalitis. The gastrointestinal upset often follows the initial flu‑like manifestations and may precede neurological signs. Occurrence of these symptoms reflects viral involvement of the central nervous system and can indicate progression toward meningitis or encephalitis.

Typical characteristics include:

Sudden onset of queasiness, sometimes accompanied by a feeling of fullness in the stomach.
Repetitive, forceful emesis that may be non‑bloody and without significant abdominal pain.
Duration ranging from several hours to a few days, often coinciding with fever spikes.

Clinical relevance lies in the need for prompt hydration and anti‑emetic therapy to prevent dehydration, which can exacerbate neurologic impairment. Monitoring of electrolyte balance is essential, as persistent vomiting may lead to hyponatremia. Early recognition of these gastrointestinal signs contributes to timely diagnosis and appropriate supportive care in patients suspected of tick‑borne viral infection.

Second Phase Symptoms («Neurological Stage»)

Meningitis Manifestations

Meningitis is a frequent manifestation of tick‑borne encephalitis and often dominates the early clinical picture. Typical features include:

Sudden onset of severe headache, frequently described as frontal or occipital.
Neck rigidity or resistance to passive flexion, indicating meningeal irritation.
Photophobia and phonophobia, reflecting heightened sensitivity to light and sound.
Nausea and vomiting, often accompanying the headache.
Fever exceeding 38 °C, usually persisting for several days.
Altered mental status ranging from mild confusion to somnolence; in severe cases, progression to coma may occur.

Additional laboratory findings support the diagnosis. Cerebrospinal fluid analysis commonly reveals a pleocytosis with a predominance of lymphocytes, elevated protein concentration, and normal or slightly reduced glucose levels. These parameters help distinguish tick‑borne encephalitis from bacterial meningitis, which typically shows neutrophilic dominance and marked hypoglycorrhachia.

Early recognition of these meningitic signs is essential for prompt antiviral therapy and supportive care, reducing the risk of subsequent neurological complications such as paresis or persistent cognitive deficits.

Severe Headache

Severe headache represents one of the earliest and most prominent manifestations of tick‑borne encephalitis. The pain typically appears abruptly, reaches high intensity, and may be diffuse or localized to the frontal region. Persistence of the headache often exceeds several days and does not respond adequately to standard over‑the‑counter analgesics.

The presence of a severe headache signals central nervous system involvement and frequently precedes the development of overt neurological deficits such as ataxia, paresis, or altered consciousness. Clinicians should therefore regard this symptom as a warning sign that warrants immediate investigation.

Associated symptoms commonly accompany the headache:

Photophobia
Nausea and vomiting
Neck stiffness
Fever exceeding 38 °C

These accompanying signs help distinguish tick‑borne encephalitis from other febrile illnesses that may present with milder cephalgia.

Diagnostic work‑up should include serologic testing for specific viral antibodies and lumbar puncture to assess cerebrospinal fluid for pleocytosis and elevated protein. Prompt identification of the severe headache in the clinical picture accelerates confirmation of the infection.

Therapeutic measures focus on symptom control and prevention of complications. High‑potency analgesics are administered to alleviate pain, while antiviral agents such as ribavirin may be considered in severe cases. Close monitoring for progression to encephalitic or meningo‑encephalitic stages is essential throughout treatment.

Stiff Neck

Stiff neck, medically described as nuchal rigidity, signals meningeal irritation and frequently appears in the early phase of tick‑borne encephalitis. The symptom emerges within days after the initial febrile stage and may persist into the neurological phase.

Typical presentation includes:

Resistance to passive neck flexion
Pain that intensifies with head movement
Absence of spinal cord compression signs

Stiff neck often coexists with headache, photophobia, and fever, forming a triad that suggests central nervous system involvement. Its presence guides clinicians toward lumbar puncture, where cerebrospinal fluid analysis reveals pleocytosis and elevated protein, confirming viral meningitis or encephalitis.

Early identification of nuchal rigidity supports timely antiviral therapy and monitoring for complications such as seizures or focal neurological deficits. Prompt management reduces the risk of long‑term sequelae associated with tick‑borne encephalitis.

Photophobia

Photophobia, defined as an abnormal intolerance to light, frequently appears during the acute phase of tick‑borne encephalitis. The symptom reflects irritation of the meninges and involvement of the optic pathways, indicating central nervous system inflammation.

