Articular cartilage blood vessels in swine osteochondrosis

Perfusion studies in swine with early lesions of osteochondrosis demonstrated that lamellar areas of chondrocyte necrosis within reserve zones of growth areas occurred only in regions of nonperfused articular cartilage. Articular cartilage with a similar anatomical location was perfused in some animals. Occasionally, nonperfused articular cartilage showed vascular alterations within cartilage canals without evidence of significant perivascular or lamellar necrosis. By light microscopy, some vessels within or adjacent to nonperfused articular cartilage had normal morphology; however, ultrastructural abnormalities were found in some vessels of all cartilage canals adjacent to necrotic cartilage lamella. Minimal alterations were in the few cartilage canal vessels that appeared normal by light microscopy, and the surrounding chondrocytes showed only minimal alterations. Early cartilage canal alterations were seen in the endothelium of cartilage canal capillaries, and ultrastructural changes in these vessels were similar to those described with experimentally induced, direct vascular injury. Vascular injury was followed by leakage of plasma and cells into the interstitial space of the cartilage canal. Necrosis of the vessel wall and interstitial tissue caused the cartilage canals to appear empty or to be filled with fibrin-like material. Although the vascular changes could be considered as part of the normal process of cartilage maturation and cartilage canal chondrification, observations suggest that in domestic swine the attendant cartilage necrosis and chondrolysis is exuberant. It is suggested that alterations in cartilage canal vessels play a major role in the pathogenesis of articular cartilage lesions that are found in osteochondrosis of swine.     

Ultrastructure of normal epiphyseal cartilage of the articular-epiphyseal cartilage complex in growing swine

Normal epiphyseal cartilage from the articular-epiphyseal cartilage complex (A-E complex) of the distal parts of the femur and humerus of growing commercial crossbred boars was collected, embedded in plastic, and studied by light and electron microscopies. The morphology of this cartilage was determined to provide a basis for comparison with cartilage affected with osteochondrosis, an important clinical disease in swine. Normal epiphyseal cartilage from the A-E complex in growing swine was divided into 4 major regions of cells: resting, proliferating, hypertrophic, and calcifying regions. Cells in the resting zone contained prominent lipid and densely aggregated glycogen. As the cells proliferated and matured, the lipid and glycogen became less prominent. The lipid droplets became smaller and scarcer, and the glycogen became dispersed in the cytoplasm. Proliferating and hypertrophic cells clustered in roughly egg-shaped groups of 4 to 8 cells/plane of section. In the calcifying region, the interterritorial matrix (between cell clusters) calcified, and the territorial matrix (uniting cells in a cluster) remained uncalcified. Calcified matrix extended the depth of one cell group from the area of capillary penetration, and the capillaries invaded by entering a cluster of cells. Territorial matrices in all regions of A-E complex epiphyseal cartilage were composed of randomly oriented collagen fibrils with a granular fibrillar proteoglycan network dispersed between the fibrils. Heterogeneity of chondrocytes was characterized by the presence of both light- and dark-staining cells in the proliferating through calcifying regions and by 3 morphologically distinct light cell types in the late hypertrophic and calcifying regions.     

Biochemical changes in articular cartilage opposing full- and partial-thickness cartilage lesions in horses

Using arthroscopic technique, identical diameter defects were created in the proximal articular surface of both intermediate carpal bones of 6 horses. One of each pair of defects was deepened to penetrate the subchondral plate. Removed cartilage was assayed for [35S] sulfate incorporation, total hexosamine content, and DNA content. Six weeks later, cartilage was harvested and similarly analyzed from the distolateral portion of the radius directly opposite the created lesions and the distomedial portion of the radius distant from the lesion. The repair tissue filling the full-thickness defect and the cartilage at the periphery of the partial-thickness lesion also were analyzed. There was a marked increase in synthetic activity (35S sulfate incorporation) opposite the full-thickness defect, compared with the cartilage opposite the partial-thickness defect. A marked decrease in glycosaminoglycan content in the cartilage opposite the full-thickness defect was found as compared with that opposite the partial-thickness defect. The repair tissue filling the full-thickness defect was highly cellular, high in synthetic activity, but low in glycosaminoglycan content. Insignificant changes occurred in the cartilage adjacent to the partial-thickness defect. On the basis of these results, we suggest that full-thickness defects at 6 weeks result in more detrimental change to the cartilage opposite it than do partial-thickness lesions of the same diameter.     

Scanning electron microscopy of the lesions of swine dysentery.

