Contemporary topics in laboratory animal science最新文献

Six common marmosets from a colony of 50 died over a period of 3 weeks, with the predominant finding of gram-negative bacterial septicemia. Four of these animals died peracutely; the other two were found when they were moribund, and they subsequently died despite clinical intervention. Gram-negative bacterial rods were present in the blood vessels of stained tissues from five of the six marmosets. Three marmosets also had severe fibrinopurulent peritonitis. In addition, one of the marmosets with peritonitis also had purulent mesenteric lymphadenitis with large colonies of gram-negative bacterial rods within dialated colonic crypts. Klebsiella pneumoniae was isolated from multiple organs in three of the marmosets. Clinical evaluation of the entire colony identified four marmosets with anorexia, nasopharyngeal discharge and diarrhea. These marmosets were treated with enrofloxacin immediately, and they responded well. K. pneumonia could not be cultured from nasal or fecal samples obtained from the colony animals. Because of the peracute nature of the disease, animals often die before exhibiting clinical symptoms, and antibiotics are seldom helpful. In this outbreak we saw both of the major forms of Klebsiella infection in common marmosets: the peracute form with bacteremia and minimal inflammatory reaction around blood vessels, and the chronic form with bacteremia, fibrinopurulent peritonitis, and mesenteric lymphadenitis.

The purpose of this study was to evaluate the baboon as an animal model for evaluating red blood cell (RBC) preservation by comparing the 24-h posttransfusion survival of baboon RBCs preserved in citrate phosphate dextrose/ADSOL (CPD/AS-1) solution at 4 degrees C for 49 days to that of human RBCs preserved under similar conditions. CPD/AS-1 originally was approved by the Food and Drug Administration for 49-day storage of RBCs, but this period subsequently was reduced to 42 days. Adult male baboons (Papio anubis and P. cynocephalus) were autotransfused with RBCs that had been harvested using CPD and that had been resuspended and stored in AS-1 solution at 4 degrees C for as long as 49 days. The 24-h posttransfusion survival was measured using the 51Cr/125I-albumin method. The 24-h posttransfusion survival (mean +/- standard deviation) was 74% +/- 7% for seven units of CPD/AS-1-treated RBCs stored for 35 days, 65% +/- 15% for 12 units stored for 42 days, and 43% +/- 16% for seven units stored for 49 days. The mean 24-h posttransfusion survival rate for autologous baboon RBCs stored in CPD/AS-1 at 4 degrees C for 35 days (74%) was similar to that for autologous human RBCs stored in a similar manner. Further storage for 42 and 49 days resulted in lower values for baboon RBCs compared with human RBCs.

Tribromoethanol typically is used alone as a general anesthetic agent for rodent surgeries. In the present study, the alpha2-adrenergic agonists xylazine and medetomidine were combined with tribromoethanol to examine their use as alternate and safe anesthetic regimes in rats. We also tested the effect of atipamezole, an alpha2-adrenergic antagonist, in reversing the anesthetic effect of the tribromoethanol-medetomidine combination. Male Sprague-Dawley rats were used to evaluate the effects of tribromoethanol (400 mg/kg intraperitoneally [i.p.]) or tribromoethanol (150 mg/kg) and medetomidine (0.5 mg/kg i.p.). Tribromoethanol (400 mg/kg)-treated rats were anesthetized for an average of 10 min, whereas rats that received tribromoethanol (150 mg/kg) and medetomidine (0.5 mg/kg) remained anesthetized for an average of 55 min. Recovery time was approximately 6 min for the tribromoethanol (400 mg/kg) group compared with 21 min for the animals that received tribromoethanol and medetomidine. In a second study, three groups of rats were given tribromoethanol (150 mg/kg) and medetomidine (0.5 mg/kg). Group 1 received atipamezole (an alpha2-antagonist; 2.5 mg/kg i.p.) 10 min after anesthetic induction, and group 2 received the same dosage at 20 min post-induction. Group 3 was allowed to recover without atipamezole treatment. The anesthetic effects in animals from groups 1 and 2 were reversed after administration of atipamezole, whereas group 3 remained anesthetized. This study demonstrates the safe and effective use of tribromoethanol-medetomidine as an anesthetic in the rat.

This reports the in vitro portion of a study designed to establish guidelines for the preparation, storage, and use of tribromoethanol (TBE). We evaluated: 1) the purity of TBE powder from three suppliers; 2) nine methods of preparation of a 25-mg/ml (working) solution for formation of particulates and breakdown products; 3) formation of particulates and breakdown products and pH change in 1-g/ml (stock) solutions and working solutions stored under four conditions (25 degrees C and 5 degrees C in light and in dark); and 4) stock and working solutions of TBE that caused lethal effects in mice. These objectives were met by using nuclear magnetic resonance spectroscopy, gas chromatography-mass spectroscopy, particle-size and turbidity analyses, and pH strips. TBE powder from three suppliers varied in purity. No significant differences in breakdown product formation, particle size, or turbidity were noted between the nine preparation methods evaluated. Stock solutions and the working solution stored at 5 degrees C in the dark maintained a pH of 6.5 to 7.0, whereas the pH dropped for all other working solutions. A low level of dibromoacetaldehyde (DBA), a potential breakdown product reported to cause toxic effects, was detectable in all newly prepared solutions. Regardless of the storage condition or pH, DBA concentration did not increase measurably in any of the solutions after 8 weeks. The stock and working solutions that demonstrated lethal effects in mice had a pH of 6.5 and did not differ notably from newly prepared, non-lethal solutions, when evaluated for DBA. A decrease in pH could not be correlated to an increase in DBA or potential lethality, as suggested in the literature. The toxicity associated with the lethal TBE in this study appears to be a result of a chemical reaction or breakdown product that has not yet been reported.

