Amikacin resistance in Staphylococcus pseudintermedius isolated from dogs.

Staphylococcus pseudintermedius is the most common microorganism isolated from canine pyoderma and postoperative wound infections. The prevalence of methicillin-resistant S. pseudintermedius (MRSP) has increased, and recently, isolates that are resistant not only to methicillin but also to other classes of antibiotic drugs, including aminoglycosides, have become common. A total of 422 S. pseudintermedius isolates collected from 413 dogs were analyzed for amikacin and methicillin resistance using broth microdilution and disk diffusion testing. Methicillin-resistant isolates were significantly (P < 0.0001) more likely to be resistant to amikacin (37%, 31/84) than were methicillin-susceptible isolates (7%, 22/338). Additionally, resistance to non-ß-lactam antibiotics was significantly associated with resistance to amikacin irrespective of methicillin resistance. Among the 422 isolates, 32 that tested positive for amikacin resistance by broth microdilution or disk diffusion testing were investigated further for the presence of aminoglycoside-modifying enzyme genes using multiplex PCR. Of these isolates, 66% (21/32) were methicillin resistant. In contrast to previous studies of Staphylococcus aureus, the most prevalent gene detected was aph(3')-IIIa found in 75% (24/32) of isolates followed by aac(6')/aph(2") and ant(4')-Ia in 12% (4/32) and 3% (1/32), respectively. Understanding the differences in antimicrobial resistance gene carriage between different species of Staphylococcus may improve antimicrobial drug selection for clinical therapy and provide insights into how resistance develops in S. pseudintermedius.

Comparison of the clinical performance of the Acuvue disposable contact lens and CSI lens in patients with giant papillary conjunctivitis.

Anecdotal reports have suggested that the use of disposable contact lenses is an effective treatment for giant papillary conjunctivitis. In a prospective randomized double-masked study, we compared the clinical performance of the Acuvue (Vistakon, Jacksonville, Florida) disposable contact lens to the traditional daily-wear lens of choice, CSI (Pilkington Barnes Hind, Sunnyvale, California), in 37 patients with previously diagnosed giant papillary conjunctivitis who were examined at one-month intervals for six months. A survey questionnaire for grading symptoms disclosed significant improvement in itching, discharge, and blurred vision in both groups early in the study. Evaluation of patient preference showed that the CSI lens was strongly preferred with regard to lens handling (76% vs 8%). In contrast, the Acuvue lens was strongly preferred with regard to lens comfort (62% vs 11%). For the variable of overall lens preference, there was no significant difference between the two lenses (CSI, 43% and Acuvue, 41%). Multiple regression analysis disclosed that both lens comfort (P < .002) and lens handling (P = .05) contributed significantly to the choices made regarding the dependent variable of overall lens preference. Lens comfort (beta = .71) was observed to be approximately 50% more powerful than lens handling (beta = .48). There was no significant difference in the rate or cost of torn lenses between groups, suggesting that the Acuvue lens can withstand the physical manipulation associated with daily-wear use for up to one month. The results of this study suggest that the use of disposable contact lenses for the treatment of giant papillary conjunctivitis is at least as effective as the traditional daily-wear lens of choice.

Argon laser fenestration of a Softperm contact lens.

Contact lens fenestration can increase tear exchange. We describe a case in which a patient with 15 D of against-the-rule astigmatism was fit with a Softperm contact lens but was unable to wear it for more than 1 hour because of corneal edema. After fenestrating the Softperm lens with an argon laser the patient was able to wear her lens for 10 hours without signs of corneal decompensation.

Anion exchanger is present in both luminal and basolateral renal membranes.

