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Biomedical subjects

J M Kruger

Publications and source records attributed to J M Kruger.

At least 19 recordsLinked to original sources
PubMed2000

Use of pamidronate disodium to reduce cholecalciferol-induced toxicosis in dogs.

OBJECTIVE: To determine whether pamidronate disodium can reduce cholecalciferol-induced toxicosis in a dose-related manner. ANIMALS: 20 clinically normal, 8- to 12-month-old male Beagles. PROCEDURE: All dogs were given 8 mg of cholecalciferol (CCF)/kg of body weight once orally, then were randomly assigned to 4 groups of 5 dogs each. Dogs were treated with IV administration of 0.9% NaCl solution (SC group), 0.65 mg of pamidronate/kg in 0.9% NaCl solution (LP group), 1.3 mg of pamidronate/kg in 0.9% NaCl solution (MP group), or 2.0 mg of pamidronate/kg in 0.9% NaCl solution (HP group) on days 1 and 4 after administration of CCF. Dogs were observed for 14 days, and serial blood samples were collected for serum biochemical, electrolyte, and 25-hydroxyvitamin D3 analyses. Urine samples were collected for determination of specific gravity. Glomerular filtration rate (GFR) was determined by plasma iohexol clearance. Histologic examination of renal tissue was performed. RESULTS: One dog in the SC group was euthanatized 3 days after administration of CCF because of severe clinical signs of toxicosis. Dogs in the HP group had significantly higher mean GFR (day 3), serum potassium concentrations (day 14), and urine specific gravity (days 7 and 14) and significantly lower mean serum creatinine concentrations and total calcium X phosphorus concentration product (days 4 and 7) than dogs in the SC group. Dogs in the HP group had no abnormal findings on histologic examination of renal tissue, dogs in the LP and MP groups had trace to mild mineralization of renal tissue, and dogs in the SC group had moderate mineralization and cellular necrosis of proximal renal tubules. CONCLUSIONS AND CLINICAL RELEVANCE: Pamidronate disodium is a potentially useful drug to reduce CCF-induced toxicosis and other causes of hypercalcemia associated with increased bone resorption in dogs.

Animals↗
PubMed1999

Medical dissolution and prevention of canine struvite urolithiasis. Twenty years of experience.

Two types of canine struvite uroliths have been recognized: infection-induced struvite is the most common type; sterile struvite is uncommonly recognized. Infection-induced struvite is most commonly associated with urease-producing staphylococcal UTI. For dogs that qualify, medical dissolution is an effective method of treatment. Medical dissolution protocols encompass: (1) eradication or control of UTI; (2) use of calculolytic diets; and (3) administration of urease inhibitors to patients with persistent UTI caused by urease-producing microbes.

Animals↗
PubMed1999

Canine calcium phosphate uroliths. Etiopathogenesis, diagnosis, and management.

Uroliths composed predominantly of calcium phosphates have been infrequently identified in dogs. Factors incriminated in the etiopathogenesis of calcium phosphate urolithiasis include an alkaline urine pH, hypercalciuria, decreased urine concentrations of crystallization inhibitors, and increased urine concentrations of crystallization promoters. Disorders associated with calcium phosphate urolith formation in dogs include primary hyperparathyroidism, hyperadrenocorticism, and idiopathic hypercalciuria. Medical therapy of patients with recurring calcium phosphate uroliths should be directed at removing or minimizing factors contributing to urine supersaturation with calcium phosphate.

Animals↗
PubMed1999

Canine urate urolithiasis. Etiopathogenesis, diagnosis, and management.

Etiopathologic factors predisposing to urate lithogenesis in Dalmatian and non-Dalmatian dogs represent diverse pathologic and/or physiologic processes involving purine nucleotide and ammonia synthesis, biodegradation, and excretion. Predisposing factors for urate urolith formation include hyperuricemia, hyperammonemia, hyperuricosuria, hyperammonuria, aciduria, and genetic predisposition. Medical therapy of dogs forming urate uroliths should be directed at modifying these predisposing factors through dietary modification, administration of allopurinol, and/or surgical correction of portovascular anomalies if present. The precise mechanisms resulting in urate urolith formation in dogs have not been determined.

Animals↗
PubMed1999

Use of pamidronate to reverse vitamin D3-induced toxicosis in dogs.

