Hepatic abscesses were induced experimentally in 5 steers by inoculating Fusobacterium necrophorum via ultrasonography-guided, percutaneous catheterization of the portal vein. Hepatic ultrasonography was performed to determine the onset and progression of abscessation. Blood samples were collected before and after inoculation for performing leukocyte counts and hepatic function tests. Ultrasonographic evidence of liver abscesses was observed as early as 3 days after inoculation. Abscesses appeared as hyperechoic centers (cellular debris and pus) surrounded by hypoechoic or anechoic areas (fluid). Increases in rectal temperature, leukocyte counts, fibrinogen, globulin, bilirubin, gamma-glutamyltransferase, and sorbitol dehydrogenase concentrations were detected. Hepatic dysfunction was evidenced by decrease in serum albumin concentration and low sulfobromophthalein clearance. The ultrasonographic diagnosis of abscesses correlated well with necropsy findings.

During this investigation, the use of iohexol was compared with iotrolan for canine cisternal myelography. Iohexol and iotrolan myelography was done in 6 dogs by cisternal puncture with a 6-week interval between both procedures; each dog served as its own control. Cerebrospinal fluid (CSF) was collected for baseline analysis from each dog immediately before the contrast agent was injected. Cerebrospinal fluid samples were obtained at 1, 3, 7, and 14 days after injection of each contrast medium for cytologic and chemical analysis. Total CSF leucocyte count and glucose concentration did not change significantly in comparison with baseline data in any of the samples. After the injection of iohexol, protein concentration increased significantly in the 24-hour sample, and lactate dehydrogenase activity increased significantly in the 3-day sample. Significant difference was not found between the different samples collected at 1, 3, 7, and 14 days, compared with both contrast media. None of the dogs had seizure activity during a 5-hour postmyelographic observation period. Pathologic changes were not found by gross or microscopic examination of the spinal cord. Although a degradation in time of radiographic quality of all myelograms took place, the average radiographic score decreased more rapidly with iohexol. The average score at 90 minutes with iotrolan was comparable with the score at 45 minutes with iohexol, and the average score at 150 minutes with iotrolan was better than the score at 90 minutes with iohexol. At 5 and 10 minutes after cisternal injection, no significant difference wasobservable between the myelograms, but from 45 minutes onward, myelograms with iotrolan were superior.

An Escherichia coli bacterial prostatitis was experimentally induced to determine the effect of bacterial infection on prostatic tissue zinc concentrations in castrated and gonadally intact male dogs. Five of the 22 mixed-breed dogs (group 1) had no culture evidence of infection 2 weeks after the instillation of bacteria into the prostate gland. The remaining 17 infected dogs were allotted to 2 groups; 1 group of dogs was subjected to castration (group CA, 7 dogs), and the other group of dogs was subjected to sham operation (group SO, 10 dogs). The groups were divided into groups of dogs with prostatic infection at necropsy (groups CA-I and SO-I), and those dogs without prostatic infection at necropsy (groups CA-N and SO-N). Urine, prostatic fluid, and prostatic tissue (week 0, 7, +/- 12) specimens were obtained for bacteriologic culturing to determine whether prostatic infection was present. Prostatic tissue was obtained at necropsy (week < 6, 7, or 12) for analysis of zinc concentration by atomic absorption spectrophotometry. The logarithmic mean prostatic tissue zinc concentrations were compared between groups. Group CA had a significantly lower prostatic zinc concentration than all other groups. Zinc concentrations were not statistically different between any of the other groups. Castration did decrease the prostatic tissue concentration of zinc, a known natural antibacterial factor. However, resistance to infection and resolution of infection were not correlated with prostatic tissue zinc concentrations in this experimental model.

Evaluation of pudendal reflexes and effects of pudendal branch conditioning on those reflexes was carried out in 2 studies. In the first study of pudendal reflexes, 20 adult male and female mixed-breed cats underwent surgical isolation of the anal branch, urethral branch, and distal trunk (consisting primarily of the dorsal nerve of the penis/clitoris) of the pudendal nerve. Reflexes were tested in all possible ipsilateral and contralateral test-response combinations. Latency values and effects of increasing stimulus rate on response amplitude were recorded. Reflexes were detected in all combinations, with response latencies between 6.3 and 13.0 ms. Response amplitudes were diminished at stimulus rates of 3 to 5 Hz, and responses were apparently abolished at 4 to 16 Hz, suggesting that pudendal reflexes are polysynaptic. In the second study of conditioning effects, 9 adult male and female mixed-breed cats underwent preparation similar to that for study 1. A train of conditioning stimuli was applied to branches of the pudendal nerve prior to attempting to induce reflex responses, as performed in study 1. Conditioning completely abolished reflex responses for a period of 70 to 130 ms. Reflex responses were diminished in amplitude, compared with those observed during preconditioning trials, for 180 to 300 ms after conditioning.

