CNS Disease in the Cat: Current Knowledge of Infectious Causes

Abstract

The information in this review, which summarises current knowledge of infectious diseases affecting the CNS, is collated from publications on the infectious diseases comprising previous research papers, review articles, case series, case reports and textbooks, supplemented by the clinical experience of the authors.

Congenital vestibular disease in captive Sumatran tigers (Panthera tigris ssp. sumatrae) in Australasia

“…There was no evidence for an infectious agent in the tiger cubs reported here. Infectious causes of vestibular disease in domesticated felids usually have a progressive course, or are accompanied by other signs of disease, neither of which was documented in these cases (Beatty et al, 2000;Gaskell et al, 2007;Gunn-Moore and Reed, 2011). No microbial agents were visualised on examination of the CSF and the lack of eosinophils in the CSF suggests that parasitic or protozoan infections are unlikely.…”

Doenças neurológicas em gatos: 155 casos

“…Outras doenças menos frequentes incluem: meningoencefalomielites bacterianas, fúngicas e parasitárias, lesões pelo vírus da imunodeficiência felina, vírus da leucemia felina e panleucopenia felina (Bradshaw et al 2004, Marioni-Henry et al 2004, Gunn-Moore & Reed 2011. As doenças inflamatórias/infecciosas constituíram a segunda categoria de enfermidades mais encontrada nesse estudo (52 gatos [33,5%]), sendo 37 gatos (71,7%) com diagnóstico definitivo e 15 (28,3%) com diagnóstico presuntivo.…”

Feline Immunodeficiency

“…Factors that influence the length of the asymptomatic stage include the pathogenicity of the infecting strain (also depending on the FIV subtype), exposure to secondary pathogens, and the age of the cat at the time of infection. In the last, symptomatic stage (FAIDS phase) of infection, clinical signs are a reflection of opportunistic infections, skin infections such as demodicosis and pediculosis, neoplasia such as B cell lymphosarcoma and squamous cell carcinoma, myelosuppression, and neurologic disease, similar to those observed in people infected with human immunodeficiency virus (HIV) (Hartmann, 1998;Sellon e Hartmann, 2006;Elder et al, 2010;Gunn-Moore & Reed, 2011;Hartamann, 2011;Korman et al, 2012;Sobrinho et al, 2012). The chronic gingivostomatitis is the most common clinical sign in infected cats and significantly degrade the quality of life of animals Pathologic abnormalities described in FIV positive cats with alterations in the morphology of lymph node: hyperplastic during acute phase, follicular involution in the terminal phase of infection; thymus: cortical involution, atrophy, lymphoid follicular hyperplasia and germinal center formation; intestinal tract: villous blunting, pyogranulomatous colitis, lymphoplasmacytic stomatitis; liver: periportal hepatitis; bone marrow: dysplastic changes, granulocytic hyperplasia and the formation of marrow lymphoid aggregates; kidney: tubulointerstitial infiltrates, glomerulosclerosis; central nervous system: Perivascular cuffing, gliosis, myelitis, loss and reorganization of neurons, axonal sprouting, vacuolar myelinopathy; lung: interstitial pneumonitis, alveolitis; skeletal muscle: lymphocytic myositis, myofiber necrosis, perivascular cuffing; reproductive failure occurs in FIV infected cats (Sellon e Hartmann, 2006;Gunn-Moore & Reed, 2011;Hartmann, 2011).…”

“…The duration of the following asymptomatic phase varies but usually lasts many years, viral replication is controlled by the immune response, but there is a progressive decline in CD4+ T lymphocyte numbers, resulting in a decreased CD4 + /CD8 + T lymphocyte ratio ( Fig. 1) (Hartmann, 1998;Sellon e Hartmann, 2006;Gunn-Moore & Reed, 2011;Hartamann, 2011). The most infected cats exhibit an increase in CD8+ T cells along with a strong humoral antibody response which allows them to control this initial phase of the infection (Elder et al, 2010).…”

“…FIV and HIV share many features in their genomes in comprising three major open reading frames (ORF), gag, pol and env, especially in the pol gene and FIV also has a very similar life cycle to that of HIV (Table 2) (Savarino et al, 2007;Elder et al, 2008;Elder et al, 2010 The similarities and discrepancies in the physiopathology of feline and human viruses in their respective natural hosts presents striking analogies, and several intriguing differences (Tables 3 and 4). FIV and HIV share a common pattern on clinical signs, having initially a nonspecific acute phase, followed by an asymptomatic phase and a phase in which the immune system is compromised and the animal is subjected to secondary infections (Sellon e Hartmann, 2006;Gunn-Moore & Reed, 2011;Hartmann, 1998;Hartamann, 2011;Magden et al, 2011;O'Brien et al, 2012).…”