Urinary aldosterone to creatinine ratio in cats before and after suppression with salt or fludrocortisone acetate

Background: The endocrine diagnosis of primary hyperaldosteronism in cats currently is based on an increased plasma aldosterone to renin ratio, which has several disadvantages for use in veterinary practice. Objectives: To establish a reference range for the urinary aldosterone to creatinine ratio (UACR) and to determine whether oral administration of either sodium chloride or fludrocortisone acetate is effective for use in a suppression test. Animals: Forty‐two healthy cats from an animal shelter and 1 cat with primary hyperaldosteronism from a veterinary teaching hospital. Methods: Morning urine samples for determination of the basal UACR were collected from 42 healthy cats. For the suppression tests, urine samples for the UACR were collected after twice daily oral administration for 4 consecutive days of either sodium chloride, 0.25 g/kg body weight (n = 22) or fludrocortisone acetate, 0.05 mg/kg body weight (n = 15). Results: The median basal UACR was 7.2 × 10^?9 (range, 1.8–52.3 × 10^?9), with a calculated reference range of <46.5 × 10^?9. Administration of sodium chloride resulted in adequate salt loading in 10 of 22 cats, but without significant reduction in the UACR. Administration of fludrocortisone resulted in a significant decrease in the UACR (median, 78%; range, 44–97%; P < .001) in healthy cats. In the cat with an aldosterone‐producing adrenocortical carcinoma, the basal UACR and the UACR after fludrocortisone administration were 32 × 10^?9 and 36 × 10^?9, respectively. Conclusions and Clinical Importance: Using the UACR for an oral fludrocortisone suppression test may be useful for the diagnosis of primary hyperaldosteronism in cats.     

Dog-associated risk factors for human plague

Plague is a rare but often fatal zoonosis endemic to the western United States. Previous studies have identified contact with pets as a potential risk factor for infection. We conducted a matched case-control study to better define the risks associated with pets at both the household and individual levels. Using a written questionnaire, we surveyed nine surviving plague patients, 12 household members of these patients, and 30 age- and neighbourhood-matched controls about household and individual exposures. Overall, 79% of households had at least one dog, 59% had at least one cat and 33% used flea control, with no significant differences between case and control households. Four (44%) case households reported having a sick dog versus no (0%) control households [matched odds ratio, (mOR) 18.5, 95% confidence interval (CI) 2.3-infinity], and four (44%) patients reported sleeping in the same bed with a pet dog versus three (10%) controls (mOR 5.7, 95% CI 1.0-31.6). Within case households with multiple members, two (40%) of five patients slept with their dogs versus none (0%) of 12 healthy family members (P=0.13). The exposures to cats were not significant. Sleeping in the same bed as a pet dog remained significantly associated with infection in a multivariate logistic regression model (P=0.046). Our findings suggest that dogs may facilitate the transfer of fleas into the home and that activities with close extended contacts with dogs may increase the risk of plague infection.     

Injection of the insertion of the deep digital flexor tendon in horses using radiographic guidance

Insertional tendinopathies of the DDFT have been reported both as the sole lesion and as part of a multifocal lesion (Dyson et al. 2003). Computed tomography (CT) and magnetic resonance imaging allow specific diagnosis of deep digital flexor tendon lesions within the hoof capsule; however, direct intralesional treatment of such lesions is difficult because of the hoof's rigid structure. A technique designed to mimic intralesional injection of insertional tendinopathies of the DDFT in the standing horse using radiographic guidance was assessed. Radiographic and contrast CT imaging and sectioning of the limbs confirmed accurate injection in all cases although inadvertant administration of injectate into adjacent structures was also evident.     

Water transport in the kidney and nephrogenic diabetes insipidus

Nephrogenic diabetes insipidus is caused by an inability of the kidney to concentrate urine despite adequate concentration of vasopressin in blood and is characterized by polyuria, polydipsia, and hyposthenuria in the presence of plasma hyperosmolality. Nephrogenic diabetes insipidus is the result of defects in water homeostasis in the kidney. Nephrogenic diabetes insipidus occurs when the kidneys cannot or do not respond to vasopressin. There are 2 categories of nephrogenic diabetes insipidus. Congenital nephrogenic diabetes insipidus is a rare, inherited, irreversible cause of polyuria and polydipsia in humans that is even rarer in animals. Acquired nephrogenic diabetes insipidus is more common and is often secondary to illness or medication that interferes with the action of vasopressin in the renal tubules. Unlike congenital nephrogenic diabetes insipidus, acquired or secondary nephrogenic diabetes insipidus is often reversible with correction of the associated or causative problem.     

An avian model of limb deviation induced by periosteal surgery

A model of limb deviation induced by hemi-circumferential periosteal stripping of the distal tibiotarsus of domestic chicks is described. This model has been developed to study the effects of periosteal stripping on the cellular, mechanical, vascular, and biochemical status of the immature bone and growth plate. It is hoped that such studies may further elucidate the mechanisms involved in altered bone growth following periosteal stripping techniques which are used in human and equine orthopaedics for the management of leg length discrepancies and angular limb deformities respectively (Auer and Martens 1980, Warrell and Baker 1987). Hemi-circumferential periosteal stripping of the left distal tibiotarsus of 28-day-old chicks resulted in significant change in metaphyseal-diaphyseal angle with time, compared to both the controls and the untreated right legs (P<0.0001). This model of limb deviation developed rapidly and consistently, and the procedures were well tolerated by the birds over the short survival time (maximum 28 days).     

