The tarsocrural joints of 11 horses were inoculated with 1.2 to 2.16 x 10(6) viable Staphylococcus aureus organisms susceptible to a trimethoprim-sulfadiazine (TMP-SDZ) combination with minimal inhibitory concentration (MIC) of 0.25 microgram of TMP/ml and 4.75 microgram of SDZ/ml. Antimicrobial treatment consisted of oral administration of a TMP-SDZ combination-30 mg/kg of body weight given once daily (group-1 horses) or 60 mg/kg given as 30 mg/kg every 12 hours (group-2 horses). Paired serum and synovial fluid samples were obtained before intra-articular inoculation with the S aureus, after inoculation with S aureus but before antimicrobial treatment, and after inoculation at various hourly intervals after oral administration of the TMP-SDZ combination. The TMP-SDZ combination was administered daily in the 2 dosages for 21 days. Samples were collected after day 3 of repetitive drug administration so that drug steady-state concentration would have been achieved. Serum and synovial fluid samples were analyzed for TMP and SDZ concentrations. Administration of the TMP-SDZ combination at a dosage of 30 mg/kg once daily was not effective in maintaining TMP or SDZ concentrations above the MIC of TMP-SDZ for the S aureus (0.25 and 4.75 microgram/ml for TMP and SDZ, respectively) in the infected synovial fluid or in maintaining adequate TMP concentration in the serum. The alternative use of the TMP-SDZ combination at a dosage of 60 mg/kg given as 30 mg/kg every 12 hours was effective in maintaining serum and synovial fluid concentrations of TMP and SDZ that were greater than the MIC for the infective organism. Sulfadiazine concentration was significantly (P less than or equal to 0.05) lower in the infected synovial fluid sample than that in the corresponding serum sample. We concluded that administration of 60 mg of TMP-SDZ/kg given as 30 mg/kg every 12 hours is more effective than 30 mg/kg given once daily for the treatment of equine infectious arthritis caused by organisms for which the MIC of TMP-SDZ is less than or equal to 0.25-4.75 microgram/ml.

Neutralizing and nonneutralizing antibodies to bovine viral diarrhae (BVD) virus were detected in 3 cows persistently infected with noncytopathic BVD virus after vaccination with modified-live cytopathic BVD virus. Neutralizing antibodies detected in serum samples from each persistently infected cow at 3 weeks after vaccination were highly specific for certain isolates of cytopathic BVD virus and reacted only with a viral protein with a molecular weight of 53,000. Neutralizing antibodies to 1 of 3 isolates of noncytopathic BVD virus were detected in a serum sample obtained at 12 weeks after vaccination from 1 of 3 persistently infected cows. Nonneutralizing antibodies were detected in all cows at 7 to 12 weeks after vaccination.The nonneutralizing antibodies were less specific for isolates of BVD virus and reacted with viral proteins with molecular weights of 115,000, 80,000, 53,000, and 47,000.

Thirty-three cattle with fatal respiratory tract disease were examined for gross and histologic lesions and for the presence of viral and bacterial agents in the lungs. Fifteen cattle had lesions characteristic of atypical interstitial pneumonia (AIP), and 18 had other respiratory tract diseases, including infectious bovine rhinotracheitis, shipping fever pneumonia, bronchopneumonia, pulmonary abscess, and edema of the trachea. Gross necropsy findings in the cattle with AIP were uncollapsed and emphysematous lungs; histopathologic findings included interstitial edema, thickening of alveolar walls, hyaline membrane formation, and hyperplasia of type-II pneumonocytes. The infective agents found in the lungs of the 33 cattle included bovine respiratory syncytial virus, bovine herpesvirus type 1, Pasteurella sp, mycoplasmas, and Corynebacterium pyogenes. Bovine respiratory syncytial virus was detected by use of immunofluorescence and immunoperoxidase on lung tissue sections; bovine herpesvirus type 1 was detected by these techniques and by isolation of the virus. Bovine respiratory syncytial virus was significantly (P = 0.01) associated with lesions of AIP (11 of 15), compared with those of other respiratory tract diseases (5 of 18).

