Tick-borne encephalitis in dogs: symptoms and treatment

Overview

TBE virus targets nerve tissue and can cause inflammation of the brain and its surrounding membranes. Inflammation can also extend into the spinal cord. Infection and clinical disease are different: antibodies to the virus can also be found in healthy dogs.

At one veterinary pathology unit in northern Europe, 2 canine TBE cases leading to euthanasia were confirmed over 20 years. The unit examines about 200 dogs after death each year. These isolated findings do not establish disease incidence in the wider dog population.

Infection may also be identified during investigation of pregnancy problems without severe neurological illness in the mother.

Causes

The virus circulates between ticks and wildlife

TBE virus belongs to the flavivirus group. Small rodents are important natural reservoirs, infecting ticks that feed on their blood. In Europe, the castor bean tick, Ixodes ricinus, is an important transmitter. The virus can occur in tick larvae, nymphs and adults.

It can remain in a tick as it develops into its next life stage. Transmission from a tick to a host occurs during a blood meal. TBE virus can be transmitted within an hour of feeding starting.

The virus can damage large motor nerve cells, so symptoms are not confined to brain function. Inflammation of the spinal cord's grey matter, or poliomyelitis, may appear particularly as neck weakness. Here, the term describes the location and type of spinal cord inflammation.

Direct contact with a dog is not the usual route

Direct transmission from dogs to people is not expected, as both mainly acquire infection from ticks. However, transmission through the placenta from a dog to her offspring has been demonstrated.

Placental damage can disrupt the foetus's oxygen and nutrient supply. Foetal growth and development may stop as a result.

Risk factors

Exposure is associated with outdoor activity in areas where ticks carry the virus. Disease occurrence is influenced by climate-dependent tick activity. In one northern European study of 342 ticks collected from dogs and cats, TBE virus was found in one tick, or 0.3%. This result applies to that collection and does not mean the same proportion occurs in every outdoor area.

In a Swiss group of 54 canine cases, age ranged from 1–13 years, with a mean of 5.61 years. Patients presented between March and October. Only 23 of 54 owners recalled tick exposure, so an unnoticed bite was possible.

Typical symptoms

Early symptoms may include fever, weakness, tiredness and reduced appetite. Some dogs also have digestive symptoms before obvious neurological illness.

• Temperature may exceed 39°C and your dog is clearly unwell.

• Your dog staggers or stumbles, or its balance and coordination deteriorate.

• The neck may be painful or so weak that holding up the head becomes difficult.

• Your dog may have focal or generalised seizures.

• One or more legs may become weak or paralysed.

• Your dog may be unusually sensitive to touch or other stimuli.

• Behaviour, alertness and responses to the surroundings may change markedly.

In the Swiss group, 34 of 54 dogs had general symptoms before neurological signs. These had been noticed 1–10 days before hospital admission.

TBE symptoms can also include cranial nerve dysfunction. Spinal reflexes may be weaker than usual on examination. Seizures occurred during the illness in 17 of the 54 dogs.

In the same group of 54, 28 dogs, or 51.8%, had unsteadiness or balance problems. Neck pain occurred in 21 dogs, or 38.8%. Limb weakness or paralysis occurred in 15 dogs, or 27.7%.

Complications and consequences

Severe disease can be life-threatening

TBE can cause severe inflammation of the brain, its membranes and the spinal cord at the same time. A rapidly fatal course may last 3–7 days. Acute illness may last 1–3 weeks. Cardiac and respiratory arrests have also been described in severe cases.

However, not every dog dies: 67% survived in a follow-up study of 54 dogs. TBE-related death or euthanasia occurred in 18 of 54 dogs, or 33%. TBE-related deaths also occurred during the 4 months after discharge. Older age was associated with a greater risk of death. Seizures were also associated with a greater risk of death.

Residual problems after recovery may include facial nerve paralysis, hindleg weakness or a mild head tremor. Recurrent seizures may complicate treatment while the dog is still in hospital.

A possible risk during pregnancy

In a case investigated in Sweden, a bitch delivered 1 live and 3 dead puppies by caesarean section. The live-born puppy also died despite attempts at resuscitation. TBE virus was found in the dead puppy's placenta. This finding makes TBE a possible cause of foetal death, but its frequency is not yet known.

In the Swedish pregnancy case, foetal deaths were detected from day 49 of pregnancy. Caesarean section was performed on day 56. The mother later had another litter of 5 healthy puppies.

Diagnosis at the vet

Symptoms and exposure guide investigations

The vet combines symptom timing, outdoor and travel history and neurological examination findings. Many other diseases cause the same symptoms, so finding a tick alone is not enough for diagnosis. Investigations may rule out conditions such as distemper, toxoplasmosis and neosporosis.

Blood tests may show changes consistent with inflammation, such as anaemia or increased neutrophil white blood cells. Cerebrospinal fluid is examined for cells, protein and, when needed, antibodies to the virus. Sampling requires anaesthesia, so a critically ill dog may not be able to undergo it.

Antibody testing and PCR answer different questions

A positive blood antibody result indicates exposure but can also occur in a symptom-free dog. IgM and IgG antibodies may remain in the blood for several months after infection. Conversely, a test early in acute disease may be negative because antibodies have not yet formed.