Patients may report:

Discomfort or pain when exposed to bright environments
Need to keep eyes closed or seek dim lighting to relieve symptoms
Worsening of headache intensity together with light sensitivity

The presence of photophobia often accompanies other neurological signs such as fever, headache, neck stiffness, and altered mental status. Its detection assists clinicians in distinguishing encephalitic involvement from peripheral infections that rarely produce light sensitivity.

Management focuses on supportive care, antipyretics, and, when indicated, antiviral therapy. Monitoring the intensity of photophobia can provide a practical gauge of disease progression and response to treatment.

Encephalitis Manifestations

Tick‑borne encephalitis typically follows a biphasic course. The initial phase presents with nonspecific systemic signs such as high fever, severe headache, muscle aches, and fatigue. These symptoms resolve after several days, after which a second phase may emerge, indicating central nervous system involvement.

Neurological manifestations include:

Meningeal irritation characterized by neck stiffness and photophobia
Altered mental status ranging from confusion to stupor
Focal neurological deficits such as weakness, sensory loss, or speech disturbances
Seizures, both generalized and focal
Cerebellar signs, including ataxia and tremor
Cranial nerve palsies, most frequently affecting the facial nerve
Persistent cognitive impairment and memory difficulties in severe cases

Long‑term sequelae may involve chronic motor dysfunction, gait instability, and reduced neuropsychological performance. Early recognition of the described signs is essential for prompt supportive care and reduction of lasting disability.

Altered Mental Status

Tick‑borne encephalitis frequently progresses to central nervous system involvement, and altered mental status represents a principal manifestation of this neuroinvasion. Patients may present with a spectrum of cognitive disturbances that reflect cortical and subcortical dysfunction.

Typical alterations include:

Confusion and impaired orientation
Reduced attention and slowed thought processes
Lethargy progressing to stupor
Acute coma in severe cases

These changes often emerge during the second phase of the disease, coinciding with meningeal irritation, focal neurological deficits, and seizures. The severity of mental status impairment correlates with viral load in the cerebrospinal fluid and predicts a higher risk of long‑term sequelae, such as persistent cognitive deficits and motor impairment. Prompt recognition of altered mental status facilitates early supportive care and may improve functional outcomes.

Seizures

Tick‑borne encephalitis (TBE) may progress to acute central‑nervous‑system involvement, during which seizures represent a serious neurologic manifestation. Seizures occur most frequently in the meningo‑encephalitic phase, when inflammation of cortical and subcortical structures disrupts neuronal excitability.

Typical seizure presentations include:

Generalized tonic‑clonic episodes, often brief but may evolve into status epilepticus.
Focal seizures with motor or sensory signs, reflecting localized cortical irritation.
Myoclonic jerks, occasionally preceding more extensive convulsive activity.

The onset of seizures usually follows the appearance of headache, fever, and altered consciousness by 2‑7 days. Electroencephalography commonly reveals diffuse slowing with occasional epileptiform discharges, supporting the diagnosis of TBE‑related epilepsy. Cerebrospinal fluid analysis shows lymphocytic pleocytosis and elevated protein, but the presence of seizures does not alter the basic laboratory criteria.

Management requires immediate seizure control with benzodiazepines, followed by antiepileptic drugs such as levetiracetam or valproate. Antiviral therapy is not indicated; supportive care and monitoring for complications remain the cornerstone of treatment. Prognosis improves when seizures are promptly recognized and treated, reducing the risk of long‑term neurological deficits.

Motor Weakness and Paralysis

Motor weakness is a frequent manifestation of tick‑borne encephalitis, often emerging during the meningo‑encephalitic phase. Weakness may be focal, affecting a single limb, or generalized, involving multiple muscle groups. The deficit typically presents as reduced muscle strength without accompanying sensory loss, distinguishing it from peripheral neuropathies.

Typical presentations include:

Flaccid paresis of the face, arm, or leg
Asymmetric limb weakness progressing to quadriparesis
Sudden loss of voluntary movement in one or more extremities
Persistent motor deficit that may evolve into irreversible paralysis in severe cases

Weakness usually appears within days of the onset of fever and meningitis signs, reaching peak severity over a short period. Recovery is variable; rapid improvement occurs in mild cases, while prolonged rehabilitation is required when extensive motor pathways are damaged. Early neuroimaging and electrophysiological studies aid in differentiating central motor impairment from peripheral causes and guide therapeutic decisions.

