Non-surgical correction of infection-induced struvite uroliths and a vesicourachal diverticulum in an immature dog

Infection-induced struvite urocystoliths and a vesicourachal diverticulum affecting a nine-week-old male mixed breed dog were eliminated with the aid of dietary and antimicrobial therapy. Urocystoliths dissolved within nine days of initiation of medical therapy, while the vesicourachal diverticulum resolved within 39 days of initiation of therapy.     

An Outbreak of Pseudomonas Mastitis in Dairy Cows

An outbreak of mastitis in a dairy herd is described in which the causative organism was Pseudomonas aeruginosa. Cases occurred either in dry cows or in animals which had very recently calved. The fact that all four quarters were involved is a very strong indication that the bacteria had been introduced in the dry cow therapy.     

Surgical removal of canine uroliths

Surgery is indicated for patients with obstructive uropathy; calcium oxalate, calcium phosphate, silica, and perhaps cystine uroliths; uroliths refractory to medical dissolution; nephrolithiasis and progressive renal dysfunction; anatomic defects predisposing to urinary tract infection; and problems precluding medical management. The goals of surgical management include removal of all uroliths while preserving organ function, eliminating partial or complete obstruction to urine outflow, and correction of anatomic abnormalities that predispose the patient to infection and or urolithiasis.     

A model aerosol exposure system for induction of porcine Haemophilus pleuropneumonia.

One group of six pigs and another group of three pigs were separately exposed in a polyethylene enclosed chamber for ten minutes, respectively, to Haemophilus pleuropneumoniae serotype 1 and Bacillus subtilis aerosols generated by an ultrasonic nebulizer. Haemophilus pleuropneumoniae and B. subtilis were deposited throughout the lungs immediately following aerosol exposure. The number of H. pleuropneumoniae and B. subtilis deposited varied within and between lungs in each group. The mean numbers of both organisms deposited in the posterior (caudal and accessory) lobes were significantly greater than those in the anterior (cranial and middle) lobes (P less than 0.001). The four principals that received H. pleuropneumoniae aerosols and the two contact controls developed fatal fibrinous pneumonia which simulated that seen in natural infections. Since this exposure system consistently resulted in clinical disease it has good potential as a model for the study of pathogenesis of the disease and more specifically for the evaluation of vaccines.     

Is sulfotep a proctolin receptor antagonist?

Proctolin-induced, dose-dependent (10^?8-2 × 10^?6 M) contraction of the isolated foregut of Schistocerca gregaria was antagonised non-competitively by sulfotep (2 × 10^?6-10^?5 M). A higher dose of sulfotep (5 × 10^?5 M) caused restoration of the proctolin dose-response curve to its control value. Neostigmine (10^?5 M) caused non-competitive inhibition of proctolininduced tissue contraction. Increasing the dose of neostigmine to 10^?4 M restored the proctolin response to control values. Sulfotep (10^?5 M) and neostigmine (10^?4 M) caused inhibition of acetylcholinesterase (AChE) activity in tissue homogenates obtained from guts pretreated with either drug for 20 min. The stimulatory effect of sulfotep (5 × 10^?5 M) on proctolin-induced gut contraction was abolished by pretreatment of tissues with atropine (10^?6 M). Under these conditions, 5 × 10^?5 M sulfotep caused further antagonism of the action of proctolin. The results suggest that sulfotep is a proctolin receptor antagonist in the locust foregut. However, higher concentrations inhibit tissue AChE activity, thereby allowing endogenous acetylcholine to activate muscarinic receptors. This leads to enhanced tissue contractility which masks the antagonistic effect of sulfotep on proctolin-induced contraction.     

Actions of formamidines,local anesthetics,octopamine and related compounds upon the electrical activity of neurohaemal organs of the stick insect (Carausius morosus) and sense organs of fly larvae (Musca domestica; Calliphora erythrocephala)

The pesticides, chlordimeform and amitraz, and their metabolites, demethylchlordimeform, N¹-(2,4-dimethylphenyl)-N-methylformamidine, and 2,4-dimethylformanilide, are effective at concentrations as low as 3 μM in raising the firing rate of endogenously active neurosecretory fibres in the isolated neurohaemal organs of Carausius morosus. Molecules such as bunamidine and cetrimide, with cationic detergent properties, produced sporadic bursting which did not elevate the overall firing rate to any great extent. Indeed, bunamidine could induce complete block of action potentials at concentrations as low as 30 μM. The local anesthetics, procaine, lidocaine, and benzocaine, do not induce block of activity at least up to a level of 1 mM. They have no effect at concentrations lower than 100 μM. Between 100 μM and 1 mM lidocaine and benzocaine produce a small increase in firing rate. Procaine produced a pronounced increase in the frequency of firing. The phenolic amines, octopamine, synephrine, and tyramine, markedly increased electrical activity. The catecholamines, dopamine, noradrenaline, and adrenaline, by contrast, only produced a weak excitation. Neither α- nor β-adrenergic blocking agents were effective in antagonizing the electrical activity induced by chlordimeform or phenolic amines until relatively high concentrations of about 1 mM were used. Chlordimeform was able to induce high-frequency bursts from sense organs associated with the epidermis and body-wall musculature in larvae of Musca domestica and Calliphora erythocephala. Octopamine did not induce any similar bursting activity in these sense organs. These results are discussed in relationship to current views on the mode of action of the N-aryl amidines. It is concluded that the excitatory effects of these compounds upon neurohaemal organs and sense organs are more likely to result from a direct action upon voltage sensitive channels of the nerve membranes, rather than by an effect mediated by interactions with octopamine receptors.     

Canine primary hyperparathyroidism and its association with urolithiasis

Primary hyperparathyroidism results from autonomous secretion of parathyroid hormone by a single or multiple parathyroid glands. Clinical signs result from various combinations of hypercalcemia, hypercalcemic nephropathy, urolithiasis, or mobilization of calcium and phosphorus from bone. Following parathyroidectomy, the prognosis for dogs with primary hyperparathyroidism is good if the disorder is diagnosed before renal disease is advanced.