OBJECTIVES: To determine whether pamidronate disodium can reduce vitamin D3-induced hypercalcemia in dogs and whether combination treatment with calcitonin is more effective than treatment with pamidronate alone. ANIMALS: 20 clinically normal male Beagles. PROCEDURE: All dogs were given 8 mg of cholecalciferol (CCF)/kg of body weight once orally, then were assigned randomly to 4 groups of 5 dogs each. Dogs were given 0.9% NaCl solution IV (group 1), calcitonin SC and 0.9% NaCl solution IV (group 2), pamidronate and 0.9% NaCl solution IV (group 3), or a combination of all 3 agents (group 4). Dogs were observed for 28 days, and serial blood and urine samples were collected for determination of serum biochemical, electrolyte, and 25(OH)D3 values, CBC, and urine mineral excretion. Samples of kidney, stomach, lung, aorta, liver, duodenum, and brain were evaluated by light microscopy and quantitative mineral analysis. RESULTS: Two dogs in group 1 were euthanatized 4 days after CCF administration because of severe clinical signs of disease. Dogs in group 3 lost less weight and had significantly lower serum phosphorus, total and ionized calcium, and urinary zinc concentrations, compared with dogs in group 1. On day 4, serum urea nitrogen concentration was significantly lower in dogs of groups 3 and 4, compared with dogs in group 1. Mild to moderate mineralization of kidneys and stomach were observed in the 2 group-1 dogs euthanatized on day 4. CONCLUSIONS: Pamidronate administration effectively prevents CCF-induced hypercalcemia and mineralization of soft tissues. CLINICAL RELEVANCE: Pamidronate is a potentially useful antidote against CCF toxicosis in dogs.

Analgesics↗
PubMed1998

Cost-effectiveness of the arthritis self-help course.

OBJECTIVE: To evaluate the cost-effectiveness of the Arthritis Self-Help Course in reducing the pain of arthritis, the leading cause of disability in the United States and a common problem among older adults. METHODS: A decision model was used to examine the cost-effectiveness of the Arthritis Self-Help Course among individuals with arthritis over a 4-year analytic horizon from 2 perspectives, namely, society and the health care system. The Arthritis Self-Help Course was assumed to reduce pain by 20% and physician visits for arthritis by 40% among individuals receiving conventional medical therapy. Estimates for program costs, costs for physician visits, and time and transportation costs were derived from the published literature and expert opinion. Sensitivity analyses were conducted on all relevant parameters. Arthritis pain and costs (program, physician visit plus/minus time and transportation) were expressed as cost per person per unit reduction in pain. Because nearly all analyses showed the program to be cost saving, we simply report the reduction in joint pain and the cost savings, because standardizing cost savings is not a useful concept. RESULTS: From both the societal and health care system perspectives, the Arthritis Self-Help Course was cost saving in base-case analyses (reducing pain by 0.9 units while saving $320 and $267, respectively) and throughout the range of reasonable values used in univariate sensitivity analyses. Cost savings were due primarily to reduced physician visits. CONCLUSIONS: The Arthritis Self-Help Course is a cost-saving intervention that further reduces arthritis pain among individuals receiving conventional medical therapy. The benefits for both patients and health care providers warrant its more widespread use as a normal adjunct to conventional therapy.

Adult↗
PubMed1997

Vaccination of cats for feline rhinotracheitis results in a quantitative reduction of virulent feline herpesvirus-1 latency load after challenge.

We recently described the construction of a feline herpesvirus-1 (FHV-1) recombinant vaccine strain, FHV beta-galgLgE delta, containing a deletion in both the gI and the gE genes. We also reported comparative tests of its safety and efficacy in cats. These cats were unvaccinated or subcutaneously vaccinated with FHV beta-galgLgE delta, its isotypic parent strain (FHV-1SA), or a commercial FHV-1 vaccine strain (FHV-1CV) and subsequently challenged with a virulent field strain of FHV-1. Here we report the determination of FHV-1 field virus latency load after challenge in the same experimental animals. FHV-1 specific quantitative PCR was carried out on feline genomic DNA isolated from trigeminal ganglia, olfactory bulbs, and brain stems. We have determined that a reduction in field virus latency load in cats vaccinated subcutaneously with wild-type FHV-1 strains prior to challenge is dependent upon glycoproteins gL and gE deleted in FHV beta-galgLgE delta.

Animals↗
PubMed1997

Measurement of serum iohexol by determination of iodine with inductively coupled plasma-atomic emission spectroscopy.

We used inductively coupled plasma-atomic emission spectroscopy to measure serum iodine to determine plasma clearance of iohexol, an iodinated radiographic contrast agent. We determined I at 178.276 nm on the phosphorus 178.287 nm channel of the polychromator by utilization of spectrum shifter offset software, while correcting for P with the sequential P 214.914 nm emission line. Determination of I on the polychromator provided excellent precision in the measurement of serum I, even though the interelement correction of P was done with a sequential P line. Total imprecision (CV) (n = 13) was 16% (at 13.7 mg/L I), 8.6% (28.7 mg/L), 3.6% (59.0 mg/L), 2.6% (120.5 mg/L), 1.7% (237.8 mg/L), 1.2% (478.7 mg/L), and 1.8% (597 mg/L). The linear range was 15 to 600 mg/L. Iohexol added to serum (mg/L I) and recoveries (%) were 15 (91.3%), 30 (95.7%), 60 (98.3%), 120 (100.4%), 240 (99.1%), 480 (99.7%), and 600 (99.5%). Studies on dogs and cats administered a single intravenous injection of iohexol indicated that a dose of 300 mg I/kg body weight was sufficient for measurement of glomerular filtration rate by using a single compartment model for plasma clearance with three samples drawn 3 to 7 h after treatment. With this protocol, correlation coefficients were > 0.99 on the beta phase of the plasma disappearance curve.

