D-penicillamine-associated neutropenia in a Doberman pinscher.

Copper-associated hepatitis in dogs results from elevated copper levels secondary to increased intake or decreased clearance. Treatment is through establishing a negative copper balance and can include chelation therapy. Traditionally, chelation therapy in dogs is uses D-penicillamine, which has been shown to have severe side effects in humans. Side effects have not been well-documented in dogs but can include nephrotoxicity and dermatologic reactions. This article is the first to report neutropenia in a dog secondary to chelation therapy using D-penicillamine. In this case, a complete blood (cell) count (CBC) collected before initiation of chelation therapy was normal and neutropenia was documented 4 mo after starting therapy. A cytologic examination of bone marrow confirmed a myeloid hypoplasia. Following discontinuation of D-penicillamine, the neutropenia resolved. Based on this case report, periodic CBC rechecks following the initiation of D-penicillamine chelation therapy are recommended to guide treatment decisions. Key clinical message: Dogs with confirmed copper-associated hepatitis should be treated cautiously with D-penicillamine for chelation therapy. D-penicillamine may adversely affect bone marrow, causing a leukopenia characterized by neutropenia. It is recommended that clinicians periodically monitor neutrophil counts while treating dogs with D-penicillamine.

Neutropénie associée à la D-pénicillamine chez un Doberman pinscher. L'hépatite associée au cuivre chez le chien résulte de niveaux élevés de cuivre secondaires à une augmentation de l'apport ou à une diminution de la clairance. Le traitement consiste à établir un bilan négatif du cuivre et peut inclure une thérapie par chélation. Traditionnellement, la thérapie par chélation chez le chien utilise la D-pénicillamine, dont il a été démontré qu'elle a de graves effets secondaires chez l'homme. Les effets secondaires n'ont pas été bien documentés chez les chiens, mais peuvent inclure une néphrotoxicité et des réactions dermatologiques. Cet article est le premier à rapporter une neutropénie chez un chien secondaire à un traitement par chélation utilisant la D-pénicillamine. Dans ce cas, une numération globulaire complète (CBC) recueillie avant le début du traitement par chélation était normale et une neutropénie a été documentée 4 mois après le début du traitement. Un examen cytologique de la moelle osseuse a confirmé une hypoplasie myéloïde. Après l'arrêt de la D-pénicillamine, la neutropénie a disparu. Sur la base de ce rapport de cas, des vérifications périodiques de la CBC après le début du traitement par chélation de la D-pénicillamine sont recommandées pour guider les décisions de traitement.Message clinique clé :Les chiens atteints d'hépatite associée au cuivre confirmée doivent être traités avec prudence avec de la D-pénicillamine pour le traitement par chélation. La D-pénicillamine peut affecter négativement la moelle osseuse, provoquant une leucopénie caractérisée par une neutropénie. Il est recommandé aux cliniciens de surveiller périodiquement le nombre de neutrophiles lors du traitement des chiens avec de la D-pénicillamine.(Traduit par Dr Serge Messier).

Suspected immune-mediated neutropenia and corticosteroid responsive pancytopenia in a Portuguese water dog.

An 8-year-old spayed Portuguese water dog was presented with dysuria, lethargy, and anorexia. A profound neutropenia and pancytopenia were identified. Bone marrow aspirates revealed neutrophilic hyperplasia, a significant left shift, and toxic changes, suggesting immune-mediated destruction as a likely underlying mechanism. Immunosuppressive therapy was instituted and clinical signs improved.

Neutropénie à médiation immunitaire suspectée et pancytopénie répondant aux corticostéroïdes chez un Chien d'eau portugais. Un Chien d'eau portugais femelle stérilisée âgée de 8 ans a été présentée avec de la dysurie, de la léthargie et de l'anorexie. Une neutropénie profonde et de la pancytopénie ont été identifiées. Des aspirations de la moelle osseuse ont révélé une hyperplasie neutrophilique, un virage important vers la gauche et des changements toxiques suggérant une destruction à médiation immunitaire comme mécanisme sous-jacent probable. Une thérapie immunosuppressive a été instituée et les signes cliniques se sont améliorés.(Traduit par Isabelle Vallières).

Ulcerative dermatitis, thrombocytopenia, and neutropenia in neonatal foals.

This report describes transient ulcerative dermatitis, severe thrombocytopenia, and mild neutropenia in 6 foals from 4 mares from geographically diverse regions of the United States. The foals presented at <4 days of age with oral and lingual ulcers, and crusting and erythema around the eyes, muzzle, and perineal, inguinal, axillary, trunk, and neck regions. There was a severe thrombocytopenia (0-30,000 platelets/microL), leukopenia (1900-3200 white blood cells/microL), and mild neutropenia (500-1800 neutrophils/microL). Four of the 6 foals had petechiae and ecchymotic hemorrhages and 3 had bleeding tendencies. Results of examination of a bone marrow biopsy from 1 foal were normal and results of a platelet surface immunoglobulin test in another were negative. Histopathology of the skin in all foals showed subepidermal clefting with subjacent vascular dilation, dermal hemorrhage, and superficial papillary necrosis. The foals were treated supportively with broad-spectrum antibiotics (5/6), corticosteroids (3/6), gastric ulcer prophylaxis (6/6), whole-blood transfusion (4/6), and platelet-rich plasma (1/6). The skin lesions and thrombocytopenia (>50,000 platelets/microL) improved in 2 weeks (4/6). Two foals had a decline in their platelet counts when the steroids were decreased and needed protracted treatment. All foals survived and were healthy as yearlings. Two mares that had 2 affected foals each, upon subsequent pregnancies to different stallions, had healthy foals when an alternate source of colostrum was given. The findings in the cases in this report suggest a possible relationship between colostral antibodies or some other factor in the colostrum and the thrombocytopenia and skin lesions, although further investigation is warranted to confirm or refute this hypothesis.