Speech and Swallowing Difficulties

Speech and swallowing difficulties are frequent neurological manifestations of tick‑borne encephalitis. The infection can involve the brainstem and cranial nerves, producing motor deficits that affect oral and pharyngeal muscles. Dysarthria, characterized by slurred or slow speech, often appears early in the meningo‑encephalitic phase. Dysphonia, a change in voice quality, may accompany vocal‑cord paresis. Impaired coordination of swallowing muscles leads to dysphagia, increasing the risk of aspiration and malnutrition.

Typical presentations include:

Reduced articulation speed and precision (dysarthria)
Hoarseness or loss of voice (dysphonia)
Difficulty initiating or completing a swallow (dysphagia)
Coughing or choking during meals
Sensation of throat blockage or foreign body

These symptoms reflect involvement of the nucleus ambiguus and other brainstem nuclei responsible for phonation and deglutition. Early identification allows prompt supportive care, such as speech‑language therapy and modified diets, to prevent complications.

Myelitis Manifestations

Tick‑borne encephalitis is a flavivirus infection transmitted by Ixodes ticks that may extend beyond cerebral involvement to affect the spinal cord. Involvement of the spinal cord presents as myelitis, a serious neurological complication that can develop during the second, meningo‑encephalitic phase of the disease.

Typical clinical features of myelitis include:

Acute or sub‑acute motor weakness, often asymmetric, affecting one or more limbs;
Sensory disturbances such as numbness, paresthesia, or loss of proprioception in a dermatomal distribution;
Autonomic dysfunction, most frequently urinary retention or overflow incontinence;
Hyperreflexia and spasticity, occasionally accompanied by pathological reflexes (e.g., Babinski sign);
Pain localized to the spinal region or radiating along affected nerve roots.

The presentation frequently resembles transverse myelitis, with rapid progression over hours to days. Magnetic resonance imaging of the spine typically reveals hyperintense T2‑weighted lesions spanning one or several vertebral segments. Cerebrospinal fluid analysis shows pleocytosis with a predominance of lymphocytes and elevated protein, supporting an inflammatory process. Early antiviral therapy and high‑dose corticosteroids are recommended to limit neuronal damage, although recovery varies; residual motor or sensory deficits persist in a proportion of patients.

Limb Weakness and Numbness

Limb weakness and numbness are frequent neurological manifestations of infection transmitted by ticks. Weakness typically emerges abruptly, affecting one or both extremities, and may progress over hours to days. Numbness often accompanies motor deficits, presenting as reduced sensation to touch, temperature, or vibration in the same region.

Key clinical features include:

Asymmetric or symmetric paresis, most often in the distal muscles of the arms or legs.
Paresthetic sensations preceding or following motor impairment.
Absence of facial involvement in early stages, distinguishing the presentation from other viral encephalitides.
Possible coexistence with headache, fever, or neck stiffness during the meningeal phase.

Pathophysiology involves inflammatory infiltration of the central nervous system, leading to demyelination of corticospinal tracts and peripheral nerve irritation. The resulting conduction block explains both motor weakness and sensory deficits.

Diagnostic work‑up relies on:

Detailed neurological examination confirming motor and sensory loss.
Electromyography showing reduced motor unit potentials.
Magnetic resonance imaging revealing hyperintense lesions in the spinal cord or brainstem.
Serological testing for specific antibodies confirming recent exposure.

Prognosis depends on the severity of motor involvement; complete recovery occurs in many cases, while persistent deficits are reported when lesions affect the spinal cord extensively. Early antiviral therapy and supportive care, including physiotherapy, improve functional outcomes and reduce long‑term disability.

Muscle Atrophy

Tick‑borne encephalitis (TBE) presents with a range of neurological signs; muscle atrophy frequently follows the acute encephalitic phase.

Muscle atrophy denotes a reduction in muscle fiber size caused by loss of innervation or prolonged disuse. In TBE, viral injury to motor neurons and spinal anterior horn cells leads to denervation, while severe headache, fever, and altered consciousness often limit patient mobility, accelerating wasting.

Typical manifestation includes visible thinning of limb muscles, accompanied by decreased strength. Atrophy may be focal, affecting the extremities most involved in the initial inflammatory process, or more generalized when widespread neuronal damage occurs. The condition usually emerges weeks after the peak of encephalitic symptoms and persists unless rehabilitative measures are instituted.

Diagnostic relevance rests on identifying atrophic changes during neurological examination, corroborated by electromyography that reveals reduced motor unit potentials. Magnetic resonance imaging may show cortical or subcortical lesions consistent with TBE, while the presence of muscle wasting signals peripheral nervous system involvement.

