Abstract
The first known case of what is now called bat white-nose syndrome (WNS) was documented in February, 2006 in New York State. Since then, WNS has spread throughout the northeastern portion of the US, causing a population decline of up to 75% in some areas. The condition affects hibernating bats and is characterized grossly by prominent white fungal growths on the muzzle, ears, and/or wing membranes. Histological examination of necropsy specimens revealed a cutaneous fungal infection. Fungal hyphae replaced hair follicles and adnexae, with penetration into surrounding tissues. Epidermal erosions were also associated with fungal growth. The bats were severely emaciated, with little or no identifiable fat that is necessary for them to survive hibernation. A fungus was isolated from affected bats, but the morphology of this fungus had not been previously described. It was identified as a member of the Geomyces group and has distinct single curved conidia. The optimal temperature for growth is between 5°C and 10°C, which falls well within the temperature range of bat hibernacula. At this time it is uncertain whether the fungus is the primary cause of death in the bats or if this represents an opportunistic infection due to some other cause.
Blehert DS, Hicks AC, Behr MK, Meteyer CU, Berlowski-Zier BM, Buckles EL, Coleman JT, Darling SR, Gargas A, Niver R, Okoniewski JC, Rudd RJ, Stone WB. Bat white-nose syndrome: an emerging fungal pathogen?. Science
Until now it was unclear how often temporal lymph nodes were present in the bovine, and their cell populations were previously uncharacterized. The authors performed anatomical dissection of the temporal region of 62 cattle to determine the frequency and distribution of nodal tissue, define the area drained by the lymph nodes, and characterize the cell populations in these nodes. Lymph nodes and hemal nodes were found in 77% of the 124 temporal regions and were usually bilateral. The ratio of lymph nodes to hemal nodes was 3:2. Using injections of India ink, they demonstrated that the drainage area encompassed the forehead, upper eyelid, base of the horn, and the temporal muscle. Analysis of cell populations by immunohistochemistry and flow cytometry showed that the temporal lymph nodes and hemal nodes are very similar to other cranial lymph nodes. The name proposed for the temporal lymph node is lymphonodus temporalis. This paper also provides an excellent general review of bovine lymph nodes and hemal nodes.
Casteleyn CR, Breugelmans S, Simoens P, Van den Broeck W.
This review article discusses some of the technical and interpretive pitfalls that can be encountered when using immunohistochemistry in the evaluation of pathological specimens. Specific areas that may cause difficulties are fixation and tissue processing, protease and heat-induced epitope retrieval, endogenous enzyme activity, effects of avidin and biotin, issues with the primary antibody, and problems with the detection system. Each section is thoroughly referenced and provides a detailed explanation of the potential problems. With the ever-increasing reliance on immunohistochemical assays in diagnostic pathology, this review will help us understand how to avoid technical difficulties that could potentially result in erroneous interpretations.
Bussolati G, Lenonardo E.
In humans, chronic ingestion of arsenic can lead to cardiovascular and respiratory diseases. The investigators hypothesized that chronic exposure to low levels of sodium arsenite (AsIII) would cause early vascular changes that may play an important role in the pathogenesis of chronic arsenic toxicity. C57BL/6 mice were exposed to 50 ppb AsIII in drinking water for four, five, or eight weeks. Microarray analyses performed on lung tissues from exposed and control mice demonstrated significant differences in expression of 65 genes. Specifically, in the extracellular matrix (ECM) category 91% of the genes, including elastin and collagen, were significantly decreased in exposed mice. These results were verified with real-time RT-PCR. Histological examination showed that the ECM surrounding small arteries in the heart and lungs had areas of disruption, and alpha-smooth muscle actin was decreased in walls of blood vessels in exposed mice. The findings of altered gene expression and disruption of ECM in the target organs of chronic arsenic toxicity support the initial hypothesis that an early vasculopathy is a component of the etiopathogenesis of chronic arsenic ingestion.
Hays AM, Lantz RC, Rodgers LS, Sollome JJ, Vaillancourt RR, Andrew AS, Hamilton JW, Camenisch TD, et al.