Canine and Feline Epilepsy. Luisa De Risio
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Diagnostic investigations
Haematological and biochemical findings are nonspecific and include absolute lymphopaenia, hypoalbuminaemia and hyperglobulinaemia during the acute phase of illness. CSF analysis may reveal mononuclear pleocytosis (>5 WBC/μl) and elevated protein concentration (>25 mg/dl). Eosinophilic intracytoplasmic inclusions may be found in CSF or peripheral blood cells although their detection is rare. CSF can be normal in dogs with acute noninflammatory demyelinating encephalomyelitis. A CDV-specific antibody ratio (CDV-specific IgG in CSF/CDV specific IgG in serum) higher than canine adeno- or parvovirus-specific antibody ratio (IgG in CSF/IgG in serum) can help to identify intrathecal production of CDV-specific IgG (see antigen-specific antibody index, Chapter 10). MRI of the brain may be normal or may reveal lesions that are hyperintense on T2WI, isointense or hypoin-tense on T1WI with inconsistent contrast enhancement, and loss of cortical grey/white matter demarcation. The lesion distribution varies depending on the stage of CDV encephalitis (Bathen-Noethen et al., 2008; Griffin et al., 2009).
The diagnosis of CD can be achieved by molecular assays, such as reverse transcriptase polymerase chain reaction (RT-PCR) and real-time RT-PCR on blood, CSF, urine, conjunctival swabs or tissue specimens (Elia et al., 2006; Saito et al., 2006), as well as detection of viral antigen by direct fluorescent antibody assay (dFA) (on neural tissue, cerebrospinal fluid cells (infected lymphocytes), footpad biopsy, or other tissues) or by immunohistochemistry (IHC) on biopsy specimens (e.g. nasal mucosa, foot pad, haired skin of the dorsal neck) or post-mortem.
Treatment
Treatment consists of supportive care and antibiotics and is aimed at preventing the secondary bacterial infections that are frequent in immunosuppressed animals. Anti-epileptic treatment is performed as for other types of structural brain disorders (see introduction to this chapter and Chapters 12–24). Seizures secondary to CDV encephalitis have been reported to be difficult to control with phenobarbital (Tipold et al., 1992).
Modified-live vaccines are recommended for immunization of dogs to prevent CDV.
Although vaccine-induced disease is always suspected in dogs that develop distemper shortly after immunization, in most cases, the disease is induced by wild-type CDV infecting pups before active immunization is elicited (Martella et al., 2008).
Prognosis
Prognosis is variable depending on the clinical syndrome associated with CDV infection and generally varies from persistent neurological deficits (particularly myoclonus) to death.
Feline infectious peritonitis
Feline infectious peritonitis (FIP) and viral non-FIP encephalitides (i.e. non-suppurative encephalitides of unknown, although probable viral, aetiology based on histological findings) are the two most commonly recognized infectious CNS disorders of cats (Gunn-Moore and Reed, 2011).
FIP is a highly fatal, progressive and immune-augmented disease of cats caused by infection with feline coronavirus (FCoV). Although the terms feline infectious peritonitis virus (FIPV) and feline enteric corona-virus (FECV) have been used to refer to the virus causing FIP and the ubiquitous benign enteric virus, respectively, the term FCoV should be used to describe all coronaviruses in cats. FCoV is an RNA virus and belongs to the genus Coronavirus of the family Coronaviridae. It has been proposed that FCoV along with swine and canine coronaviruses becomes part of a new species called Geselavirus (Addie, 2012). FCoV causes a ubiquitous enteric infection in cats, which leads to FIP in approximately 1–3% of cats. The etiopathogenesis of FIP is complex and still unclear. A widely cited patho-genetic hypothesis is the ‘in vivo mutation transition hypothesis’ also called the ‘internal mutation hypothesis’. This postulates that viral mutations occur in healthy FCoV-infected cats giving rise to virulent virions that are able to replicate within macrophages and disseminate systemically leading to FIP (Pedersen, 2009). The precise nature of the mutation responsible for this pathogenetic hypothesis has not been identified yet. An alternative ‘circulating avirulent and virulent FCoV hypothesis’ suggests that distinctive benign and pathogenic strains of FCoV circulate in a population, and susceptible individuals exposed to the virulent strains develop FIP (O’Brien et al., 2012). It is likely that FIP etiopathogenesis is more complex than either hypothesis alone would suggest.