Management focuses on early physiotherapy, progressive resistance training, and nutritional support to stimulate hypertrophy. Regular monitoring of muscle mass and strength guides therapy adjustments and helps prevent long‑term disability.

Key points:

Atrophy results from viral‑induced motor neuron loss and immobilization.
Onset follows the acute encephalitic stage, often weeks later.
Clinical assessment includes visual inspection, strength testing, EMG, and imaging.
Rehabilitation programs are essential for functional recovery.

Factors Influencing Symptom Severity and Progression

Viral Strain Virulence

Tick‑borne encephalitis, a flaviviral infection transmitted by Ixodes ticks, typically progresses through an incubation period of one to two weeks followed by a biphasic clinical course. The initial phase presents with nonspecific systemic signs, after which a second phase involves the central nervous system.

Typical manifestations during the neurological phase include:

High fever
Severe headache
Neck stiffness
Photophobia
Nausea and vomiting
Altered mental status
Seizures
Focal neurological deficits
Ataxia
Flaccid or spastic paralysis

Virulence varies among the three recognized TBE virus subtypes—European, Siberian, and Far‑Eastern. The Far‑Eastern subtype exhibits the highest pathogenicity, producing more frequent encephalitic forms, extensive neuronal damage, and elevated case‑fatality rates. The Siberian subtype causes a higher proportion of severe meningitis and encephalitis, whereas the European subtype often results in milder meningitic presentations. Strain‑specific differences also influence the likelihood of biphasic disease progression and the duration of neurological symptoms.

Identification of the infecting viral strain provides prognostic information, guides intensity of monitoring, and may inform decisions on supportive care and antiviral research.

Host Immune Response

Tick‑borne encephalitis (TBE) triggers a rapid innate reaction followed by a specific adaptive response that shapes the clinical picture. Early detection of viral RNA by pattern‑recognition receptors initiates production of type‑I interferons and pro‑inflammatory cytokines, limiting viral spread and contributing to fever and malaise.

Dendritic cells present viral antigens to naïve T lymphocytes.
Natural killer cells exert cytotoxic activity against infected neurons.
Complement activation amplifies inflammation and promotes opsonization.

The adaptive phase is dominated by virus‑specific CD8⁺ cytotoxic T cells and CD4⁺ helper T cells that secrete interferon‑γ and interleukin‑2, supporting viral clearance. B‑cell activation generates neutralizing IgM and, later, IgG antibodies that facilitate virus elimination and confer long‑term protection.

Cytokine storms and blood‑brain barrier disruption, driven by these immune mechanisms, underlie common neurological manifestations such as meningitis, encephalitis, and meningo‑encephalomyelitis. Elevated concentrations of interleukin‑6 and tumor necrosis factor‑α in cerebrospinal fluid correlate with headache, neck stiffness, and altered mental status. Persistent T‑cell infiltration can produce focal deficits, including ataxia and cranial nerve palsies.

Effective immune control reduces viral load but may also cause collateral neuronal damage, explaining the transition from acute febrile illness to severe neurological impairment in a subset of patients.

Age and Co-morbidities

Tick‑borne encephalitis manifests with a spectrum of neurological signs; patient age and existing medical conditions markedly shape the clinical picture.

In younger individuals, especially children, the disease often begins with nonspecific flu‑like symptoms and may progress to mild meningitis. Adults frequently experience more pronounced headache, high fever, and nausea, while elderly patients show a higher incidence of severe meningoencephalitis, seizures, and prolonged consciousness disturbances.

Key age‑related patterns include:

Children: brief prodrome, limited focal deficits, rapid recovery.
Middle‑aged adults: pronounced fever, neck stiffness, occasional cranial nerve palsy.
Seniors: extensive encephalitic involvement, gait instability, persistent cognitive impairment.

Pre‑existing health problems amplify the severity of TBE. Immunosuppression, chronic cardiovascular disease, diabetes mellitus, and chronic pulmonary disorders each increase the risk of extensive brain inflammation and unfavorable outcomes.

Influence of common co‑morbidities:

Immunocompromised status: delayed viral clearance, higher viral load, extended hospitalization.
Cardiovascular disease: heightened risk of autonomic dysfunction and arrhythmias during the acute phase.
Diabetes: greater propensity for hyperglycaemic crises and secondary infections.
Chronic lung disease: increased likelihood of respiratory complications in severe encephalitic cases.

