Cost-effectiveness of FDA variance for blood collection from individuals with hereditary hemochromatosis at a 398-bed hospital-based donor center.

Hereditary hemochromatosis (HH) is treated by therapeutic phlebotomy to reduce excess body iron. This 398-bed, hospital-based donor center wanted to determine whether there was a financial advantage to requesting FDA approval to allow transfusion of blood components from eligible individuals with HH. Donor center records from 2008 were reviewed to identify all therapeutic phlebotomy patients with a diagnosis of HH. HH patients were contacted and asked to complete the AABB Uniform Donor History Questionnaire (UDHQ) to determine their eligibility as potential allogeneic blood donors. Financial ramifications attributable to loss of revenue from the therapeutic phlebotomies($100/collection) were compared with the potential gain in revenue from collecting units for transfusion ($429/collection) in a 12-month period. Nineteen HH patients were identified and screened for allogeneic eligibility. Seventeen patients (89%) met the eligibility criteria for allogeneic donors, and two patients (11%) did not. Retrospective review of donor records indicated that a total of 60 units were collected from these HH patients from January 2008 through December 2008. Fifty-five of the 60 units collected (92%) were eligible for allogeneic use, potentially generating gross revenue of $23,595. After deducting expenses for infectious disease testing and loss of revenue for the nonqualified therapeutic phlebotomies, the net revenue from the collection of 55 RBC units that could have potentially been used for allogeneic transfusion was $20,345. In contrast, the current revenue generated by the collection of 60 therapeutic phlebotomies was only $6,000. In 2008, using eligible HH individuals as allogeneic blood donors would have resulted in an increase in revenue of $14,345 for our blood center.This study demonstrates that even at a medium-size, hospital-based donor center, obtaining a variance from the FDA to establish an HH blood donor program is a cost-effective endeavor, which does not compromise donor or patient safety.

Diagnostic testing for pituitary pars intermedia dysfunction in horses.

Pituitary pars intermedia dysfunction is a slowly progressive disorder that afflicts most breeds of horses. Because it shares features with human Cushing disease, it has been referred to as equine Cushing disease. A variety of tests of pituitary-adrenocortical function were performed on horses with evidence of pituitary pars intermediate dysfunction, and results were compared with those in healthy control horses. Diurnal variations in plasma cortisol concentration were not statistically different between control horses and those with pituitary pars intermedia dysfunction. An ACTH stimulation (1 U of natural ACTH gel/kg of body weight, IM) test or a combined dexamethasone suppression test (10 mg, IM) and ACTH stimulation (100 mg of synthetic ACTH, IV) test also failed to distinguish horses with pituitary pars intermedia dysfunction from control horses. A significant (P < 0.001) dose-related suppression of cortisol concentration in response to increasing doses (5, 10, 20, and 40 micrograms/kg) of dexamethasone was observed in control horses but not in those with pituitary pars intermedia dysfunction. On the basis of plasma cortisol concentration, the dexamethasone suppression test, using 40 micrograms/kg, whether initiated at 5 PM with sample collection at 15 (8 AM) and 19 (12 PM) hours after dexamethasone administration, or initiated at 12 AM with sample collection at 8 (8 AM), 12 (12 PM), 16 (4 PM), 20 (8 PM), and 24 (12 AM) hours after dexamethasone administration, reliably distinguished between control horses and those with pituitary pars intermedia dysfunction.(ABSTRACT TRUNCATED AT 250 WORDS)

Mortality of harbor seal pups at different sites in the inland waters of Washington.

