The normal radiographic anatomy of the equine larynx was determined by use of xeroradiography and dissection. The body and laminae of the thyroid cartilage, the muscular process of the arytenoid cartilages, and the dorsal lamina and arch of the cricoid cartilage had radiographic evidence of mineralization (calcification) and/or ossification in clinically normal horses. There was a significant (P less than 0.01) increase in the degree of mineralization of the thyroid and arytenoid cartilages with advancing age. Horses with diagnosis of arytenoid chondrosis (arytenoid chondral dysplasia, arytenoid chondropathy) by use of endoscopy had radiographic changes that included: enlargement with increased density of the arytenoid cartilage region, abnormal patterns of mineralization (dystrophic mineralization or osseous metaplasia), abnormal contour of the corniculate process(es) and laryngeal masses, sometimes obliterating part or all of the lateral laryngeal ventricles.

Lesions in 32 calves that died or were euthanatized during the course of severe natural infection with bovine respiratory syncytial virus (BRSV) are described. All calves had been dyspneic for 1 to 2 days. At necropsy, lesions that could be related to dyspnea included congested and cyanotic mucosae and widespread petechiae. The lungs had various lesions in the cranioventral (CV) and caudodorsal (CD) portions. The CV portion of the lungs was consolidated, firm, and edematous. Histologically, the main characteristic was degenerative, necrotic bronchiolitis, with few syncytial cells. Signs of repair, such as epithelial hyperplasia, fibrosis, and bronchiolitis obliterans, often were observed. The CD portion of the lungs was markedly distended, owing to severe edema and emphysema. Bronchiolar lesions were lacking in the CD portion. In 14 calves, hyaline membranes were seen in the CV and CD portions. Results of immunofluorescence for BRSV were positive in 24 calves, but only in the CV portion of the lungs. The calves had variable concentrations of BRSV-specific IgG1 and IgM in serum, lung lavage fluid, or both. The BRSV-specific IgA, on the contrary, was seldom detected. Thus, 2 discrepancies existed. Although the clinical picture appeared to be acute, bronchiolar lesions and serotest results suggested infection of longer duration. Also, although virus and viral cytopathologic features were detected only in the CV portion of the lungs, the CD portion had extensive lesions that consisted of emphysema and edema.

Premature calving, typified by early expulsion (17 to 43 days) of weak or dead calves and accompanied by retained placentas, was induced in 8 of 9 pregnant cows fed a mixture of Ponderosa pine needles and alfalfa hay. Five control cows of comparable gestation age fed only alfalfa hay maintained normal pregnancies until they were euthanatized at the time the pine needle-treated cows were producing premature calves. Serum specimens from all cows were assayed for progesterone concentration and ovaries and placentomes were examined for histopathologic changes. There were no bacterial, fungal, chlamydial, or viral agents determined to be associated with the premature births. Serum progesterone concentration in the treated cows decreased progressively and were 0.4 to 1.5 ng/ml at the time of premature calving. Histopathologic changes were evident in the placenta and corpora lutea of treated cows only. The number of binucleate trophoblastic giant cells in placentomes was less than normal and the number of necrotic luteal cells in corpora lutea was greater than normal.

Changes in renal function, determined by pharmacokinetics of phenolsulfonphthalein (PSP), and renal morphologic features were examined in adult pony mares given 20 mg of gentamicin sulfate/kg of body weight, IV, q 8 h (group A) n = 7 or isotonic saline solution, IV, q 8 h, n = 5 (group B) for 14 days. Susceptibility of ponies to gentamicin-induced nephrotoxicosis was varied. Two group-A ponies developed acute renal failure and were euthanatized before treatment day 14, whereas 5 group-A ponies did not develop physical or behavioral abnormalities after 14 days of gentamicin administration. All group-A ponies but none of group-B ponies developed ultrastructural abnormalities of the proximal tubular epithelium, consistent with gentamicin-induced nephrotoxicosis. Significant (P less than 0.05) differences were not detected in pharmacokinetic values of either group. Clearance of PSP was reduced in 4 group-A ponies that developed the most severe gentamicin-induced nephrotoxicosis. Changes in clearance of PSP were significantly (P less than 0.05) correlated with changes in the serum creatinine concentration.

