Efficacy of abamectin against gastrointestinal tract nematodes and lungworms of cattle was determined in 4 experiments. The first 2 experiments were controlled trials in which efficacy was determined at necropsy in calves with either experimentally induced (n = 14) or naturally acquired (n = 16) infections. Half the calves in each experiment were treated with abamectin (200 micrograms/kg of body weight, sc), and half were left untreated as controls. Efficacy was > 99% against adult stages of Dictyocaulus viviparus, Haemonchus placei, Ostertagia ostertagi, Trichostrongylus axei, Cooperia punctata, Trichuris discolor, and C oncophora, and was 92.4% against Nematodirus helvetianus. The second 2 experiments were clinical trials in which efficacy was determined by fecal egg count reduction in naturally infected yearling heifers (n = 75) or 2-year-old heifers (n = 75). Within replicates of 5, 4 heifers were assigned at random to treatment with 200 Kg of abamectin/kg and 1 was left untreated as a control. Abamectin was 100% effective in eliminating strongylate nematode eggs from the feces of these heifers. In all experiments, adverse reactions were limited to small, clinically unimportant injection site swellings in 29% of abamectin-treated calves. Abamectin was judged to be safe and effective in these trials.

The safety of moxidectin 1% injectable anthelmintic (0.6 mg/kg of body weight, 3 times the recommended dose) was evaluated in 145 reproductively sound, beef cows undergoing estrous cycle. Five treatment groups received moxidectin 1% injectable at specific times relative to a synchronized estrus (day 0): preovulatory treatment (day -2, treatment group 1), treatment at ovulation (day 0, group 2), and treatment after ovulation (days 7, 14, and 28, group 3, 4, and 5, respectively). Two groups of control cows received an injection of vehicle only at times corresponding to treatment in the other groups (6 at days -2, 7, and 28; 7 at days 0, 7, and 14). A final control group (8) received neither product or vehicle. Adverse clinical reactions were not observed in moxidectin- or vehicle-treated cows. Cows were bred by artificial insemination between days -2 and 25 and, subsequently, by breeding-sound bulls through day 65 of the study. Treatment and control groups did not differ in pregnancy rate or time to conception. Moxidectin (at 3 times the therapeutic dose) did not have deleterious effects on cow reproductive performance as examined (eg, at folliculogenesis, ovulation, and the early embryonic phase of development).

The capability of diclazuril, a benzeneacetonitrile anticoccidial agent, to inhibit development of tachyzoites of Toxoplasma gondii was examined in cultured human foreskin fibroblast cells and in Hsd:ICR mice. Treatment of infected cell cultures with 10.0, 1.0, 0.1 or 0.01 micrograms of diclazuril/ml for 3 days resulted in > 99% reduction in tachyzoite counts, compared with controls. Treatment with 0.005 micrograms of diclazuril/ ml resulted in > 97% reduction in tachyzoite counts, compared with controls. Treatment of host cells with 10.0, 1.0, 0.1, and 0.01 micrograms of diclazuril/ml for 24 hours prior to tachyzoite inoculation resulted in 97, 31, 0, and 0% reduction in tachyzoite counts, compared with controls, respectively, 3 days after inoculation. All mice that were treated orally with 10.0 mg of diclazuril/kg of body weight and 80% of mice treated orally with 1.0 mg of diclazuril/kg 1 day prior to and for 10 days after tachyzoite inoculation were protected against acute toxoplasmosis. Mice treated with 10.0 mg of diclazuril/kg did not develop protective immunity, whereas mice treated with 1.0 mg of diclazuril/kg survived challenge exposure.

Exogenous creatinine clearance rate was determined in 8 partially (approx 75%) nephrectomized dogs fed 2 concentrations of dietary sodium, beginning 9 weeks after partial nephrectomy was performed. In a double crossover design, dogs were then fed low-sodium diet (0.18% sodium on a dry-weight basis) or high-sodium diet (1.3% sodium on a dry-weight basis) in 2 sequences (L/H/L or H/L/H) for 3 consecutive 4-week observation periods. Glomerular filtration rate (GFR) was measured by exogenous creatinine clearance before and after partial nephrectomy, and every 2 weeks during the experimental diet periods. Initial mean +/- SD GFR (3.76 +/- 0.78 ml/min/kg of body weight) decreased precipitously after nephrectomy (1.25 +/- 0.45 ml/min/kg); however, during the postnephrectomy and experimental diet periods, GFR gradually increased in all dogs to nearly half the prenephrectomy values (1.87 +/- 0.22 ml/min/kg). Significant differences in GFR were not observed when dogs were fed the IM or the H/L/H sequence. Therefore, it was concluded that abrupt change from high dietary sodium (1.3%) to restricted dietary sodium (0.18%), or vice versa, does not cause deterioration of renal function in dogs with moderate renal impairment. However, caution should be used in extrapolating these findings to dogs with clinically evident (azotemia, isosthenuria) renal failure.