Recognition of age‑dependent symptomatology and the impact of co‑morbidities guides diagnostic vigilance and therapeutic prioritisation, ensuring timely intervention for high‑risk groups.

Differential Diagnosis and Complications

Distinguishing from Other Infections

Tick‑borne encephalitis (TBE) presents with a biphasic illness that aids separation from other infectious diseases. The initial phase, lasting 2–7 days, mimics nonspecific viral infections with fever, malaise, headache and myalgia. After a brief asymptomatic interval, the second phase emerges with neurological involvement that distinguishes TBE.

Key clinical elements that separate TBE from meningitis, viral encephalitis, and Lyme disease include:

Abrupt onset of high‑grade fever accompanied by severe neck stiffness during the second phase, whereas bacterial meningitis often shows rapid progression with marked photophobia and altered consciousness.
Predominance of cerebellar ataxia and dysarthria, uncommon in most viral encephalitides that favor seizures and focal cortical deficits.
Presence of peripheral paresis or facial nerve palsy without accompanying rash, differentiating TBE from Lyme disease, which typically includes erythema migrans and arthritic symptoms.
CSF analysis revealing moderate pleocytosis with lymphocytic predominance, normal to mildly elevated protein, and absent bacterial growth; this pattern contrasts with the neutrophilic dominance seen in bacterial meningitis and the higher protein levels observed in herpes simplex encephalitis.

Temporal pattern, specific neurological signs, and cerebrospinal fluid profile together provide a reliable framework for distinguishing TBE from other infections that affect the central nervous system.

Long-Term Neurological Sequelae

Cognitive Impairment

Cognitive impairment represents a frequent neurological manifestation of tick‑borne encephalitis. It emerges during the meningo‑encephalitic phase and may persist after the acute illness. Patients often exhibit reduced attention span, slowed information processing, and difficulties with short‑term memory retrieval. Disorientation and impaired executive functions, such as planning and problem‑solving, are also reported.

Typical features include:

Decreased concentration and inability to sustain mental effort.
Impaired recall of recent events while remote memory remains relatively preserved.
Slowed speech output and reduced verbal fluency.
Deficits in abstract reasoning and difficulty adapting to new tasks.

Neuropsychological testing frequently reveals lower scores on tests of working memory, digit span, and symbol‑digit substitution. Magnetic resonance imaging may show transient hyperintensities in the basal ganglia and thalamus, correlating with the severity of cognitive deficits. Recovery varies; some individuals regain baseline performance within weeks, whereas others experience prolonged or permanent impairment. Early recognition and supportive rehabilitation improve functional outcomes.

Chronic Fatigue

Tick‑borne encephalitis (TBE) is a viral infection transmitted by Ixodes ticks, presenting with a biphasic course that may involve the central nervous system. After an initial febrile phase, neurological involvement can produce meningitis, encephalitis, or meningoencephalitis.

Chronic fatigue frequently follows the acute neurological episode. Patients report persistent exhaustion lasting weeks to months, unrelieved by rest, and accompanied by reduced physical and mental performance. The fatigue often coexists with sleep disturbances, impaired concentration, and mild mood changes, but without overt motor weakness.

Clinical relevance of prolonged fatigue includes:

Indicator of incomplete recovery from CNS inflammation
Potential contributor to reduced quality of life and functional capacity
Factor in differential diagnosis with post‑viral fatigue syndromes

Management emphasizes supportive care: graded activity programs, sleep hygiene, and evaluation for secondary complications such as depression or autonomic dysfunction. Early recognition of chronic fatigue aids in tailoring rehabilitation and monitoring long‑term outcomes.

Psychiatric Disorders

Tick‑borne encephalitis frequently presents with neuropsychiatric manifestations during the acute encephalitic phase. Central nervous system involvement can lead to alterations in cognition, affect, and behavior that mimic primary psychiatric disorders.

Typical psychiatric features include:

Acute anxiety and panic attacks
Mood disturbances such as depression or irritability
Psychotic symptoms, including hallucinations and delusions
Delirium with fluctuating consciousness and disorientation
Sleep disorders, notably insomnia or hypersomnia
Cognitive deficits affecting memory and attention

These manifestations often coexist with classic neurological signs, such as headache, fever, and focal deficits, and may persist as part of the post‑encephalitic syndrome. Early recognition of psychiatric symptoms facilitates prompt antiviral therapy and appropriate psychiatric management.