This study compared the short-term clinical and pathologic effects of spiral and total ring prostheses, applied to the cervical and thoracic portions of the trachea of dogs via a combined intercostal thoracotomy and ventral cervical midline approach. The effect of intraluminal placement of synthetic monofilament nonabsorbable suture also was evaluated. Eleven small-breed dogs were randomly allotted to 3 groups. Group 1 (n = 3) were controls that had been treated by sham operation, group 2 (n = 4) had polypropylene spiral prostheses applied to the cervical and thoracic portions of the trachea, and group 3 (n = 3) had total ring prostheses applied to the cervical and thoracic portions of the trachea. All dogs were euthanatized and necropsied 8 weeks after surgery. Clinical complications were minimal and limited to mild, short-term lameness and coughing. Three and 6 weeks after surgery, radiographs were within normal limits in all dogs. Tracheoscopy confirmed maintenance of tracheal lumen diameter and integrity of the mucosal epithelium in all dogs. Gross and microscopic postmortem findings were similar in groups 2 and 3. Mild adhesions were present between prostheses and adjacent structures. Similar adhesions were present where prostheses had been applied and subsequently removed in group-1 dogs. Histopathologic abnormalities included mild to moderate adventitial and periprosthetic fibrosis and mild adventitial inflammation associated with polypropylene spiral prostheses and total ring prostheses. The majority (70%) of intratracheal sutures evaluated were covered by microscopically normal ciliated mucosal epithelium by 8 weeks after surgery. Polypropylene spiral prostheses and total ring prostheses applied to the cervical and thoracic portions of the trachea of dogs in the manner described appear to be tolerated well and produce a minimal tissue response over the study period.

Two federally licensed attenuated live transmissible gastroenteritis (TGE) virus vaccines (an IM vaccine and an oral-IM vaccine) and 1 nonlicensed nonattenuated live TGE virus vaccine were evaluated and compared in sows free of TGE virus-neutralizing antibodies. Litters from the sows were challenge exposed at 3 and 5 days of age, and results were combined according to the vaccine administered to the sows. The survivability of pigs suckling sows vaccinated with the nonattentuated vaccine was significantly (P less than 0.01) greater than that of pigs suckling sows vaccinated with the IM attenuated vaccine, significantly (P less than 0.05) greater than that of pigs suckling sows vaccinated with the oral-IM attenuated vaccine, and significantly (P less than 0.05) greater than that of pigs suckling sows that had not been vaccinated. The differences, however, between survivability of litters from sows vaccinated with the IM attentuated vaccine or the oral-IM attenuated vaccine and that of litters from the sows not vaccinated were not significant (P greater than 0.10). The nonattenuated TGE vaccine, although giving a higher level of protection than the attenuated vaccine was eventually overwhelmed. Dexamethasone did not increase the incidence of diarrhea, and levamisole did not potentiate the lactogenic immunity in sows after given their first dose of the nonattenuated vaccine. Survivability in litters suckling sows that developed diarrhea after given their first dose of the nonattenuated vaccine was not greater than that in litters suckling sows that did not develop diarrhea. The best results were obtained when 3-day-old suckling pigs were challenge exposed with virulent TGE virus.

A 4% pilocarpine gel applied topically to eyes was evaluated in glaucomatous Beagles and normotensive Miniature Schnauzers to determine its efficacy in reducing intraocular pressure (IOP) and to assess any side effects. Pilocarpine gel significantly (P less than 0.05) reduced IOP for 24 hours after treatment, compared with baseline (pre-drug) values, untreated fellow eyes, and placebo-treated eyes. The IOP remained significantly lower (P less than 0.05) during 3 treatment days, as well as the first 2 days after treatment. The pupil sizes were significantly smaller (P less than 0.01) in all treated dogs after the first administration of pilocarpine, compared with baseline values, untreated eyes, and placebo-treated eyes. The subsequent pilocarpine gel administrations induced significant miosis (P less than 0.01), compared with baseline values, but the extent of miosis and duration were significantly less (P less than 0.01) as the number of treatments increased. Conjunctival irritation and blepharospasm were observed mainly in the first 2 days of treatment and were minimal after subsequent applications. There was no contralateral effect on IOP or pupil size, compared with baseline values and placebo-treated eyes.

Clinical electromyographic studies were performed in dogs (6 weeks to 5.5 years old) with a degenerative myopathy analogous to Duchenne muscular dystrophy. Spontaneous activity, consisting primarily of complex repetitive discharges (pseudomyotonic discharges), was found in all dogs tested, but was most prominent in dogs greater than or equal to 10 weeks old. Myotonic discharges also were found, but were less frequent. Motor unit potentials were generally abnormally brief and frequently polyphasic. Ulnar nerve conduction velocities determined in two 4-month-old dogs were similar to those of unaffected littermates. It was concluded that canine X-linked muscular dystrophy is a primary myopathic process in which complex repetitive discharges and myotonic discharges are a prominent feature. The basis for this spontaneous activity is not known.

