The severity of pulmonary thromboembolism and pulmonary hypertension induced by heartworms dying after administration of 2 adulticides was evaluated. Because melarsomine dihydrochloride (RM340) has been shown to be more effective in killing Dirofilaria immitis (heartworms) than the traditional approved adulticide, thiacetarsamide, an attempt was made to determine whether this new adulticide induced more severe lung disease. Before adulticide treatment, 32 dogs with naturally acquired heartworm infections received physical examinations, semiquantitative antigen concentration tests, CBC, platelet counts, serum biochemistry analyses, arterial blood gas determinations, thoracic radiography, pulmonary arteriography, and pulmonary hemodynamic tests. Eight dogs with a low burden and 9 dogs with a high burden of heartworms were treated with thiacetarsamide, and 7 dogs with a low burden and 8 dogs with a high burden were treated with RM340. Except for the heartworm-burden test, tests were repeated at regular intervals during the first 7 weeks after treatment. None of the dogs coughed or had dyspnea after treatment. Six of 9 dogs with high worm burdens and 4 of 8 dogs with low worm burdens had surviving heartworms after thiacetarsamide treatment, in contrast to only 3 of 15 RM340-treated dogs. Differences between the 2 adulticide treatments were minimal as determined by thoracic radiography, pulmonary hemodynamic tests, clinical laboratory analyses, pulmonary arteriography, or necropsy. The RM340 treatment was a more effective adulticide, but it did not increase the severity of hypertension and thromboembolism.

Fifteen 2-week-old kittens were randomly assigned to 1 of 3 milk treatment groups as the sole source of nutrition for 4 weeks: queen's milk, commercially available kitten milk replacer (CMR), and an experimental milk replacer (EXP). Kittens fed queen's milk suckled ad libitum, whereas CMR- and EXP-fed kittens were tube-fed every 6 hours. Kittens were weaned at 6 weeks of age and were fed a feline growth diet ad libitum for an additional 4 weeks. Kittens were examined at 2, 4, 6, 8 and 10 weeks of age; the procedure included an ophthalmic examination and blood sample collection for CBC and serum biochemical and amino acid analyses. Kittens fed CMR and EXP diets had weight gain greater than that for queen's milk-fed kittens. The kittens fed CMR, however, had diarrhea throughout most of the milk-feeding trial and developed diffuse anterior and posterior lens opacification and vacuolation at the posterior Y-sutures. The lens opacities noticed in the kittens during the milk treatments resolved to a residual perinuclear halo, and a few incipient cortical opacities were observed by the end of the growth diet-feeding period. Serum arginine concentration was significantly (P < 0.05) lower in the CMR-fed kittens, but was not different during the growth diet-feeding period. We concluded that the EXP diet supported normal growth in 2- to 6-week-old kittens; CMR supported normal kitten growth rate, but resulted in diarrhea and cataract formation; and serum amino acid data indicated that low arginine concentration may have been related to the CMR-induced cataract formation.

Critical tests were conducted in horses (n = 11) with naturally acquired infections of benzimidazole (BZ)-resistant population-B small strongyles in 1989 and 1990. Anthelmintics administered were thiabendazole (44 mg/kg of body weight, n = 4), oxibendazole (10 mg/kg, n = 3), and oxfendazole (OFZ, 10 mg/kg; n = 4). All compounds were paste formulations administered orally except for 1 of the OFZ treatments, which was a suspension formulation given by stomach tube. Aggregate mean efficacy was calculated for all species of small strongyles, drug-resistant and nonresistant. The highest efficacy was for oxibendazole (98%) and OFZ 94%); efficacy for thiabendazole was 63%. Five genera and 16 species of small strongyles were recovered from the 11 horses, ranging from 7 to 13 species (mean, 11). Of these, 7 species were found to have resistance in variable degrees to most of the anthelmintics. These strongyles were Cyathostomum catinatum, Cyathostomum coronatum, Cylicocyclus nassatus, Cylicostephanus calicatus, Cylicostephanus goldi, Cylicostephanus longibursatus, and Cylicostephanus minutus. The large strongyle, Strongylus vulgaris, was present in afl 11 test horses, and efficacy was 100% for all drugs. Seven of the BZ-treated foals (at least 1 horse from each BZ-treatment group), were infected with S edentatus; removal was 100%.

