Ten horses were euthanatized before, during, or after surgery to correct severe volvulus of the large colon. At surgery, the colonic serosa changed from blue-gray, blue or purple toward a more normal pink in seven horses after the volvulus was corrected. The mucosa consistently remained black or dark red. Results of postmortem colonic microangiography revealed perfusion of the serosa and the circular and longitudinal muscle layers, but mucosal perfusion was limited by thrombosis in the muscularis mucosae and submucosa. There was evidence of thrombosis of the mesenteric colic vessels in six horses. Damage to the colonic vascular system, especially thromboembolism in the submucosa, may be an important limitation to colonic viability after surgical correction of volvulus of the large colon.

Angiography↗

PubMedDate not supplied

A comparison of three techniques for closure of pelvic flexure enterotomies in normal equine colon.

Six enterotomies 3 cm long, spaced at 3 cm intervals, were made in the antimesenteric border of the pelvic flexure of the ascending colon in five adult horses. Ten incisions each were sutured with a Utrecht pattern (single layer), a full-thickness simple continuous oversewn with a Cushing pattern (two layer), and a mucosal simple continuous with a seromuscular simple continuous oversewn with a Cushing pattern (three layer). In all horses, chromic gut and polyglactin 910 were each used once for each pattern. On day 6, the pelvic flexure was excised and the colonic vessels were injected with a radio-opaque mass. Sections of each enterotomy were studied by light microscopy and high detail radiography. The single-layer closure led to serosa-to-mucosa healing and a thin bowel wall, and the three-layer closure resulted in distortion of the bowel wall by hematoma formation and submucosal contamination with ingesta. The two-layer closure resulted in good alignment and improved healing. There was less inflammatory reaction with polyglactin 910 than with chromic gut.

Animals↗

PubMedDate not supplied

Oxalate nephrosis and renal sclerosis after renal transplantation in a cat.

A 10-year-old castrated domestic shorthair cat received two renal allografts, 14 days apart, for the treatment of chronic renal failure. Oxalate nephrosis developed in both allografts, and they became nonfunctional. During the transplantation period, the cat was not exposed to exogenous sources of oxalate, and there was no evidence of primary type 2 hyperoxaluria before surgery. Urologic surgery, in particular renal transplantation, has been identified as a factor that can precipitate renal failure in human patients with decompensated renal function and hyperoxaluria. If hyperoxaluria was present before surgery in this cat, it was most likely caused by increased absorption or decreased metabolism of dietary oxalate.

Animals↗

PubMedDate not supplied

The accuracy of intraoperative diagnoses based on examination of frozen sections. A prospective comparison with paraffin-embedded sections.

The accuracy of diagnoses based on examination of frozen sections was determined by comparing the results to those obtained by examination of tissues prepared using conventional methods (formalin fixation, paraffin-embedded tissue). One hundred ninety-four specimens were examined using the frozen section technique; 37 were examined to confirm a tentative diagnosis or to document lymph node metastasis and the remainder were examined to diagnose an unknown pathologic process. Of the 194 specimens examined, an accurate, specific diagnosis was obtained in 161 (83%); in 19 (10%), the pathologic process was correctly identified, but a specific diagnosis was not obtained; and in 2 (1%) the diagnosis was deferred. The remaining 12 (6%) were incorrectly diagnosed by the frozen section technique. When the number of specimens in which a specific diagnosis was obtained was combined with the number of specimens in which the pathologic process was correctly identified, the overall accuracy rate of the frozen section technique was 93%. There was no difference in the accuracy of the frozen section technique based on the reason for submission of the sample, source of tissue submitted, or the type of pathologic process (i.e., inflammatory or neoplastic). Of the 12 incorrect diagnoses, 4 (33%) were because of sampling errors and 8 (67%) were caused by interpretation errors.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMedDate not supplied

Persistent experimental Salmonella dublin intramammary infection in dairy cows.

Experimental intramammary infections were induced in five post-parturient Holstein cows by inoculation of low numbers (5000 colony forming units) of virulent Salmonella dublin via the teat canal of mammary gland quarters. Rectal temperature, pulse and respiratory rates, milk yield, and milk quality as assessed by the California Mastitis Test (CMT) and somatic cell counts (SCC) were recorded every 12 hours at milking. Bacteriologic cultures of foremilk quarter samples and feces were obtained daily, as were complete blood counts. ELISA titers for IgG and IgM recognizing S. dublin lipopolysaccharide (LPS) were obtained weekly on serum and quarter milk samples. All cows excreted S. dublin intermittently from infected quarters, but no changes were detected in rectal temperature, appearance of the mammary gland or secretions, CBC, milk yield, and pulse and respiratory rates. Somatic cell counts were modestly increased in infected quarters as compared with uninfected quarters (P = .015, paired t test); however, CMT scores after infection remained low, and were not significantly different from pre-infection scores (P greater than .10, sign test). After infection, administration of dexamethasone resulted in signs of clinical mastitis and increased excretion of S. dublin from mammary quarters (P = .0004, paired t test). One cow had necrotizing mastitis and S. dublin septicemia and was euthanatized. In the four surviving cows, clinical improvement was observed after systemic gentamicin therapy and intramammary infusion with polymyxin B, but all cows continued to excrete S. dublin intermittently from one or more quarters and occasionally from feces for the remaining period of observation. All infected cows demonstrated a rise in IgG and IgM ELISA titers recognizing S. dublin LPS in serum and milk. At necropsy (13-25 weeks postinfection), S. dublin was recovered only from the mammary tissue or supramammary lymph nodes in three of four cows. In one cow, mammary gland and lymph-node samples were negative for S. dublin despite positive milk cultures. In all cows, histopathologic examination revealed multifocal areas of chronic active mastitis. These lesions were similar to histopathologic findings from mammary gland carriers with naturally acquired S. dublin infection.

Animals↗

PubMedDate not supplied

The oncogenic potential of some avian adenoviruses causing diseases in chickens.

The oncogenic potentials of three different strains of avian adenoviruses (the Tipton strain of the inclusion body hepatitis virus, the DPI-2, and the Indiana C viruses) were investigated in newborn hamsters. Animal inoculations were via two routes, subcutaneous and intracerebral. All three viruses proved nononcogenic for the hamsters observed over a period of 225 days. However, lesions of hepatitis similar to those of inclusion body hepatitis of chickens were seen in three hamsters inoculated with the DPI-2 virus.

Adenoviridae↗

PubMedDate not supplied

Role of the bursa of Fabricius in the pathogenicity of inclusion body hepatitis and infectious bursal disease viruses.

Chickens were chemically bursectomized with cyclophosphamide at 3 days old, and studies made of the effects of infection by inclusion body hepatitis virus (IBHV) and infectious bursal disease virus. In another experiment, 3-week-old chickens were infected with infectious bursal disease virus before inoculation with IBHV. Interference with the bursa of Fabricius by cyclophosphamide or by infectious bursal disease virus enhanced the pathogenicity of IBHV. In contrast, cyclophosphamide effects on the bursa protected chickens against infectious bursal disease.

Animals↗