Replication of feline infectious peritonitis virus (FIPV) in feline cell cultures was inhibited after incubation of cells with either human recombinant leukocyte (alpha) interferon (IFN) or feline fibroblastic (beta) IFN for 18 to 24 hours before viral challenge exposure. Compared with virus control cultures, FIPV yields were reduced by ranges of 0.1 to 2.7 log10 or 2 to 5.2 log10 TCID50 in cultures treated with human alpha- or feline beta-IFN, respectively; yield reductions were IFN dose dependent. Sensitivity to the antiviral activities of IFN varied with cell type; feline embryo cells had greater FIPV yield reductions than did similarly treated feline kidney or feline lung cells. Comparison of the virus growth curves in IFN-treated and virus control cultures indicated marked reduction in intracellular and extra-cellular FIPV in IFN-treated cultures. Compared with virus control cultures, intracellular and extracellular infectivity in IFN-treated cultures was delayed in onset by 12 and 30 hours, respectively, and FIPV titers subsequently were reduced by 3 to 3.5 and 5 log10 TCID50, respectively. Frequently, immunofluorescent and electron microscopy of IFN-treated cells or cell culture fluids did not reveal virus; however, even in cultures without viral cytopathic changes, small amounts of virus occasionally persisted in cells.

Nitrofurazone solution containing 0.2% nitrofurazone and 99.8% polyethylene glycol was given to 4 healthy horses (2 L in 2 L of lactated Ringer solution, intraperitoneally). Horses developed hypovolemia, hyperosmolality, and mixed respiratory and metabolic acidosis. These changes were largely attributable to polyethylene glycol, but a contribution of nitrofurazone cannot be excluded. Intraperitoneal infusion of nitrofurazone solution in horses is contraindicated.

A subpopulation of purified, interepithelial lymphocytes from porcine small intestinal mucosa contained cytoplasmic granules. Toluidine blue staining revealed metachromatic granules in 13.64% (606/4,450) cells. The cells had scant organelles, a single large nucleus with obvious invagination of the nuclear membrane, and prominent chromatin. Each cell contained 1 to 10 cytoplasmic membrane-bound granules, 0.6 to 1.5 microns in diameter. These findings indicated that the granular mucosal lymphocytes are related morphologically to mucosal mast cells. The presence of serotonin in the granules, confirmed by the serotonin releasing test, provided functional evidence that granular mucosal lymphocytes are related to mucosal mast cells.

Cardiovascular effects (vasodilatation, hypotension) of morphine administration have been attributed to central actions and peripheral histamine release. In the study reported here, we compared plasma histamine (Hm) concentrations after morphine sulfate and oxymorphone HCl administration in conscious dogs. Five healthy adult dogs (mean body weight, 10.1 kg) were randomly administered morphine (2 mg/kg of body weight, IV or oxymorphone (0.2 mg/kg, IV) by a 5-second bolus injection at weekly intervals. Venous blood samples (5 ml) were collected from jugular veins before and at 1, 2, 5, 15, 30, and 60 minutes after drug administration. Behavioral changes were recorded. Plasma was analyzed by a radioenzymatic technique, using purified histamine N-methyltransferase as an enzyme catalyst (sensitivity of assay, 40 pg Hm/ml). Mean base-line Hm value for all dogs was 0.55 ng/ml. The mean Hm value was significantly higher (P < 0.05) than the base-line value at 1, 2, 5, 15, and 60 minutes after morphine administration (531.4, 251.0, 113.0, 31.5 and 1.0 ng of Hm/ml, respectively), but there were no significant increases in histamine values from base-line values at any time after oxymorphone administration. All dogs given morphine and 1 dog given oxymorphone showed excitatory behavior; 2 dogs given morphine and 3 dogs given oxymorphone salivated profusely.