We examined the mortality rates and causes of death of harbor seal (Phoca vitulina) pups in three regions of the inland waters of Washington (USA) in 1984. One hundred eight pups were collected during 239 searches of the shoreline areas near harbor seal haulout sites or through public reports. Minimum neonatal (up to 1 mo after birth) mortality rates at these regions ranged from 12% to 26% of the pups born. Neonatal mortality was highest in the Strait of Juan de Fuca; 33 of the estimated 105 (31%) pups born at the primary site died. Causes of death varied by location. In southern Puget Sound predation by coyotes (Canis latrans) was the primary cause of death, accounting for eight of 43 (19%) of the dead pups examined; starvation was the next most common cause of death. Mortality at study sites in the Strait of Juan de Fuca was related to premature parturition; 19 of 49 (39%) of the pups found dead were born prematurely. Nine species of bacteria were identified in samples taken from 42 pups; Proteus sp. and Escherichia coli were the most common.

Pyrrolizidine alkaloid-induced liver disease in horses: an early diagnosis.

Nine adult horses were fed alfalfa hay cubes containing approximately 10% Senecio vulgaris until all horses had consumed approximately the same amount of toxic components of S vulgaris, pyrrolizidine alkaloids (PA). The amount of PA consumed was determined by the amount that induced clinical signs of PA toxicosis in 3 horses. The 6 other horses were given similar amounts per kilogram of body weight. An initial decrease of feed intake was observed when horses' diets were changed from alfalfa cubes to alfalfa/Senecio cubes, and feed intake was decreased further over 89 to 98 days. From 50 to 159 days, body weight decreased in all horses. Liver disease was induced in all 9 horses after they ate an average of 233 +/- 9.2 mg of PA/kg of body weight. Eight horses died or were euthanatized. Treatment with branched chain amino acids had no effect on mortality, but appeared to reduce neurologic problems. Clinical signs of PA-induced liver disease included ataxia, head pressing, and decreased feed intake. Other clinical signs of toxicosis were observed individual horses, but did not develop in most horses. Megalocytic hepatopathy developed. Liver abnormalities proceeded as PA was consumed and were severe in 8 of 9 horses before clinical signs of toxicosis appeared. Sulfobromophthalein sodium clearance did not decrease until PA-induced liver disease was advanced. Bile acid (BA) concentrations increased to greater than or equal to 50 mumol/L, in the 8 horses that died. One horse had hepatopathy and increased BA concentration, but survived. In this horse, BA concentration peaked at 33 mumol/L and then decreased.(ABSTRACT TRUNCATED AT 250 WORDS)

Dactylaria gallopava encephalitis in two grey-winged trumpeters (Psophia crepitans).

Encephalitis caused by Dactylaria gallopava is reported in two 17-to-18-day-old grey-winged trumpeters (Psophia crepitans). One of the chicks was housed in a tropical exhibit, and the other was in an adjacent room. Fir bark litter and aerosol infection were the suspected source and route of infection. The occurrence of this disease in a species other than the domestic chicken and turkey suggests the presence of a broader avian population at risk than previously indicated. Adult trumpeters and both young and old passerines housed in the same exhibit were not affected.

Equine ehrlichiosis in northern California: 49 cases (1968-1981).

Case records of horses with equine ehrlichiosis (Ehrlichia equi) at the University of California Veterinary Medical Teaching Hospital and Ackerman Creek Large Animal Clinic were analyzed for evaluation of clinical signs, time of onset, hematologic values, response to treatment, and recovery. Equine ehrlichiosis was found to be seasonal in horses in the foothills of northern California, with higher incidence than reported previously. The horses developed fever, anorexia, depression, limb edema, icterus, and ataxia. Hematologic changes were leukopenia, thrombocytopenia, icterus, anemia, and inclusion bodies in the neutrophils and eosinophils. Diagnosis was made by observing the characteristic inclusion bodies, using a standard Wright's stain. Mortality was low, although complications of opportunistic secondary infection and injury due to ataxia did develop. Treatment with tetracycline resulted in prompt clinical improvement within 24 hours. Chronic cases were not detected. Equine ehrlichiosis should be differentiated from diseases with similar clinical signs including encephalitis, liver disease, purpura hemorrhagica, equine infectious anemia, and equine viral arteritis.

