Continuous, low-dose oral exposure to sodium chlorate reduces fecal generic Escherichia coli in sheep feces without inducing clinical chlorate toxicosis.

Our objectives were to determine an effective, yet safe, daily dose of sodium chlorate for reducing fecal shedding of generic Escherichia coli in mature ewes. In a completely randomized experimental design, 25 Targhee ewes (age ∼ 18 mo; BW = 62.5 ± 7.3 kg, mean ± SD) were assigned randomly to 1 of 5 sodium chlorate treatments, which were administered in the drinking water for 5 consecutive days. Treatments were control group (no sodium chlorate) and 4 targeted levels of daily sodium chlorate intake: 30, 60, 90, and 120 mg · kg(-1) BW · d(-1) for 5 d. Individual ewe ad libitum intake of water (with treatments) was measured daily, and BW was measured at the beginning of and 15 and 51 d after the 5-d treatment period. Serum chlorate, whole blood methemoglobin and packed-cell volume (PCV), and fecal generic E. coli and general Enterobacteriaceae coliforms were measured from corresponding samples collected at the end of the 5-d treatment period. Average daily intakes of sodium chlorate from drinking water treatments were 95%, 91%, 90%, and 83% of the target treatment intakes of 30, 60, 90, and 120 mg · kg(-1) BW · d(-1), respectively. Daily sodium chlorate intake remained constant for all treatment groups except for ewes offered 120 mg NaClO3 · kg(-1) BW · d(-1), which decreased (quadratic; P = 0.04) over the course of the 5-d treatment period. This decrease in sodium chlorate intake indicated that the 120-mg NaClO3 level may have induced either toxicity and/or an aversion to the drinking water treatment. Serum chlorate concentrations increased (quadratic; P < 0.001) with increasing sodium chlorate intake. At the end of the 5-d treatment period, mean (least squares ± SEM) serum chlorate concentrations for ewes offered 30, 60, 90, and 120 mg NaClO3 · kg(-1) BW · d(-1) were 15.6 ± 14.1, 32.8 ± 15.8, 52.9 ± 14.1, and 90.3 ± 14.1 µg/mL, respectively. Whole blood methemoglobin and PCV were similar (P = 0.31 to 0.81) among the control group and ewes offered sodium chlorate. Likewise, BW was not affected by sodium chlorate (P > 0.27). Ewes consuming approximately 55 mg NaClO3 · kg(-1) BW · d(-1) or more (i.e., ewes offered 60, 90, and 120 mg) had a >1.4 log unit reduction in fecal E. coli and Enterobacteriaceae coliforms compared with control ewes. We suggest that for a short-term, 5-d dosing strategy, 55 to 81 mg NaClO3 · kg(-1) BW · d(-1) is an effective, yet safe, daily oral dose range for mature ewes to achieve a 97% to 99% reduction in fecal shedding of generic E. coli.

Sodium chlorate reduces the presence of Escherichia coli in feces of lambs and ewes managed in shed-lambing systems.