Thirty weanling pigs were examined by scanning electron microscopy at various time intervals after oral inoculation with crude colon contents from pigs affected with dysentery. The earliest recognizable change was a corrugated appearance of the mucosal surface of the large intestine. Large spirochetes, morphologically similar to Treponema hyodysenteriae, were first observed within the crypts of Lieberkühn where they seemed to proliferate onto the luminal surface. Then mucus, fibrin, erythrocytes, and disrupted epithelium appeared. Large spirochetes were always abundant in those lesions, but variable numbers of other mixed bacterial forms were also present. The earliest changes could be correlated with the appearance of large spirochetes in the feces and with early clinical signs, but not with a specific postinoculation time. Once bloody diarrhea was present, no consistent pattern was observed in development, location, or form of the lesions. With time, the lesions merely came to involve an increasingly greater surface area of the large intestine.     

Scanning electron microscopy of sarcoptic mange lesions in swine

Scanning electron microscopy revealed that lesions of sarcoptic mange in swine, pass through 3 different stages. During the first 3 weeks of infestation, adult female mites tunnel into the epidermis. During the following 3 or 4 weeks, the surface openings of these tunnels become covered with keratinized epidermal crust which increases in thickness. After 7 weeks of infestation, the crust falls off, the tunnel openings become apparent again and most of the mites vacate these tunnels.     

Acute aflatoxicosis in swine: clinical pathology, histopathology, and electron microscopy

Feeder pigs weighing 12 to 15 kg each were given a single oral dose of aflatoxin, 1.2 mg/kg of body weight. Liver-specific serum enzyme activities were compared with gross, microscopic, and ultrastructural hepatic changes in individual pigs euthanatized at 24, 48, and 72 hours after they were given aflatoxin. The greater the morphologic change in liver of the treated pigs, the greater the increase in liver-specific serum enzyme activities. Isocitric dehydrogenase, alkaline phosphatase, sorbitol dehydrogenase, and aspartate aminotransferase activities increased in 6 of 8 treated pigs by 24 hours. Increase in gamma-glutamyl transpeptidase activity was not significant. Microscopic and ultrastructural changes in centrilobular hepatocytes included glycogen deletion, mitochondrial and endoplasmic reticulum swelling, membrane disruption, and nuclear fragmentation at 24 hours. The centrilobular areas had marked extravasation of erythrocytes at 24 hours without basal lamina changes. At 72 hours, the centrilobular hepatocytes had increased lipid vacuoles and acceptable amounts of glycogen. Marked infiltrations of monocytes, plasma cells, and lymphocytes were also present at this time.     

Scanning electron, light, and transmission electron microscopy of intestine of gnotobiotic calf.

Adjacent areas of upper, middle, and lower parts of the small intestine and spiral colon from a 48-hour-old gnotobiotic calf were compared by scanning electron microscopy (SEM), light microscopy (LM), and transmission electron microscopy (TEM). As visualized by all 3 methods, small intestinal histologic features, except for apical location of villous epithelial cell nuclei in sections of upper and middle parts of small intestine, were similar to those described for other species. The colonic surface visualized by SEM was composed of flattened ridges separated by furrows into which opened the crypts of Lieberkühn. The epithelial surfaces of the ridges and the furrows had an extensive microvillous covering and scattered goblet cell openings.     

Acute monensin toxicosis in sheep: light and electron microscopic changes

Monensin was administered orally to 3 sheep at dosages of 12 (the LD50), 16, and 24 mg/kg of body weight, respectively. Clinical signs of monensin toxicosis were observed in the sheep in 24 to 36 hours of administration. Clinical signs included CNS depression, anorexia, diarrhea, and stiffness. Increased serum creatine phosphokinase and aspartate aminotransferase activities identified possible muscle damage. Sheep were euthanatized at 54 hours after dosing; at necropsy, there were skeletal muscle hemorrhages, pale myocardium, and pulmonary edema. Ultrastructural lesions were in the liver, diaphragm, and myocardium; diaphragm and myocardium were most severely affected. Mitochondrial swelling and cristolysis, swollen sarcoplasmic reticulum, and disruption of myofibrillar architecture were prominent. These ultrastructural changes are consistent with the hypothesis that monensin causes muscle cell necrosis due to its ionophorous properties and disruption of cellular Na+:Ca2+ balance. It is proposed that this upset of normal ionic processes allows increased intracellular calcium, which directly leads to the functional and structural mitochondrial changes observed.     

