Canine encephalitis — inflammation of the brain

Ellen Andrews
Sunday, June 2, 2019

Encephalitis is described as inflammation of the brain and can be defined as infectious and non-infectious. Susceptibility to the condition can depend on the genetic makeup of the dog and the location in which they live, as geographic-specific pathogens can play a large part in causing infectious encephalitis. The disorder is diagnosed as non-infectious immune-mediated encephalitis when there is no pathogen as the cause. This article explores the condition of the canine central nervous system, discussing the type, cause, clinical signs, diagnosis and treatment. It outlines the importance of nursing care for the neurologically impaired patient.

Clinical signs such as depression, head tilting, circling and seizures can indicate various diseases or conditions when seen separately, however, if a combination of neurological signs are presenting together, it can mean the patient has inflammation of the brain, known as encephalitis.

Encephalitis is divided into two categories; infectious and non-infectious. Infectious encephalitis includes bacterial, fungal, viral or parasitic, whereas non-infectious encephalitis of unknown origin (Coates and Jeffery, 2014) is commonly as a result of an immune-mediated disease. All variations of the disease have a guarded prognosis (Lowrie et al, 2013) and veterinary staff should work quickly to diagnose and treat the condition. Diagnosis is most effectively achieved via analysis of cerebrospinal fluid (CSF). Treatment depends on the pathogen or cause of the condition and most commonly involves broad spectrum antibiotics, antivirals and immunosuppressive corticosteroids (O'Neill et al, 2005).

Due to the nature of the condition, veterinary nurses play an important role in the treatment and care of patients; intensive nursing and monitoring of neurological changes can also help in early detection and treatment of the condition.

Infectious encephalitis

Approximately 60% of encephalitis cases do not have a definable infectious cause (Olby and Platt, 2013). Infectious encephalitis includes: bacterial, viral, fungal, parasitic. The incidence of infectious agents causing encephalitis depends on the geographic location. Dogs in some areas are prone to encephalitis causing disease, such as Rocky Mountain spotted fever which occurs in the southwestern states of the USA (Yaglom et al, 2018) but is not present in the UK.

Encephalitis can also be the result of introduction of bacterial infection due to an injury to the protective barriers. The protective barriers include: the skin, bone, meninges, muscle tissue and the blood–brain barrier (a layer of specialised endothelial cells that encompass the brain, designed to block out substances that could be damaging to the central nervous system (CNS) (Webb and Muir, 2000). This method of contracting the infection is less likely if the protective barriers are intact.


Bacterial infections of the CNS most commonly occur due to bacteria being carried in the blood from areas within the body. Bacterial encephalitis in dogs is usually the result of direct extension of a non-CNS infection, such as from the lung or from splenic abscesses, ear infections, urinary infections, vertebral osteomyelitis and sinusitis (Webb and Muir, 2000). Bacterial infections that can cause encephalitis include septicaemia and bacterial endocarditis.

Other pathways of bacterial infection in the canine can include: injury or bite wound adjacent to the face, spine or neck which break the protective barriers; contaminated surgical equipment; or foreign body such as a grass seed migrating through tissue and entering the CNS.


Viral infections that can lead to encephalitis are: rabies; canine herpesvirus, adenovirus, West Nile virus, distemper and parvovirus. These diseases have an impact on organs and body systems, such as respiratory, neurological, blood and gastrointestinal systems. The virus invades the blood stream and can enter the tissue of the brain causing inflammation. Canine distemper virus frequently causes neurological disease via lesions in the brain causing necrosis in the white matter in multifocal areas (Vandevelde et al, 1980).


Parasitic infections that can lead to encephalitis are caused by the aberrant migration of parasites into the CNS, for example heartworms or roundworms, or tick-borne infections which cause rickettsiosis and Lyme disease. Rickettsiosis or Rocky Mountain spotted fever is a severe disease transmitted by the American Levi tick (Figure 1), and is associated with widespread vasculitis (Yaglom et al, 2018). According to Pfeffer and Dobler (2011) an increase in the amount of tick-borne encephalitis (TBE) transmitted via the Castor Bean tick and the Taiga tick is due to the increase in domestic dogs travelling to endemic areas throughout Europe, creating higher exposure to infection.