Assessment of tolerant sunfish populations (Lepomis sp.) inhabiting selenium-laden coal ash effluents. 1. Hematological and population level assessment.

Sunfish were collected from coal ash effluent-receiving streams and Ohio River watershed reference sites to assess the effects of exposure to low-level selenium concentrations. Selenium, copper, and arsenic concentrations were statistically higher in tissue samples from exposed fish than in reference fish. Leukopenia, lymphocytosis, and neutropenia were evident in exposed fish and were indicative of metal exposure and effect. White blood cell counts and percent lymphocyte values were significantly correlated with liver selenium concentrations. Plasma protein levels were significantly lower in exposed fish than in fish from the Ohio River, indicating that exposed fish may have been nutritionally stressed. Condition factors for fish from the ash pond-receiving streams were the same as, or lower than, those of fish from the reference sites. There was no evidence that the growth rate of fish in the receiving streams differed from that of fish in the reference streams. Despite liver selenium concentrations which exceeded reported toxicity thresholds and evidence of significant hematological changes, there were no significant differences in fish condition factors, liver-somatic indices, or length-weight regressions related to selenium.

Clinical and clinical laboratory correlates in sea otters dying unexpectedly in rehabilitation centers following the Exxon Valdez oil spill.

Following the Exxon Valdez oil spill, 347 oiled sea otters (Enhydra lutris) were treated in rehabilitation centers. Of these, 116 died, 94 within 10 days of presentation. Clinical records of 21 otters dying during the first 10 days of rehabilitation were reviewed to define the laboratory abnormalities and clinical syndromes associated with these unexpected deaths. The most common terminal syndrome was shock characterized by hypothermia, lethargy, and often hemorrhagic diarrhea. In heavily and moderately oiled otters, shock developed within 48 hours of initial presentation, whereas in lightly oiled otters shock generally occurred during the second week of captivity. Accompanying laboratory abnormalities included leukopenia with increased numbers of immature neutrophils (degenerative left shift), lymphopenia, anemia, azotemia (primarily prerenal), hyperkalemia, hypoproteinemia/hypoalbuminemia, elevations of serum transaminases, and hypoglycemia. Shock associated with hemorrhagic diarrhea probably occurred either as a direct primary effect of oiling or as an indirect effect secondary to confinement and handling in the rehabilitation centers. Lightly oiled otters were less likely to die from shock than were heavily oiled otters (22% vs. 72%, respectively). Heavily oiled otters developed shock more rapidly and had greater numbers of laboratory abnormalities, suggesting that exposure to oil was an important contributing factor.

Effects of poly I:C in porcine iron deficient neutropenia.

Withholding iron dextran treatment normally given to pigs at 1-3 days of age to prevent anemia resulted also in neutropenia. Polyinosinic acid:polycytidylic acid (poly I:C) at 0.5 mg/kg IV at 25 days of age resulted in induction of putative interferon 2 to 24 hours later, with significantly (P less than 0.05) lower concentrations in iron-deficient (Fe-) female pigs than in iron-supplemented (Fe+) female pigs. Poly I:C caused several transient toxic manifestations, including elevations in blood urea nitrogen, creatinine, aspartate aminotransferase, potassium (K), total bilirubin and phosphorus (P), marked leukopenia (both neutropenia and lymphopenia), and declines in serum albumin, calcium, cholesterol, glucose and globulin. Certain blood chemistries before poly I:C were significantly (P less than or equal to 0.05) different: albumin, globulin, cholesterol and K were higher in females than in males; albumin, globulin, glucose, P and K were higher in Fe- than in Fe+ pigs; and total carbon dioxide was higher in Fe+ than in Fe- pigs.

Effects of large doses of phenylbutazone administration to horses.

The effects of large doses of phenylbutazone were evaluated in clinically normal horses. The drug was given to 4 groups of 2 horses each at the rate of 30 mg/kg of body weight, orally, or 30, 15, or 8 mg/kg IV daily for up to 2 weeks. All horses became anorectic and depressed after 2 to 4 phenylbutazone treatments, and the horses given 15 or 30 mg/kg died on or between days 4 and 7 of treatment. A decrease in total blood neutrophil count occurred in all horses, and was associated with toxic left shift in horses given the 2 larger dosage schedules. The horses also had progressive increases in serum urea nitrogen, creatinine, and phosphorus concentrations, accompanied by decreasing serum calcium concentrations. There was a progressive decrease in total serum protein in all 8 horses. Gastrointestinal ulcerations, renal papillary necrosis, and vascular thromboses were the predominant postmortem findings.