Distribution of the rabies virus in the central nervous system of naturally infected foxes]

Quantitative distribution of rabies virus and the character of immunofluorescence in various parts of the central nervous system [CNS] and salivary glands were investigated in 21 naturally infected foxes. A mean death period was recorded in mice infected with the virus obtained from various parts of the CNS and salivary glands of the investigated foxes. The highest average titer of the virus was found out in the salivary glands - 4.46 log MLD50 per 0.03 ml i. c. The average titer was 2.30 log in the cornu ammonis, 1.99 log in the lobus olifactorius, 1.80 log in the spinal cord of the sacro-lumbar region, 1.73 log in the cortex, 1.71 log in the medulla oblongata, and 1.64 log in the cerebellum. The highest intensity of specific fluorscence was recorded in the thalamus, lobus piriformis, and cornu ammonis. In these regions, numerous round fluorescent inclusion bodies similar to Babes-Negri bodies occurred. Babes-Negri bodies in the cornu ammonis of foxes were proved in 81% of cases. Mice infected with the virus obtained from the salivary glands showed the shortest mean death period - 12.2 days and from the cornu ammonis it was 14.6 days. In virus infection from the other parts of the CNS the mean death period ranged from 16.0 to 17.4 days.     

Cellular response to rabies virus infection

The effects of rabies virus on host cells were studied and compared to those obtained with another rhabdovirus, vesicular stomatitis virus [J. Virol. 34, 777-781 (1980)]. We show here: (1) that rabies infection has no effect on cell morphology, while infection with vesicular stomatitis virus caused cell retraction. Thus, only vesicular stomatitis virus induced a depolymerization of the microfilaments; and (2) that microtubules and microfilaments do not play a major role in rabies virus production, as it is suggested by results obtained with several effectors (colcemid, colchicine and cytochalasin-B) which directly or indirectly affect cytoskeleton organization. The same properties were observed with directly or indirectly affect cytoskeleton organization. The same properties were observed with vesicular stomatitis virus. Furthermore, the use of cytochalasin-B shows that an inhibition of glycosylation of the virion spike protein occurs only in rabies infected cells. As vesicular stomatitis viral glycosylation is normal in cytochalasin-B treated cells, results obtained indicate that two types of interactions can occur between a virion and the host-cell depending on the rhabdovirus type.     

Cryptococcal infection of the central nervous system of a dog in the United Kingdom

Cryptococcal infection of the C.N.S. is described in a two-year-old Borzoi dog. The animal showed limb weakness progressing over a period of five months to spastic paraplegia with head tremor, stiffness of the neck and nystagmus. On post-mortem examination there was severe hydrocephalus and granulomatous ependymitis. Cryptococci were found in the lesions and were identified on the basis of morphology and reaction to specific fluorescent antibody. This is believed to be the first case of canine cryptococcosis reported in the United Kingdom.     

Ovine arthrogryposis and central nervous system malformations associated with in utero Cache Valley virus infection: spontaneous disease

Gross appearance and histologic lesions seen in 15 newborn lambs in an outbreak of congenital arthrogryposis with hydrocephalus or hydranencephaly (CAH) in Texas are described. Severe arthrogryposis with skeletal muscle hypoplasia was seen in limbs of affected lambs. Spinal column deformities were also present. Multiple central nervous system (CNS) malformations were present in CAH lambs including micrencephaly, cerebellar hypoplasia, micromelia, hydrocephalus, hydranencephaly, and porencephaly. Histologic lesions consisted primarily of areas of necrosis and loss of the paraventricular neuropil and motor neurons in the CNS and a resolving myositis with poorly developed myotubular myocytes in skeletal muscle. Seroepidemiologic studies on the flock and serologic data from heart blood taken from the stillborn affected lambs indicated that the outbreak was due to in utero infection with Cache Valley Virus.     