Figure 1. The American Levi tick is a carrier of Rocky Mountain spotted fever and Lyme disease each potentially resulting in infectious encephalitis.

Other parasitic infections that can lead to inflammation of the brain includes toxoplasmosis. Toxoplasmosis is most commonly suspected of causing disease in the UK and constitutes an important part of the differential diagnosis for infectious inflammatory CNS diseases (Coelho et al, 2019). Toxoplasmosis results in systemic infection affecting most organs, and leads to cysts that enter the tissue and most commonly the CNS (Lappin, 2004). Another differential diagnosis with very similar presentation to toxoplasmosis is neosporosis caused by Neospora caninum, an intracellular parasite (Dubey and Lindsay, 1996). Neosporosis can cause severe neuromuscular disorders such as ascending paralysis (Dubey, 2003).

Non-infectious encephalitis

When encephalitis is not caused by an infection, an underlying autoimmune disease is likely to be the cause. A healthy immune system acts to protect the body from any infections or foreign bodies. When an animal's immune system is unable to differentiate between an infection or a foreign body and itself, it begins to attack healthy cells within the body.

There are three main types of non-infectious encephalitis: granulomatous meningoencephalomyelitis (GME); necrotising meningoencephalitis; and hepatic encephalopathy. The pathological features of GME and necrotising meningoencephalitis are similar, both are inflammatory diseases of unknown cause (Suzuki et al, 2003). They differ in their breed disposition, distribution of lesions and the presence or absence of necrosis.

Hepatic encephalopathy is a metabolic disorder caused by liver disease.

The risk of death is high with non-infectious encephalitis; a study conducted by Lowrie et al (2013) on the outcomes of meningoencephalitis indicated that 56% were fatal.


GME is a nonsuppurative CNS inflammatory autoimmune disease of undetermined aetiology in dogs (Olby and Platt, 2013). GME most commonly affects small breed dogs aged between 4–8 years. Previously described as reticulosis, GME is defined by Adamo et al (2007) as large perivascular cuffs of lymphocytes and monocytes in the meninges of the brain and the spinal cord.

Necrotising meningoencephalitis (Pug encephalitis)

Necrotising meningoencephalitis is most commonly caused by an autoimmune attack on the CNS. The disease is categorised by inflammatory changes consisting of the infiltration of white blood cell (lymphocytes, plasmacytes and histiocytes) within the CNS (Suzuki et al, 2003). Levine et al (2008) state that the hallmark of the disease is extensive necrosis, which varies in severity from microscopic neuronal necrosis to gross cavitation most frequently found in the cortex but occasionally seen in the brainstem.

The disorder is found to be linked to genetic susceptibility and is most commonly found in Pugs (Uchida et al, 1999) (Figure 2) and can occur in other small breed dogs such as Maltese, Shih Tzu, Papillon and Chihuahua. In some breeds such as the Yorkshire Terrier and French Bulldog, the lesions are found in the white matter, this disease is called necrotising leukoencephalitis (Park et al, 2012) and can be a differential diagnosis. Patients found to have necrotising encephalitis are most commonly under 4 years of age.

Figure 2. Pug dogs are commonly more susceptible to immune-mediated necrotising meningoencephalitis along with Maltese and Yorkshire Terriers.

Hepatic encephalopathy

Hepatic encephalopathy refers to a neurological syndrome with hyperammonaemia caused by severe liver failure or disturbance of ammonia metabolism caused by a liver shunt (Morita et al, 2004). A build up of ammonia in the brain can have a toxic affect on astrocytes, which are cells in the CNS responsible for monitoring normal neurotransmitter uptake, regulation of the blood–brain barrier and development of the nervous system (Zhan et al, 2016). This leads to neuronal disfunction or necrosis (Morita et al, 2004).

Clinical signs

Clinical signs of encephalitis are varied and can present in a similar manner to other conditions. Neurological conditions can cause intra cranial pressure, this is referred to as Cushing reflex. Signs of this include: increased systolic and pulse pressure; bradycardia; and respiratory irregularity (Fodstad et al, 2006).