Packed cell volume and plasma total protein (TP), serum albumin (Alb) and globulin (Glb), and plasma ionized calcium (PCa) concentrations, blood viscosity (BV), and plasma viscosity (PV) were measured in 42 horses at rest and after the cross country jumping phase of a horse trial competition. The BV and Pv were determined at 6 shear rates (230, 115, 46, 23, 11.5, 5.75 s 1), using a digital rotational cone and plate microviscometer. A paired t-test was used to determine differences between PCV, TP, Alb, Glb and PCa values at rest and after exercise. The PCV, TP, Alb, and Glb values increased (P < 0.05) in horses after exercise. The PCa concentration decreased (P < 0.05) in horses after exercise. Mean BV and Pv in the 42 horses at rest and after exercise were fitted to an asymptotic function. Significant (P < 0.05) correlation at aH shear rates was seen between BV at rest and PCV, TP, Alb, Glb, and PCa values at rest; and between BV after exercise and PCV, TP, Alb, Glb, and PCa values after exercise. Significant correlation was not seen between PV at rest and TP, Alb, Glb, and PCa at rest, or between PV after exercise and TP, Alb, Glb, and PCa concentrations after exercise at any shear rate.

The role of porcine parvovirus (PPV) in inducing reproductive failure in swine has been extensively documented. However, information is not available as to the risk of ppv transmission by embryo transfer. Using the polymerase chain reaction (PCR) technique, PPV-specific DNA was detected in association with 4-day-old porcine embryos incubated in vitro in the presence of NADL-8 strain of PPV, despite attempts to rid the embryos of virus by either washing or treatment with pronase or trypsin. The presence of PPV in embryos collected from acutely infected swine was not detected by PCR, although PPV DNA was detected in the proximal portion of the reproductive tract during the early stages of infection. Viral-specific nucleic acid was not detected in embryos transferred from infected donors to seronegative recipients and retrieved and assayed on the 15th and 32nd days of gestation. Results of the use of PCR to detect PPV associated with swine female reproductive tract and embryos ascribe minimal risk to the transmission of PPV to seronegative recipients through embryo transfer.

Parenchymal cells were isolated from the liver of male calves, and monolayer cultures formed were treated with glucocorticoids to examine whether haptoglobin, appearance of which is associated with hepatic lipidosis (fatty liver) in cattle, is induced by steroid hormones. Without addition of dexamethasone, only trace amounts of haptoglobin were detected in culture medium. With addition of dexamethasone (10(-12) to 10(-4)M), considerable amounts of haptoglobin were released into the medium. Maximal release was observed at concentrations of 10(-8) to 10(-6)M dexamethasone. Haptoglobin release was similarly induced by cortisol, although the effect was less potent than that of dexamethasone. Actinomycin D (a known protein synthesis inhibitor) dose-dependently reduced amounts of haptoglobin released in response to 10(-8)M dexamethasone. Dexamethazone also induced annexin I, which is known to be synthesized in response to glucocorticoids. Dexamethasone treatment resulted in reduced protein kinase C activity in the cell cytosol, which has been shown to be an early event in dexamethasone-treated cells. Other than glucocorticoids, estradiol induced haptoglobin release, whereas progesterone was less effective. The association of haptoglobin with hepatic lipidosis can be reasonably explained by the fact that haptoglobin production by the liver is induced by glucocorticoids and estradiol, and these steroid hormones are triggers for development of hepatic lipidosis in cattle.

The alpha 1-proteinase inhibitors of trypsin, Spi1, Spi3A, and Spi3B, in bronchoalveolar lavage fluid (BALF) and serum of horses were separated by electrophoresis, and their proportions were quantified in 12 control horses and 12 with chronic obstructive pulmonary disease (COPD). A significantly lower proportion of Spi3B (P < 0.05) and higher proportion of Spi1 (P < 0.02 to P < 0.01) were detected in BALF, compared with serum, in control and COPD-affected horses and appeared to be attributable to reduced Spi3 activity in BALF. There was no significant difference between the control and COPD groups in this respect, indicating that the decrease in Spi3 may be a physiologic phenomenon. The differences observed may be associated with proteolytic damage to or preferential complex formation by Spi3.

Anthelmintic efficacy of doramectin, a macrocyclic lactone of the avermectin family, was evaluated against larval parasitic nematodes in calves. The investigational product was given sc at a dosage of 0.2 mg/kg of body weight to 10 calves infected 6 days previously with third-stage larvae of the genera Haemonchus, Ostertagia, Cooperia, and Nematodirus. Ten additional calves with identical larval exposure were given saline solution SC also at 6 days after inoculation, and served as the nonmedicated controls. At 14 or 15 days after treatment, the calves were slaughtered in complete replicate for nematode recovery and subsequent quantifications. In comparing nematode numbers at necropsy for the saline- and doramectin-treated groups, nematocidal effectiveness as directed against fourth-stage larvae was: 100% for Haemonchus placei and Cooperia spp, > 99% for Ostertagia ostertagi, and 64.5% for Nematodirus helvetianus. All treatments were easily administered, and adverse behavioral or tissue reactions were not seen to result from doramectin administration.

Efficacy of fenbendazole at 2 dosages for treating naturally acquired giardiasis in dogs was assessed. Giardia cysts were not detected in the feces of 6 of 6 group-1 dogs (as determined by use of the zinc sulfate concentration technique) after fenbendazole treatment (50 mg/kg of body weight, PO, q 24 h, for 3 doses). Cysts were not detected in the feces of 6 of 6 group-2 dogs after fenbendazole treatment (50 mg/ kg of body weight, PO, q 8 h, for 3 days). However, cysts were not detected in the feces of only 1 of 6 group-3 (nontreated control) dogs. Signs of toxicosis were not observed in any dog. These results indicate that the current label dosage (for the treatment of Toxocara canis, Toxascaris leonina, Ancylostoma caninum, Uncinaria stenocephala, Trichuris vulpis, and Taenia pisiformis, but not Giardia spp) of fenbendazole (50 mg/kg, PO, q 24 h, for 3 doses) is also effective for treating giardiasis in dogs.