Our objective was to establish doses of orally administered NaClO(3) that reduced the presence of generic Escherichia coli in intestines of ewes and neonatal lambs managed in a shed-lambing system. Neonatal lambs (n = 32; age = 7.1 ± 1.2 d; BW = 6.8 ± 1.0 kg) and yearling ewes (n = 44; BW = 74.8 ± 5.6 kg) were used in 2 experiments. In both experiments, lambs and ewes were randomly assigned to 1 of 4 groups, and groups were randomly assigned to 1 of 4 treatments. In Exp. 1, neonatal lambs were given single, aqueous, oral doses of saline (control; NaCl, 30 mg·kg of BW(-1)) or 30, 60, or 90 mg of NaClO(3)·kg(-1) of BW. At 25.9 ± 1.3 h after treatment, lambs were euthanized, and intestinal contents were collected aseptically. In Exp. 2, ewes were given single, aqueous, oral doses of saline (NaCl, 150 mg·kg of BW(-1)) or 150, 300, or 450 mg of NaClO(3)·kg(-1) of BW. At 24.0 ± 0.8 h after treatment, fecal samples were collected aseptically from the rectum of each ewe. For both experiments, generic E. coli were enumerated from intestinal contents and feces within 4 to 12 h after collection. In Exp. 1, the effect (P = 0.08) of NaClO(3) on the presence of generic E. coli in colon contents was dose-dependent. This effect was linear (P < 0.01) and negative, which indicated that as NaClO(3) dose increased, generic E. coli that could be isolated from colon contents decreased. Specifically, lambs dosed with 60 and 90 mg of NaClO(3)·kg(-1) of BW had fewer E. coli cfu·g(-1) of content than control lambs (P < 0.06). Lambs dosed with 90 mg of NaClO(3)·kg(-1) of BW had fewer E. coli cfu·g(-1) of content than lambs dosed with 30 mg of NaClO(3)·kg(-1) of BW (P = 0.09). Sodium chlorate dose did not influence (P = 0.58) the presence of generic E. coli in contents collected from the cecum. In Exp. 2, the effect (P < 0.0001) of NaClO(3) on the presence of E. coli in fecal contents from ewes was dose-dependent. This effect was quadratic (P < 0.0001) and negative; ewes dosed with 150, 300, and 450 mg of NaClO(3)·kg(-1) of BW had fewer E. coli cfu·g(-1) of feces than control ewes. No differences in E. coli cfu·g(-1) of feces were detected between NaClO(3) treatments (P = 0.88 to 0.97). Based on these results, a single oral dose of at least 60 and 150 mg of NaClO(3)·kg(-1) of BW in neonatal lambs and yearling ewes, respectively, significantly decreased the presence of generic E. coli in contents from the lower intestine.

Effect of Lomodex-MgSO(4) in the prevention of reperfusion injury following unilateral testicular torsion: an experimental study in rats.

Fertility in patients treated for unilateral testicular torsion has been shown to be significantly reduced in all the reported series to date, implying that the present-day treatment requires further refinement in the form of adjunct pharmacotherapeutic intervention (Lomodex and MgSO(4)) in addition to scrotal exploration. Prepubertal Holtzman strain rats (35 days old) were used for our study. Two sets were formed with six groups of rats in each set. Rats were treated as follows: group 1, sham-operated group; group 2, torsion (4 h); group 3, torsion + detorsion (1 h); group 4, torsion + ATP-MgCl(2) + detorsion; group 5, torsion + Lomodex-MgSO(4) + detorsion; group 6, torsion + normal saline + detorsion. Whereas the first set of animals was sacrificed immediately at the end of experiment, animals in set 2 were sacrificed 8 weeks after the end of the experiment to look for the development of antisperm antibodies. Parameters studied were thiobarbituric acid reductase (TBAR) assay, histology of testicular tissue, and sperm agglutination test. Student's t-test was used for significance. With detorsion (149.95+/-30.68) there was a significant rise in the TBAR values (P<0.05) compared with torsion (57.39+/-14.47). Treatment with both Lomodex-MgSO(4) (40.74+/-6.39) and ATP-MgCl(2) (48.30+/-18.35) yielded TBAR levels comparable to those in the sham group (31.35+/-11.96). Similar injury was also seen on the contralateral testis, with detorsion (114.28+/-10.68) much more detrimental than torsion (40.59+/-15.02) and rescue seen following treatment with Lomodex-MgSO(4) (27.55+/-8.64) as well as ATP-MgCl(2) (38.61+/-12.23). Regarding th histology, with detorsion there was evidence of severe distortion of tubules, with almost all the tubules showing maturation arrest and a few tubules completely devoid of any germinal cells. Treatment with Lomodex-MgSO(4) as well as ATP-MgCl(2) showed preservation of tubular morphology. Our study failed to document the presence of agglutinating antibodies (antisperm antibodies) in any of the groups. Unilateral testicular torsion has bilateral effects and is a form of ischemia-reperfusion injury. Treatment of torsion by detorsion alone does not prevent testicular damage. The results of the present study show that administration of Lomodex + MgSO(4) prior to detorsion results in prolonged testicular salvage with a potential of subsequent improvement in semen quality and fertility and reduction in long-term morbidity. The presence of agglutinating antibodies could not be detected in the present study.

[Pseudo-Acanthosis nigricans in a 12 year old boy after kidney transplantation]. / Pseudo-Acanthosis nigricans bei einem 12 Jahre alten Jungen nach Nierentransplantation.

Cutaneous lesions under immunosuppressive therapy require a specific diagnostic approach. We present the case of a 12 year old boy who developed pseudo-acanthosis nigricans 3 months after renal transplantation.