Quantitation of an epithelial S-phase response in the rat forestomach and glandular stomach following gavage dosing with ethyl acrylate.

Gavage dosing of the irritant, ethyl acrylate (EA), has been found to induce hyperplasia in the rat forestomach, but no signs of toxicity in the glandular stomach or in organs remote from the site of dosing. To quantitatively describe this effect as a background for subsequent modeling studies, pulse measurements of the number of S-phase cells were made following a single gavage dose of EA. The time-course of the S-phase response in the forestomach epithelium following a high dose (200 mg/kg or a 4% solution in corn oil) indicated that the number of S-phase nuclei was decreased relative to control animals immediately following gavage dosing with a minimum at 6 hr, but that the number of S-phase nuclei increased significantly above control values by 20 hr and remained significantly elevated until at least 48 hr following the gavage dose. A single-dose dose-response study with gavage doses of 0, 2, 10, 20, 50, 100, or 200 mg/kg EA and S-phase analysis at 24 hr following gavage dosing indicated that a significant increase in S-phase nuclei was evident at doses of 20 mg/kg or higher. Dosing with EA for 2 weeks at dose levels of 0, 10, 50, or 200 mg/kg caused a prolonged elevation of S-phase nuclei only at the 200 mg/kg dose level during the 24 hr following the last gavage dose. Lower doses did not induce a significant increase in the S-phase nuclei. In contrast to the forestomach, the S-phase response of the glandular stomach was transient following a single 200 mg/kg gavage dose, and only a marginal response was observed following multiple 200 mg/kg doses. No effects were observed at lower doses. Comparison of these results to prior determinations of the effect of EA on the concentration of nonprotein sulfhydryls (primarily glutathione) in the forestomach and glandular stomach indicate a correlation of the stimulation in S-phase activity in the forestomach with the repletion and overshoot of tissue nonprotein sulfhydryl levels.

Disseminated Halicephalobus deletrix infection in a horse.

A 13-year-old Quarter Horse gelding was referred for evaluation of a draining tract and fracture of the right hemimandible of 4 weeks' duration. Two days prior to admission, the horse had developed pigmenturia. Radiography of the mandible revealed a fracture of the vertical ramus of the right hemimandible, loss of the right lower second premolar, and osteomyelitis involving an extensive portion of the hemimandible. Ultrasonography of the left kidney revealed loss of normal renal architecture. Histologic examination of tissue obtained from the right hemimandible revealed granulomatous osteomyelitis and multiple metazoan parasites identified as Halicephalobus deletrix. The horse was treated with antimicrobial and deworming agents, and the mandible was surgically debrided. The horse became atactic 8 days after surgery and was euthanatized. Necropsy identified parasitic migration in the right hemimandible, kidneys, and CNS.

Thoracic neoplasia in equids: 35 cases (1967-1987).

Thirty-two horses and 3 ponies had neoplasia involving the thoracic cavity. Lymphosarcoma of the thorax was found in 19 (54.2%) of the equids. The other 16 equids had metastatic adenocarcinoma (7 horses; 20%), metastatic squamous cell carcinoma (5 equids; 14.3%), metastatic hemangiosarcoma (3 equids; 8.6%) or undifferentiated sarcoma (1 horse; 2.9%). Thoracic neoplasia was diagnosed before death in 15 equids (42.9%).

Mycotic omasitis and rumenitis as sequelae to sepsis in dairy cattle: six cases (1979-1986).

Medical records of 6 cows with mycotic rumenitis or omasitis, but no history of grain engorgement, were reviewed. A diagnosis was made at necropsy in all cows, although the condition was suspected before euthanasia in 3 cows. Common clinical findings included inappetence, rumen stasis, fluid rumen contents, and scant, pasty, or loose feces. Postmortem findings included severe ulcerative rumenitis or omasitis, with thrombosis of blood vessels in the submucosa, and branching, septate fungal hyphae abundant in inflamed tissues. In these cows, mycotic omasitis and rumenitis were thought to be sequelae of sepsis, with reflux of abomasal fluid into the forestomach and broad spectrum antimicrobial therapy as possible predisposing factors for mycotic infections.

Disseminated granulomatous disease in a cat caused by larvae of Toxocara canis.

The gross and histological findings of a case of disseminated granulomatous disease caused by larval nematode infection in a cat are presented. The larvae were identified as those of Toxocara canis and the lesions associated with infection of cats with various ascaridoid larvae are discussed.