Serum samples obtained from feeder calves before and after entry into the market system (days 0 to 7) were assayed for antibodies to Pasteurella haemolytica biotype A, serotype 1 capsular polysaccharide (CPS) and lipopolysaccharide/outer membrane protein (LPSp) by isotype in a kinetic-augmented, antigen-capture ELSIA. These test results, plus indirect hemagglutination (IHA) antibody titers, and hemolysin-in-gel test (HIGT) findings were compared with clinical performance data during the initial 4 weeks in the feedlot (receiving period). High concentrations of HIGT antibody, at the point of initial assembly of feeder calves at weaning and during the subsequent 7-day marketing period, were associated with freedom from bovine respiratory disease (BRD) during the receiving period. High or rapidly increasing concentrations of anti-CPS IgG1 during the marketing period were also associated with less BRD. However, high concentrations of anti-LPSp IgG1 during the marketing period were associated with increased BRD during the receiving period. There was no correlation between the concentrations of antibody determined by IHA tests early in the marketing period and freedom from BRD during the receiving period. High concentrations of antibody determined by this test at entry into the feedlot (day 7) were associated with a high incidence of BRD. Calves vaccinated with a P haemolytica bacterin had significantly (P less than 0.05) higher HIGT values and concentrations of anti-LPPp IgG1 and IHA antibody than did nonvaccinated calves on entry into the feedlot (day 7). Vaccination appeared to have little effect on the amount of anti-CPS IgG1. Of all the tests used to quantitate antibody, the HIGT correlated best with clinical performance. High concentrations of HIGT antibody during the marketing period predicted freedom from BRD during the receiving period. When calves were vaccinated with tissue culture-derived and conventional P haemolytica bacterins in oil adjuvant at 28-day intervals and tested for antibody responses by isotype on days 0, 28, and 35, there were clear and highly significant increases in anti-LPSp IgG1 activity. Also, the amount of anti-LPSp IgM and the HIGT and IHA antibody titers increased significantly. In all tests, the antibody response was highest to the tissue culture-derived bacterin. High concentrations of HIGT antibody, as found in vaccinated animals, were correlated with resistance to transthoracic inoculation of virulent P haemolytica.

An in vitro method to label equine RBC with technetium 99m was modified to achieve quantitative labeling of cells in concentrated whole blood. After a blood sample was incubated with a reducing agent (stannous citrate), an oxidizing reagent (NaOCl) and a chelating agent (EDTA) were added to inactivate residual Sn2+ in the plasma. This step prevented premature reduction of pertechnetate in plasma. Labeling of RBC from 9 healthy horses, using a standard whole blood protocol, resulted in only moderate labeling efficiency (44 to 85%) and indicated a linear relationship between labeling efficiency and PCV. Effects of increased incubation time, increased incubation temperature, prelabeling sedimentation, and double addition of NaOCl/EDTA were investigated in whole blood from 10 healthy horses. Labeling efficiency was improved by each independent factor and by combination of factors. Highest labeling efficiencies (96 to 97%) were achieved when blood samples were sedimented for 20 minutes before being labeled, regardless of incubation time or incubation temperature. Morphologic features of RBC were unaffected by labeling procedures. In vivo whole blood clearance time for labeled cells was determined in 5 healthy horses. Sedimented blood samples were labeled, using a standard 15-minute incubation time at 20 to 22 C. Mean clearance half-time for 5 horses was approximately 20 hours. More than 95% of 99mTc activity was associated with the cells during the 24 hours after reinjection.

Leukotoxin activity from culture supernatants of Pasteurella haemolytica serotype 1 in logarithmic growth phase caused rapid (less than 5 min) release of intracellular K+, uptake of extracellular Ca2+, and swelling of cultured bovine lymphoma cells (BL3 cells). Release of 51CrO(4)(2-) and lactate dehydrogenase (LDH) from BL3 cells began after 15 minutes of incubation with leukotoxin at 37 C and was completed between 60 and 120 minutes of incubation. In addition, leukotoxin exposure of BL3 cells resulted in cell aggregation and adherence to glass surfaces. Scanning electron microscopy indicated that after 10 minutes of leukotoxin exposure, BL3 cells increased in size, and large membrane defects developed between 20 and 60 minutes of exposure. The rate of release of LDH from leukotoxin-exposed BL3 cells was proportional to the amount of leukotoxin added. At high cell concentrations, the activity of LDH released at completion was directly proportional to the amount of leukotoxin added. Leukotoxin-induced release of LDH required a divalent cation, whereas K+ release and cell swelling did not. The addition of Ca2+, Mn2+, and Ba2+ resulted in increased leukotoxin-induced release of LDH. Divalent cation concentrations of 0.5 to 2.5 mM resulted in 50% of maximal stimulation. Ethylene glycol-bis(beta-aminoethyl ether) N,N,N',N'-tetraacetic acid blocked increased release of LDH caused by Ca2+ addition, but had no effect on K+ release or cell swelling. Leukotoxin action on BL 3 cells (K+ release, cell swelling, Ca2+ uptake, and release of LDH) was prevented by incubation at 4 C.