Peanut agglutinin (PNA) and surface immunoglobulin (SIg) were investigated as markers for T and B lymphocytes in blood and lymphoid tissues of dogs of various ages. In the blood study, 4 age groups (n = 8 dogs/group) were used. The mean (+/- SD) percentages of PNA-positive (PNA +) cells were 68.4 +/- 8.6% (group 1, < 1 year old), 70.3 +/- 9.2% (group 2, 1 to 2 years old), 72.0 +/- 3.7% (group 3, 5 to 6 years old), and 63.8 +/- 10.1% (group 4, 10 to 11 years old). The mean percentages of SIg-positive (SIg+) cells in blood were 32.1 +/- 10.6% (group 1), 43.2 +/- 7.0% (group 2), 34.3 +/- 4.8% (group 3), and 35.0 +/- 6.8% (group 4). The mean total percentages of PNA+ and SIg+ cells were 100 +/-6% (group 1), 113.5 +/- 4.9% (group 2), 106.3 +/- 5.3% (group 3), and 98.9 +/- 9.2% (group 4). The proportions of PNA+ and SIg+ cells in dogs of group 2 were significantly (P < 0.05) different from those in dogs of the other groups. Serial changes in PNA+ and SIg+ cells were investigated in blood of 6- to 29-week-old pups (n = 8). A significant (P < 0.05) transient decrease in PNA+ cells and a corresponding increase in SIg+ cells was observed in pups between 14 and 17 weeks old. Lymphoid tissue specimens and blood samples were obtained from 2- to 6-month-old dogs (n = 11) and from 6- to 12-month-old dogs (n = 10). Percentages reflected the combined data from both groups because there were no significant differences between the 2 age groups. The mean percentages of PNA+ cells were: blood, 68.4 +/- 8.6%; thymus, 86.6 +/- 16.3%; spleen, 29.5 +/- 16.0%; lymph node, 48.5 +/- 16.0%; and bone marrow, 30.8 +/- 26.4%. The mean percentage of SIg+ cells were: blood, 32.1 +/- 10.6%; thymus, 3.1 +/- 5.5%; spleen, 69.3 +/- 10.3%; lymph node, 55.4 +/- 15.2%; and bone marrow, 65.4 +/- 22.4%. The procedureto identify T lymphocytes in blood and lymphoid tissue was easy to perform, was reproducible, and could be performed on as few as 10(6) cells. Percentages of T lymphocytes identified compared favorably with those of other studies.

In vitro testing of bacterial susceptibility to a combination of ticarcillin and clavulanic acid was done, using 406 aerobic gram-positive and gram-negative isolates (considered to be pathogens) cultured from equine and small animal specimens. A microdilution broth technique of susceptibility testing was performed, using trays with wells containing a range of doubling concentrations of dehydrated ticarcillin (range, 0.50 to 128 microgram/ml) with fixed concentration of clavulanic acid (4 microgram/ml). The following isolates of equine origin were (90%) susceptible to concentrations of ticarcillin and clavulanic acid combinations of less than or equal to 16 and 4 microgram/ml, respectively: Staphylococcus aureus, S intermedius, Klebsiella pneumoniae, Enterobacter aerogenes, Ent agglomerans, Ent cloacae, Escherichia coli, Actinobacillus sp, Corynebacterium pseudotuberculosis, Rhodococcus equi, Proteus vulgaris, and Bordetella bronchiseptica. Isolates of small animal origin (90%) susceptible to less than or equal to 16 and 4 microgram of ticarcillin-clavulanic/ml included S aureus, S intermedius, Ent aerogenes, Ent agglomerans, Pasteurella multocida, B bronchiseptica, Pr mirabilis, and Serratia sp.

The effect of T-2 toxin, a radiomimetic immunosuppressive agent, on resistance to the facultative intracellular bacterial pathogens Listeria monocytogenes (strain EGD), Mycobacterium bovis (BCG Copenhagen 1331), and Salmonella typhimurium was determined. Female Swiss ICR mice were given a single dose of T-2 toxin (4 mg/kg of body weight) by gastric gavage. On the seventh day after toxin administration, the mice were infected by intraperitoneal inoculation with L monocytogenes, S typhimurium, or M bovis. Mice given the toxin also were exposed to respirable droplet nuclei containing L monocytogenes or M bovis. The effect of the toxin on the course of infection was monitored by observing mortality or by enumeration of bacteria in te spleen or lungs of infected mice. The toxin increased resistance to infection with L monocytogenes initiated by intraperitoneal inoculation, but reduced resistance to M bovis infection initiated by intraperitoneal inoculation. The toxin had no appreciable effect on the course of salmonellosis or on resistance to infection initiated by inhalation of L monocytogenes or M bovis aerosols. Therefore, it was concluded that T-2 toxin does not necessarily reduce resistance to infection in mice. The toxin's effect on the course of in vivo bacterial infections depends on the nature of the infective agent and the route of inoculation.