Fasting and postprandial gastroesophageal sphincter pressure (GESP) and plasma gastrin immunoreactivity were measured in 6 dogs from 9 through 60 months after treatment for and recovery from gastric dilatation-volvulus (GDV). The GESP was not significantly increased in these dogs, compared with that in clinically normal dogs in either the fasting or postprandial state. Corresponding plasma gastrin immunoreactivity was not significantly increased in dogs of the GDV-recovered group, compared with that in clinically normal dogs (fasting or postprandial). An exaggerated increase in GESP in response to food-induced gastrin release was not observed in dogs of the GDV-recovered group. Exogenously administered pentagastrin (3-micrograms/kg bolus, IV) increased fasting GESP in clinically normal dogs over a 4-minute test period (P = 0.01). Gastric distention in response to oral administration of isosmolar saline solution (500 ml) did not significantly increase GESP or plasma gastrin immunoreactivity in clinically normal dogs. In anesthetized clinically normal dogs, gastric distention in response to use of balloons filled to exert intragastric pressure of 30 mm of Hg also did not cause significant increase in plasma gastrin immunoreactivity. Increased GESP, secondary to hypergastrinemia or gastric distention, is an unlikely cause of eructation failure in dogs with GDV.

Serum from dogs with surgically induced renal impairment was incorporated into the medium for erythroid bone marrow cultures. A significant correlation was found between serum activities of erythropoietin and numbers of erythroid colony-forming units grown in culture. Serum creatinine concentrations had no correlation, and serum parathyroid hormone activities had a negative correlation with numbers of erythroid colony-forming units that was below the level of significance. Purified 1-84 parathyroid hormone added to bone marrow cultures was found to be stimulatory to erythroid colony-forming unit growth in higher concentrations, but decreased the number of burst-forming units. Unmeasured substances in the canine serum appeared to have a greater effect on the canine erythroid bone marrow cultures than did creatinine or parathyroid hormone values.

Electron microscopy revealed several unique features in canine bone marrow, compared with that of other species. The marrow was fatty and extensively trabeculated and was enclosed by a complete layer of endosteal bone-lining cells. Branched reticular cells were closely associated with each other and, occasionally covered part of the sinus wall as an adventitial layer. The extent of adventitial coverage varied markedly and was less extensive, compared with that of other species. On average, only 23% of the sinus wall was covered by adventitial layer, in contrast to 65% reported in laboratory animals. Unilaminar sinuses, with no adventitial coverage, accounted for greater than 38% of all sinuses. Quantitative analysis indicated that 60% of the latter sinuses contained apertures, as opposed to 35% of sinuses with adventitial coverage (P less than 0.05). Moreover, the number of apertures in unilaminar sinuses was significantly (P less than 0.009) greater than that in multilaminar sinuses. Apertures were observed every 59 micromoles in unilaminar sinuses, in contrast to every 109 micromoles in multilaminar sinuses. Approximately 75% of the apertures were occupied by cells in transit, and only 25% were free of cells. Macrophages were distributed throughout the marrow and were closely associated with all blood cell lines. Occasionally, cells that entered the lumen were not fully mature. Erythroblasts were seen migrating across the wall and within the lumen of sinuses. The less-extensive adventitial coverage in canine bone marrow might indicate that the rate of cell delivery from the marrow into the circulation was relatively high in this species. The prevalence of unilaminar sinuses, along with the larger number of apertures, suggested that these sinuses were more accessible to the migrating cells and that the cellular traffic across them was intense.

The seroprevalence and seasonal trend of antibody titers against equine monocytic ehrlichiosis (Potomac horse fever) were determined in apparently healthy horses in selected areas of Illinois in 1986. Sera from 1,367 horses (6 months to 29 years old) were evaluated for the presence of antibodies against Ehrlichia risticii with indirect immunofluorescence. The majority (88%) of the horses were Thoroughbred or Standardbred racehorses. The number of horses with antibodies against E risticii was 229/1,367 (16.75%). The titers in these horses ranged from 1:10 to 1:640. As the year progressed, the number of seropositive horses (titers greater than or equal to 1:10) and the magnitude of the titers increased significantly, both reaching a maximum in July and August, respectively (P less than 0.05). A relationship between seropositivity and gender was not detected. In the year prior to sampling, 56.8% of the seropositive horses had not been ill, whereas 0.8% had diarrhea, an episode of acute abdominal pain, or laminitis. It was concluded that a large number of horses in Illinois are exposed to E risticii, that maximal exposure occurs in July, and that the most common form of the disease in Illinois is not associated with clinical signs.

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.

