Canine and Feline Epilepsy. Luisa De Risio
mg/dl) and pleocytosis (100–10,000 WBC/μl) containing mainly neutrophils, lymphocytes and macrophages. CSF collection may be difficult or impossible due to the high viscosity of the fluid caused by the high protein and inflammatory cell content, therefore additional care should be taken when collecting CSF in cats with suspected FIP and ideally MRI should be performed before attempting CSF collection. In cats with CNS, FIP, MRI may show T2 and FLAIR hyperintensity and contrast enhancement of ventricular lining, choroid plexus and meninges compatible with ependymitis, choroiditis and meningitis (Fig. 5.7a–e). Concurrent hydro-cephalus is common, and herniation of the cerebellum secondary to increased intracranial pressure is possible (Negrin et al., 2007). Detection of FCoV antigen within macrophages in body fluids, as well as in cytologic or biopsy specimens by direct immunofluorescence or immunohistochemistry confirms the diagnosis of FIP, however false negatives can occur (Hartmann, 2005). RT-PCR identification of FCoV in blood or effusions does not provide a definitive diagnosis of FIP and RT-PCR on CSF has low sensitivity (31% in one study) (Foley et al., 1998). Quantitative RT-PCR may help to increase sensitivity and specificity in the diagnosis of CNS FIP (Nghiem and Schatzberg, 2010). Characteristic histopatho-logic CNS lesions of FIP are a pyogranulomatous meningoencephalitis and lymphoplasmacytic periventriculitis.
Treatment
Treatment is aimed at suppressing the inflammatory and immune-mediated response of the cat’s immune system to virulent FCoV. Treatment protocols include glucocorticoids and feline interferon-ω for effusive FIP, and polyprenyl immunostimulant (or alternatively glucocorticoids) and feline interferon-ω for non-effusive FIP (Addie, 2012).
Prognosis
Prognosis is guarded to poor in cats with effusive FIP and in cats with non-effusive FIP resulting in neurologic signs. Prevention of FIP should focus on preventing infection with FCoV (whenever possible). Safety and efficacy of vaccination requires further evaluation (Hartmann, 2005; Addie, 2012).
Bacterial diseases of the CNS in dogs and cats
Bacterial diseases of the CNS can be caused by aerobic and anaerobic organisms (Table 5.4) and can result in meningitis, encephalitis, myelitis, abscessation (focal or multifocal) or empyema.
Multiple organism infections can occur. Bacterial CNS infections are relatively uncommon in dogs and cats. Bacteria can gain access to the CNS haematogenously from a distant septic focus (e.g. endocarditis, urinary tract infections, pulmonary infections), by extension of infection from structures adjacent to the nervous system, such as the nasal passages, sinuses, internal ears, dental roots and eyes, or by direct penetration into the CNS such as occurs with bite wounds, migrating plant foreign bodies, and previous trauma or surgery (Radaelli and Platt, 2002; Dennis et al., 2005; Sturges et al., 2006; Kent, 2012). A compromised immune system can predispose to bacterial colonization of the CNS (Smith et al., 2007).
Table 5.4. Bacterial diseases of the CNS in dogs and cats.
| Organisms | Gram reaction | Shape |
| Aerobic/facultative anaerobic organisms | ||
| Staphylococcus spp. | Positive | Coccus |
| Streptococcus spp. | Positive | Coccus |
| Corynebacterium spp. | Positive | Rod |
| Pasturella spp. | Negative | Rod |
| Escherichia coli | Negative | Rod |
| Proteus spp. | Negative | Rod |
| Pseudomonas spp. | Negative | Coccus |
| Salmonella spp. | Negative | Rod |
| Klebsiella sp. | Negative | Rod |
| Bartonella spp. | Negative | Rod |
| Brucella canis | Negative | Coccus |
| Nocardia spp. | Positive | Rod |
| Other aerobic organisms | ||
| Anaerobic organisms | ||
| Bacteroides spp. | Negative | Rod |
| Fusobacterium spp. | Negative | Rod |
| Peptostreptococcus spp. | Positive | Coccus |
| Eubacterium spp. | Positive | Coccus |
| Actinomyces spp. | Positive | Rod |
| Other anaerobic organisms |
Fig. 5.7. MRI of the brain of a 4-month-old, male, domestic short hair cat with FIP resulting in multifocal CNS signs and mild abdominal effusion. Transverse FLAIR images at the level of caudate nucleus (a), pons (b) and medulla oblongata show hyperintensity of the lining (ependyma) of both lateral ventricles (a), meninges (b, c) and choroid plexus of the fourth ventricle (c). Sagittal T1W (d) and T1WC (e) images of the caudal fossa and adjacent regions. Note the diffuse meningeal enhancement around the brain stem and of the ependymal lining of the dilated fourth ventricle.
Clinical signs
General physical examination in animals with bacterial CNS infection may be normal or reveal fever and the involvement of other organs such as the lungs, gastrointestinal tract, urinary tract, prostate, skin and ears. Severely systemically affected animals may present with hypovolaemic shock and signs of disseminated intravascular coagulation. Animals with cerebral abscessation may show signs of a previous bite wound, trauma or surgery on the head.
Neurological signs vary depending on the location and extent of the infection and associated inflammation and include spinal hyper-algesia, behavioural or personality changes, altered mental status, ataxia, paresis, postural reaction deficits, cranial nerve dysfunction and seizures (Radaelli and Platt, 2002). Onset of signs is generally acute and rapidly progressive. Fever and cervical hyperalgesia have been reported in about 40% and 30% of dogs with bacterial meningoencephalomyelitis, respectively (Radaelli and Platt, 2002). Seizures have been reported in 11 to 30% of dogs with bacterial meningoencephalomyelitis (Radaelli and Platt, 2002). Death may occur due to brain herniation and acute respiratory insufficiency in animals with severe brain oedema or mass effect.
Diagnostic investigations
Haematology may reveal a systemic inflammatory response. Abnormalities including neutrophilic leucocytosis with or without a left shift or leukopaenia, and thrombocytopaenia have been reported to occur in about 57% of dogs with bacterial meningoencephalomyelitis (Radaelli and Platt, 2002). Haematological abnormalities appear uncommon in cats with cerebral abscess (Costanzo et al., 2011). Serum biochemistry abnormalities may be present and reflect involvement of other organs.
MRI or CT of the brain may reveal various parenchymal and meningeal signal changes in animals with meningoencephalitis, a space-occupying mass lesion in animals with cerebral abscessation as well as abnormalities of contiguous structures (e.g. otitis media-interna, sinusitis, retrobulbar mass) representing the source of the infection. The CT and MRI characteristics of cerebral abscessation can change over time reflecting the different stages of abscess development (Costanzo et al
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