Nephrotoxicity of sodium arsenate in dogs.

Nephrotoxicity of sodium arsenate was evaluated in dogs to determine the pathophysiologic basis for renal lesions caused by this heavy metal. Examination of biopsy specimens indicated that the low dose of the As salt (0.73 mg/kg of body weight) produced histologic changes consisting of mild degeneration and vacuolation of renal tubular epithelium. Vacuolation involved mainly the ascending thick portion of the nephron. Clinical pathologic changes were not demonstrable at this dosage level according to glomerular filtration rate (creatinine clearance), fractional reabsorption of sodium, potassium, and chloride; plasma osmolar and free water clearance; and urinalysis. The medium dose (7.33 mg/kg) resulted in alterations determined by urinalysis, but did not markedly affect other clinical pathologic measurements. Histopathologic changes were equal to or greater than those seen with the low dose. Tubular necrosis was observed in the cortical portion of the nephron and the ascending thick limb. The high dose (14.66 mg/kg) consistently produced marked changes in all parameters evaluated. Clinical pathologic alterations were compatible with acute tubular necrosis involving all segments of the nephron. Histologically, moderate glomerular sclerosis and severe tubular necrosis were observed. During recovery from the high dose of As, a gradual compensatory healing process was observed that was evident in all clinical pathologic parameters and was confirmed from sequential renal biopsy specimens.

Nontuberculous mycobacterial disease in rhesus monkeys.

In a colony of rhesus monkeys (Macaca mulatta), 42 cases of nontuberculous mycobacterial-related disease were identified from 1970 to 1978. The disease affected young and old colony-born and wild-caught monkeys of both sexes. Serotypes 1, 2, 4, 8, and 18 of the Mycobacterium avium-intracellulare group were isolated from different monkeys. The lesions were primarily intestinal in 36 monkeys. Lesions of the large intestine, small intestine, and mesenteric lymph nodes were characterized by diffuse accumulations of large macrophages containing many acid-fast bacteria. Acid-fast bacteria could not be identified histologically in four monkeys with typical histories of diarrhea and weight loss, positive skin reactions to the tuberculin test with M. avium tuberculin, and isolation of the organism from tissues on one or more occasions. Two monkeys had histologically positive lesions limited to the lungs, although chronic colitis of undetermined cause was present.

Nontuberculous mycobacterial disease in rhesus monkeys.

In a colony of rhesus monkeys (Macaca mulatta), 42 cases of nontuberculous mycobacterial-related disease were identified from 1970 to 1978. The disease affected young and old colony-born and wild-caught monkeys of both sexes. Serotypes 1, 2, 4, 8, and 18 of the Mycobacterium avium-intracellulare group were isolated from different monkeys. The lesions were primarily intestinal in 36 monkeys. Lesions of the large intestine, small intestine, and mesenteric lymph nodes were characterized by diffuse accumulations of large macrophages containing many acid-fast bacteria. Acid-fast bacteria could not be identified histologically in four monkeys with typical histories of diarrhea and weight loss, positive skin reactions to the tuberculin test with M. avium tuberculin, and isolation of the organism from tissues on one or more occasions. Two monkeys had histologically positive lesions limited to the lungs, although chronic colitis of undetermined cause was present.

Effect of pyrrolizidine alkaloid-induced hepatic disease on plasma amino acid patterns in the horse.

Plasma amino acid patterns were studied in 6 clinically normal adult horses during the course of hepatic disease induced by feeding them plants containing pyrrolizidine alkaloids. At death, there were significant (P less than 0.01) increases in glutamine, proline, tyrosine, asparagine, lysine, histidine, alanine, phenylalanine, methionine, aspartic acid, and ornithine values. There were no significant changes in glycine, valine, isoleucine tryptophan, and arginine values. There were significant (P less than 0.01) decreases in citrulline. Ammonia increased 4-fold. Alpha-Aminoadipic acid and alpha-aminobutyric acid were not detectable in the plasma of clinically normal horses, but were in the plasma of horses with severe hepatic disease. The ratio of branched chain amino acids (isoleucine + leucine + valine) to phenylalanine plus tyrosine progressively decreased from a normal of +/- 0.5 to 1.3 +/- 0.3 (mean +/- SD) just prior to death. The relative changes in plasma amino acid pattern in horses with hepatic diseases seem similar to those changes occurring in man and other animals with hepatic disease.

