Rectal swab specimens were collected from 362 apparently healthy dogs of different origin, age, breed, and sex. Specimens were obtained in summer, autumn, and winter. Ninety-five thermophilic Campylobacter spp were isolated: C jejuni biotype I, n = 57, C jejuni biotype II, n = 1, C coli, n = 36, and C laridis, n = 1. Biotypes of C jejuni recovered were the same as those associated with Campylobacter-induced enteritis in human beings. Prevalence of C jejuni was significantly (P < 0.05) greater: in dogs < 6 months old than in adult dogs; in dogs living under high density and cohabitation housing conditions for long periods; and in autumn.

Free, autogenous, full-thickness skin grafting was performed on 10 dogs; 5 dogs were given an iron chelator, deferoxamine-10% hydroxyethyl pentafraction starch (DEF-HES; 50 mg/kg of body weight, IV), and 5 dogs were given 10% hydroxyethyl pentafraction starch (HES) in 0.9% saline solution (5 ml/kg, IV). The percentage of viable graft on day 10 was higher, but not significantly so, in DEF-HES-treated dogs (mean +/- SD, 72.6 +/- 24.8%; median 76.5%) than in HES-treated dogs (mean +/- SD, 46.7 +/- 34.3%; median, 48.8%). A trend for a positive correlation between the percentage of viable graft (on day 10) and the percentage of original graft area (on day 28) was observed in HES- and DEF-HES-treated dogs; this trend was significant in HES-treated dogs (P = 0.012). Both groups had significant positive correlation between percentage of viable graft on day 10 and percentage of haired skin on day 28 (HES, P = 0.000002; DEF-HES, P = 0.0148). A unique finding in DEF-HES treated dogs was the consistent observation of foamy macrophages in the dermis adjacent to the grafts, in deep subcutaneous tissue below the grafts, and in normal dermis.

The mechanism of estrogen-induced myelotoxicosis is unknown, although evidence indicates that estrogen does not directly damage the bone marrow granulocyte-macrophage progenitor cells and that the thymus is a probable mediator of the bone marrow suppression. Estrogen-induced production of a myelopoiesis-inhibitory factor by canine thymic stromal cells in vitro has been observed. Then, presence of a myelopoiesis-inhibitory factor in canine serum was investigated immediately after estrogen administration in vivo. Maximal reduction in colony-forming units-granulocyte/macrophage growth by sera from individual dogs varied. Individual dog sensitivity to estrogen-induced myelotoxicosis is seen clinically, and the cause is unknown. This serum factor could have a role in the eventual bone marrow hypoplasia seen in estrogen-treated dogs and is possibly the same factor produced by cultured thymic stromal cells exposed to estrogen.

Pepsinogen and protein concentrations were determined in blood samples, collected from the left gastroepiploic artery and vein, and in abomasal lymph from 15 steers naturally infected with Ostertagia ostertagi and 4 uninfected steers. In steers with type-1 ostertagiosis, the concentration gradient between the mucosal interstitium and the blood alone could account for higher than normal serum pepsinogen concentrations. High interstitial pepsinogen concentrations may have resulted from increased epithelial permeability or increased pepsinogen production and secretion. However, in steers with type-2 ostertagiosis, the concentration gradient could not entirely account for the high serum pepsinogen concentrations, suggesting that capillary permeability or surface area may have been altered. Lymphatic uptake contributed pepsinogen to the blood in all infected steers.

Cardiovascular and at accompany markedly long periods (12 hours) of halothane anesthesia were characterized. Eight spontaneously breathing horses were studied while they were positioned in left lateral recumbency and anesthetized only with halothane in oxygen maintained at a constant end-tidal concentration of 1.06% (equivalent to 1.2 times the minimal alveolar concentration for horses). Results of circulatory and respiratory measurements during the first 5 hours of constant conditions were similar to those previously reported from this laboratory (ie, a time-related significant increase in systemic arterial blood pressure, cardiac output, stroke volume, left ventricular work, PCV, plasma total solids concentration, and little change in respiratory system function). Beyond 5 hours of anesthesia, arterial blood pressure did not further increase, but remained above baseline. Cardiac output continued to increase, because heart rate significantly (P < 0.05) increased. Peak inspiratory gas flow increased significantly (P < 0.05) in later stages of anesthesia. There was a significant decrease in inspiratory time beginning at 4 hours. Although PaO2, and PaCO2, did not significantly change during the 12 hours of study, PVO2 increased significantly P < 0.05) and progressively with time, beginning 6 hours after the beginning of constant conditions. Metabolic acidosis increased with time significantly [P < 0.05] starting at 9 hours), despite supplemental IV administered NaHCO3. Plasma concentrations of eicosanoids: 6-ketoprostaglandin F1 alpha (PGF1 alpha, a stable metabolite of PGI2), PGF2 alpha, PGE, and thromboxane (TxB2, a stable metabolite of TxA2) were measured in 5 of the 8 horses before and during anesthesia. Significant changes from preanesthetic values were not Significant changes from preanesthetic values were not detected. Dynamic thoracic wall and lung compliances decreased with time.

