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Thirty-six of 50 young equids examined at necropsy for gross pathologic and histopathologic evidence of osteochondrosis were determined to have lesions characteristic of this disorder in the distal joints of the tarsus. Abnormalities ranged from retained endochondral cores underlying undisturbed articular cartilage surfaces to clefts, subchondral osseous cyst-like lesions, and cartilage ulceration. Our findings supported the conclusion that osteochondrosis may cause spavin in the juvenile equid.

The efficacy of eliminating parotid salivary secretions by retrograde infusion of 10% formalin, 2% chlorhexidine, or 2% or 3% silver nitrate solutions was evaluated in 10 horses. Solutions were kept within the parotid salivary gland for 90 seconds after infusion through parotid duct cannulae and then allowed to drain freely. Severed parotid ducts and surgical incisions were left to heal by second intention. All agents eliminated glandular secretions. There was less necrosis and suppurative inflammation after formalin infusion than after chlorhexidine and silver nitrate. Silver nitrate (2% and 3%) caused the most necrosis and inflammation.

Campylobacter jejuni was inoculated intravenously into pregnant ewes on gestation days 114 and 123 to reproduce ovine abortion. All ewes aborted 7–12 days post-inoculation. High numbers of C. jejuni were isolated from ewe tissues (caruncle, bile, cecal feces), fetal tissues, and placenta. C. jejuni colonies were identified in caruncles and placenta by light microscopy and immunoperoxidase techniques. Histologically, inoculated ewes had a severe purulent endometritis with vasculitis. Placentas from inoculated ewes and field cases showed necrosis and purulent inflammation; however, placentas from inoculated ewes had large numbers of bacterial colonies compared to few bacteria found in field cases. Histologically, only one fetus from the inoculated ewes showed lesions (purulent bronchopneumonia), whereas all fetuses from field cases had a distinct bronchopneumonia, and one fetus showed multifocal hepatic necrosis. These results suggest that C. jejuni (serotypes Penner 1 and Lior 2) is an important abortifacient organism for sheep.

The congenital absence of myenteric ganglia in the terminal portion of the ileum, cecum, and entire colon of white foals with overo spotted parents was reported. Males as well as females were affected. The foals were generally normal at birth but did not defecate. Signs of colic were noticed between 5 and 24 hours after birth, with death occurring at 23 to 132 hours.

Nasomaxillary fibrosarcoma was diagnosed in 3 young horses. Clinical signs included epiphora, facial swelling, dyspnea, unilateral serosanguineous nasal discharge, or an external mass. Physical examination, radiography, and cytology were important diagnostic adjuncts. The definitive diagnosis in each case was based on biopsy. In one case, surgical removal of the tumor and extensive curettage of the affected sinus resulted in extended remission from neoplastic disease.

One hundred nineteen hepatic tissue samples from 117 Bedlington Terriers were divided into 6 groups depending on the severity of histopathologic hepatic changes. Group 0 comprised dogs with microscopically normal livers. Group I dogs had copper-positive, lipofuscin-containing lysosomes present in centrilobular hepatocytes. Microfoci of hepatic necrosis, in addition to the increased numbers of the copper-positive, lipofuscin-containing lysosomes in centrilobular and periportal hepatocytes, were present in group II dogs. Group III dogs had more copper-positive, lipofuscin-containing lysosomes present translobularly and morphologic changes consistent with chronic active hepatitis. Mixed micro- or macronodular cirrhosis and translobular presence of copper-positive, lipofuscin-containing lysosomes characterized group IV dogs. Dogs in group V had massive hepatic necrosis and morphologic changes that were consistent with the changes in group III and IV dogs. Histochemical staining for copper was useful in making the microscopic diagnosis of this disease and was shown to be necessary in early diagnosis (group I) when other clinical and pathologic values associated with this syndrome were not consistently abnormal. Copper histochemical stains varied in sensitivity. Timm's silver sulfide was more sensitive for copper than was rubeanic acid, which was more sensitive than rhodanine staining. The brown pigment associated with the copper in the lysosomes was shown to be lipofuscin pigment with the aid of histochemical staining with orcein, Prussian blue, periodic acid-Schiff, and acid-fast stains together with fluorescent microscopy (excitation maxima: 365 nm; emissions: 420 + nm). Since these were positive only in later stages of the hepatic disease, they were not especially useful in its early diagnosis. The severity of the histopathologic hepatic changes was shown to increase with age and was associated with increasing hepatic copper concentration. These observations illustrate that this inherited, chronic hepatic degeneration in the Bedlington Terrier is progressive. Clinical chemical tests were diagnostically useful only in later stages of the disease. Alanine transaminase activity was of most value, but was not always abnormal, even when severe hepatic damage was present. Clinical signs of hepatic disease were seen in dogs in groups III, IV, and V. Death due to hepatic failure occurred only in dogs in groups III, IV, and V. Hemosiderin was present in increased amounts in the liver, bone marrow, spleen, and lymph nodes of affected Bedlington Terriers, indicating that a possible defect in iron metabolism and/or an increase in RBC turnover existed.(ABSTRACT TRUNCATED AT 400 WORDS)

The effect of copper on thiobarbituric acid (TBA) reaction values, an index of lipid peroxidation, was examined in Bedlington Terriers, healthy dogs, and rats. High hepatic concentrations of copper appeared to lower TBA values in the inherited, chronic, progressive hepatic degeneration of Bedlington Terriers, a disease associated with copper toxicosis. The suspected TBA inhibition was confirmed when Cu2+ was added to homogenates of healthy dog or rat liver or a malondialdehyde standard. The amount of copper added approximated that in diseased Bedlington Terriers. Because of the interference by copper, the TBA test was judged to be an inappropriate test for the evaluation of lipid peroxidation in samples containing high copper concentrations such as those in diseased Bedlington Terriers.

A conifer twig was responsible for severe fibrinopyogranulomatous adhesive pleuritis and pneumonia in a horse. At necropsy, the twig was found in a terminal bronchus and extended into the lung parenchyma, through the pleura, and into the accumulated exudate. Inhalation of plant material may be a more common cause of pleuritis than previously recognized. Meticulous examination at necropsy would be necessary to make the diagnosis.

Surgical incisions were made in the skin and superficial digital flexor tendons in horses. A low intensity laser therapy device was used to treat the limbs. After laser therapy was completed, skin and superficial digital flexor tendons from incised laser-irradiated, incised-control, and nonincised-control limbs were compared microscopically. Qualitative differences between laser irradiated and nonirradiated tissues were not found. The laser therapy device used in this study may be of insufficient power to affect wound healing.

Pulmonary lobar hypertrophy was diagnosed in a 4-hour-old Quarter Horse full-term foal that had respiratory arrest shortly after birth. The gross and microscopic appearances were consistent with polyalveolar lobe, a congenital anomaly of human infants.

A clinical, viral, hematologic , and genetic study was conducted over a 4-year period on a family of Appaloosas with high incidence of clinical ataxia and pathologic features of equine degenerative myeloencephalopathy. Marginal to deficient serum vitamin E (alpha-tocopherol) and blood selenium values were the only other consistent antemortem abnormalities in the affected horses. Members of this family were all descendants of a clinically normal mare and were raised in 3 separate environments with variable quality of feed. All horses had access to pasture grasses. Normal chromosomal karyotypes were found in 11 affected and/or related horses examined. Equine herpesvirus type 2 was isolated from 4 of the horses, but evidence for a role of this virus in the pathogenesis of the disease was not found. The role of antioxidant deficiency in the pathogenesis of neurologic dysfunction in this equine family and in others reported to be affected with equine degenerative myeloencephalopathy remains speculative.