Pathological and Immunohistochemical Analyses of Naturally Occurring Equine Glanders Using an Anti-BpaB Antibody.

Glanders is caused by the gram-negative bacterium Burkholderia mallei. In this study, we investigated the histopathology and immunohistochemical localization of B. mallei in natural cases of equine glanders. Four horses showing clinical signs of nasal discharge and multiple cutaneous nodules or papulae in the hindlimbs and abdomen were reported in Mongolia. They tested positive for B. mallei infection on complement fixation, Rose Bengal agglutination, and mallein tests. Gross and histological lesions observed in these cases were similar to those previously reported in equine glanders. Immunohistochemistry using a monoclonal antibody to B. mallei BpaB showed localization of the bacterial antigen in the cytoplasm of neutrophils, macrophages, epithelioid cells, and multinucleated giant cells in the pyogranulomas and abscesses in target organs. Some alveolar type II cells and bronchiolar epithelial cells also contained the antigen. These results suggest that the anti-BpaB antibody is useful for identifying B. mallei-infected cell types in naturally infected horses.

Immunohistochemical phenotyping of macrophages and T lymphocytes infiltrating in peripheral nerve lesions of dourine-affected horses.

Dourine is a deadly protozoan disease in equids caused by infection with Trypanosoma equiperdum. Neurological signs in the later stage of infection may be caused by peripheral polyneuritis and related axonal degeneration. This neuritis involves T lymphocytes, B lymphocytes, and macrophages, and is observed in cases without obvious neurological signs. However, the pathogenesis of neuritis remains unclear. We identified M2 macrophages and CD8 T cells as the predominant phenotypes in neuritis of dourine-affected horses with or without neurological signs. In contrast, the populations of M1 macrophages and CD4 T cells were small. This result indicates that inflammation was chronic and suggests that dourine-associated neuritis occurs at the early stage of infection.

Adverse effects of inhaled sand dust particles on the respiratory organs of sheep and goats exposed to severe sand storms in Mongolia.

Sand storms in Mongolia have increased in frequency and scale, resulting in increased exposure of the inhabitants of Asian countries, including Japan and Korea, to Asian sand dust (ASD), which results in adverse effects on the respiratory system. However, there is no information on the health risks of severe sand storms in domestic animals in Mongolia. The aim of the study was to investigate the effects of sand dust particles on the respiratory organs, including the lungs and tracheobronchial lymph nodes, of sheep and goats exposed to severe sand storms in Mongolia. Seven adult sheep and 4 adult goats that had been exposed to sand storms and 3 sheep with no history of exposure were included in this study. Lung tissues and tracheobronchial lymph nodes were subjected to histopathological and immunohistochemical examination. The mineralogical contents of the lungs and lymph nodes were determined using inductively coupled plasma atomic emission spectroscopy. Fibrosis and granulomatous lesions comprising macrophages containing fine sand dust particles were observed exclusively in the lungs of sheep and goats exposed to sand storms. The activity of macrophages was also demonstrated by the presence of IL-6, TNF, and lysozyme. In addition, silicon, which is the major element of ASD (kosa aerosol), was detected exclusively in the lung tissues of the exposed animals. Our findings suggest that exposure to sand dust particles may affect the respiratory systems of domestic animals during their relatively short life span.

Cerebellar ataxia suspected to be caused by Oxytropis glabra poisoning in western Mongolian goats.

In the last five years in western Mongolia, a neurological disorder and resultant economic loss have developed in goats, sheep, cattle and horses: association of the disease with ingestion of Oxytropis glabra, a toxic plant, was suggested. Affected goats showed neurological signs, including ataxia, incoordination, hind limb paresis, fine head tremor and nystagmus. Three goats, one with moderate clinical signs and the other two with severe clinical signs, were necropsied and examined to describe and characterize the histologic, immunohistochemical and ultrastructural lesions. Although no gross pathological changes were observed in a variety of organs including the central nervous system of these goats, microscopic examination of the cerebellum demonstrated degenerative changes in all these goats, such as vacuolar changes and loss of Purkinje cells, torpedo formation in the granular layer, increased number of spheroids in the cerebellar medulla, and loss of axons and myelin sheaths of Purkinje cells. The chemical analysis of the dried plant detected 0.02-0.05% (dry weight basis) of swainsonine. This is the first report describing the clinical and pathological findings in Mongolian goats suspected to be affected by O. glabra poisoning.

A novel dense granule protein, GRA22, is involved in regulating parasite egress in Toxoplasma gondii.

The intracellular protozoan parasite Toxoplasma gondii is capable of invading any nucleated cell and replicates within a parasitophorous vacuole (PV). This microenvironment is modified by secretory proteins from organelles named rhoptries and dense granules. In this report, we identify a novel dense granule protein, which we refer to as GRA22. GRA22 has no significant homology to any other known proteins. GRA22 possesses a signal peptide at the N-terminal end which is responsible for dense granule and PV localization. The RH strain GRA22 contains 12 copies of tandem repeats consisting each of 21 amino acids located between the 42nd and 293rd amino acid residues from a full length of 624 amino acids. On the other hand, ME49 strain GRA22 has 10 copies of tandem repeats. The Neospora caninum GRA22 ortholog completely lacks this repetitive sequence. GRA22 knock out parasites show a similar growth rate as the parental strain. However, the timing of egress is earlier than that of the parental strain. These results suggest that GRA22 is involved in regulating parasite egress in T. gondii.