Fifteen 2-week-old kittens were randomly assigned to 1 of 3 milk treatment groups as the sole source of nutrition for 4 weeks: queen's milk, commercially available kitten milk replacer (CMR), and an experimental milk replacer (EXP). Kittens fed queen's milk suckled ad libitum, whereas CMR- and EXP-fed kittens were tube-fed every 6 hours. Kittens were weaned at 6 weeks of age and were fed a feline growth diet ad libitum for an additional 4 weeks. Kittens were examined at 2, 4, 6, 8 and 10 weeks of age; the procedure included an ophthalmic examination and blood sample collection for CBC and serum biochemical and amino acid analyses. Kittens fed CMR and EXP diets had weight gain greater than that for queen's milk-fed kittens. The kittens fed CMR, however, had diarrhea throughout most of the milk-feeding trial and developed diffuse anterior and posterior lens opacification and vacuolation at the posterior Y-sutures. The lens opacities noticed in the kittens during the milk treatments resolved to a residual perinuclear halo, and a few incipient cortical opacities were observed by the end of the growth diet-feeding period. Serum arginine concentration was significantly (P < 0.05) lower in the CMR-fed kittens, but was not different during the growth diet-feeding period. We concluded that the EXP diet supported normal growth in 2- to 6-week-old kittens; CMR supported normal kitten growth rate, but resulted in diarrhea and cataract formation; and serum amino acid data indicated that low arginine concentration may have been related to the CMR-induced cataract formation.

Thirty young ponies were examined endoscopically for evidence of gastric ulceration. Seven ponies had noninduced gastric ulcers present at the initial examination and were eliminated from the study. In an attempt to induce gastric ulcers experimentally, flunixin meglumine (1.1 mg/kg of body weight, IM, q 8 h) was administered for 7 days to the 23 ponies with endoscopically normal gastric mucosa. During the 7 days of flunixin administration, 11 ponies developed gastric ulcers that were appropriate for study. The 11 ponies were randomly allotted to 2 groups. Group-A (n = 5) and group-B (n = 6) ponies received ranitidine (4.4 mg/kg, PO, q 8 h) and corn syrup, respectively, until ulcers healed or for a maximum of 40 days. General anesthesia was induced every 3 to 5 days for visual evaluation of ulcer healing by use of a video endoscope. The earliest complete healing of gastric lesions observed in a corn syrup-treated pony was at 17 days. At 40 days, 3 of 5 and 3 of 6 ponies of the ranitidine and corn syrup-treated groups, respectively, had healed ulcers. Results of this study indicate that: noninduced gastric ulcers may be common in young ponies, flunixin meglumine may be effective in inducing gastric ulcers for gastric healing studies in young ponies, and ranitidine (4.4 mg/kg, q 8 h) is not significantly effective in accelerating healing of experimentally induced gastric ulcers in ponies under conditions of this study.

Saline (0.9% NaCl) solution or 1 of 3 nonsteroidal anti-inflammatory drugs (NSAID) was administered IV to 5 neonatal calves 15 minutes after the start of a 3-hour IV infusion of Escherichia coli lipopolysaccharide (LPS; 2 micrograms/kg/h). Four additional calves were given a 3-hour IV infusion of saline solution alone. Clinical attitude, mean arterial blood pressure, PCV, WBC, and plasma lactate, glucose, and eicosanoid concentrations (thromboxane B2, 6-keto-PGF(1 alpha)) were monitored for 12 hours. Flunixin meglumine (1.1 mg/kg of body weight, IV), ketoprofen (2.2 mg/kg, IV), and ketorolac tromethamine (1.1 mg/kg, IV) each ameliorated the clinical signs of endotoxemia and LPS-induced lacticemia, but failed to significantly alter the degree of leukopenia or hypoglycemia associated with infusion of LPS. Although the 3 NSAID prevented eicosanoid production, they provided only partial protection against LPS-induced hypotension. Each NSAID modified the response to LPS, but none was clearly superior to the others in modulating the clinical signs or physiologic alterations induced by infusion of LPS in neonatal calves.

