Tropical theileriosis in Bos taurus and Bos taurus cross Bos indicus calves: response to infection with graded doses of sporozoites of Theileria annulata.

This work extends basic knowledge of tropical theileriosis in taurine and crossbred cattle. Infection of Bos taurus and Bos taurus cross Bos indicus (Sahiwal) calves with graded doses of sporozoites of Theileria annulata (Hissar), an Indian stock of the parasite, showed the following to be dose dependent in both cattle types: the time to appearance and population size of macroschizonts, microschizonts and piroplasms, time and severity of pyrexia, anaemia manifested by erythrocyte counts and haematocrit. All infections were accompanied by a prompt and severe panleucopenia. This effect was dose related in both the taurine and the Sahiwal crossbred calves. Lymphocyte counts returned to preinfection levels in the blood of animals which recovered, but death from theileriosis was characteristically accompanied by a persistent and severe lymphocytopenia. Flow cytometry using monoclonal antibodies to bovine mononuclear cells was used to identify the lymphocyte subsets involved in lymphocytopenia. The outcome of infection was dose dependent in the crossbred calves but not in taurine calves. Although the results obtained did not differ qualitatively between the two cattle types, they provided some preliminary evidence for resistance to tropical theileriosis in Sahiwal crossbred calves.     

Influence of diet on urine pH and the Feline urological syndrome

The hypothesis that feline urine pH can be manipulated by use of varying amounts of natural food components was tested. A relatively simple experimental model was constructed whereby soybean meal in a basal calculogenic diet was substituted by other components at varying levels and the changes in urine pH measured. In a different phase of the experiment the result of rapid change of diet was used to show the speed of response of urine pH. The effect of urine acidifying compounds was also demonstrated by the model. The prophylactic effect of three food components on urine pH was compared, with corn gluten meal the most potent. The model also demonstrated that feline urological syndrome (FUS) is possible in the presence of reduced levels of magnesium confirming previous work noting that the effect of urine pH is greater in the prevention of the condition than magnesium levels per se.     

The distribution of C-bands in canine transmissible venereal tumor cells

Colchicine-arrested metaphase preparations, derived from canine transmissible venereal tumor (TVT) cells grown in culture, were characterized based on the occurrence and distribution of constitutive heterochromatin. Analysis of the data with regard to the distribution of C-bands in the pericentric, interstitial and telomeric segments revealed a nonrandom distribution along the arms of many chromosomes with the bulk of the bands occurring in the centromeric region. The frequency of C-banded regions differed from those reported for normal dog cells and both primary and transplanted tumors. These results suggest that similar nondifferentially-stained TVT karyotypes do not necessarily exhibit identical distribution of constitutive heterochromatin.     

Piroxicam Therapy in 34 Dogs With Transitional Cell Carcinoma of the Urinary Bladder

Thirty-four dogs with histopathologically confirmed, measurable, nonresectable transitional cell carcinoma of the urinary bladder were treated with piroxicam (0.3 mg/kg PO sid) and were evaluated for tumor response and drug toxicity. Dogs were evaluated at the Purdue University Veterinary Teaching Hospital by means of physical examination, thoracic and abdominal radiography, cystography, complete blood count, serum biochemistry profile, and urinalysis. In selected cases, prostaglandin E₂ (PGE₂) concentrations in plasma and in supernatants of stimulated monocytes, and natural killer cell activity were quantified, Dogs were evaluated before therapy and at 28 and 56 days after initiation of therapy. Dogs with stable disease or remission at 56 days remained on the study and were evaluated at 1 to 2 month intervals. Tumor responses were 2 complete remissions, 4 partial remissions, 18 stable diseases. and 10 progressive diseases. The median survival of all dogs was 181 days (range, 28 to 720+ days), with 2 dogs still alive. Piroxicam toxicity consisted of gastrointestinal irritation in 6 dogs and renal papillary necrosis (detected at necropsy) in 2 dogs. Monocyte production of PGE₂ appeared to decrease with therapy in dogs whose tumors were decreasing in size, and increased in dogs with tumor progression. A consistent pattern in natural killer cell activity was not observed. In vitro cytotoxicity assays against 4 canine tumor cell lines revealed no direct antitumor effects of piroxicam. In summary, antitumor activity, which was not likely the result of a direct cytotoxic effect, was observed in dogs with transitional cell carcinoma of the bladder treated with piroxicam.     