Thirty young ponies were examined endoscopically for evidence of gastric ulceration. Seven ponies had noninduced gastric ulcers present at the initial examination and were eliminated from the study. In an attempt to induce gastric ulcers experimentally, flunixin meglumine (1.1 mg/kg of body weight, IM, q 8 h) was administered for 7 days to the 23 ponies with endoscopically normal gastric mucosa. During the 7 days of flunixin administration, 11 ponies developed gastric ulcers that were appropriate for study. The 11 ponies were randomly allotted to 2 groups. Group-A (n = 5) and group-B (n = 6) ponies received ranitidine (4.4 mg/kg, PO, q 8 h) and corn syrup, respectively, until ulcers healed or for a maximum of 40 days. General anesthesia was induced every 3 to 5 days for visual evaluation of ulcer healing by use of a video endoscope. The earliest complete healing of gastric lesions observed in a corn syrup-treated pony was at 17 days. At 40 days, 3 of 5 and 3 of 6 ponies of the ranitidine and corn syrup-treated groups, respectively, had healed ulcers. Results of this study indicate that: noninduced gastric ulcers may be common in young ponies, flunixin meglumine may be effective in inducing gastric ulcers for gastric healing studies in young ponies, and ranitidine (4.4 mg/kg, q 8 h) is not significantly effective in accelerating healing of experimentally induced gastric ulcers in ponies under conditions of this study.

The effects of preanesthetic medication on ease of duodenal endoscopic intubation in dogs was evaluated. One of 12 combinations of preanesthetic medications (using atropine, glycopyrrolate, morphine, meperidine, acepromazine, and 0.9% NaCl solution) was administered IM to each of 12 dogs in a trial. Twelve endoscopic trials were performed so that each dog received each treatment combination once. Anesthesia was induced with thiamylal administered IV and maintained with halothane vaporized in oxygen. Electrocardiographic recordings, indirect blood pressure measurements, end-tidal carbon dioxide partial pressures, and halothane concentrations were monitored during the anesthetic period. The ease with which the fiberoptic endoscope was passed into the proximal portion of the duodenum was qualitatively scored on the basis of time and maneuvering effort. None of the preanesthetic combinations made intubation of the duodenum significantly easier than that with 0.9% Nacl solution (control). Only the combination of morphine and atropine induced gastropyloric conditions that resulted in significantly higher (more difficult) endoscopic scores than those after preanesthetic medication with 0.9% NaCl solution.

Enzyme-linked immunosorbent assays for the detection of Toxoplasma gondii antigen-containing IgM immune complexes (T gondii-specific IgM-IC) and IgG immune complexes (T gondii-specific IgG-IC) in the serum of cats were developed. Serum from clinically ill, naturally infected cats; healthy, naturally infected cats; and healthy cats experimentally inoculated with T gondii was assayed. All combinations of T gondii-specific IgM, IgG, antigens, IgM-IC, and IgG-IC were detected in naturally infected and experimentally infected cats. Clinically ill cats and cats with ocular signs of toxoplasmosis were more likely than healthy cats to have T gondii-specific IC in serum. It was concluded that T gondii-specific IC form in the serum of cats, may play a role in clinical disease development, and affect the results of T gondii-specific IgM, IgG, and antigen serologic assays.

