Canaliculitis due to Gemella haemolysans in a single isolate. / Canaliculitis por Gemella haemolysans en aislamiento único.

CASE REPORT: An 84 year-old woman was referred for evaluation of a painless swelling with small purulent discharge in her left upper canaliculus, and an associated epiphora of one-month duration. The patient was diagnosed with acute primary canaliculitis. She was treated with topical and oral antibiotics, as well as topical corticoids for three months, with little response. Surgical treatment with left upper canaliculotomy and curettage was then performed, and Gemella haemolysans was identified from the curetted material. The patient had no recurrence of the disease two months after the surgery. DISCUSSION: This is the first time that Gemella haemolysans is described as unique agent causing primary canaliculitis.

Morphological changes and virus distribution in the ileum of colostrum-deprived calves inoculated with non-cytopathic bovine viral diarrhoea virus genotype-1.

Eight colostrum-deprived calves were inoculated intranasally with a non-cytopathic strain of bovine viral diarrhoea virus (BVDV) genotype-1 and killed in batches of two at 3, 6, 9 and 14 days post-inoculation (dpi). Two non-inoculated animals with similar background served as controls. All infected calves developed mild pyrexia and transient leucopenia due primarily to lymphopenia. Viraemia was correlated with body temperature and inversely related to leucocyte count. Ileal Peyer's patches developed mild follicular lymphoid depletion from 3dpi. This change was accompanied by cellular fragmentation and pyknosis, characteristic of apoptosis, which was most prominent from 6dpi. Lymphocyte apoptosis was confirmed by ultrastructural examination. Stellate cells and macrophages located in the lymphoid follicles were identified as infected by virus from 3dpi and the number of these infected cells increased until 9dpi. Fewer lymphocytes expressed BVDV antigen. Macrophages had morphological features consistent with activation of secretory and phagocytic function from 3dpi. These findings suggest that BVDV is only directly responsible for the destruction of a small number of lymphocytes. Although lymphocyte infection coincided with the onset of apoptosis, the intensity of infection was disproportionate to the marked depletion of gut-associated lymphoid tissue, particularly during the early stages of this process. Characterization of the indirect pathogenic mechanisms involved in the lymphoid depletion associated with BVDV infection will require additional study.

Cytokine expression in paraffin wax-embedded tissues from conventional calves.

The cross-reactivity of antibodies against human tumour necrosis factor (TNF)alpha, interleukin (IL)-1alpha, IL-1beta and porcine IL-6, and the distribution of immunolabelled cells were evaluated on paraffin wax-embedded tissues from five healthy calves. The tissues were fixed in 10% buffered formalin or Bouin's solution and processed for structural studies and immunohistochemical studies by the avidin-biotin-peroxidase technique. Bouin's solution proved to be the more suitable fixative and Tween 20 the most effective antigen unmasking technique for increasing detectable antigenicity. Constitutive expression of TNFalpha, IL-1alpha, IL-1beta and IL-6 by different cell populations, mainly macrophage-like cells, was detected. Lymphoid organs displayed a higher presence of immunolabelled cells than did lung, liver or kidney. TNFalpha and IL-1alpha appeared as the predominant cytokines, especially in the gut-associated lymphoid tissue of the ileum and in the regional mesenteric lymph nodes. The results will facilitate investigation of the role of these cytokine-producing cells in inflammatory disease processes in calves.

Neuropathologic study of experimental classical swine fever.

The aim of this study was to report on the lesions occurring in the central nervous system (CNS) during experimental classical swine fever (CSF) to clarify the spatial and chronologic distribution of the lesions and virus antigen in the CNS. To learn more about the pathogenetic mechanisms of the lesions during CSF in the CNS and to investigate the role of the virus in these mechanisms, cellular infiltrates and infected cells have been characterized. Twenty-eight pigs were inoculated with the virulent CSF virus isolate Alfort 187 and slaughtered from 2 to 15 postinoculation days; 4 animals of similar background served as a control group. Immunohistochemistry, electron microscopy, and the transferase-mediated deoxyuridine triphosphate nick-end labeling method were used to detect viral antigens and apoptosis. The results showed the presence of nonpurulent meningoencephalitis, occasional microhemorrhages, and apoptosis of the lymphocytes forming the perivascular and interstitital infiltrate in swine with CSF. Macrophages appeared to display little involvement in CNS lesions. The infected cells observed at the early stage of disease were lymphocytes and microglial cells in the rostral portion of the telencephalon, with infection of these cells in other areas in the next stages. The relationship between these lesions and the presence of viral antigen varied according to the type of lesion: hemorrhages were not associated with the presence of antigen in endothelial cells, but infiltrate-cell apoptosis was temporally and spacially associated to viral infection. However, the link between viral infection and the presence of cell infiltrate was far from clear.

The role of B cells in the immune response to pestivirus (classical Swine Fever virus).

Pigs inoculated with the Alfort 187 isolate of classical swine fever (CSF) virus were used to study the immunological mechanisms associated with the humoral immune response in the disease. Quantitative and qualitative changes in the B-cell population (lambda light chain [C-lambda]-positive, immunoglobulins [Ig]-M-positive, and IgG-positive were demonstrated in the spleen, thymus and ileocaecal lymph node. Blood and serum samples were used to examine changes in leucocytes, albumin/globulin ratios and specific antibodies against CSF virus titration. Despite the lymphoid depletion shown by infected animals, an increase in B cells and potentially immunoglobulin-producing C-lambda+ plasma cells was observed in the lymphoid organs from the onset of disease. The increase in C-lambda+ B cells was matched by a parallel increase in IgM+ cells, which attained peak values from 7 days post-inoculation (dpi), while IgG+ cells increased from 11 dpi onwards. The enhanced biosynthetic capacity of these cells may have been linked to the initiation of a humoral response to CSF virus, and to the progressive decline in the albumin/globulin ratios of inoculated animals. Activation, proliferation and differentiation of B cells coincided with the presence of viral antigen, and with an intense phagocytic and biosynthetic activity of monocytes-macrophages and T lymphocytes. The previously reported increase of cytokine (TNFalpha, IL-1alpha and IL-6) production by monocytes-macrophages, and the release of IL-2, IL-4 and IFNgamma by T lymphocytes, may play a role in the initiation of the humoral immune response in CSF. These changes may have influenced the late appearance of virus-specific antibodies in the study, as well as the progressive increase of immunoglobulins.

BSE infection in bovine PrP transgenic mice leads to hyperphosphorylation of tau-protein.

We observed the changes in the central nervous system (CNS) of transgenic mice expressing bovine prion protein (Bo-PrP) as a contribution to our knowledge of the pathogenesis of bovine spongiform encephalopathy (BSE). The main result was the detection of hyperphosphorylated tau. This protein was detected for the first time, using immunohistochemical techniques, in the neurons and glial cells of mice experimentally infected with BSE. The results highlighted the involvement of tau protein in the pathogenesis of BSE and the close link between hyperphosphorylated tau deposits and prion protein. Ultrastructural examination revealed a novel arrangement of intraneuronal tau deposits not hitherto reported.