Esophageal phytobezoar in a horse

A 23-year-old Thoroughbred stallion was admitted to the hospital for treatment of acute esophageal obstruction. Clinical examination and contrast radiography confirmed the presence of an esophageal obstruction. The horse was euthanatized, and examination revealed a bolus of feed material occluding the esophageal lumen 6 cm caudal to the thoracic inlet, with underlying necrosis of the esophageal mucosa. A large pulsion diverticulum was identified in the caudocervical portion of the esophagus. Apparently, the phytobezoar was formed within the esophageal diverticulum and subsequently became dislodged, occluding the esophagus.     

Recovery of Campylobacter jejuni in feces and semen of caged broiler breeder roosters following three routes of inoculation

We previously reported the recovery of Campylobacter (naturally colonized) from the ductus deferens of 5 of 101 broiler breeder roosters, and four of those five positive roosters had previously produced Campylobacter-positive semen samples. Those results prompted further evaluation to determine if inoculation route influenced the prevalence or level of Campylobacter contamination of semen, the digestive tract, or reproductive organs. Individually caged roosters, confirmed to be feces and semen negative for Campylobacter, were challenged with a marker strain of Campylobacter jejuni either orally using 1.0 ml of a diluted cell suspension (log(10)4.3 to 6.0 cells), by dropping 0.1 ml of suspension (log(10)5.3 to 7.0 cells) on the everted phallus immediately after semen collection or by dip coating an ultrasound probe in the diluted cell suspension (log(10)4.3 to 6.0 cells) and then inserting the probe through the vent into the colon. Six days postinoculation, individual feces and semen samples were again collected and cultured for Campylobacter. Seven days postinoculation, roosters were killed, the abdomen aseptically opened to expose the viscera, and one cecum, one testis, and both ductus deferens were collected. The samples were then suspended 1:3 (weight/volume) in Bolton enrichment broth for the culture of Campylobacter. Samples were also directly plated onto Cefex agar to enumerate Campylobacter. Campylobacter was recovered 6 days after challenge from feces in 82% of samples (log(10)4.1 colony-forming units [CFU]/g sample), 85% of semen samples (log(10)2.9 CFU/ml), and on the seventh day postchallenge from 88% of cecal samples (log(10)5.8 CFU/g sample). Campylobacter was not directly isolated from any testis sample but was detected following enrichment from 9% (3/33) of ductus deferens samples. Roosters challenged with Campylobacter orally, on the phallus, or by insertion of a Campylobacter dip-coated ultrasound probe were all readily colonized in the ceca and produced Campylobacter-positive semen and feces on day 6 after challenge. The low prevalence of recovery of Campylobacter from the ductus deferens samples and failure to recover from any testis sample suggests that semen may become Campylobacter positive while traversing the cloaca upon the everted phallus. The production of Campylobacter-positive semen could provide a route in addition to fecal-oral for the horizontal transmission of Campylobacter from the rooster to the reproductive tract of the hen.     

Influence of dietary crude protein concentration and source on potential ammonia emissions from beef cattle manure

Emissions of ammonia, as well as other gases and particulates, to the atmosphere are a growing concern of livestock producers, the general public, and regulators. The concentration and ruminal degradability of CP in beef cattle diets may affect urinary and fecal excretion of N and thus may affect ammonia emissions from beef cattle feed yards. To determine the effects of dietary CP concentration and degradability on potential ammonia emissions, 54 steers were randomly assigned to nine dietary treatments in a 3 x 3 factorial arrangement of treatments. Treatments consisted of three dietary CP concentrations (11.5, 13, and 14.5%) and three supplemental urea:cottonseed meal ratios (100:0, 50:50, and 0:100 of supplemental N). Steers were confined to tie stalls, and feces and urine excreted were collected and frozen after approximately 30, 75, and 120 d on feed. One percent of daily urine and feces excretion were added to polyethylene chambers containing 1,550 g of soil. Chambers were sealed, and ammonia emissions were trapped in an acid solution for 7 d using a vacuum system. As the protein concentration in the diet increased from 11.5 to 13%, in vitro daily ammonia emissions increased (P < 0.01) 60 to 200%, due primarily to increased urinary N excretion. As days on feed increased, in vitro ammonia emissions also increased (P < 0.01). Potential ammonia losses were highly correlated (P < 0.01) to urinary N (r2 = 0.69), urinary urea-N (r2 = 0.58) excretion, serum urea-N concentration (r2 = 0.52), and intake of degradable protein N (r2 = 0.23). Although dietary composition can affect daily ammonia losses, daily ammonia emissions must be balanced with effects on animal performance to determine optimal protein concentrations and forms in the diet.     

