Detection of Vancomycin-Resistant Enterococcus Spp. (VRE) from Poultry.

Twenty-eight isolates of E. faecalis and 5 isolates of E. hirae were isolated from chicken samples obtained from markets in Sri Serdang, Selangor. They were tested for susceptibility to vancomycin and other antimicrobial agents. All of the isolates showed multiple resistance to the antibiotic tested. All Enterococcus spp. were resistant (100%) to ceftaxidime, cephalothin, erythromycin, gentamicin, kanamycin, nalidixic acid and streptomycin. Resistance was also observed to norfloxacin (97%), tetracycline (91%), penicillin (85%), bacitracin (82%), chloramphenicol (61%) and the least resistance was to ampicillin (27%). High prevalence to vancomycin resistance was detected among the E. faecalis (27of 28) and E. hirae (4 of 5) isolates. The multiple antibiotic resistance index ranging between 0.64 to 1.0 showed that all strains tested originated from high-risk contamination. Plasmid profile analysis of Enterococcus spp. revealed plasmid DNA bands ranging in size from 1.3 to 35.8 megadalton but some isolates were plasmidless. No correlation could be made between plasmid patterns and antibiotic resistance.

Random amplified polymorphic DNA analysis to differentiate strains of Vibrio vulnificus isolated from cockles and shrimps.

A random amplified polymorphic DNA (RAPD) fingerprinting method has been developed to differentiate Vibrio vulnificus strains isolated. Twenty-nine strains isolated from cockles and twenty-one strains isolated from shrimps were analyzed. A total of 10 primers were screened with Vibrio vulnificus strains to identify those capable of generating DNA polymorphisms and two primers were selected. Primer GEN 1-50-01 and GEN 1-50-08 produced polymorphisms in most strains tested, with the band sizes ranging from 10.0 to 0.25 kb pair. Dendrogram analysis showed that primer GEN 1-50-01 produced 10 clusters and 24 single strains at a 40% similarity, whereas primer GEN 1-50-08 produced 11 clusters and 20 single strains at a 40% similarity. This study revealed the potential use of PCR fingerprinting in epidemiological studies.

Reversal of medetomidine sedation in sheep by atipamezole and yohimbine.

The antagonistic effect of the alpha 2-adrenoceptor antagonists atipamezole and yohimbine on medetomidine-induced sedation was studied in male Awassi sheep. The animals were sedated with an im injection of 40 micrograms medetomidine/kg bw. After recumbency, the sheep were injected iv with either 5 ml physiological saline solution (control), 0.2 mg atipamezole/kg or 0.2 mg yohimbine/kg. The saline-treated animals remained sedated and recumbent for 61.3 +/- 3.0 (mean +/- SE) min. Atipamezole or yohimbine significantly reduced the recumbency period to 2.8 +/- 0.9 or 4.3 +/- 0.9 min, respectively. Atipamezole or yohimbine significantly increased the medetomidine-induced reductions in the heart rate, respiratory rate and ruminal contractions. Rectal temperature was neither affected by medetomidine nor by the subsequent administrations of antagonists. These data suggest the usefulness of atipamezole or yohimbine in antagonizing the sedative effects of medetomidine in sheep.

Medetomidine sedation in sheep.

The sedative effect of medetomidine was evaluated in 6 male Awassi sheep. Medetomidine at 40 micrograms/kg, i.m. induced sedation and recumbency in the sheep within 9 +/- 1 and 17 +/- 4 minutes, respectively. The duration of recumbency was 58 +/- 1 minutes. Medetomidine produced good analgesia and marked muscle relaxation in the recumbent animals for 30 to 45 minutes. The side effects of medetomidine were bradycardia, respiratory depression, stasis of the rumen with tympany, salivation and polyuria. The animals recovered from the sedative and side effects of medetomidine 1.5 to 2 hours after gaining the righting reflex without any apparent adverse effect. The results suggested that medetomidine could be a useful sedative analgesic in sheep.

Effect of diphenhydramine on organophosphorus insecticide toxicity in mice.

Male mice were treated orally with the organophosphorus insecticides fenamiphos and dichlorvos at 10 and 150 mg/kg, respectively. The insecticides produced signs of toxicosis characteristic of cholinesterase inhibition, and induced death in all treated mice. Pretreatment of mice with diphenhydramine HCl (20 and 30 mg/kg, subcutaneously) 15 min before either insecticide significantly (P less than 0.05) reduced the incidence of toxic manifestations (excessive salivation, Straub tail, and whole body tremor), delayed the onset of death, and increased the percentage of survivors. Doses of diphenhydramine less than 20 mg/kg were not so effective. The data indicated a protective property of diphenhydramine against organophosphorus insecticide-induced toxicosis.

Interaction of diphenhydramine with cholinesterase inhibitors in mice.

Physostigmine (1.5 mg/kg, s.c.) and neostigmine (1.0 mg/kg, s.c.) injection into male mice produced signs of toxicosis characteristic of cholinesterase inhibition and evoked death in 95 and 94% of the animals respectively. Diphenhydramine injections (5-30 mg/kg, s.c.) 15 min before physostigmine or neostigmine significantly increased the latency period to onset of death and the percentage of survivors. Diphenhydramine injection (20 mg/kg, s.c.) between -30 and +2 min (but not at +5 and +10 min) relative to physostigmine prevented lethality in 100% of the animals. The data indicated that diphenhydramine which possesses anticholinergic effects protected mice against physostigmine- and neostigmine-induced toxicosis.