Isolation of antigenic proteins from erythrocytes parasitised with Babesia divergens and a comparison of their immunising potential

Soluble proteins present in the supernatant prepared from a sonicated lysate of concentrated erythrocytes infected with Babesia divergens were separated by isoelectric focussing into acidic and non acidic fractions. The acidic fraction was further separated by passage through Concanavalin A Sepharose (Con A) into two fractions, the first (Fraction 2) consisting of proteins plus one glycoprotein which did not bind to Con A, the second of glycoproteins (Fraction 1) which were eluted after binding to Con A. One group of six cows was treated with three injections of Fraction 2 with incomplete Freunds adjuvant (IFA); two other groups received the same number of injections of Fraction 1, one with IFA, the other with glucan as adjuvant. These cows plus an untreated control group were infected with 10(5) erythrocytes infected with a heterologous isolate of B. divergens. Only the group treated with Fraction 2 (Group 1) resisted lethal multiplication of the parasite. There were significant differences in magnitude of parasitaemia, reduction of packed cell volume and antibody titres between Group 1 and the other groups.     

Cellular morphology of Clostridium spiroforme

The helically-coiled bacterium, Clostridium spiroforme, has been shown to consist of an ordered aggregation of numerous individual semi-circular cells joined end to end.     

Nitrogenous constituents in plasma of foals weaned at three, four or six months of age

A study was conducted to measure the nitrogenous constituents in the blood of foals weaned at 3, 4 or 6 months of age (four foals per weaning age).Jugular blood was sampled from one week prior to weaning until one month post-weaning, and was analyzed for total protein, albumin, creatinine, urea Nitrogen and free amino acid content. Results indicated that the concentrations of most of the constituents in the blood of foals were not altered by the age of weaning, however, free amino acids decreased as age at weaning increased and creatinine was significantly higher in foals weaned at 6 months of age. Plasma creatinine, lysine and methionine levels generally decreased between pre-weaning and one month post-weaning. These data establish baseline values for blood nitrogenous constituents in foals at weaning.     

Nephrotic syndrome: a platelet hyperaggregability state

Nephrotic syndrome characterized by hypoalbuminemia and hyperlipidemia is associated with an increased incidence of thromboembolism and increased platelet hyperaggregability. Although plasma coagulation proteins are also abnormal, changes are too inconsistent to attribute thromboembolic complications to the coagulation cascade alone. Antithrombin III (ATIII) has been shown to be deficient in nephrotic syndrome. There is, however, an increase in alpha 2 macroglobulin. It is clear that platelet to platelet interactions require exposure of platelet fibrinogen receptors, the binding of fibrinogen to these receptors, platelet crossbridging, and subsequent platelet aggregation. Fibrinogen is consistently elevated in nephrotic syndrome. Hyperlipidemia and hypoalbuminemia in nephrotic syndrome increases the availability of thromboxane A2 (TxA2) by increasing the availability of TxA2 precursors and the removal of TxA2 inhibitors. Thromboxane A2 is a known inducer of platelet aggregation probably through the exposure of platelet fibrinogen receptors. Recently, fibronectins a group of adhesive proteins, were implicated in platelet to platelet interactions. Since thrombin increases the expression of platelet surface fibronectin, fibronectin may be involved in thrombus formation in nephrotic syndrome. Thromboembolic formation in nephrotic syndrome is a composite mechanism involving the coagulation cascade, platelet-platelet interactions, and platelet-surface interactions.     

Cell surface markers of the canine natural killer (NK) cell

Studies were performed to determine which of several cell surface markers are expressed on canine peripheral blood leukocyte (PBL) natural killer (NK) cells. Chromium-51 release assays showed a decrease in NK activity after depletion of PBL by carbonyl iron ingestion and adherence to IgG-antibody-coated ovine erythrocytes (EA gamma) and to IgM-antibody-complement-coated ovine erythrocytes (EA mu C). Effector cell adherence to and subsequent lysis of canine thyroid adenocarcinoma (CTAC) target cell monolayers provided direct visual identification of the putative canine NK cell. These surface immunoglobulin-negative cells, individually identified by their physical adherence to dead CTAC target cells, failed to form nonimmune rosettes with guinea pig erythrocytes or rosettes with EA mu or EA mu C. However, 39.0 +/- 4.2% of these adherent cells formed rosettes with EA gamma and 73.3 +/- 0.8% expressed the canine T-lymphocyte marker, Thy-1.     