Comparison of proteoglycan and collagen in articular cartilage of horses with naturally developing osteochondrosis and healing osteochondral fragments of experimentally induced fractures

OBJECTIVE: To compare articular cartilage from horses with naturally developing osteochondrosis (OC) with normal articular cartilage and healing cartilage obtained from horses with experimentally induced osteochondral fractures. SAMPLE POPULATION: 109 specimens of articular cartilage from 78 horses. PROCEDURE: Morphologic characteristics, proteoglycan (PG), and type II collagen were analyzed in articular cartilage of OC specimens (group 1), matched healing cartilage obtained 40 days after experimentally induced osteochondral fractures (group 2), and matched normal cartilage from the same sites (group 3). RESULTS: 79 specimens of OC cartilage were obtained from horses. Ex vivo PG synthesis was significantly greater in the femoral cartilage, compared with synthesis in the tibial cartilage, and significantly greater for groups 1 and 2, compared with group 3. For groups 1 and 2, femoral fragments had significantly greater PG content, compared with PG content in tibial fragments. Keratan sulfate content was significantly less in group 3, compared with groups 1 and 2. Cartilage from the OC specimens had loss of structural architecture. The OC tissue bed stained positive for chondroitin sulfate and type II collagen, but the fracture bed did not. CONCLUSIONS AND CLINICAL RELEVANCE: Our analyses could not distinguish articular cartilage from horses with OC and a healing fracture. Both resembled an anabolic, reparative process. Immunohistochemical analysis suggested a chondromyxoid tissue in the OC bed that was morphologically similar to fibrous tissue but phenotypically resembled hyaline cartilage. Thus, tissue in the OC bed may be degenerative cartilage, whereas tissue in the fracture bed may be reparative fibrous callus.     

Combined scanning electron and light microscopy of biopsy samples of bovine uterus.

Uterine biopsies from normal cyclic cows were optimally prepared for examination in a scanning electron microscope. After examination in the scanning electron microscope the same tissues were routinely processed for paraffin sectioning and reexamined with the light microscope. Results indicate that the scanning electron microscope is satisfactory for examination of the fine surface structure of the endometrium and the light microscope for subsurface structures of the bovine uterus.     

Effect of diet on longitudinal bone growth and osteochondrosis in swine

Weanling gilts were fed either a 12% or 16% protein diet for 10 weeks. Animals fed the 12% protein diet had reduced body weights and reduced longitudinal bone growth as measured in the distal radial growth plate. There was no difference in the growth plate widths between the two animal groups, but there was a significant reduction in the daily rate of cell production in the proliferative zone of animals fed the 12% protein diet. No effect of diet on the rate of expansion of the epiphysis at the articular-epiphyseal junction of the distal femur or humerus could be detected. All animals in both groups had morphologic cartilage lesions consistent with early changes associated with osteochondrosis (OCD), and there was no difference in the lesion morphology between the dietary groups. Areas of disorderly endochondral ossification in the radial growth plate were associated with perpendicular growth cartilage infractions. Growth plate lesions were characterized by increased widths of the maturing cartilage zone without increased width of the proliferative zone or an increase in the daily rate of cell production. Focal growth plate lesions developed because of a transitory inhibition of cartilage mineralization and resorption. Disorderly foci of endochondral ossification beneath articular cartilage were characterized by an area of chondrocyte necrosis which prevented normal cartilage matrix mineralization. Lamellae of cartilage necrosis were also present within the reserve zone of the articular cartilage. These were associated with abnormalities of the cartilage canal vessels, and chondrocyte necrosis was considered to precede degenerative changes in articular cartilage matrix.(ABSTRACT TRUNCATED AT 250 WORDS)     

Immune electron microscopy of transmissible gastroenteritis virus and rotavirus (reovirus-like agent) of swine.

Immune electron microscopy (IEM) was developed as a diagnostic aid for detecting and identifying transmissible gastroenteritis virus and rotavirus (reovirus-like agent) in fecal and intestinal contents from cases of gastroenteritis in young pigs. Variables involved in use of direct IEM and its sensitivity were determined. Aggregates of virus coated with specific antibody were seen in virus samples mixed with homologous convalescent antiserum, but not in control samples containing preexposure serum or antibody directed against a heterologous virus. At least a ten fold enhancement of the sensitivity of direct IEM for virus detection was accomplished using indirect IEM employing rabbit anti-porcine IgG to further aggregate virus-antibody complexes. The technique was used to investigate the size and morphology of the porcine rotavirus. Particles ranged from 55 to 70 nm in diameter and had capsomere structures. Morphologically, the porcine rotavirus resembled the calf and human rotaviruses. By IEM, employing specific antiserums for each virus, porcine rotavirus was found to be antigenically related to these 2 viruses, but not to the reovirus type 3.