Immune‐mediated neutropenia suspected in five dogs

Perkins, M; Canfield, P.J.; Churcher, R K; Malík, Richard

doi:10.1111/j.1751-0813.2004.tb14641.x

Cited by 16 publications

(23 citation statements)

References 14 publications

(48 reference statements)

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“…Steroid-responsive neutropenia (also termed immune-mediated neutropenia) has been assumed to have an immune-mediated cause. [1][2][3][4][5] This assumption is based largely on the exclusion of other causes of neutropenia and of a rapid and sustained response of most patients to prednisone therapy. A bone marrow immunofluorescent antibody test that used anti-IgG and anti-C3 antibodies was reported to be positive in 1 dog with steroid-responsive neutropenia and provided some support for an immune-mediated etiology.…”

Section: Discussionmentioning

confidence: 99%

“…2 Affected dogs are frequently asymptomatic, although persistent fever and lethargy are not infrequently observed. [1][2][3][4][5] Some affected dogs have concurrent or subsequent immune-mediated diseases, including immune-mediated hemolytic anemia, immunemediated thrombocytopenia, suppurative meningitis, or suppurative polyarthritis, providing further support for a predisposition to immune-mediated disease. 3,4 Bone marrow cytologic findings in dogs with steroid-responsive neutropenia are typically characterized by granulocyte hyperplasia.…”

Section: Discussionmentioning

confidence: 99%

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Pure white cell aplasia in a dog

Weiss

Henson

2007

Veterinary Clinical Pathol

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A 3-year-old Irish Wolfhound was evaluated because of acute onset of lethargy and fever. Severe neutropenia (0/microL; reference interval 2500-11,200/microL) was associated with granulocyte aplasia in the bone marrow (myeloid:erythroid ratio, 0.009:1). Antineutrophil antibodies were assessed by an indirect immunofluorescence assay using flow cytometry. When normal canine leukocytes were incubated with the patient's serum and anti-IgG, a marked shift was observed in the forward-angle light scatter of the neutrophil population, and the monocyte cluster disappeared, possibly the result of fragmentation or lysis. Both neutrophil fluorescence intensity (309 +/- 11 median channel units [MCU], control values 107-152 MCU) and the percentage of neutrophils with increased fluorescence intensity (61 +/- 5%, control values 3.8-13.7%) were increased in the patient's serum, consistent with the presence of antineutrophil antibodies. Repeated episodes of neutropenia occurred while treatment with steroidal and nonsteroidal immunosuppressive therapy was initiated and modified. The neutrophil count eventually stabilized in the low-normal range, and the dog was maintained for the next 15 months on prednisone (0.4 mg/kg PO q 48 h) and azathioprine (2 mg/kg daily). During this period, the dog developed immune-mediated hemolytic anemia and thrombocytopenia, decubital ulcers, nasal aspergillosis, and eventually, multi-organ septicemia, which led to euthanasia on day 784. A diagnosis of pure white cell aplasia was made in this dog, based on the many similarities to human patients with pure white cell aplasia, including severe neutropenia with selective granulocyte aplasia, serum antineutrophil antibodies, remission dependent on treatment with immunosuppressive therapy, and recurrent bacterial infections.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Pure white cell aplasia in a dog

Weiss

Henson

2007

Veterinary Clinical Pathol

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“…[5][6][7][8][9] The retrospective study reported here was designed to evaluate the clinicopathologic features and potential risk factors for idiopathic neutropenia in dogs. To the authors' knowledge, only 9 dogs have been described as having corticosteroid-responsive, idiopathic neutropenia.…”

Section: Discussionmentioning

confidence: 99%

Evaluation of clinicopathologic features, response to treatment, and risk factors associated with idiopathic neutropenia in dogs: 11 cases (1990–2002)

Brown¹,

Parnell²,

Schulman³

et al. 2006

javma

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“…27,28 Infrequent reports have documented immune-mediated neutropenia in dogs and cats, whereas immune-mediated neutropenia is well described in human beings. 8,9,27,28,30 In infants, 3 main disorders related to immune-mediated neonatal neutropenia have been documented and include ANN, neonatal autoimmune neutropenia, and autoimmune neutropenia of infancy. 27 The pathophysiology of ANN is analogous to NI but involves the foal's neutrophils rather than erythrocytes.…”

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confidence: 99%

Alloimmune neonatal neutropenia and neonatal isoerythrolysis in a Thoroughbred colt

et al. 2011

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A 3-day-old, 59-kg Thoroughbred colt was presented to the Lloyd Veterinary Medical Center (Ames, Iowa) for suspected neonatal isoerythrolysis (NI). The colt's dam was a 5-year-old primiparous mare without reported medical disorders during gestation or parturition. Upon initial examination, the colt was quiet and lethargic but still responsive, with a rectal temperature of 38.0°C, heart rate of 160 beats/min, and respiratory rate of 80 breaths/min. Marked jaundice of the mucous membranes and sclera was observed. interval: 0.5-3.9 mg/dl). Agglutination of red cells was not observed on the blood smear. After identification of an appropriate donor via major and minor cross-match, a blood transfusion consisting of 1.5 liters of packed red cells was performed over 6 hr; no adverse reactions were observed. Administration of amikacin (25 mg/kg, intravenously [IV], every 24 hr) and ceftiofur (5 mg/kg, IV, every 12 hr) also was initiated. The colt rapidly appeared much brighter and energetic with the hematocrit rising to 19% shortly after blood transfusion was complete. The hematocrit slowly increased during hospitalization and was 29% at the time of discharge on day 30 (Fig. 1). Blood typing of the mare identified the Aa, Ca, Qa, Qb, and Qc antigens on maternal red blood cells; Ca, Ka, Qa, Qb, and Qc antigens were identified on the colt's red blood cells, suggesting the Ka erythrocyte antigen as the cause of NI in this colt.Despite the gradually increasing hematocrit, leukopenia characterized by marked neutropenia was identified on both automated a and manual evaluation of blood smears during the initial 5 days of hospitalization (Fig. 1). A thorough diagnostic investigation to identify a possible source of infection that could result in persistent neutropenia was conducted including repeated physical examinations and thoracic and abdominal ultrasonography. The colt was consistently bright and alert and maintained a normal body temperature; no abnormal findings were observed via ultrasonography, and blood cultures did not yield bacterial growth. Because an obvious source of infection could not be identified in conjunction with continued and profound neutropenia along with the absence of immature or toxic neutrophils, an immune-mediated neutropenia was considered. On day 5 of hospitalization, Abstract. A 3-day-old Thoroughbred colt was originally presented for treatment of neonatal isoerythrolysis, which was treated with a blood transfusion. However, persistent neutropenia was observed despite the absence of detectable infection. Subsequently, a granulocyte agglutination test was performed by incubating the colt's neutrophils with the mare's serum; results were positive, leading to a clinical diagnosis of alloimmune neonatal neutropenia. The diagnosis was further supported via flow cytometric analysis. The colt was hospitalized and treated prophylactically with antimicrobials and 4 separate doses of recombinant human granulocyte colony-stimulating factor (rhG-CSF; 1.4-3.5 µg/kg, subcutaneously) in attempts to maintain the...

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Immune‐mediated neutropenia suspected in five dogs

Cited by 16 publications

References 14 publications

Pure white cell aplasia in a dog

Pure white cell aplasia in a dog

Evaluation of clinicopathologic features, response to treatment, and risk factors associated with idiopathic neutropenia in dogs: 11 cases (1990–2002)

Alloimmune neonatal neutropenia and neonatal isoerythrolysis in a Thoroughbred colt

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