Comparative healing of mesenteric and antimesenteric incisions in the bovine jejunum.

Paired incisions (n = 6 pairs) were made in the jejunum of each of 8 Holstein cows. Pairs consisted of 2-cm transverse incisions, 35 cm apart, at the antimesenteric region and at the mesenteric region. Bursting-wall tension was used to test mechanical strength, and cellular and vascular events of healing were evaluated using histologic examination and microangiography. Healing was evaluated at postoperative hour (POH) 48 in 4 of the cows (group 1) and at POH 96 in the remaining 4 (group 2). Evidence of leakage of intestinal contents was not found in any of the cows. At POH 48 and 96, bursting-wall tension was significantly (P less than 0.001) greater in the intestinal segments with antimesenteric incisions than in those segments with mesenteric incisions. Disruption of normal vasculature was seen at mesenteric and antimesenteric sites; ingrowth of vessels, reformation of vascular plexuses, and development of collateral circulation were observed at POH 96. Granulation tissue was observed at POH 96 at the antimesenteric and mesenteric sites, and early stages of mucosal reepithelialization were seen in several sections at POH 48. Better apposition of tissue layers was seen in antimesenteric incisions, but mucosal eversion was evident in several mesenteric incisions. Some sections examined from cows at POH 96 had complete bridging of mucosa, submucosa, and muscularis layers at the antimesenteric location. Inflammatory cells were observed along the incision and at the mucosal and serosal surfaces in many of the sections. Deposition of new collagen was not appreciable in any section at POH 48 or 96.

Comparative toxicology of tetrachlorobiphenyls in mink and rats. II. Pathology.

Young female pastel mink and young female Sprague-Dawley rats were injected intraperitoneally on 3 sequential days with 50 mg/kg of either 2,4,2',4' tetrachlorobiphenyl (TCB) or 3,4,3',4'-TCB and sacrificed after 7 days. Two control groups were established for each species; one allowed free access to food, and one pair-fed to the 3,4,3',4'-TCB-treatment group. Heart blood was collected from each mink immediately after sacrifice. A complete set of tissues was collected from all animals and placed in buffered formalin. The rats displayed no clinical signs of illness following the administration of either congener, nor were there any significant gross or microscopic lesions created in this species. Mink in the 2,4,2',4'-TCB and control groups remained free of clinical signs and significant gross or microscopic lesions. Mink in the 3,4,3',4'-TCB group developed anorexia within 48 hr after the initial injection, and depression and melena by Day 4. Necropsy on Day 7 revealed a severe necrotizing enteritis with moderate to marked villus atrophy and fusion in the small intestines of all mink in this treatment group. The epithelial necrosis generally spared the basal one-third of the mucosa, and the deep crypt epithelium was often moderately hyperplastic. The mechanism by which 3,4,3',4'-TCB causes this unique lesion is unknown.

Comparative toxicology of tetrachlorobiphenyls in mink and rats. I. Changes in hepatic enzyme activity and smooth endoplasmic reticulum volume.

Mink have been shown previously to be extraordinarily sensitive to polychlorinated biphenyls (PCBs) and related classes of halogenated hydrocarbons. This study explored several aspects of the acute response of mink to two purified tetrachlorobiphenyl (TCB) congeners and compared their response with that of the rat, a less sensitive and more thoroughly studied species. Young female pastel mink and young female Sprague-Dawley rats received three daily intraperitoneal injections with equimolar doses of either 2,4,2',4'-TCB or 3,4,3',4'-TCB, and were sacrificed after 7 days. Two control groups were used for each species; one was allowed free access to food and the other was pair-fed to the 3,4,3',4'-TCB treatment group. Rats remained clinically normal, while mink treated with 3,4,3',4'-TCB developed severe anorexia, diarrhea, and melena. Both species had significant increases in hepatic cytochrome P-450 content and the characteristic shift in the spectral maxima from 450 to 448 nm in the 3,4,3',4'-TCB- but not in the 2,4,2',4'-TCB-treated animals. Rats but not mink had increased activities of several hepatic monooxygenases in response to both congeners while microsomal epoxide hydrolase was increased in rats after 2,4,2',4'-TCB and in mink after 3,4,3',4'-TCB. Significant increases in the relative volume of smooth endoplasmic reticulum within hepatocytes of 2,4,2',4'-TCB-treated rats but not mink were confirmed by ultrastructural morphometry. Accumulation of both congeners was greater in adipose tissue than in the liver of either species. In both species, concentrations in adipose tissue were much greater for 2,4,2',4'-TCB than for 3,4,3',4'-TCB. PCB toxicosis in mink, as in other species, appeared to be dependent on isomeric arrangement of chlorine substituents. However, unlike other species, the toxicosis was not associated with biochemical or morphological evidence of hepatic enzyme induction. Moreover, the target organ of 3,4,3',4'-TCB toxicosis in mink was the small intestinal mucosa.