Animals↗
PubMed1996

Glycoproteins gl and gE of feline herpesvirus-1 are virulence genes: safety and efficacy of a gl-gE deletion mutant in the natural host.

Feline rhinotracheitis virus (FRV) is an important upper respiratory tract pathogen of cats. FRV is a member of the subfamily Alphaherpesvirinae and is designated feline herpesvirus-1 (FHV-1). Besides upper respiratory clinical signs, FHV-1 may cause generalized infections in neonates or abortions in pregnant queens. Recently we described a recombinant FHV-1 strain with a deletion in the genes for glycoproteins gl and gE (FHB beta-galglgE delta) and reported that cats vaccinated subcutaneously with high doses of the recombinant FHV-1 strain responded with only mild clinical signs and developed strong immunity against subsequent virulent virus challenge. Here we compare the intranasal and subcutaneous routes of administration of this strain and assess its ability to induce protective immunity and prevent virus shedding after challenge. Cats vaccinated subcutaneously or intranasally with high doses of the recombinant FHV-1 strain responded with only mild clinical signs and developed strong immunity against subsequent virulent virus challenge. This was especially evident when the mutant vaccine was administered oronasally. In contrast, intranasal administration of two other FHV-1 isolates induced severe clinical signs in cats. We conclude from testing this FHV-1 mutant in the natural host that deletion of gE and a portion of gl genes strongly reduces viral virulence but that immunogenicity is maintained.

Administration, Inhalation↗
PubMed1996

Medical management of feline urethral obstruction.

A step-by-step priority of procedures is recommended when attempting to restore urethral patency in an obstructed male cat. In order of priority they are: (1) massage of the distal urethra, (2) attempts to induce voiding by gentle palpation of the urinary bladder, (3) cystocentesis, (4) retrograde urethral flushing, (5) combinations of 1 through 4, (6) diagnostic radiology to determine if the cause of urethral obstruction is intraluminal, mural or extramural, and if absolutely necessary, (7) surgical procedures.

Animals↗
PubMed1996

Feline perineal urethrostomy: a potential cause of feline lower urinary tract disease.

Perineal urethrostomies are associated with complications that may mimic primary causes of feline lower urinary tract disorders. Though postoperative urethral strictures may be minimized by proficiency with an effective surgical technique, removal of the distal urethra may result in bacterial urinary tract infections in 25% to 30% of patients after surgery. Urinary tract infections caused by urease-producing microbes may induce struvite urolith formation. Thus the prophylactic benefits of minimizing recurrent urethral obstruction by urethrostomy must be weighed against a long-term predisposition to recurrent bacterial urinary tract infection and urolith formation.

Animals↗
PubMed1996

Management of nonobstructive idiopathic feline lower urinary tract disease.

Consistently effective treatment and prevention of nonobstructive idiopathic lower urinary tract disease (LUTD) in male and female cats remains an enigma. Because clinical signs associated with this form are frequently self-limiting, considerable debate exists about the efficacy of various symptomatic therapies advocated for management of idiopathic feline LUTD. Any form of therapy might appear to be beneficial, as long as it was not harmful. The self-limiting nature of some forms of idiopathic feline LUTD underscores the need for controlled prospective double-blind clinical studies to prove the value of various forms of therapy.

Analgesics↗
PubMed1996

Hypercalcemia and renal failure. Etiology, pathophysiology, diagnosis, and treatment.

Hypercalcemia is a frequent disorder of calcium metabolism in dogs and cats. Hypercalcemia-induced alterations in renal function and morphology are linked to many of the clinical manifestations observed in hypercalcemic patients. Since many renal effects induced by hypercalcemia are potentially reversible, early recognition and characterization of the problem facilitates rapid therapeutic intervention.

Animals↗
PubMed1996

Feline lower urinary tract disorders. Definition of terms and concepts.

Lower urinary tract disorders of male and female cats may be caused by a variety of fundamentally different causes. The term Feline urologic syndrome should be abandoned and substituted with descriptive etiopathogenic terms whenever possible. If the underlying cause cannot be identified, the term Idiopathic lower urinary tract disease is recommended.

Animals↗
PubMed1996

Viral infections of the feline urinary tract.

The exact cause of hematuria, dysuria, and urethral obstruction remains unknown in a large percentage of naturally occurring cases of feline lower urinary tract disease (FLUTD). One attractive hypothesis implicates viruses as the cause of some idiopathic forms of FLUTD; supporting this hypothesis is the fact that a gamma herpesvirus, a calicivirus, and a retrovirus have been isolated from urine and tissues obtained from cats with this type of disease. Although the clinical course and laboratory findings of cats with idiopathic FLUTD are suggestive of an infectious cause, the question of whether viruses have a pathologic role in some forms of naturally acquired FLUTDs has not been completely answered.

Animals↗