The relationship of muscle and bone structure to limb weakness was examined in 60 Duroc pigs from 3 lines divergently selected for thoracic limb weakness. The lines were designated high, control, or low, with the low line having inferior thoracic limb structure. At approximately 100 kg, 10 pigs of each line and gender were scored for thoracic limb structure and movement. Right and left thoracic limbs were collected at slaughter. A computerized morphometric image analysis system was used to determine cross-sectional areas of muscles, bones, and soft tissues at levels through the brachium, antebrachium, metacarpus, and digits. The statistical model that was used to analyze the data included the effects of line, sire, gender, and side (left vs right), with weight as a covariate. Total bone area was similar for all 3 lines of pigs at all cross-sectional levels, but significant differences in muscle and other soft tissue areas were observed, including significantly greater extensor area for the antebrachium (P less than 0.001) in low-line pigs than in control- and high-line pigs, smaller total area (P less than 0.05) of the metacarpus in low-line pigs than in control and high-line pigs, and less total area of the medial digit (P less than 0.01) in low-line pigs than in control- or high-line pigs. Total area of bone and soft tissue for each cross-sectional region was significantly greater (P less than 0.05) in boars than in gilts. Side differences also were observed in total cross-sectional areas of bone and soft tissue of the antebrachium, metacarpus, and digits. Pigs selected for inferior thoracic limb structure had less total soft tissue cross-sectional areas in distal limb regions than did control- or high-line pigs. Limb weakness may be related to altered distribution of soft tissue supporting structures of the thoracic limb.

To determine the drug dose required to inhibit platelet reactivity by at least 50%, 2 drug regimens were evaluated in heartworm-negative, heartworm-infected, and heartworm-infected dogs embolized with dead heartworms. Aspirin, or a combination of aspirin and dipyridamole, were administered to 2 groups of Beagles (n = 5 each) for 5 to 9 days; a third group of 5 Beagles served as nontreated controls. For heartworm-negative dogs, mean (+/- SD) aspirin dosage that inhibited collagen-induced platelet reactivity by at least 50% was 6 (+/- 2) mg/kg of body weight given once daily. The aspirin/dipyridamole combination dosage was 1 mg of each drug/kg given every 12 hours. All dogs (n = 15) were implanted with 7 adult heartworms each and remedicated (or not treated) beginning at 21 days after heartworm implantation. In heartworm-infected dogs, mean aspirin dosage required to inhibit collagen-induced platelet reactivity > 50% was 10 (+/- 6) mg/kg. Mean dosage of aspirin/dipyridamole combination was 1.6 +/- (0.5) mg of each drug/kg given every 12 hours. When platelet reactivity in response to collagen was determined to be inhibited by at least 50% in all medicated dogs, each dog (n = 15) was embolized with 7 dead adult heartworms to mimic heartworm adulticidal treatment. Platelet reactivity was monitored for 21 days after treatment, and drug dose was adjusted to maintain platelet inhibition by at least 50%. In embolized dogs, mean aspirin dosage was 17 (+/- 14) mg/kg given once daily. Mean dosage of the aspirin/dipyridamole combination was 2.8 (+/- 1.3) mg of each drug/kg given every 12 hours. All dogs (n = 15) were euthanatized 21 days after heartworm embolization. Each lung lobe was evaluated for severity of lesions and presence of organized or fibrinous thrombi. Lesion severity in the aspirin- and aspirin/dipyridamole-treated dogs was not significantly different from that in control dogs.

Phosphonoformate (PFA), a noncompetitive inhibitor of reverse transcriptase (RT), inhibited feline leukemia virus FeLV) infection of 2 feline cell lines and inhibited progeny virus RT activity in a chronically FeLV-infected cell line. Feline leukemia virus infection of 3201 cells, an FeLV-negative lymphoma cell line, was inhibited by > 70% at a concentration of only 1 micromole PFA and by > 90% at concentrations of 64 to 256 micromole PFA, as evidenced by RT activity. However, FeLV antigen expression by 3201 cells remained relatively constant over noncytotoxic concentrations of PFA. Because the persistence of viral antigen expression with concomitant suppression of RT activity appears to be unique and because 3201 cells express small amounts of an endogenous retrovirus (RD and 114) contain endogenous FeLV proviral sequences, a possible role of endogenous retroviruses acting as helper viruses was suggested. Feline leukemia virus infection of 81C cells, a sarcoma-positive, leukemia-negative fibroblast cell line, was inhibited by > 50% at a concentration of 64 micromole PFA and by > 98% at concentrations of 256 to 512 micromole PFA, as indicated by suppression of focus formation. The feline lymphoid cell line FL-74 is a large producer of FeLV. When FL-74 cells were cultured in the presence of 256 micromole PFA, virus production (virus budding and viral antigen) was not affected, but progeny virus lost RT activity and infectivity. Direct addition of PFA (256 micromole to FeLV also reduced RT activity and infectivity. These data indicate that PFA can directly and rapidly inactivate retrovirus independent of cellular processing, presumably by inhibiting RT. Long-term PFA administration may curtail spread of retroviral infections within and between hosts via extracellular inactivation of newly produced virus particles. Results of this study also suggest that PFA might be used prophylactically to treat materials potentially contaminated with retroviruses.