Monoclonal antibodies recognizing the O-polysaccharide portion of Brucella abortus strain 2308 provided BALB/c mice with passive protection against challenge exposure with the homologous strain. Numbers of colony-forming organisms in the spleen were reduced by IgM and IgG monoclonal antibodies. Active immunization of mice, using B abortus 2308S lipopolysaccharide, resulted in production of IgM antibody at 14 days. Clearance of organisms in the actively immunized mice after challenge exposure at 14 days was nearly identical to that in passively immunized mice. Mice either passively or actively immunized were effectively protected from 0 to 28 days. Bacterial colonization of the spleen was observed to increase in both groups of mice at 56 days and indicated that humoral responses were effective in eliminating the organism in the early stages of infection, but other immune mechanisms were necessary for protection of mice in the later stage of infection with virulent strains of B abortus.

Monoclonal antibodies (MAB) to porcine immunoglobulins were produced by fusion of SP2/0 cells with splenic lymphocytes of mice that had been immunized with porcine IgG or IgA. Of 16 MAB selected for detailed study, 13 reacted with heavy chains (7 anti-gamma, 6 anti-alpha) and 3 reacted with light chains of native immunoglobulin. Several of the same MAB (3 anti-gamma chain, 1 anti-alpha chain, 3 anti-light chain) also reacted with denatured immunoglobulin by use of immunoblotting analysis. Collective results of competitive ELISA, immunodiffusion, and immunoblotting analysis indicated that the 7 MAB of anti-gamma chain specificity were directed to 3 epitopes, the 6 MAB of anti-alpha chain specificity were directed to at least 2 epitopes, and the 3 MAB of anti-light chain specificity were directed to at least 2 epitopes that may have been located on different types of light chains. When tested by immunodiffusion with 5% polyethylene glycol incorporated in the agar matrix, all anti-gamma chain and antilight chain MAB, but no anti-alpha chain MAB, had precipitating activity. When polyethylene glycol was not used, only 4 MAB (all of the anti-gamma chain specificity and of IgM isotype) had precipitating activity. These MAB, with specificity for gamma and alpha chains and those reported earlier with mu-chain specificity, should be invaluable in the detection and quantification of porcine immunoglobulin isotypes. These MAB have potential applications in delineating the porcine immune response to selected immunogens.

Live Pasteurella haemolytica biotype A, serotype 1 isolates (n = 3) and Escherichia coli K-12, strain W3110, were reacted with bovine pulmonary lavage cell (PLC) suspensions. The comparative effects of the different bacteria on the functional and metabolic activity of alveolar macrophages (AMO) in the PLC suspensions were assessed simultaneously by use of 51Cr release, luminol-dependent chemiluminescence (LDCL), and AMO bactericidal assays. The bovine PLC reponsed differently to E coli, than to the 3 P haemolytica isolates in each of the 3 experimental test systems; however, responses to each of the P haemolytica isolates were not found to be significantly different. Unopsonized live P haemolytica cells adversely affected the functional and metabolic response of PLC, whereas there was no evidence of a cytotoxic (cytocidal) influence of E coli. A difference in 51Cr release for reaction mixtures containing E coli and P haemolytica was not detected at zero time; however, at each subsequent time, reaction mixtures phagocytically stimulated with P haemolytica had significantly increased amount of 51Cr release (P less than 0.05), compared with those mixtures containing E coli. Bovine AMO in the PLC suspensions were able to effectively kill E coli in vitro, but were unable to prevent survival and subsequent growth of P haemolytica. The luminol-dependent chemiluminescence profiles for reaction mixtures phagocytically stimulated with E coli provided evidence of sustained production of oxygen radicals with antimicrobial capabilities by bovine AMO in the PLC. Production of these highly reactive antimicrobial oxidants appeared initially in cultures containing P haemolytica but, subsequently, their production declined precipitously and ceased altogether.