Antigen-specific IgG(T) responses in natural and experimental cyathostominae infection in horses

Equine clinical larval cyathostominosis is caused by simultaneous mass emergence of previously inhibited larvae from the mucosa of the colon. Clinical signs include diarrhoea, colic, weight loss and malaise, and in up to 50% of cases, the disease results in death. Cyathostominae spend a large part of their life cycle as larval stages in the intestinal mucosa. Definitive diagnosis is difficult due to the lack of diagnostic methods for pre-patent infection. In the present study, the enzyme-linked immunosorbent assay (ELISA) was used to investigate isotype responses to larval cyathostominae somatic antigen. Measurement of anti-larval IgG(T) responses appeared to have the most immunodiagnostic potential. An increase in IgG(T) response was detected to crude larval antigen by 5 weeks post-infection (PI) in individual infected ponies. Subsequently, IgG(T) responses to larval and adult somatic extracts were examined by Western blotting using sera from experimentally-infected horses and helminth-naive animals (n=6). Two antigen complexes, designated A and B, in larval somatic antigen were recognised specifically by the infected animals by 7 weeks PI. Sera taken from 23 endemically-infected animals, whose cyathostominae burdens had been enumerated, were also used to identify putative diagnostic antigens. Eighteen horses had positive mucosal worm burdens (range 723-3,595,725) and all but two of these animals had serum IgG(T) antibody specific to either complex. Moreover, IgG(T) responses specific to antigen complexes A and B were absent in all five parasite negative horses that were tested. Serum IgG(T) responses to either of the two complexes were identified in five clinical cases tested. IgG(T) responses to adult antigen somatic extracts were more heterogeneous, with no clear pattern between experimentally-infected ponies and helminth-free controls. The results indicate that increases in serum IgG(T) to mucosal larvae occur in the pre-patent period and that two antigenic complexes within somatic preparations of these stages have immunodiagnostic potential.     

Persistence of carotenoid pigments in the blood of concentrate-finished grazing sheep: its significance for the traceability of grass-feeding

Carotenoid pigments are good biomarkers of grass feeding in sheep. However, grazing lambs are often stall-finished because of grass shortage. We investigated the nature of the carotenoids present in sheep blood and their persistence in this tissue. Four treatments were compared: 1) feeding a concentrate-based diet (n = 10 lambs), 2) grazing followed by a long stall-finishing period (n = 10), 3) grazing followed by a short stall-finishing period (n = 10), and 4) grazing to slaughter weight (n = 10). The concentrate supply was regulated to have similar average daily gain for all treatments. The 40 lambs were allocated to either the grazing or the stall treatments on the basis of their birth date, birth weight, and body weight. The 30 grazing lambs were further allocated to long-stall, short-stall, or grass treatment on the basis of their body weight and plasma carotenoid content. Plasma content of total carotenoids was measured by spectrophotometry during the grazing and the stall periods for all lambs and at slaughter weight for the eight heaviest lambs of each treatment. Analysis of the nature and the concentration of individual carotenoids was performed by HPLC on pasture and stall diets and on blood of grazing lambs. The carotenoid content of the stall diet was 2 to 3% that of the pasture diet. Lutein, zeaxanthin, and beta-carotene accounted for 43 to 58%, 3 to 17%, and 0 to 7% of total plasma carotenoids in grazing lambs, respectively. Two unknown polar carotenoids, expressed in lutein equivalent, accounted for 10 to 22% and 0 to 9% of total carotenoids. Plasma carotenoid content during the grazing and the finishing periods varied among animals (P < 0.001). At slaughter weight, plasma carotenoid content was higher for grass-fed than for stall-fed, long-stall finished, or short-stall finished lambs (P < 0.001), and reliably distinguished grass-fed lambs from all the others. Plasma carotenoid content decreased exponentially with the interval from starting on the stall diet (P < 0.005). The deceleration parameter of the model increased linearly with lamb average daily gain during the stall-finishing period, suggesting that the turnover of carotenoids in the blood may depend on the level of intake of the stall-finishing diet. After 4 to 13 d on the stall diet, depending on the initial plasma carotenoid concentration, plasma carotenoid concentration of previously grazed, stall-finished lambs fell to the values of lambs fed a concentrate diet without grazing. Such a low persistence is of interest for discriminating grazing lambs from stall-finished grazing lambs.     

Familial non-rcd1 generalised retinal degeneration in Irish setters

Four Irish setters were diagnosed with bilateral retinal degeneration and cataracts at an age ranging from six to 11 years. In three of these dogs, progressive night blindness was reported from an age of eight to 11 years. In the fourth dog, aged six, no signs of visual impairment had been noticed. In all four dogs, the rod-cone dysplasia type 1 (rcd1) mutation was excluded as a cause, using an allele-specific PCR. From their three-generation pedigrees, a familial relationship was detected in three out of four dogs, which were also related to four additional Irish setter dogs with a history and clinical signs suggestive of late-onset progressive retinal degeneration. These results suggest the existence of a possibly hereditary, late-onset, progressive retinal atrophy in the Irish setter breed, that is distinct from rcd1.