Antiparasitic activity of several compounds was evaluated over a long period (about 25 years) in the same flock of sheep. Haemonchus contortus was of special interest, including its relation to drug resistance, especially to thiabendazole and other benzimidazoles, in addition to phenothiazine. Eleven compounds were evaluated in 15 controlled tests, done between 1966 and 1989 in naturally infected lambs (n = 145) born and raised on the same pasture. Sheep were first placed on the pasture in 1962, and a few more were added thereafter. Internal parasites in these sheep were classified in 3 general categories: indeterminate exposure to parasiticides; H contortus, resistant to thiabendazole; and H contortus, resistant to phenothiazine. The parasitic infections probably became more homogeneous after several years because of few introductions of outside sheep after initial establishment of the flock. Activity against naturally acquired internal helminths was evaluated for cambendazole (CBZ: dosage, 20 mg/kg of body weight), fenbendazole (FBZ: 5 or 7.5 mg/kg), mebendazole (MBZ: 10 mg/kg); oxfendazole (OFZ: 3.5 or 10 mg/kg), oxibendazole (OBZ: 10 mg/kg); parbendazole (PBZ: 15 mg/kg), phenothiazine (PTZ: 550 mg/kg); pyrantel pamoate (PRT: 25 mg base/kg), tetramizole (TET: 15 mg/kg); thiabendazole (TBZ: 30 or 44 mg/kg), and trichlorfon (TCF: 100 mg/kg). Thiabendazole was used more often (9 tests) than the other compounds. Thiabendazole was more active against mature H contortus in later years than when first used in 1966, although it was never 100% effective. Efficacy against immature H contortus for TBZ did not exceed 86%. Activity against immature and mature stages of this parasite was good overall for the other benzimidazoles. Results indicated no definite side resistance of non-TBZ benzimidazoles for this species. Removal of both stages of H contortus was generally low for PTZ. For the other nonbenzimidazoles (PRT, TET, and TCF), efficacy against immature and mature H contortus was 93 to 100%, except for 1 test with PRT (79% on mature worms) and 1 with TCF (77% on immature worms). With regard to other abomasal parasites, activity for the compounds tested against 2 species of Ostertagia was greater than or equal to 97%, with 1 exception; numbers of these parasites in nontreated lambs were less than numbers of H contortus. All compounds, except PTZ and TCF, were effective against a third species, Trichostrongylus axei. Activity against several species of intestinal parasites, most present in low numbers, was determined for 5 compounds (TCF, TBZ, CBZ, PTZ, and PRT) in 5 rests. Thiabendazole, CBZ, and PRT were highly effective against trichostrongylus, with a few exceptions. Trichlorfon and PTZ had overall less activity against trichostrongylus than did the other products. Against trichurids, PRT and TCF were highly efficacious.

During the breeding season, the effect of constant administration of an agonist analog of gonadotropin-releasing hormone (GnRH; goserelin acetate) on reproductive activity of mares was determined. Twenty-four mares undergoing estrous cycles were allocated at random to 6 groups (n = 4/group) and, on May 29 (day 0), received no treatment (group 1, controls), 120 micrograms (group 2), 360 micrograms (group 3), 600 micrograms (group 4), or 1,200 micrograms (group 5) of GnRH agonist/d for 28 days via a depot implanted subcutaneously. The final group of mares (group 6) was treated with 120 miocrograms of GnRH agonist/d for 84 days (3 occasions at 28-day intervals). During a pretreatment period (April 19 to May 29) and for 90 days after initiation of GnRH agonist treatment, follicular development and ovulation were monitored by transrectal ultrasonography of the reproductive tract at 2- to 3-day intervals. On each occasion a blood sample was collected for determination of luteinizing hormone (LH) and progesterone. Estrous behavior was monitored by teasing of mares with a stallion. Initiation of agonist treatment was random, relative to the stage of the estrous cycle, and all mares ovulated within 11 days before or after implantation. in 3 of 4 nontreated control mares, estrous cycles were observed throughout the study, with interovulatory intervals ranging from 18 to 26 days. In the remaining mare, concentration of progesterone was high after asynchronous double ovulation during the pretreatment period, suggestive of persistent corpus luteum. In group-2 mares, ovulation occurred in all mares 7 days before and 2 days after initiation of treatment; however, the next anticipated ovulation was delayed in 3 of 4 mares (interovulatory interval, 33 to 70 days). Estrous cycles were not disrupted in the remaining mare. At higher doses (groups 3-5), 1 mare each from groups 3 and 5 ovulated between days 0 and 2 of treatment initiation, but faded to ovulate during the remainder of the study (anovulatory for > 88 days). Similarly, an additional 2 mares of groups 2 and 3 ovulated within 2 days of GnRH agonist treatment. A second ovulation occurred in these mares 32 to 35 days later, thereafter, both mares were anovulatory for the remainder of the study. In the remaining 8 mares, interovulatory intervals were either lengthened (n = 6 mares, range, 32 to 82 days) or were unaffected (n = 2) by treatment. One group-6 mare had a lengthened interovulatory interval, 1 was anovulatory for > 90 days, and the remaining 2 mares were unaffected by treatment. During the 28-day treatment period, serum concentration of LH decreased (P < 0.05) only in mares of groups 3-5. In group-6 mares, concentration of LH was unchanged during each 28-day period after depot GnRH agonist administration. Thus, constant administration of a GnRH agonist to mares during the breeding season disrupted their estrous cycles. Anovulation or lengthening of the interovulatory interval by GnRH agonist treatment was associated with persistence of a corpus luteum or an extended follicular phase.