Renal ultrasonographic changes were evaluated in 5 dogs administered 10 ml of commercial antifreeze (95% ethylene glycol)/kg of body weight, PO, and in 2 dogs given placebos. Studies were made prior to and after ingestion on an hourly basis over a period of 8 to 10 hours. All dogs were anesthetized immediately after toxin or placebo ingestion for the duration of the study. Renal cortical echogenicity was evaluated in comparison with that of the adjacent liver and spleen. Echogenicity of the renal medulla and definition of the corticomedullary juction were assessed. Within 4 hours after ethylene glycol administration, renal cortical echogenicity of all intoxicated dogs increased from normal to surpass that of the liver and approach or equal that of the spleen. Medullary echogenicity in all intoxicated dogs progressively increased over the course of the study, with changes recognized within 5 hours after ethylene glycol administration. An ultrasonographic pattern consisting of nearly equal, marked increase in cortical and medullary echogenicity and relatively hypoechoic corticomedullary junction and central medullary regions was recognized concurrent with the development of anuria in 3 of the 5 intoxicated dogs. Mild, transient increases in cortical and medullary echogenicity were observed in anesthetized control dogs. However, no statistical difference (P less than 0.05) was detected between baseline, peak, and terminal echogenicity values in these dogs. Blood and urine samples were collected hourly from intoxicated dogs to coincide with ultrasonographic studies. Most clinicopathologic values derived from these samples were not statistically different (P less than 0.05) from those reported in a study that used a similar intoxication protocol in nonanesthetized dogs.

Ultrastructural examination of optic nerve capillaries in the canine lamina cribrosa revealed many spherical, membrane-bound, electron-dense inclusions that closely resembled Weibel-Palade bodies, in pericytes and endothelial cells of preglaucomatous, early, moderately, and advanced affected Beagles with hereditary primary open-angle glaucoma. This ultrastructural difference between the laminar capillary endothelial cells of normal and glaucomatous Beagles could represent a functional vascular disorder, because Weibel-Palade bodies are associated with microcirculatory abnormalities.

Neoplastic cells were isolated from 2 sibling Great Dane/Labrador Retriever mixed-breed dogs in which telangiectatic type osteosarcomas arose concurrently. Cells from various sites in the same osteosarcoma appeared similar in culture, but there were differences between the 2 osteosarcomas in growth characteristics and appearance of cells. Cells from 1 osteosarcoma had a small, but significant (P less than 0.05), cyclic adenosine monophosphate response to parathyroid hormone stimulation, indicating a low order of osteoblastic differentiation. Cells from the other osteosarcoma had no response to parathyroid hormone stimulation. Cells from both osteosarcomas and a concentrated cell-free filtrate from the osteosarcoma with osteoblastic differentiation were injected into nude mice, but osteosarcomas were not induced. Results of ultrastructural examination of osteosarcoma samples for viral particles were negative and supernatant fluids from cultured cells were considered negative for viral reverse transcriptase activity.