Binding of the anion-exchange inhibitor 3H2-labeled 4,4'-diisothiocyano-2,2'-stilbene disulfonic acid (DIDS) to highly purified luminal and basolateral beef kidney tubular membranes was characterized. Specific binding of [3H2]DIDS is present in both luminal and basolateral membranes. Scatchard analysis revealed a Kd for [3H2]DIDS of 5.5 microM and 19.3 microM and a maximal number of binding sites of 10.9 nmol and 31.7 nmol DIDS/mg protein in basolateral and luminal membranes, respectively. To assess the role of this putative anion exchanger on transport we measured 35SO4 uptake by luminal and basolateral membranes. In both luminal and basolateral membranes sulfate uptake was significantly greater in the presence of an outward-directed Cl gradient, OH gradient or HCO3 gradient than in the absence of these gradients. There was an early anion-dependent sulfate uptake of five to ten times the equilibrium uptake at 60 min. The sulfate taken in could be released by lysis of the vesicles indicating true uptake and not binding of sulfate. No significant difference in SO4 uptake was found in the presence and in the absence of valinomycin, indicating that the anion exchanger is electroneutral. The anion-dependent sulfate uptake was completely inhibited by either DIDS or furosemide in both luminal and basolateral membranes. Dixon analysis of HCO3-dependent SO4 uptake by luminal membranes in the presence of different concentrations of DIDS revealed a Ki for DIDS of 20 microM. The similar values of the Kd for [3H2]DIDS binding and the Ki for DIDS inhibition of SO4 uptake might suggest an association between DIDS binding and the inhibition of SO4 transport. In addition, an inward-directed Na gradient stimulated sulfate uptake in luminal but not in basolateral membranes. The Na-dependent sulfate uptake in luminal membranes was also inhibited by DIDS. We conclude that, in addition to the well-known Na-dependent sulfate uptake in luminal membranes, there exists an anion exchanger in both basolateral and luminal membranes capable of sulfate transport.

Adipose tissue mobilization is unaffected by obesifying hypothalamic knife cuts.

Unilateral electrolytic lesions of the medial hypothalamus have previously been reported to spare starvation-induced lipid mobilization from the ipsilateral retroperitoneal fat pad. This suggests that deficient lipid mobilization contributes to the enhanced lipid deposition which results when such lesions are bilateral. In contrast, unilateral parasagittal hypothalamic knife cuts, which also obesify when bilateral, failed to prevent starvation-induced ipsilateral lipid mobilization. This finding indicates that impairment of neurally mediated lipid mobilization is probably neither a necessary nor a sufficient feature of hypothalamic obesity.

Fanconi's syndrome associated with carburetor fluid intoxication.

A patient who ingested carburetor fluid developed methanol intoxication followed by hypouricemia, hypophosphatemia, glycosuria, and hyperchloremic metabolic acidosis. Renal clearances of phosphate, uric acid, glucose, and bicarbonate were found to be elevated indicating the presence of Fanconi's syndrome. The authors postulate that the Fanconi's syndrome observed in our patient was the result of the organic solvents present in the mixture.

The Lee Obesity Index vindicated?

Correlations are reported for rats between the Lee Obesity Index and percent body fat. At weaning, rats were divided into 4 groups; supermarket diet and ovariectomy, supermarket diet and sham surgery. Lab Chow pellets and ovariectomy, and Lab Chow pellets and sham surgery. Four other groups received the treatments as adults. Eighteen and fifteen weeks later, respectively, the rats were measured for Obesity Index and were sacrificed for carcass analysis. The Obesity Index correlated well with percent body fat for animals made obese by diet; but it was not generally reliable for ovariectomized rats or for pellet fed sham operated controls. The Percent body fat also correlated well with body weight and with a simple weight/length ratio for rats made obese by diet. Thus, while the Obesity Index can reliably predict percent body fat, it may be no better at doing this than are some simpler measures.

Evidence for vagal involvement in the eating elicited by adrenergic stimulation of the paraventricular nucleus.

We examined the role of the vagus nerves in mediating the eating and preprandial drinking seen after injection of norepinephrine (NE) into the region of the paraventricular hypothalamic nucleus of satiated rats. Complete subdiaphragmatic vagotomy (confirmed by gastric secretion tests) abolished the NE-elicited eating response, whether the diet used was lab chow, milk, or a milk-chow misture, and attenuated, by 38%, the NE-elicited drinking response. These effects occurred independently of changes in body weight or daily food intake imposed by vagal surgery. The vagotomized rats retained the capacity to rapidly increase eating in response to food deprivation or insulin injection challenges, indicating that the effect of vagotomy on NE-induced eating was not due to some non-specific impairment. Efferent vagal blockade of intact rats with systemic injections of atropine methyl nitrate (0.4 mg/kg) prior to central NE infusions yielded similar results. Finally-selective section of the coeliac branch of the vagus produced a 49% reduction of NE, elicited eating, as compared with a 29% reduction in water intake, while selective section of the gastric plus hepatic vagal branches, leaving only the coeliac branch intact, did not significantly affect either ingestive response. Both of these selectively vagotomized groups displayed an unimpaired capacity to increase food intake in response to systemic insulin injections. These results suggest participation of efferent vagal mechanisms in the adrenergic feeding, and, to a lesser extent, drinking phenomena and are consistent with a particular role for some function under coeliac vagal control (perhaps insulin secretion) in modulating the effects of NE on feeding behavior.

