A preliminary trial of the sedation induced by intranasal administration of midazolam alone or in combination with dexmedetomidine and reversal by atipamezole for a short‐term immobilization in pigeons

ObjectiveTo assess the sedative and immobilization effect of intranasal administration (INS) of midazolam (MID) without or with INS dexmedetomidine (DXM), and some physiological changes induced by the drugs. The ability of INS atipamezole to reverse the DXM component was also assessed.Study designProspective ‘blinded’ experimental study.AnimalsIn total, 15 pigeons.MethodsPigeons were sedated by INS MID alone at a dose of 5 mg kg⁻¹ (group MID, n = 6) or in combination with INS DXM at a dose 80 μg kg⁻¹ (group MID-DXM, n = 6). Measurements were made of heart rate (HR), respiratory rate (f_R) and cloacal temperature (CT). The degree of sedation was assessed at 15 minutes prior to, immediately after, and at intervals until 100 minutes after drug administrations. Following MID-DXM, INS atipamezole (250 μg kg⁻¹) was administered and the same indices measured 5 and 10 minutes later.ResultsMID had no effect on HR and f_R, and although CT decreased, it remained within physiological range. MID-DXM caused significant falls in HR, f_R and CT that persisted until the end of sedation. Atipamezole antagonized sedation and cardiorespiratory side effects of MID-DXM within 10 minutes of application. In addition, for MID compared to MID-DXM, the lowest sedation scores [10 (7–14) and 10.5 (5–14) versus 2 (1–4) and 2 (1–5)] were achieved in the 10th and 20th minute versus the 20th and 30th minute of the sedation, respectively.Conclusions and clinical relevanceMID alone, given INS had minimal side effects on vital functions but caused inadequate immobilization of pigeons for restraint in dorsal recumbency. MID-DXM caused an effective degree of immobilization from 20 to 30 minutes after administration, at which time birds tolerated postural changes without resistance. Atipamezole antagonized both side effects and sedation, but complete recovery had not occurred within 10 minutes after its application.     

Lack of a type-2 glycosyltransferase in the fish pathogen Flavobacterium psychrophilum determines pleiotropic changes and loss of virulence

Flavobacterium psychrophilum is an important fish pathogen, responsible for Cold Water Disease, with a significant economic impact on salmonid farms worldwide. In spite of this, little is known about the bacterial physiology and pathogenesis mechanisms, maybe because it is difficult to manipulate, being considered a fastidious microorganism. Mutants obtained using a Tn4351 transposon were screened in order to identify those with alteration in colony morphology, colony spreading and extracellular proteolytic activity, amongst other phenotypes. A F. psychrophilum mutant lacking gliding motility showed interruption of the FP1638 locus that encodes a putative type-2 glycosyltransferase (from here on referred to as fpgA gene, Flavobacterium psychrophilum glycosyltransferase). Additionally, the mutant also showed a decrease in the extracellular proteolytic activity as a consequence of down regulation in the fpgA mutant background of the fpp2-fpp1 operon promoter, responsible for the major extracellular proteolytic activity of the bacterium. The protein glycosylation profile of the parental strain showed the presence of a 22 kDa glycosylated protein which is lost in the mutant. Complementation with the fpgA gene led to the recovery of the wild-type phenotype. LD₅₀ experiments in the rainbow trout infection model show that the mutant was highly attenuated. The pleiotropic phenotype of the mutant demonstrated the importance of this glycosyltranferase in the physiology and virulence of the bacterium. Moreover, the fpgA mutant strain could be considered a good candidate for the design of an attenuated vaccine.     

Pre-operative fibrous osteodystrophy and severe,refractory, post-operative hypocalcemia following parathyroidectomy in a dog

A 13-year-old dog exhibited dramatic, radiographic osteopenia consistent with fibrous osteodystrophy secondary to primary hyperparathyroidism. Following parathyroidectomy, the dog developed severe, prolonged hypocalcemia, but was successfully treated and discharged 32 d after surgery. A variety of factors may have contributed to this dog’s hypocalcemia including hypoparathyroidism and hungry bone syndrome.