Clinical examination findings can include signs such as: a high temperature if the cause is infectious; bradycardia; irregular respiration; goose stepping gate; fever; uneven pupil size; and other CNS deficits such as lack of ocular response to light, neck pain, ataxia, weakness, proprioceptive issues, agitation and depressed consciousness including coma (Olby and Platt, 2013).

Clinical signs found from a full neurological examination depend on the location of the lesion within the CNS (Figure 3). The areas that can be affected include the forebrain, optic nerve, cerebellum, brainstem, midbrain, medulla oblongata, spinal cord, or meninges. Where two or more of these areas are affected it is referred to as multifocal. Olby and Platt (2013) suggest, as a general rule, that inflammatory diseases tend to be acute in onset and progressive, with a multifocal, asymmetrical distribution within the CNS.

Figure 3. Longitudinal section of the canine brain. Clinical signs of encephalitis depend on the location of lesions within the brain.

When the forebrain is involved, generalised or partial seizures, blindness, circling, pacing, depression and head pressing would likely be seen.

If the lesion is present in the brainstem symptoms include loss of coordination, head tilting, facial nerve paralysis (Horner's syndrome) and tremors.

Where the medulla oblongata or the hindbrain is affected, symptoms might include cranial nerve deficits, such as depressed palpebral, gag and corneal reflexes (Filippo et al, 2011).

As canine encephalitis is a result of other underlying autoimmune or infectious diseases, there will undoubtedly be other clinical signs present in the patient.


Normal screening such as blood work, radiographs and urinalysis will most often take place due to the presentation of the patient. However, these diagnostic tests may reflect no abnormalities as the activity in the CNS may be separate from the rest of the body. The diagnosis of inflammatory causes of CNS disease relies on combining the patient's history, genetic disposition, presenting signs and neurological examination with the results of blood work, infectious disease titres, CSF analysis (including culture and polymerase chain reaction (PCR) analysis) and advanced imaging such as magnetic resonance imaging (MRI) investigations (Platt, 2006).

To diagnose encephalitis, a biopsy can be taken of the inflamed part of the brain. Brain biopsies are very complicated and due to this, extremely rare; 30% of cases undergoing brain biopsy experience complications and only 82% are diagnostic (Flegel et al, 2012) They are most commonly undertaken at academic hospitals or veterinary speciality referral hospitals using computed tomography (CT) imaging as a guide (Talarico and Schatzberg, 2010). An MRI or a CT scan can be conducted for diagnosis. An MRI can have low sensitivity for diagnosis of inflammatory disease, therefore should always be completed in conjunction with CSF analysis. In standard practice, a CSF sample must be taken, and a fluid analysis conducted. In the absence of intra-cranial imaging; a lumbar puncture is the preferred method of CSF collection due to the possible presence of intra-cranial pressure or risk of herniation. Diagnosis is based on finding an increased total nucleated cell count, high levels of lymphocytic and neutrophilic inflammation, and elevated protein levels.

A CFS or blood culture can be actioned to isolate the causative organism (Coelho et al, 2019). If the cause of the inflammation is not infectious, it is uncommon for the origin of the disease to be identified.


Treatment is aimed at the primary disease process and can depend on the cause of the inflammation in the presenting patient.

If bacterial encephalitis is diagnosed, broad-spectrum antibiotics should be administered. This should be continued for several weeks after the clinical signs subside.

When immune-mediated disease is suspected as the cause of encephalitis the standard protocol is to treat with immunosuppressive doses of corticosteroids, such as prednisolone, initially, then tapering off the corticosteroids to the lowest possible dose to control signs (Menaut et al, 2008). It is uncommon for corticosteroid therapy to be terminated as, once the dose is reduced, clinical signs recur (O'Neill et al, 2005). Research has shown that patients treated with prednisolone in conjunction with cytarabine have the longest survival time (Cornelis et al, 2019).

Many patients presenting with encephalitis are in a critical condition and therefore require further treatment such as intravenous fluids, anti-inflammatory drugs, antiemetics, anticonvulsants, antifungals, antibiotics and nutritional support.

Much of the treatment of the condition is in managing the clinical signs. Treatment should be administered rapidly and may not always be successful (Lowrie et al, 2013). If treatment is successful, some clinical signs may remain in place indefinitely, for example blindness, which is dependent on the amount of damage to the CNS.