After IV administration of 0.5 mg of glucagon/cat, glucose tolerance and insulin secretory response were evaluated in 10 lean cats, 10 obese cats, and 30 cats with diabetes mellitus. Blood samples for glucose and insulin determinations were collected immediately before and at 5, 10, 15, 30, 45, and 60 minutes after IV administration of glucagon. Baseline serum insulin concentration and insulin secretory response were used to classify diabetes mellitus in the 30 cats as type I or type II. Mean (+/- SEM) baseline and 30-minute serum glucose concentrations in obese cats were significantly (P < 0.05) decreased, compared with values in lean cats, but were similar at all other blood sample collection times. Serum glucose concentration in diabetic cats was significantly (P < 0.05) greater than values in obese and lean cats at all blood sample collection times. Two statistically different insulin responses to IV administration of glucagon were seen in diabetic cats. Of the 30 diabetic cats, 23 had minimal insulin secretory response after glucagon administration (ie, serum insulin concentration was at or below sensitivity of the insulin assay). Seven diabetic cats had baseline serum insulin concentration similar to that of obese cats and significantly (P < 0.05) greater than that of lean cats and of the other 23 diabetic cats. In these 7 diabetic cats, serum insulin concentration increased after glucagon administration. Total insulin secretion was not significantly different between these 7 diabetic cats and the lean and obese cats, and was significantly (P < 0.05) greater than total insulin secretion in the other 23 diabetic cats. Results support existence of type-I and type-II diabetes mellitus in cats.

In each of 4 horses, sterile synovitis was induced by intra-articular injection of 3 micrograms of Escherichia coli endotoxin (lipopolysaccharide, LPS) into one antebrachiocarpal joint; an equal volume (2 ml) of phosphate-buffered saline solution (PBSS) was injected into the opposite, control carpus. Blood and 1.5 ml of synovial fluid were obtained at postinjection hours (PIH) 0, 2, 4, 8, 12, 18, 42, 66, and 144. Synovial fluid sample collection was accomplished by use of an indwelling, intra-articular catheter through PIH 12, and by arthrocentesis subsequently. Joint fluid samples were analyzed for cell counts, protein concentration, cytologic variables, and tumor necrosis factor (TNF), interleukin 6 (IL-6), and prostaglandin E2 (PGE2) values. Tumor necrosis factor and IL-6 activities and WBC count were also measured in blood. To monitor local inflammation, skin temperature of each carpus was imaged, using a thermographic scanner prior to each sample collection time. Horses had minimal systemic effects. Mean (SEM) rectal temperature increased significantly to 39.02 +/- 0.15 C only at PIH 18 after intra-articular injection of LPS. One horse had signs of mild depression from PIH 7 to 18, but its vital signs did not change appreciably. Each horse had mild signs of discomfort in the LPS-injected limb from PIH 1 to 3 until PIH 8 to 10. Mean peak surface temperature of the LPS-injected carpi was significantly higher than that of control carpi from PIH 8 to 144 (P < 0.05). Mean synovial fluid WBC count in the LPS-injected and control carpi increased after injection and peaked by PIH 8 (193,125 +/- 8,528 cells/microliter, LPS-treated; 16,425 +/- 8,336 cells/microliter, controls). Mean values for LPS-treated (principal) joints were significantly greater than values for control joints from PIH 2 until after PIH 66 (P < 0.05). Mean synovial fluid protein concentration increased in the principal and control joints, with values for the principal joints remaining significantly greater than values for control joints from PIH to 144 (P < 0.05). Mean TNF activity in synovial fluid was maximal at PIH 2 (10,573 +/- 5,924 U/ml). Interleukin-6 activity increased more gradually and peaked at PIH 8 (1.78 +/- 0.71 X 10(6) U/ml). Tumor necrosis factor activity did not increase above the minimal detectable value of 6 U/ml in the control joints. Mean PGE2 concentration in the principal joints peaked by PIH 2 (3.6 +/- 0.37 ng/ml) and remained significantly (P < 0.05) greater than the value for control joints from PIH 2 through 66. These results indicate that a humane model of synovitis was created by intra-articular injection of LPS and can be used to establish the basic responses of synovial TNF, IL-6, and PGE, in horses with early inflammatory joint disease.