An increase in antibody levels in samples taken 2–3 weeks apart can strengthen the diagnosis. PCR looks for viral genetic material, but the virus is present in blood only briefly and often in smaller amounts by the time symptoms appear. In a small tested group, cerebrospinal fluid RT-qPCR was negative in 7 of 8 dogs.

Antibodies against different flaviviruses can cross-react in laboratory tests. The laboratory therefore confirms that the method is suitable for dogs and advises on interpretation. Blood and cerebrospinal fluid collected at the same time can be compared to assess the antibody ratio.

The same follow-up study excluded 3 dogs whose cerebrospinal fluid antibodies were initially negative but whose TBE was later confirmed. In 2 of these dogs, antibody results became positive 1 or 2 weeks after the first examination. The third dog's disease was confirmed by brain tissue examination after death.

The cerebrospinal fluid antibody level did not predict death in this canine follow-up study.

MRI does not always show a change

Brain MRI may show changes consistent with inflammation, often symmetrically distributed. Brain MRI was abnormal in 11 of 17 dogs examined, or 64.7%. These changes are not specific to TBE. Brain tissue changes and detection of the virus after death can confirm the diagnosis.

Pregnancy problems also call for placental examination

Investigations of foetal death must consider causes including Brucella canis and canine herpesvirus. In the Swedish TBE-associated case, viral genetic material was found in the placenta but not in the puppy's liver, kidney or lung samples. A separate staining method located the virus in placental cells. Placental tissue death alone does not prove TBE, as similar small lesions also occur in placentas of healthy puppies.

Treatment

Symptoms are treated according to disease severity

There is no specific treatment for TBE in dogs; care is supportive and planned by the vet. Fluids, nursing care and rehabilitation are tailored to the patient's needs. Seizures may be treated with medicines such as phenobarbital or levetiracetam. If the response is inadequate, more intensive seizure treatment may be needed in hospital.

Antibiotics are used to treat any secondary bacterial infection. The benefit of glucocorticoids, or corticosteroid medicines, in TBE is unclear. Their effectiveness could not be established in a follow-up study without an untreated comparison group.

The amount of help needed at home also depends on whether your dog can move and how well neurological functions recover.

Rehabilitation may continue after the hospital stay

In the Swiss follow-up study of 54 dogs, hospitalisation lasted an average of 8 days, with a range of 1–36 days. Dogs with hindleg weakness regained unaided walking at 6 days, with a range of 2–12 days. For dogs with weakness or paralysis of all limbs, the corresponding time was 12 days, with a range of 3–26 days. Neck weakness resolved in the 9 dogs affected within 2–71 days.

Prevention

There is no specific TBE vaccine in use for dogs. The protective efficacy of human vaccines has not been established in dogs. Reducing tick exposure is the main preventive measure. A parasite control product is chosen according to the animal species and the product's authorised use.

Check the coat regularly as well and remove any ticks found. No tick control product provides completely reliable protection. A tick remover or tweezers makes removal easier.

Do not apply grease or other substances to a tick on the skin to remove it. External parasite protection and coat checks complement each other.

Important for dog owners

Record tick sightings, walking areas, travel abroad and when symptoms began. Tell the vet whether fever, reduced appetite or digestive symptoms preceded unsteadiness or seizures. Recording seizure duration and your dog's recovery helps describe what happened.

Routine TBE antibody testing is not necessary in a healthy dog.

Testing a tick removed from a dog for TBE is not recommended either.

At discharge, agree on help needed at home, safe movement and follow-up. Note whether appetite, walking and usual behaviour return. New seizures or a change in consciousness are reasons to contact the treating practice immediately.

Frequently asked questions

Is tick-borne encephalitis the same as Lyme disease?

TBE is caused by a virus. Lyme disease is caused by Borrelia bacteria. TBE can be transmitted within an hour of a tick starting its blood meal. Despite this rapid transmission, most canine TBE virus infections do not cause visible illness. There is no specific TBE vaccine in use for dogs.

Can TBE pass from my dog to me?

Direct transmission from dogs to people is not expected. Both people and dogs mainly acquire infection from ticks. A dog's exposure to TBE virus therefore does not mean ordinary contact with it will infect its owner. Regular coat checks for ticks are part of preventing infection in dogs.

Can a dog recover from TBE?

Yes: 67% survived in a clinical follow-up study of 54 dogs. However, residual problems may include facial nerve dysfunction, limb weakness or a head tremor. Seizures were associated with poorer survival. Older age was also associated with a greater risk of death. Rehabilitation and nursing care are tailored to the dog's individual abilities.

Does a negative TBE test rule out the disease?

Not always: antibodies may not have formed by the start of illness. PCR may also be negative, as the virus is present in blood only briefly. Tests are selected according to symptoms, sampling time and available methods.

Can TBE harm unborn puppies?

TBE virus has been demonstrated in placental tissue in a canine case involving foetal deaths. The finding supports the possibility of transmission from mother to foetus. It is not yet known how common this cause of puppy deaths is. Investigations of pregnancy problems also consider better-known infections, such as Brucella canis.