Porcine proliferative enteropathy in Estonian pig herds: histopathology and detection of Lawsonia intracellularis by PCR.

Lawsonia intracellularis is the causative agent of proliferative enteritis in pigs (PPE). This bacterium is difficult to culture from clinical samples and antemortem demonstration is therefore usually performed by PCR on faecal samples. The aim of this study was to elucidate the frequency of L. intracellularis infection in pig herds in Estonia using PCR, histopathological methods and electronmicroscopical studies. The frequency of demonstration of L. intracellularis was highest in 9-12 weeks old pigs (68.1%). It was more frequent in growing pigs with enteritis on small farms where the system of "all-in all-out" was not practiced and where standards of hygiene were poor. Gross and histopathological studies demonstrated that characteristic macroscopic changes associated with PPE were localised to the distal jejunum and ileum.Thickened longitudinal and circumferential folds occurred in the mucosa of the affected regions of the bowel. Samples from pigs aged 4 to 20 weeks exhibited the most intensive inflammatory changes. The distal part of the jejunum, ileum and the upper third of proximal colon and cecum wall were visibly thickened with reduced luminal diameter. Hyperplasia of lymphoid tissue and, in many cases, pseudomembranous or fibrinous inflammation was found. L. intracellularis was detected in 56 young pigs using histopathological methods. Additionally, in 8 of these pigs intracellular bacteria were demonstrated in ilial epithelial cells by transmission electronmicroscopical (TEM) investigation. On the basis of these TEM investigations it was concluded that L. intracellularis causes disturbances of normal growth, differentiation and apoptosis of the epithelial cells of ileum.

Application of Photoshop-based image analysis and TUNEL for the distribution and quantification of dexamethasone-induced apoptotic cells in rat thymus.

UNLABELLED: The aim of the present study was to determine the target site cells in the rat thymus after exposure to the synthetic glucocorticoid, dexamethasone, at therapeutic doses. The findings of histology and histochemistry (Feulgen, terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling--TUNEL) with quantification by computerized histomorphometry are described. MATERIAL AND METHODS: A quantified investigation of apoptotic and mitotic thymic lymphocytes in 36 young adult Wistar rats was performed at 1-7 days after a 3-day injection of dexamethasone (a total dose of 1.2 mg/rat intraperitoneally). RESULTS: At the first day after dexamethasone administration the moderate involution and atrophy of thymus histology were observed with simultaneous fall in cortical cellularity and mitotic activity of thymocytes. More rapid fall appeared in the inner cortex. The number of apoptotic (TUNEL-positive) cells was significantly increased. On the days 5 and 7 the expression of apoptosis and the cell proliferation were at almost normal level. CONCLUSIONS: The findings suggest that dexamethasone-induced apoptosis of cortical thymic lymphocytes, mainly correlated with synchronous inhibition of mitosis and cell number fall in thymus. The main target sites of dexamethasone injury were cells in the inner cortex of lobuli thymi.

Transport proteins in rats' renal corpuscle and tubules.

UNLABELLED: The localization of transepithelial transport proteins for glucose and water reabsorption in renal corpuscle and tubules epithelium was observed. MATERIAL AND METHODS: Immunohistochemistry of normal male Wistar rats' kidney has been performed. Facilitated diffusion glucose transporter GLUT4, Na(+)-dependent glucose co-transporter SGLT1, a cargo transporter TGN38, and water transporter aquaporin-2 (AQP2) were used. RESULTS: An intensive GLUT4 expression in renal proximal tubules and in convoluted segment of distal tubules has been observed. The intensive SGLT1 expression was marked in all renal tubules, and also in the glomerulus of the renal corpuscle. TGN38 was expressed mainly in the S1 of proximal tubules and a bit weaker in the distal tubules. The most intensive AQP2 expression in the proximal tubules and in the thin part of Henle's loop has been detected. In some cases AQP2 expression in the collecting tubules has been observed. The same tubules nephroni are marked heterogeneously. The distribution of transepithelial transport proteins in different parts of nephroni is also greatly heterogeneous because of weak determination of urinary system. CONCLUSION: The comparable transport-proteins distribution with technique of fluorescence immunohistochemistry in rats' renal corpuscle and tubules was elucidated. Data suggest that expression of glucose and water transepithelial transporter proteins is heterogeneous in all parts of nephron, and, probably, is in accordance with recycling of transport proteins.

Ultrastructural changes in the remnant kidney (after 5/6 nephrectomy) glomerulus after losartan and atenolol treatment.

The aim of our study was to investigate the effect of losartan on the changes in the early stages (at week 4) of experimental chronic renal failure after 5/6 nephrectomy compared with the impact of atenolol. Attention was focused on the ultrastructural changes in the renal corpuscles. Twenty-seven male Wistar rats were divided into three groups: nephrectomized group, nephrectomized losartan-treated group and nephrectomized atenolol-treated group. Rats were kept in a climate-controlled facility, where animals were housed under standard conditions on a 12-hour light/dark cycle and fed with standard rodent chow. Angiotensin receptor antagonist losartan (180 mg/L) or beta-blocking agent atenolol (750 mg/L) was added to the drinking water and treatment was started on the first day after the operation. Systolic blood pressure and 24 hour protein excretion was measured every week. Nephrectomized rats had higher proteinuria and systolic blood pressure than the treated rats. Rats were killed 4 weeks after surgery. Early stage renal disease was characterized by glomerular hypertrophy and focal segmental glomerulosclerosis. The morphological study revealed that ultrastructural changes in the atenolol-treated group were smaller than those in the nephrectomized and losartan-treated groups. Glomerular basement membrane (GBM) thickness was significantly increased in losartan-treated (206.8 nm) and atenolol-treated (198.8 nm) rats compared to nephrectomized (169.2 nm) rats. The podocytes demonstrated hypertrophy and foot process effacement, especially in nephrectomized group. In conclusion, our results show that firstly, treatment with losartan and atenolol significantly increased GBM thickening and secondly, treatment with atenolol reduced ultrastructural changes in the podocytes.