Actinomycotic mycetoma in a cat.

Actinomycotic mycetoma, a chronic, progressive infection of the subcutaneous tissue characterized by tumefaction, draining sinuses, and grains, was diagnosed in the right hindlimb of a young adult, male cat. The organisms that cause actinomycetoma are soil or plant saprophytes that gain entrance to the skin through abrasion or traumatic implantation. Streptomyces griseus, an organism generally considered to be a saprophyte, was cultured bacteriologically. Despite extensive surgery and long-term antibiotic therapy, the infection persisted, and the cat was euthanatized.

Abortion and stillbirth associated with Chlamydia psittaci var ovis in dairy goats with high titers to Toxoplasma gondii.

During two consecutive breeding seasons in a brucellosis-free dairy goat herd, approximately 40% to 70% of the does (mean herd size, 14.5) had stillbirths or aborted. None of the does aborted or had stillbirths twice. In the first breeding season, 9 of 13 does aborted in the last 2 months of gestation. Three fetuses and 2 fetal placentas from 2 does were examined. Microscopic findings included severe multifocal hepatic necrosis, mild pneumonia, and mild multifocal necrosis in the brain. Cultures for Listeria monocytogenes, Chlamydia psittaci, and Coxiella burnetii were negative. Paired sera from 3 of the does that had aborted or had stillbirths were tested for antibodies to Toxoplasma gondii. On the basis of high titers, a tentative diagnosis of toxoplasmosis was made. During the following breeding season, 6 of 16 does aborted during the last 2 months of gestation. A total of 6 fetuses and 4 fetal placentas from 5 of these does were examined. Microscopic findings included infiltration of mononuclear cells around hepatic vessels and multifocal necrosis and gliosis in the brain. Chlamydia psittaci was isolated from the tissues of 1 fetus, 2 aborting does had persistent, high antibody titers against C psittaci (1:160 and 1:320), and all except 2 other does in the herd had C psittaci titers of 1:20 to 1:40. All but 2 does had T gondii titers of 1:32 to 1:4096. Evidently there was mixed infection with C psittaci and T gondii in this herd, but the former organism probably was responsible for the abortions and stillbirths.

Ulcerative duodenitis in foals.

Seven foals aged 18 days to 3 1/2 months had either single or multiple full-circumference segments or long antimesenteric bands of necrotizing duodenitis, sharply delineated from adjacent viable duodenum. Perforation of the necrotic wall had occurred in all foals, leading to acute fibrinous peritonitis. On the mucosal surface severe diffuse, acute inflammation and ulceration involved the anterior half of the duodenum. Two further foals, aged 28 and 30 days, had lesions that are believed to be a chronic form of this disease. Both foals had a thickened duodenal wall, with large areas of mucosa replaced by granulation tissue. In addition one had several strictures associated with firm adhesions between the duodenal serosa and adjacent structures, together with ascending cholangiohepatitis and pancreatitis. Eight foals had gastric ulcers that were considered to be of less significance than the duodenal lesions. No etiologic agent could be found by aerobic or anaerobic bacterial culturing, negative contrast electron microscopy for viruses, or immunofluorescence staining for equine herpesvirus 1, equine adenovirus, or equine coronavirus. The possible involvement of non-steroidal anti-inflammatory drugs is discussed.

Endocarditis caused by Erysipelothrix rhusiopathiae in a dog.

Bacterial endocarditis was diagnosed in a 4-year-old male German shorthaired Pointer with a 4-month history of shifting lameness and intermittent fever. The dog died in spite of treatment for progressive depression and dehydration. Blood cultures were positive for Erysipelothrix rhusiopathiae strain 7, which is known to be pathogenic for dogs. The clinical diagnosis was confirmed at necropsy.20