Isolated segments of left dorsal colon and a side-to-side colocolostomy (between the left ventral colon and left dorsal colon) were surgically created in 6 adult ponies. Four segments, each separated by an empty segment, were inoculated (20 ml) with 1 of the following 4 solutions: phosphate buffered saline solution (PBSS)/1% polyethylene glycol (PEG); purified cholera toxin in PBSS/1% PEG (5 micrograms cholera toxin/ml of PBSS/1% PEG); lyophilized Salmonella typhimurium UCD 1755 culture lysate, reconstituted in PBSS/1% PEG; and viable S typhimurium UCD 1755 (10(8) organisms/ml of PBSS/1% PEG). Twenty hours following inoculation of the treatment solutions into the isolated colon segments, the ponies were reanesthetized. Fluid accumulation in the isolated segments was measured, and tissue samples from isolated segments were taken for examination by light microscopy and electron microscopy, and for measurement of mucosal cyclic adenosine monophosphate levels. There was fluid accumulation in segments inoculated with cholera toxin in 4 ponies (29.5 +/- 12.7 ml), and in segments inoculated with S typhimurium UCD 1755 culture lysate in 3 ponies. (14.0 +/- 8.7 ml). There was no fluid accumulation in segments inoculated with either the control solution (PBSS/1% PEG) or viable S typhimurium UCD 1755. There was significantly (P less than 0.05) less cyclic adenosine monophosphate in segments inoculated with cholera toxin, Salmonella lysate, and viable Salmonella, compared with control segments. Histologically, there were minimal changes in control segments, consisting of mild to moderate submucosal edema and capillary congestion. Changes in the other segments were more pronounced and included neutrophilic infiltration and exocytosis, with the changes increasing in severity in the segments inoculated with cholera toxin, S typhimurium culture lysate UCD 1755, and viable S typhimurium UCD 1755, respectively. Ultrastructurally, mucosa from control segments was normal. Mucosa from segments inoculated with cholera toxin had swollen endoplasmic reticula and basolateral separation of surface epithelial cells. Mucosa from segments inoculated with S typhimurium UCD 1755 culture lysate and viable S typhimurium UCD 1755 had swollen smooth and rough endoplasmic reticula, separation of epithelial cells, degeneration of microvilli, and goblet cell degeneration.

Thirty-eight tracheobronchial aspirates (TBA) were collected from twenty 1 to 6-month-old foals, which were free of clinical signs of respiratory tract or other infectious disease. We collected TBA from 9 of the foals 3 times when they were approximately 8, 16, and 24 weeks old. Aspirates were examined cytologically after staining with modified Wright-Giemsa, Gram, toluidine blue, and prussian blue stains. Aerobic bacterial culturing was performed on all aspirates. Of the 20 initial TBA, 4 (20%) were normal cytologically on the basis of previously defined criteria for TBA from clinically normal horses, 6 (30%) had a high percentage of eosinophils (> 5%), 8 (40%) were classified as indicative of subacute inflammation, and 2 (10%) were classified as indicative of acute inflammation. Nine (45%) were positive for mast cells and none were positive for hemosiderin-laden macrophages (hemosiderophages). Of the 9 foals from which samples were collected at 16 and 24 weeks of age, results were similar, except for an increase in the number of TBA classified as indicative of chronic inflammation (33% and 22% respectively) and the number positive for hemosiderophages (33% and 88%, respectively). One TBA was considered nondiagnostic because of pharyngeal contamination. Culturing of 12 of the 37 aspirates (32%) yielded a potential microbial pathogen. Only 2 were positive cultures from the same foal. The following organisms were isolated: beta-hemolytic Streptococci spp (4), Actinobacillus/Pasteurella spp (4), Rhodococcus equi (2), unidentified nonenteric Gram-negative rod (1), and Escherichia coli (1). Thirty-four of the 37 aspirates (92%) yielded light growth of various organisms considered to be nonpathogenic and normal inhabitants of the upper respiratory tract. It was concluded that the presence of inflammatory cells, eosinophils, and mast cells in the tracheobronchial aspirates from clinically normal foals is a common finding. These cytologic findings were consistent in the samples collected from foals at 8, 16, and 24 weeks of age. It was also concluded that bacteria with recognized pathogenicity can be isolated from TBA from clinically normal foals and were most frequently isolated from 1- to 2-month-old foals or those with cytologic evidence of inflammation, even in the absence of clinical signs of respiratory tract disease.

Scanning electron microscopy of vascular corrosion casts of the optic nerve region in normal and glaucomatous Beagles demonstrated that the blood supply to the laminar optic nerve is derived from short posterior ciliary arteries, cilioretinal arteries, and longitudinal pial vessels. The short posterior ciliary arteries formed a ring of striated pillars around the scleral canal. The central retinal artery was not present in the dog. Differences between the casts in normal and glaucomatous dogs were not detected.

Natural killer (NK) cell activity and function were determined for 11 untreated and treated dogs with lymphoma. Concurrent chromium release and single cell binding assays, methods used to measure overall cytotoxic activity and that from individual cells, respectively, were performed at effector-to-target cell ratios of 50:1 and 100:1, with incubation periods of 12 and 16 hours. Significant reduction was achieved in overall activity for untreated dogs, using a 16-hour incubation period and an effector-to-target ratio of 100:1 (P less than 0.05). Decreased activity (P less than 0.025) was also achieved for those dogs that were administered combination chemotherapy, consisting of such drugs cyclophosphamide, vincristine, prednisone, and doxorubicin. There was no significant difference in binding or cytotoxin activity by individual cells in the untreated or treated dogs, compared with the healthy controls. Short- or long-term treatment with glucocorticoids did not influence overall NK cell activity or individual cell cytotoxicity. The overall cytotoxic activity in untreated dogs was reduced, but these dogs had relatively normal numbers of NK cells compared with paracontrols. This suggests that a defect in recycling, or the ability to kill targets repetitively, may be involved. A similar defect was found in NK cells of dogs treated aggressively with combination chemotherapy.