Management of comminuted fractures of the proximal phalanx in horses: 64 cases (1983-2001)

OBJECTIVE: To report the outcome of surgical treatment of comminuted fractures of the proximal phalanx in horses. DESIGN: Retrospective study. ANIMALS: 64 horses. PROCEDURE: Medical records and radiographs were reviewed to obtain information regarding signalment, fracture classification, and treatment. Follow-up information was obtained by telephone conversation or evaluation of production records. RESULTS: Thirty-eight horses had moderately comminuted fractures of the proximal phalanx. Two horses were euthanatized immediately. Fractures of the proximal phalanx in 36 horses were repaired with open reduction and internal fixation with a successful outcome in 33 (92%) horses. Reconstruction of the fracture was performed in most horses by use of a long curved incision, transection of the collateral ligament of the metacarpophalangeal or metatarsophalangeal joint, and open exposure of the proximal articular surface of the proximal phalanx. Twenty-six horses had severely comminuted fractures of the proximal phalanx. Six horses were euthanatized immediately. One horse was euthanatized after 9 days of treatment with a cast alone. Severely comminuted fractures of the proximal phalanx in 13 horses were treated with an external skeletal fixation device, and fractures healed in 8 of those horses. Six horses with severely comminuted fractures of the proximal phalanx were treated with transfixation pins incorporated into a fiberglass cast, and fractures healed in 4 horses. CONCLUSIONS AND CLINICAL RELEVANCE: Moderately comminuted fractures of the proximal phalanx can be successfully repaired; however, fractures that are too severe to permit accurate reconstruction of the fragments remain difficult to treat and horses have only a fair prognosis for survival.     

Adipose tissue angiogenesis

A review of adipose tissue angiogenesis includes the morphological and cytochemical development of adipose tissue vasculature and the concept of primitive fat organs. Spatial and temporal relationships between fetal vascular and fat cell development are discussed, including depot- and genetic-dependent arteriolar differentiation. The relationship between connective tissue deposition and elaboration of adipose tissue vasculature is discussed with respect to regulating adipocyte development in a depot-dependent manner. In vitro studies indicated that depot-dependent vascular traits may be attributable to intrinsic growth characteristics of adipose tissue endothelial cells. These studies indicate that adipogenesis may be regulated by factors that drive angiogenesis. Fundamental aspects of angiogenesis, including basement membrane breakdown, vasculogenesis, angiogenic remodeling, vessel stabilization, and vascular permeability were reviewed. Critical angiogenic factors include vascular endothelial growth factor (VEGF), VEGF receptors, angiopoietins (Ang), ephrins, matrix metalloproteinases, and the plasminogen enzymatic system. Vascular endothelial growth factor is the most critical factor because it initiates the formation of immature vessels and disruption of a single VEGF allele leads to embryonic lethality in mice. Expression of VEGF is influenced by hypoxia, insulin, growth factors, and several cytokines. Angiogenic factors secreted and/or produced by adipocytes or preadipocytes are discussed. Vascular endothelial growth factor expression and secretion by adipocytes is regulated by insulin and hypoxia, and is associated with adipose tissue accretion. Vascular endothelial growth factor accounts for most of the angiogenic activity of adipose tissue. The proposed role of leptin as an adipogenic factor is reviewed with respect to efficacy on various aspects of angiogenesis relative to other angiogenic factors. The VEGF and leptin genes are both hypoxia inducible, but potential links between VEGF and leptin gene expression have not been examined. Finally, several studies including a study of mice treated with antiangiogenic factors indicate that adipose tissue accretion can be controlled through the vasculature per se.