A serologic survey was conducted to determine the prevalence and seroconversion rates for ovine adenovirus (OAV) serotypes 1-4 and bovine adenovirus (BAV) serotypes 2, 3, and 7 in sheep in Iowa and in surrounding states. For 2 consecutive years, paired serum samples were obtained from 1- to 2-month-old lambs as they entered a ram test station and, again, 2 months later. Sera were tested for adenovirus antibodies by use of a microtitration serum virus-neutralization test. At the time of entry, high prevalence of antibody (titer greater than or equal to 2) was detected to all tested adenoviruses except BAV-3. All adenoviruses were active in the ram test station both years, as indicated by greater than or equal to fourfold increase in adenovirus antibody titer (seroconversion) in some of the lambs. The prevalence and seroconversion rate for OAV-1 was 94.0 and 7.2%, respectively; for OAV-2, 98.6 and 15.1%; for OAV-3, 86.5 and 11.0%; for OAV-4, 98.4 and 13.2%; for BAV-2, 97.6 and 22.4%; for BAV-3, 11.4 and 3.8%; and for BAV-7, 81.6 and 4.5%. The results indicate that adenovirus infections were widespread in the sheep population and that the prevalence of active infection based on seroconversion rates was approximately 45%.

The susceptibility of 50 clinical Escherichia coli isolates to various antibacterials, including cefoxitin and cefotetan was ascertained, and the minimal inhibitory concentration (MIC) of cefoxitin and cefotetan for each of these isolates was determined. The pharmacokinetics of cefoxitin and cefotetan after a single IV or SC injection (30 mg/kg of body weight) were determined in 4 dogs. Of the 50 E coli isolates, 98% were susceptible in vitro to cefotetan, 90% were susceptible to cefoxitin, and 88% were susceptible to gentamicin. The MIC that would inhibit the growth of 90% of the E coli isolates (MIC90) was 0.25 micrograms/ml for cefotetan and 4 micrograms/ml for cefoxitin. Plasma cefotetan concentrations remained above MIC90 for (mean SD) 8.2 +/- 1.72 hours and 13.52 +/- 0.28 hours after IV and SC administration, respectively. Plasma cefoxitin concentrations remained above MIC90 for (mean +/- SD) 5.37 +/- 1.18 hours and 7.95 +/- 0.71 hours after IV and SC administration, respectively. We concluded that cefotetan was superior to cefoxitin in activity against E coli in vitro. We recommend that cefotetan be given at a dosage of 30 mg/kg, IV, every 8 hours, or SC, every 12 hours.