Suppressor activity of bovine Fc gamma positive cells during a persistent infection with Mycobacterium avium

The cell mediated immune response (CMI) was measured in calves after experimental infection with Mycobacterium avium. Using the tuberculin skin test a CMI response could be measured from four to 14 weeks after infection, and with a lymphocyte stimulation (LS) test from six to 40 weeks. One year after infection no CMI response was detected by either of the tests, in spite of the fact that in such calves M avium bacteria could be found in the intestinal lymph nodes at autopsy. After removal of mononuclear cells bearing receptors for the Fc part of IgG, the peripheral blood lymphocytes obtained from a calf infected one year earlier responded to M avium pure protein derivative in the LS test in contrast to lymphocytes obtained from uninfected calves.     

Pathological changes of tracheal mucosa in chickens infected with infectious laryngotracheitis virus

Six-week-old chickens were inoculated via the posterior thoracic air sac with infectious laryngotracheitis virus. Chickens were sacrificed on various days through day 16 postinoculation (PI), and the trachea was examined by scanning electron microscopy (SEM) and light microscopy (LM). The pathological changes observed on day 1 PI were hypertrophy and hyperplasia of goblet cells. From day 3 PI, the epithelial cells protruded collectively and fused to form syncytia, which contained many intranuclear inclusion bodies. Subsequently, epithelial syncytia desquamated, one after another, and connective tissues were exposed in places. Serofibrinous exudate and detritus were abundant on the surface of the exposed connective tissues and seemed to form a pseudomembrane. On day 5 PI, the remaining epithelial cells began to repair the devastated mucosa just under the pseudomembrane. On day 6 PI, microvillus-rich regenerating epithelial cells were arranged like paving stones. On day 8 PI, the epithelial cells proliferated extensively and formed folds with cyst-like structures. By day 16 PI, the tracheal epithelium was covered with cilia and regained its normal histologic appearance.     

Tumors of the alimentary tract

Neoplasms of the canine and feline alimentary tract represent diagnostic and therapeutic challenges for the veterinarian in practice. Careful attention to historical details and thorough and repeated examination are of paramount importance in evaluating animals with chronic digestive disturbances. By judicious use of ancillary studies such as plain and contrast radiography, endoscopy, and exploratory surgery, the clinician may arrive at a diagnosis earlier in the course of a neoplasm. This in turn may facilitate more efficacious treatment. A particularly interesting aspect of tumors of the gastrointestinal tract is their frequent association with environmental carcinogens. By being aware of these relationships, veterinarians stand a better chance of reaching the ultimate goal of cancer therapists--the prevention of malignant disease.     

Gold-induced immune thrombocytopenia in the dog

In two seven-year studies with gold compounds in dogs of both sexes, thrombocytopenia was observed after 45 to 72 months of dosing in three of 14 and two of 14 dogs in high-dose groups that received 2.4 to 3.6 mg/kg of auranofin per day orally or 0.5 to 2.0 mg/kg of gold sodium thiomalate intramuscularly once every three days, respectively. An immune basis for the disorder was suggested by the apparent consumptive nature of the thrombocytopenia (increased bone marrow megakaryocytes and large peripheral blood platelets), the response to corticosteroid therapy and the demonstration of increased platelet-associated immunoglobulin. The latter was demonstrated with a solid phase radioimmunoassay and by electron microscopy using a staphylococcal protein A-colloidal gold conjugate. Platelet-associated immunoglobulin decreased as the platelet counts rose, and in one dog monitored over periods of steroid-induced remissions and subsequent relapses, the amount of platelet-associated immunoglobulin G correlated inversely with the platelet count (r = 0.82). These findings suggest that the long-term administration of gold compounds in dogs is associated with a dose-dependent incidence of thrombocytopenia, which is immune-mediated and similar to that associated with parenteral chrysotherapy in man. The application of tests for platelet-associated immunoglobulin to canine patients with immune thrombocytopenia should be useful in the diagnosis of the disorder in clinical practice.