Читать книгу Canine and Feline Epilepsy - Luisa De Risio - Страница 268

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 predictive of FIP (Addie, 2012). In cats with neurological signs, CSF analysis may reveal elevated protein (50–350 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.