Nursing considerations

Supportive nursing actions are dependent on the severity of the patient and the symptoms that are presenting. The aim of nurses is to monitor the patient thoroughly, ensure medication is being administrated as directed by the veterinarian and manage homeostasis.

General nursing should take place such as monitoring intravenous (IV) fluid intake, fluid output, checking catheter sites, checking bandaging, intensive monitoring of any changes and recording all details to report to the case veterinarian.

Management of the neurologically impaired patient, i.e. those experiencing seizures, limited consciousness or blindness is demanding (Table 1). These patients are usually recumbent and thus at risk for bed sores, urine scalding, urine infections, muscle atrophy and joint stiffness.

Table 1.

Nursing care considerations for the neurological patient in clinic

Clinical sign Problem Action
Blindness Bumping into objects Clear the area from low lying objects that could pose a problem for the patient. Line the cage with padding to avoid the patient injuring themselves
Reluctance to leave cage Gently guide the patient from the cage with a tight leash to ensure control should the patient panic. With smaller animals, they can be guided using hands and with larger, two people can assist with movement from the cage
Stress Approach the cage of the patient slowly and cautiously ensuring you gently make yourself known so as to not startle. Ensure the patient is located in a quiet, calm and dimly lit space
Seizure Injury due to convulsions Pad the cage of seizing patients including the walls. Ensure the patient is in a cage with enough space as they are less likely to injure themselves
Urination Incontinence sheets and moisture wicking bedding under patients. Change when wet. Thoroughly wash and dry patients after soiling
Limited consciousness Pressure sores Having subsequent padding in the cage. Repositioning the patient frequently
Muscle atrophy Regular physical therapy and massage of limbs to increase blood flow
Development of condition Close monitoring of condition of patients, checking neurological signs, noting changes and report to the veterinary surgeon
Dehydration Manage intravenous fluids, checking lines, catheters, fluid input and output. Weigh the patient daily. Small amounts of water. Offer orally if the patient is at a high enough level of consciousness
Nutritional deficits Calculate patient's resting energy requirements (RER) and obtain the best way to get nutrition into the patient i.e. syringe feed or feeding tube.Divide feeding up into small feeds so as to avoid overwhelming the digestive system.Ensure the patient is cleaned after each feed, wipe away any residual food from coat and face.Avoid stressing the patient with syringe feeding, a non-invasive feeding tube may be lower stress option for the patient
Balance/proprioception Patient unable to stand or walk Aid the patient with standing and balance by supporting each end. An abdominal sling may be a helpful option with larger patients.Discourage the patient from taking more than a few steps if they are walking so as to avoid the patient falling or injuring themselves

Nurses also need to be aware of presenting or developing clinical signs of patients in hospital. For example; a patient hospitalised with distemper may begin to show neurological signs such as head tilting, pupil size change or seizing. These should be noted, and the veterinary surgeon informed — this could lead to early detection of encephalitis.

The following are examples of nursing considerations for patients with encephalitis:

  • A well-padded cage to ensure any seizure activity does not lead to injury and that a recumbent patient is not susceptible to bedsores. Baby and infant mattresses placed under patients and on cage walls can be an excellent method of protecting the seizing patient from injuring themselves during convulsions.
  • Have a seizure plan in place. Anticonvulsant medication should be dispensed to administer IV or rectally should the patient experience a seizure.
  • Monitoring for intra cranial pressure or Cushing reflex; identifying signs of blood pressure, sudden bradycardia and irregular respiration (Fodstad et al, 2006).
  • Consider a coma scale or AVPU scale to assess the level of consciousness:
  • A: alert — does the animal appear conscious and aware of its surroundings?
  • V: verbal stimuli responsive — does the animal respond to noise or voice?
  • P: Pain responsive — does the animal respond to pinching toes or ears?
  • U: Unresponsive (Hanel et al, 2016).
  • Cleaning patients of any bodily fluids such as urine, faeces, and vomit — using a sponge bath method of cleaning the patient, i.e. a warm and damp towel, is much less stressful to the patient than moving the patient to a bathing area. Any shampoo or residual soap should be completely cleaned from the coat as this can lead to skin irritation if left. Completely dry the patient to ensure body temperature does not drop and for patient comfort.
  • Change wet bedding — patients should have incontinence sheet underneath moisture wicking bedding to draw any fluid away from the patient. Bedding should be changed as soon as soiled to avoid patient discomfort, urine scald and decreased body temperature.
  • Another method of avoiding urine scald is to place a urinary catheter. Manual expression of the bladder comes with risks of bladder rupture and should only be completed under veterinary supervision.
  • Ensure the environment is calm, dimly lit and quiet — ideally the neurologically compromised patient is kept in an area of low foot traffic, noise and light. The patient should be kept as calm as possible with no sudden movements or stress. The blind patient should be approached slowly and gently — make the patient aware of your presence so as to not startle them.
  • Passive range-of-motion exercises to avoid muscle atrophy and pressure sores. For the patients with limited consciousness, this is very important. They should receive physical therapy at least three times daily and the recumbent patient should be turned regularly to avoid pneumonia and discourage bedsores. Physical therapy can be achieved by lifting the patient's legs and gently extending and contracting the limb in a natural motion. This encourages blood flow through the muscles. When turning patients, always roll the legs under to avoid any contortions.
  • In the comatose patient, eyes should be regularly lubricated to ensure there is no damage caused by a drying eye.
  • Mouth should be checked in a comatose patient to ensure the patient is not biting down on cheek or tongue. Keep the mouth clear of any blockages or build up of food, clear away any regurgitation.
  • Nutritional management — the patient's resting energy requirement (RER) should be calculated and a high quality, veterinary diet should be fed either orally or via feeding tube. The patient's mouth and coat should be cleaned after feeding to remove any food or residue. Food should not be left in the kennel as this can lead to food aversion. RER can be calculated using: RER (kcal/day) = 70 x (body weight in kg)0.75. Nutritional support should only be provided to patients that are fully conscious and not in an altered mental state.
  • When monitoring brachycephalic patients, be aware of the risk of oxygen deprivation due to their small airway — have an oxygen supply ready should the patient begin showing signs of respiratory distress. Ensure their temperature is monitored closely as these breeds can overheat.

Another consideration for nurses is to manage clients' expectations. It can be a very stressful and worrying time for clients when their pet is ill. After speaking with the veterinary surgeon, clients can feel overwhelmed and confused. It can be helpful to speak to the nurse about their concerns. Be sure to update the clients regularly on their pet's progress and the care being provided. Encourage them to come in and visit their pet — visits from owners may improve patient attitude and provide positive stimulation. This could also aid with depression if they are hospitalised for multiple days.

Owners need to be aware that with a condition such as encephalitis, clinical signs may develop and change throughout the course of the illness. Encourage the veterinary surgeon to discuss the possible development and changes to clinical signs.


There are many different causes for brain inflammation. Infectious encephalitis is far less common than immunemediated. The condition is rapidly life threatening and should be diagnosed and treated as soon as possible. Breed type and geographical location of the patient, including places the pet has travelled to, are strong indicators that the condition could be present. Encephalitis can present as acute onset of circling, head pressing, running into walls, aimless wandering, pacing, blindness, or acting confused after meals. Less severe signs can include learning/training difficulties, lethargy, or disorientation. Encephalitis is usually progressive and if left untreated, it can be fatal. CSF analysis is the most definitive diagnostic method and cytology could indicate the causal pathogen if present. Treatment is cause specific and should include treatment of the clinical signs. Intensive nursing should be undertaken with all clinical signs taken into consideration and a comprehensive nursing care plan is recommended. This should include considerations such as ensuring the patient is in a quiet, low foot traffic environment within the clinic, the kennel is well padded for the semi-conscious or seizing patient, and ensuring clients have support and are well informed of their pet's illness.


  • Encephalitis is a neurological condition defined as inflammation of the brain.
  • Encephalitis is catagorised as infectious or non-infectious.
  • Clinical signs can include head tilting, goose stepping, uneven pupils, seizures and loss of consciousness.
  • Encephalitis can be fatal.
  • Treatment is varied and mainly focused on managing the clinical signs.

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