A review of coronavirus infection in the central nervous system of cats and mice

Feline infectious peritonitis (FIP) is a common cause of death in cats. Management of this disease has been hampered by difficulties identifying the infection and determining the immunological status of affected cats and by high variability in the clinical, pathological, and immunological characteristics of affected cats. Neurological FIP, which is much more homogeneous than systemic effusive or noneffusive FIP, appears to be a good model for establishing the basic features of FIP immunopathogenesis. Very little information is available about the immunopathogenesis of neurologic FIP, and it is reasonable to use research from the well-characterized mouse hepatitis virus (MHV) immune-mediated encephalitis system, as a template for FIP investigation, and to contrast findings from the MHV model with those of FIP. It is expected that the immunopathogenic mechanisms will have important similarities. Such comparative research may lead to better understanding of FIP immunopathogenesis and rational prospects for management of this frustrating disease.     

Establishment of central nervous system infection by canine distemper virus: breach of the blood-brain barrier and facilitation by antiviral antibody

Morphologic, immunologic and virologic data implicating antiviral antibody in promoting entry of canine distemper virus (CDV) into brain and reticuloendothelial tissues are reviewed. Infection of central nervous system (CNS) endothelium precedes invasion of virus-positive and -negative leukocytes into Virchow-Robin spaces and central nervous system (CNS) parenchyma by 1-3 days. Platelets are implicated in initiation of endothelial infection in that: CDV-infected dogs are thrombocytopenic; platelets from CDV-infected dogs contain IgG-virus complexes on their plasma membranes; platelet microthrombi were observed adjacent to foci of endothelial infection, and; CDV-susceptible ferrets rendered thrombocytopenic by antiplatelet antibody exhibit delayed viral entry into CNS tissues. Renal glomerular-bound IgG, IgM and occasionally CDV antigen were demonstrated in CDV-infected dogs by immunocytochemical techniques. Distemper-infected dogs with inherited C3 deficiency exhibited enhanced renal glomerular disease associated chiefly with deposition of IgM in mesengial regions vs. their homozygous normal CDV-infected littermates. Direct infusion of virus-positive leukocytes, plasma and platelets into the CNS capillary bed via the right carotid artery should establish the primacy of each in the initiation of CNS vascular endothelial infection by CDV.     

Susceptibility of mice to bovine herpesvirus type 5 infection in the central nervous system

Bovine herpesvirus type 5 (BoHV-5) is an important pathogen that causes meningoencephalitis in cattle. Few studies have used the mouse as a model for BoHV-5 infection. Despite the fact that BoHV-5 can infect mice with immune deficiencies, little is known about viral replication, immune response, and the course of infection in the central nervous system (CNS) of wild-type mice. Therefore, the aim of this study was to evaluate the response in the CNS of BALB/c mice acutely infected with BoHV-5 at different days post-inoculation (dpi). BoHV-5, when inoculated intracranially, was able to infect and replicate within the CNS of BALB/c mice. Until 15 dpi, the mice were able to survive without showing prominent neurological signs. The infection was accompanied by a Th1 immune response, with a significant expression of the cytokines IFN-γ and TNF-α and chemokine CCL-2. The expression of these cytokines and chemokines was most significant in the early course of infection (3 and 4 dpi), and it was followed by meningoencephalitis with perivascular cuffing and periventriculitis, composed mainly of macrophages and lymphocytes. After the expression of cytokines and chemokine, the mice were able to curb BoHV-5 acute infection in the brain, since there was a decrease in the number of BoHV-5 DNA copies after 3 dpi and viable viral particles were not detected after 6 dpi. Importantly, BoHV-5 was able to infect the trigeminal ganglia during acute infection, since a large number of BoHV-5 DNA copies were detected on 1 and 2 dpi.     

Inflammatory disease of the central nervous system

Inflammatory diseases involving the central nervous system can be difficult to diagnose and frustrating to treat. The clinician can maximize successful treatment of these patients by recognizing the clinical signs in the early stages of disease, following a logical diagnostic plan to identify the specific etiologic agent involved, and formulating an appropriate and aggressive therapeutic plan. Treatment will not always be successful owing to lack of effective treatments and irreversible neurologic damage.     

Acute injury to the central nervous system

Central nervous system (CNS) trauma is divided into brain and spinal cord injury. A basic understanding of the pathophysiology of CNS trauma helps the practitioner more accurately evaluate, treat, and prognose cases of CNS trauma. The progressive nature of CNS injuries and the contribution of microvascular ischemic are explored.