Plasma granulocyte colony-stimulating factor concentrations in neutropenic, parvoviral enteritis-infected puppies.

We evaluated the temporal relationship between neutrophil numbers and plasma granulocyte colony-stimulating factor (G-CSF) concentrations in dogs infected with canine parvovirus, a common infectious cause of neutropenia. G-CSF is produced in response to neutropenia, infection, or inflammation, and results in the production and release of neutrophils from the bone marrow. Adequate numbers of functional neutrophils are necessary for protection from infection, and the timely production of G-CSF is a crucial response to certain diseases. The relationship between peripheral neutrophil numbers and plasma G-CSF concentrations during the course of an infectious disease characterized by neutropenia has not been described previously in dogs. Eight mixed-breed puppies were given an oronasal challenge with canine parvovirus, and peripheral neutrophil numbers as well as plasma G-CSF concentrations were measured daily. G-CSF was not detectable in plasma of any dog before the onset of neutropenia, but G-CSF became detectable just after the onset of neutropenia in the 7 dogs that developed clinical illness. Neutropenia persisted or worsened for at least 2 days after plasma G-CSF became detectable in all 7 dogs. Neutrophil nadir, the highest plasma G-CSF concentrations, and the most severe clinical illness occurred concurrently in most dogs. Although 1 dog died while still neutropenic, plasma G-CSF concentrations declined before resolution of neutropenia in the other 6 dogs, and were again below the limits of detection in 5 of the 6 dogs at the time of resolution.

Recombinant human granulocyte colony-stimulating factor for treatment of puppies with neutropenia secondary to canine parvovirus infection.

OBJECTIVE: To determine the effect of treatment with recombinant human granulocyte colony-stimulating factor (rhG-CSF) for puppies with neutropenia secondary to canine parvovirus infection. DESIGN: Randomized controlled clinical trial. ANIMALS: 23 puppies. PROCEDURE: Diagnosis was confirmed by use of an ELISA for detection of canine parvovirus antigen in feces, and all puppies received standard treatment for parvoviral enteritis. All puppies had neutropenia (< 1,000 neutrophils/microliter) at the time of admission to the hospital or within 4 days afterward. Eleven puppies were treated with rhG-CSF daily until neutrophil count was > 1,500 cells/microliter; the remaining 12 puppies were not treated with rhG-CSF. RESULTS: We did not detect any significant differences between groups regarding duration of hospitalization, neutrophil count when neutropenia was first detected, lowest neutrophil count, or time until neutrophil count was > 1,500 cells/microliter. CLINICAL IMPLICATIONS: Results suggest that treatment with rhG-CSF may not be beneficial in puppies with neutropenia secondary to canine parvovirus infection.

Atraumatic rupture of the gastrocnemius muscle after corticosteroid administration in a dog.

A 6-year-old spayed female Shetland Sheepdog was referred for evaluation of lameness, muscle atrophy, and a partial plantigrade stance of the right hind limb of 5 weeks' duration. Without history of trauma, atraumatic rupture of the right gastrocnemius muscle was diagnosed. Surgical repair was unsuccessful. The dog then developed signs of hyperadrenocorticism. Results of ACTH stimulation and low-dose dexamethasone suppression tests were consistent with iatrogenic adrenal suppression. One deleterious effect of excessive use of corticosteroids on muscle and connective tissue is degenerative myopathy. Steroid-induced myopathy with subsequent rupture of the gastrocnemius muscle was suspected in this dog. Clinical signs of myopathy most often develop with use of triamcinolone acetonide; therefore, care should be taken when administering this and other corticosteroids.