Rodent pinworms rarely cause clinical disease, but infestation can affect experimental results. Our facility maintained a colony of Wistar rats for behavioral pharmacology studies that had been infested with Syphacia muris for > 15 years. The laboratory in which the animals were housed encompassed several rooms and contained a variety of complex behavioral equipment, including > 60 operant chambers. Several prior attempts to eliminate the pinworms were unsuccessful because of inadequate duration of treatment and incomplete environmental decontamination. Many of the rats in this colony were food-restricted as part of behavioral studies. Pinworms were eliminated from these animals by treating them with 450 ppm fenbendazole-containing feed for 3 consecutive weeks followed by 6 weeks of alternating every other week with standard rodent diet. Rats not on food restriction protocols were treated on the same schedule with 150 ppm fenbendazole-containing feed. Environmental decontamination of eggs from the behavioral equipment was not attempted. One year after treatment, the colony has remained free of S. muris. We adapted previously published protocols to our situation, including the problem of food-restricted rats and unfeasible environmental decontamination, to eradicate S. muris from our colony.

Murine fur mites are reported to exist in over one-third of research institutions and can be problematic to eliminate. Current treatment strategies can be labor-intensive, toxic, and may confound research studies. The ideal method would be technically simple, safe, effective, and relatively inexpensive. When we found that mice from a noncommercial vendor were infested with Myocoptes musculinus, the animals were treated topically with Cydectin pour-on (containing moxidectin 0.5%) at 0.5 [corrected] mg/kg. After one treatment, mites were eradicated from all infested mice. No toxic effects or clinical signs of illness were observed in the mice. To the authors' knowledge, this is the first report of topical moxidectin as a treatment for murine acariasis.

To perform mechanical ventilation of mice in the absence of highly expensive commercially available devices, we developed a membrane-pump-driven respirator and studied its practicability. The continuous airflow generated by the membrane pump was changed into an intermittent flow by using a multifunction timer. Tidal volume was adjusted by a rotary dimmer regulating the electric power onto the pump. The expiration air left the circuit through openings at the tube connection. Mice were ventilated with room air for 5 h with a tidal volume of approximately 200 muL. In group 1 (n = 6), ventilation was performed with a frequency of 110 min-1, in group 2 (n = 6) with a frequency of 150 min-1. Spontaneously breathing anesthetized mice (n = 6) served as controls. In addition we performed single-lung open-chest ventilation for 1 h in two animals. The parameters of arterial blood gas analyses were within the normal range except for moderate hyperventilation in group 2. Single-lung ventilation led to a significant decline (P < 0.05) of pO2 and SO2, whereas the pCO2 remained within the normal range. Respiratory rate, tidal volume and pressure limitation can be adjusted for optimal ventilation. In addition, the device provides a minimalized dead space and impedes potential alveolar damage caused by negative pressure generated by spontaneous inspiration during positive-pressure ventilation.

This study, performed in conjunction with an in vitro evaluation of tribromoethanol (TBE), consisted of three trials with three objectives. The first objective was to compare anesthetic efficacy and short-term pathologic findings of TBE, ketamine-xylazine (K-X), and sodium pentobarbital (NaP). The second objective was to evaluate how changes of TBE that occur during the perceived most favorable and least favorable storage conditions (8 weeks at 5 degrees C in the dark [5D] and 25 degrees C with exposure to light [25L], respectively) affect anesthetic efficacy and short-term pathology when compared to newly prepared TBE. The third objective was to perform a 6-week clinical assessment of animals that received newly prepared TBE. All animals that received TBE (400 mg/kg) and 14 of 15 that received K-X (K, 120 mg/kg; X, 16 mg/kg) were anesthetized, as defined by loss of pedal reflex. In comparison, only 8 of 15 animals administered NaP (60 mg/kg) were anesthetized. Anesthetic duration for animals that received K-X was 31.7 min, which was significantly (P = 0.0085) longer than animals that received TBE (18.5 min). Recovery times for TBE and K-X were not significantly different (26.5 and 27.5 min, respectively). Pathologic lesions associated with TBE administration were significantly (P = 0.001) greater than those associated with K-X. NaP was not associated with any pathologic lesions. The pH of newly prepared and 5D TBE was 6.5 to 7.0, whereas that for 25L TBE was 3.0. Anesthetic induction, duration, recovery times, and pathologic lesions were not significantly different, regardless of the pH or storage condition of the solution. It was noted, however, that the average anesthetic duration for animals administered newly prepared TBE in the second trial was longer (37.7 min) than the first trial that used newly prepared TBE. For the third trial (long-term clinical assessment), the average anesthetic duration for TBE was 46.5 min, significantly (P < 0.025) longer when compared to the first trial that used newly prepared TBE. During the third trial, 10 animals were found dead or moribund. All animals that were found moribund were necropsied and found to exhibit a marked ileus. Because of the variability in anesthetic effectiveness, pathology, and morbidity and mortality associated with the use of TBE, we do not recommend the use of this anesthetic agent in ICR mice.