FCoV has a worldwide distribution and therefore cats worldwide are susceptible to developing FIP (Kent, 2009). FCoV is endemic especially in environments in which many cats are kept together in a small space (e.g. catteries, shelters, pet stores). Although cats of any age can develop FIP, the risk is higher in kittens and cats up to 2 years of age or older than 10 years of age. The risk to develop FIP appears greater in young and immune-compromised cats as well as in cats with a high viral load (Hartmann, 2005). In addition, pure-breed cats (such as the Abyssinian, Bengal, Birman, Himalayan, ragdoll, rex) have a greater risk of developing FIP than non- pure-breed cats (Pesteanu-Somogyi et al., 2006). Infection usually takes place by ingestion (or, rarely, by inhalation) of material contaminated by infected faeces shed by a cat with FCoV infection or by a cat with FIP (Hartmann, 2005). Many healthy cats shed FCoV intermittently or continuously for up to 10 months post-infection or longer, serving as chronic carriers and thereby perpetuating reinfection of other cats (Hartmann, 2005).
Clinical signs
Clinical signs of FIP can be variable because many organs can be involved. Three different forms of FIP have been identified: (i) an effusive (also called exudative or wet) form characterized by abdominal, thoracic and pericardial effusions; (ii) a non-effusive (also called granulomatous, non-exudative, dry or parenchymatous) form characterized by granulomatous changes in different organs, including the CNS, the eyes, kidneys, mesenteric lymph nodes, bowel wall and liver; and (iii) a mixed form. The effusive and noneffusive forms can transform into each other and should be considered the gradations of the same process characterized by pyogranulomatous vasculitis (Hartmann, 2005; Addie, 2012). Neurological signs are most common with the non-effusive form of FIP and can occur either alone or in conjunction with systemic signs such as fever, vomiting, diarrhoea, anorexia, weight loss and lethargy. Neurological signs include abnormal mental status and behaviour, head tilt, seizures, ataxia (generally vestibular), nystagmus cranial nerve dysfunction, and varying degrees of proprioceptive and motor deficits. Seizures can be generalized tonic-clonic or focal, and status epilepticus can occur (Timmann et al., 2008). Ocular signs of FIP comprise anterior uveitis (often with keratic precipitates) (Plate 4), chorioretinitis, anisocoria and retinal haemorrhage, detachment and cuffing of the retinal vasculature. Clinical signs are slowly progressive and eventually fatal.
Diagnostic investigations
Definitive diagnosis of FIP ante-mortem is challenging due to the nonspecific clinical signs, lack of pathognomonic haematologic and biochemical abnormalities and low sensitivity and specificity of tests routinely used in practice (Hartmann, 2005). Haematology usually reveals a normocytic, normochromic, non-regenerative anaemia, neutrophilic leukocytosis and lymphopaenia. Approximately 50% of cats with the exudative form and 70% of cats with the granulomatous form of FIP have increased serum proteins, primarily due to hyperglobulinaemia. Protein electrophoresis reveals a polyclonal gammopathy, mainly involving the γ-globulins. Other serum biochemical changes may be observed depending on the severity of involvement of other organ systems including abnormal hepatic enzyme, bilirubin, urea nitrogen and creatinine levels. When present, effusions should be analysed and typically they are consistent with a modified transudate (protein content >3.5 g/dl, cellular content <5000 nucleated cells/ml) in cats with FIP. An effusion with protein content >3.5 g/dl, albumin/globulin ratio <0.45, and low cellulatiry consisting predominantly of neutrophils and macrophages is highly