Thoracic compliance measurements by use of readily available equipment were determined to be practical and safe in dogs. Twenty healthy dogs (age 1 to 16 years, weight 2.3 to 49.5 kg) were anesthetized for routine procedures such as dentistry or neutering. The animals were first hyperventilated to reduce pulmonary atelectasis, to check for leakage at the endotracheal tube cuff, and to induce mild hypocarbia, thus minimizing voluntary respiratory efforts. Total thoracic compliance measurements were calculated as the difference between exhaled volumes at static inspiratory pressures of 15 and 20 cm of H2O, divided by the pressure difference, and expressed as a function of body weight. The procedure was easy, took 5 to 10 minutes, and caused no recognizable ill effects in any of the dogs studied. Mean total thoracic compliance was 42.25 +/- 32 ml/cm of H2O. There was a significant correlation with weight, but no significant relationship was seen between compliance and age, or gender. The mean weight-adjusted total thoracic compliance was 1.85 +/- 0.56 ml/cm of H2O/kg. In studies in a small group of dogs with documented respiratory tract disease, 4 of 7 had a mean compliance > 2 SD below the normal range. Thus, this test may become part of the routine workup of any animal being anesthetized for procedures such as bronchoscopy to evaluate respiratory tract disease. Routine monitoring of animals on ventilators could provide early warning of complications such as pneumonia, pleural effusion, or pulmonary edema.

Forty 3- to 17-week old domestic ferrets, including 2 gnotobiotes, were inoculated orally and/or rectally with 10(6), to 10(9) colony-forming units of 1 or more of 4 strains of Campylobacter jejuni, 3 of mink and 1 of human origin. Feeding or gavage of any of the 4 strains, in milk or broth, with or without preinoculation sodium bicarbonate treatment to neutralize stomach acid, induced colonization in 38/40 ferrets; diarrhea lasted 2 to 4 days in conventional kits, 6 days in gnotobiotes. Bacteremia was detected in 4 of 18 tested, 2 to 5 days after inoculation. Two strains caused no more severe disease or prolonged colonization after 3 serial IV passages in kits than they did before passage. Multiple inoculations with a given strain resulted in progressively briefer colonization and milder disease, but subsequent inoculation with a different strain induced colonization and gastrointestinal disease similar to a primary infection. Five kits inoculated rectally after 4 previous homologous inoculations were resistant to colonization as well as to disease. Agglutinin titers of ferrets inoculated orally or rectally once were low or undetectable, but increased in response to repeated inoculation. Pretreatment with a 1% formalin enema caused mild colon irritation without clinical or histologic evidence of proliferative colitis in ferrets concurrently inoculated orally and/or rectally, whether or not they had preexisting antibodies to any strain of C jejuni. Histologic examination of tissues revealed leukocytic infiltration of intestinal lamina propria in 29 of 35 infected kits and 5 of 8 noninfected controls, and cryptosporidiosis in 5 infected kits plus 1 control. Examination of silver-stained sections of intestine from 15 infected ferrets revealed Campylobacter-like organisms on the surface of, but never inside, epithelial cells. The lack of characteristic gross or histologic lesions suggested that C jejuni is not, by itself, responsible for proliferative colitis in ferrets.

Plasma concentrations of porcine growth hormone (PGH) were similar in healthy pigs and those with atrophic rhinitis (AR), therefore, observed reduced growth rates and feed efficiency in naturally infected pigs with AR were not attributed to low concentrations of plasma PGH. Also, pituitary glands in both groups of pigs were responsive to growth hormone-releasing hormone (GHRH) challenge by increasing PGH secretion. Administration of clonidine hydrochloride to pigs naturally infected with AR failed to elicit any significant change (5.3 +/- 1.4 ng/ml) in the plasma concentration of PGH within a 45-minute bleeding interval. The pretreatment concentrations of PGH were similar in specific-pathogen-free toxin-treated and specific-pathogen-free control groups, but they increased significantly in toxin-treated pigs (20.7 +/- 8.2 ng/ml) within 15 minutes after GHRH injection. Porcine growth hormone release in toxin-treated pigs was variable; however, all pigs did not respond to GHRH administration: 3 responded with an increase in PGH release (35.6 +/- 10.6 ng/ml), 2 did not respond (6.7 +/- 0.5 ng/ml), and 1 had a decrease in PGH release (3.9 ng/ml). Therefore, the observed reduced growth rates reported in the literature may be attributed to factors at the target level of PGH action, such as insufficient or down-regulation of PGH receptors, changes or impaired ability in the PGH receptor-binding characteristics, and inability of PGH receptor complex to transduce signal. Toxins are known to modulate signal transduction pathways. It has been speculated that serotype-D Pasteurella multocida toxin may influence growth by its effect on signal transduction from PGH receptor complex on the cell membrane to the interior of the cell. This would account for the presence of high concentrations of PGH in the plasma and a functionally competent hypophysis cerebri, which responded to GHRH injection that have retarded growth in pigs affected with AR.