Horizontal stereotaxic atlas of the albino rat brain.

An atlas of the albino rat brain was prepared in the horizontal plane, extending from the olfactory bulbs through the hind brain. It was drawn to the scale of König and Klippel's rat brain atlas so as to be used in conjunction with their atlas. Corresponding histological sections were also prepared.

Circadian rhythms in vasopressin deficient rats.

Circadian rhythms in wheel running and drinking behavior were investigated using heterozygous an homozygous (diabetes insipidus) female Brattleboro rats Despite the lack of vasopressin in the suprachiasmatic nuclei of the diabetic rats, they showed coherent rhythms, both in cyclic light and in constant light. However, the periods of the free-running rhythms were longer for the diabetic rats, they were less active, and, of course, were severely polydipsic. Replacement treatment with systemic infusions of vasopressin reversed the polydipsia but did not affect the other measures.

Hypothalamic knife cut obesity in hyper or hypothyroid rats.

Recent evidence indicates that the paraventricular nucleus of the hypothalamus (PVN) contains both neurons that produce thyrotropic releasing hormone (TRH) and neurons that are destroyed or disconnected by the knife cuts that produce hypothalamic hyperphagia and obesity. This, and other evidence, suggested linkage between thyroid regulation and appetite control. As predicted, hyperthyroidism potentiated and hypothyroidism tempered the weight gains of knife cut rats. However, these effects were due entirely to increased and decreased, respectively, linear growth, not to differences in the degree of obesity. Enhanced linear growth and elevated growth hormone levels are a minor component of the enhanced weight gain of hypothalamically knife cut rats. Most of the weight gain is due to fat deposition. Only the enhanced linear growth and growth hormone aspect appear to possibly be mediated via the thyroid. In addition, obesifying knife cuts did not reduce goiterogenesis in PTU treated rats, as would be expected if the elaboration of TRH were blocked by obesifying knife cuts. Thus, neither TRH nor thyroxine is involved in the etiology of hypothalamic obesity.

Vagal mediation of hypothalamic obesity but not of supermarket dietary obesity.

In two independent experiments, complete subdiaphragmatic vagotomy did not prevent the development of the obesity that results from the addition of highly palatable foods to the diet of rats. The vagotomized animals exhibited only a 1-day delay in the onset of overeating, and this only when first exposed to the tasty diet. In independent tests of the functional completeness of the vagotomies, the vagotomized animals failed to overeat or gain excessive weight on a standard laboratory diet following bilaterally parasagittal hypothalamic knife cuts. Thus, hypothalamic knife-cut obesity requires the integrity of the vagus for its full expression, whereas dietary obesity does not.

Depriving or pair feeding intact controls induces some persisting regulatory deficits similar to those of the recovered lateral rat.

To determine the extent to which acute starvation might contribute to the chronic deficits in regulatory feeding, drinking, and body weight maintenance characteristic of rats with lateral hypothalamic brain lesions, neurologically intact rats were pair-fed (including forced feedings) and pair-watered for 2-4 wk with rats rendered transiently aphagic and adipsic by hypothalamic knife cuts. When the pair-fed rats were subsequently allowed to free-feed, their body weights remained suppressed. In addition, the pair-fed rats failed to eat in response to glucoprivation induced by insulin or 2-deoxy-D-glucose. The pair-fed rat drank less than nondeprived controls, but more than rats with knife cuts, when administered osmotic or volemic challenges to thirst. Other aspects of the recovered lateral syndrome were absent. In a second experiment, intact rats that had recovered from varying durations of semistarvation with or without subsequent forced feedings were tested for regulatory impairments. Deficits in chronic body weight maintenance were found in rats that had been starved and subsequently force-fed. Diminished responses to glucoregulatory challenges were seen in rats that had been starved but not forced-fed as well as in those that had been force-fed but not starved. This impaired eating in response to glucoregulatory challenges abated with repeated testing. Thus, both the acute failure of ingestive behaviors and therapeutic forced feedings can contribute to the impired regulatory eating and driniing that follow recovery from certain types of brain damage.