A method for quantification of serum total IgE concentration in dogs by use of an ELISA containing monoclonal mouse anti-canine IgE was developed. Microtitration plates were coated with monoclonal mouse anti-canine IgE. Test sera and reference serum dilutions were added, followed by biotinylated monoclonal mouse anti-canine IgE. Avidin-alkaline phosphatase conjugate was added, and color development was measured spectrophotometrically, using a microtitration plate reader. Quantitative results were obtained by assigning to a reference serum a value of 100 IgE units/ml. Absorbance values of unknown samples were converted into IgE units by comparison with a standard curve generated by measurement of reference serum dilutions. Intra- and interassay coefficients of variation were 5 and 7%, respectively, and assay sensitivity was 1 U/ml. The assay was used to establish a normal range for total IgE concentrations in 30 healthy dogs. Total IgE concentration in healthy dogs followed a skewed distribution and ranged from < 1 to 91.2 U/ml, with a geometric mean value of 7.1 U/ml. The IgE concentration was remarkably stable in serum samples subjected to 25 freeze/ thaw cycles or incubation at approximately 25 C (room temperature) for up to 10 days. Comparison of total IgE concentrations in 23 serum samples assayed by use of double-overlay radial immunodiffusion and ELISA yielded correlation coefficient of 0.94. Comparison of the reference serum standard curve with serial dilutions of a purified IgE solution of known concentration yielded a range of values for the IgE unit of 0.7 to 2.0 micrograms.

Thirty-two mixed-breed male and female cats were blocked by sex, arranged by body weight from greatest to least, and allocated to 4 groups of 8 (4 male, 4 female) cats, using random numbers. Cats in each of 3 groups were treated orally with a 7% suspension formulation of lufenuron at dosage of 15, 30, or 45 mg/kg of body weight. Cats in the fourth group were treated orally with an excipient suspension without lufenuron. Cats were infested with newly emerged, unfed cat fleas (Ctenocephalides felis felis) on days -7 and -3 before treatment and at approximately weekly intervals after treatment. Flea eggs were collected from beneath each cat on selected days before and after treatment and placed in an artificial rearing medium. Flea eggs and medium were kept for 35 days in an insectary to determine effects of lufenuron or excipient suspension on emergence of adults of the F1 generation. Lufenuron was 100% effective in inhibiting development of C felis at all dosages for 11 days after treatment. Thereafter, efficacy exceeded 92% in all dosages groups, On day 32, when the study was terminated, efficacy for each of the dosage groups was: 15 mg/kg, 95.2%; 30 mg/kg, 98.2%; and 45 mg/kg, 99.6%. Adverse reactions or side effects were not observed in cats, regardless of treatment dosage.

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.

Antiparasitic efficacy of ivermectin against migrating Gasterophilus intestinalis was evaluated in 36 treated and 24 nontreated (n = 12) or vehicle-treated (n = 12) ponies experimentally and naturally infected with G intestinalis and naturally infected with G nasalis. Each pony was experimentally infected with 500 G intestinalis lst instars in 2 divided doses on days -14 and -7 before treatment. On day 0, ivermectin was administered at the rate of 200 microgram/kg of body weight by IV (n = 12) or IM injection (n = 12) or given as an oral paste (n = 12). Ponies were euthanatized and necropsied 21 days after treatment. In each nontreated or vehicle-treated pony, late lst-, lst- to 2nd-instar molt, and early 2nd-instars of G intestinalis were found in the mouth, and 2nd- and 3rd instars of G intestinalis and 3rd instars of G nasalis were found in the stomach. Bots were not found in any ivermectin-treated pony and, thus, ivermectin was 100% effective against oral and gastric stages. Adverse reactions were not observed in ponies given ivermectin by IM injection or orally, but 1 pony given the vehicle IV and 1 pony given ivermectin (in the vehicle) IV had an anaphylactic reaction, resulting in death of the ivermectin-treated pony. It was speculated that the adverse reaction was caused by histamines released in response to vehicle components given by IV injection.