Alterations in plasma corticosteroids, insulin and selected metabolites in horses used in endurance rides.

The effects of prolonged exercise on plasma concentrations of corticosteroids, insulin, glucose, lactate and beta-hydroxybutrate were studied in a group of horses competing in a 160 km endurance ride. Of the 53 horses included in the study at the outset, 23 completed the course. Plasma corticosteroids increased while glucose and insulin decreased during exercise. Little change occurred in plasma lactate or beta-hydroxybutyrate. The parameters studied did not result in the finding of any consistent significant differences beteeen individuals that completed and those that did not complete the course.

Malignant lymphoma in macaques: a clinicopathologic study of 45 cases.

Malignant lymphoma was diagnosed in 42 rhesus macaques (Macaca mulatta) and 3 stumptail macaques (M. arctoides) between February 1969 and December 1977. The distribution of tumor masses in the tissues of individual animals varied widely. Solitary tumor masses were present in 14 animals and multiple masses in the remaining 31 animals. Visceral lymph nodes, gastrointestinal tract, heart, and kidneys were most commonly affected. Peripheral lymph nodes were rarely involved. Most malignant lymphomas were of an undifferentiated cell type, although tumors of histiocytic, lymphocytic, poorly differentiated, and mixed lymphocytic and histiocytic cell types were also observed. Concurrent bacterial and/or viral infections were evident in 30 of the 45 macaques with malignant lymphoma. Amyloidosis was present in 9 animals. This high incidence of malignant lymphoma suggested that their immune responses were abnormal. The development of malignant lymphoma in the macaques may have been secondary to or enhanced by immunodeficiency.

Canine hyperadrenocorticism: pretreatment clinical and laboratory evaluation of 117 cases.

The physical findings, clinical signs, age, breed and sex distributions, and laboratory data of 117 dogs with untreated Cushing's syndrome were reviewed. Poodles, Dachshunds, and Boxers of all ages were found to be at increased risk, as were dogs of all breeds greater than or equal to 6 years old. Polydipsia, polyuria, progressive bilaterally symmetric alopecia, and abdominal distention were the most frequently observed clinical signs and physical findings. Lymphopenia, eosinopenia, above normal values of serum alkaline phosphatase, serum cholesterol, and sulfobromphthalein dye retention, and below normal urine specific gravity were the most frequent abnormalities found in the laboratory data. About 50% of the dogs had urinary tract infections. Final diagnosis was established on the basis of abnormally high plasma corticosteroid values in response to an intramuscular injection of adrenocorticotropic hormone.

Vitamin D intoxication and the pathogenesis of vitamin D nephropathy in the dog.

Dogs given excess vitamin D (500 or 1,000 micrograms/kg of body weight each day for 1 to 3 weeks were observed for clinical and pathologic changes of increased blood pressure and of characteristic nephropathy associated with vitamin D toxicosis or hypercalcemia. Serum calcium and serum urea nitrogen (UN) increased throughout the treatment period, but serum phosphorus remained within the normal range. Plasma renin activity increased markedly. Blood pressure showed only insignificnat changes (P = greater than 0.05). Gross and microscopic examination of the kidneys suggested vascular-oriented changes with an ischemic basis. Glomerular vascular poles showed hypertrophy and hyperplasia of juxtaglomerular cells. Ultrastructually, an increase in the number of secretory granules was noticed in these cells. A hypothesis regarding the mechanism of renal injury during vitamin D toxicosis is presented.