Eighteen strains of Escherichia coli serogroup O115:K"V165" isolated from 1- to 8-week-old pigs with diarrhea were tested for toxigenicity, pathogenicity in pigs and mice, serum resistance, mannose-resistant hemagglutination (MRHA), F165 and other surface antigens, colicin V (Col V), aerobactin, and biotype. Twelve strains were positive for heat-stable enterotoxin (STb), MRHA-negative, and F165-negative; 5 strains were enterotoxin-negative, MRHA-positive, and F165-positive; and 1 strain was MRHA-positive, but F165- and enterotoxin-negative. Six of the 12 STb-positive strains moderately colonized the ileum of newborn colostrum-deprived pigs within 24 hours after inoculation. Two of the colonizing strains were able to induce watery diarrhea. All 12 STb-positive strains were nonpathogenic for adult mice and were serum-sensitive; 11 of 12 were Col V-negative, 9 of 12 did not produce aerobactin, and 10 of 12 belonged to biotypes other than 1 or 2. All 6 enterotoxin-negative strains colonized the small and large intestines, associated with peritoneal serosal surfaces, and induced septicemia and polyserositis in newborn colostrum-deprived pigs 1 to 2 days after inoculation. In contrast, 3 STb-positive strains poorly colonized the intestines and did not induce septicemia in pigs at 3 days after inoculation. All 6 enterotoxin-negative strains were Col V-positive, produced aerobactin, and belonged to biotype 1 or 2. Of the 5 enterotoxin-negative, F165-positive strains, only 4 were pathogenic for intraperitoneally inoculated adult mice and were serum-resistant. The enterotoxin-negative, F165-negative strain was neither serum-resistant nor mouse-pathogenic. O-agglutinable mutants of the mouse-pathogenic strains were, for the most part, no longer pathogenic for adult mice, although these strains remained unchanged for biotype and production of MRHA, F165, and Col V, and 3 of 4 mutant strains were serum-resistant. Thus, E coli strains of the same serogroup isolated from diarrheic pigs may cause either intestinal or extraintestinal disease upon reinoculation of pigs, depending on the virulence attributes produced by the strains.

Fifteen newborn germ-free pigs were inoculated with 2 strains, D-282 and T-15, of Streptococcus suis type II. Some pigs also were preinoculated with Bordetella bronchiseptica, which successfully predisposed them to S suis infection. The 2 streptococcal strains were differentiated by muramidase treatment, which released certain high molecular-weight proteins, termed muramidase-released proteins (MRP), from the cell wall of strain D-282, but not from the cell wall of strain T-15. Only strain D-282 (MRP-positive) induced clinical signs of disease and markedly increased neutrophil numbers in pigs. Streptococci were more frequently isolated from fecal swab specimens obtained from pigs inoculated with strain D-282 (MRP-positive) than from specimens obtained from pigs inoculated with strain T-15 (MRP-negative). Both strains were isolated from nasal swab specimens obtained from all infected pigs. Postmortem examination revealed fibrinopurulent meningitis, polyserositis, and polyarthritis in pigs inoculated with strain D-282; this strain was isolated from the CNS, serosae, visceral organs, heart, and joints. Whereas strains D-282 caused several pathologic changes, strain T-15, isolated from the lungs, caused only pneumonia. Both strains were isolated from the tonsils of all pigs. Virulence differed distinctly between the MRP-positive and the MRP-negative strains.

Male broiler chicks were given feed and water ad libitum from hatching through 3 weeks of age. The feed contained 0, 1.25, 2.5, and 5.0 microgram of aflatoxin/g of feed. The chicks were killed by cervical dislocation and specimens of liver and kidney were obtained for electron microscopy on days 3, 6, 9, 17, and 21. In chicks fed 5.0 microgram of alfatoxin, the primary lesions in liver were hepatocellular lipidosis, enlargement of bile canaliculi, reduction in mitochondrial size, mild lymphocytic infiltration, and hepatocellular degeneration and necrosis. Similar lesions were noticed in some chicks fed 2.5 microgram of aflatoxin, but none was observed in chicks fed at 1.25 microgram of aflatoxin. At 5 microgram of aflatoxin, the most consistent lesion in the kidney was thickening of the glomerular basement membrane. Similar glomerular lesions were observed at 2.5 microgram of aflatoxin, but not at 1.25 microgram of alfatoxin. Some foot processes of the glomerular epithelial cells were poorly developed. Fusion of foot processes was not observed and fibrous material was not evident in the basement membrane. The pseudopodia of endothelial cells lining the thickened basement membrane were depleted in number or were absent. Degenerative changes also were observed in the cells of the proximal convoluted tubules, but these were less consistent than those of the glomerulus.