Objective—To evaluate equine IgG as a treatment for
kittens with failure of passive transfer of immunity
Animals—13 specific pathogen-free queens and their
Procedure—Kittens were randomized at birth into 9
treatment groups. One group contained colostrumfed
(nursing) kittens; the other groups contained
colostrum-deprived kittens that were administered
supplemental feline or equine IgG PO or SC during
the first 12 hours after birth. Blood samples were collected
at serial time points from birth to 56 days of
age for determination of serum IgG concentrations.
The capacity of equine IgG to opsonize bacteria for
phagocytosis by feline neutrophils was determined
via flow cytometry.
Results—Kittens that received feline or equine IgG
SC had significantly higher serum IgG concentrations
than those of kittens that received the supplements
PO. In kittens that were administered supplemental
IgG SC, serum IgG concentrations were considered
adequate for protection against infection. The half-life
of IgG in kittens treated with equine IgG was shorter
than that in kittens treated with feline IgG. Feline IgG
significantly enhanced the phagocytosis of bacteria
by feline neutrophils, but equine IgG did not.
Conclusions and Clinical Relevance—Serum concentrations
of equine IgG that are considered protective
against infection are easily attained in kittens, but
the failure of these antibodies to promote bacterial
phagocytosis in vitro suggests that equine IgG may
be an inappropriate treatment for FPT in kittens.
(Am J Vet Res 2003;64:969–975)
Objective—To investigate effects of IV administration of dextrose on coagulation in healthy dogs.
Procedures—Thromboelastography and coagulation panel analysis were used to assess coagulation. Samples (S1 through S9) were collected during the study phases: phase 0 (S1 [baseline]); phase 1 (S2 and S3), infusion of crystalloid fluid without dextrose; phase 2 (S4 and S5), high-rate dextrose infusion; phase 3 (S6, S7, and S8), moderate-rate dextrose infusion; and phase 4 (S9), discontinuation of fluids for 24 hours. In phase 3, dogs were allocated to 2 groups; 1 was administered dextrose at a rate comparable to total parental nutrition (40% of resting energy requirement; group A), and 1 was administered dextrose at rates equaling 70% to 90% of resting energy requirement (group B). Blood glucose concentration was measured every 2 hours.
Results—No dogs had clinically relevant sustained hyperglycemia. Maximum amplitude and elastic shear modulus were significantly lower at S6 than at S1 through S4. Concentration of D-dimer was significantly higher at S6 than at S1, S3, and S4 and significantly higher at S5 than at S3. Prothrombin time was significantly prolonged at S3, S5, S7, S8, and S9, compared with the value at S1. Activated partial thromboplastin time was significantly prolonged at S5 and S6, compared with values at S1, S2, S3, S4, and S9.
Conclusions and Clinical Relevance—IV administration of dextrose to healthy dogs at rates comparable to or higher than those for conventional parenteral nutrition resulted in mild but clinically unimportant interference with coagulation.
Objective—To evaluate effects of blood collection method and site on results of thromboelastography in healthy dogs.
Animals—8 clinically normal purpose-bred dogs.
Procedures—Blood was collected from the external jugular vein by syringe aspiration via direct venipuncture with a 20-gauge needle, through a central venous catheter, or into an evacuated tube with a 21-gauge winged needle catheter. Blood was collected from the lateral saphenous vein by syringe aspiration via direct venipuncture with a 20-gauge needle or into an evacuated tube with a 21-gauge winged needle catheter. Kaolin-activated thromboelastographic analyses were performed, and R (reaction time), K (clot formation time), α angle, maximal amplitude, and G (global clot strength) were analyzed.
Results—No significant differences were observed with regard to sampling site. Sample collection method had no effect on thromboelastographic results for saphenous vein samples. Blood samples collected from the jugular vein by syringe aspiration had a lower R and K and higher α angle than did blood samples collected from the jugular vein by evacuated tube collection. Significant differences were observed between blood samples collected from the jugular vein by syringe aspiration and samples collected from the saphenous vein by evacuated tube collection and between samples collected from the saphenous vein by evacuated tube collection and samples collected from the jugular vein through a central venous catheter.
Conclusions and Clinical Relevance—Different sampling methods resulted in small but significant differences in thromboelastographic values. Results justify the use of standardized techniques for research purposes, but all of these sampling methods were acceptable for 1-time clinical use.
Objective—To determine whether passive transfer of
IgG in neonatal kittens affects plasma opsonic capacity
and neutrophil phagocytic and oxidative burst
responses to bacteria in vitro.
Animals—22 kittens from 6 specific pathogen-free
Procedure—Kittens were randomized at birth into the
following treatment groups: colostrum-fed,
colostrum-deprived, or colostrum-deprived supplemented
with feline or equine IgG. Blood samples
were collected at intervals from birth to 56 days of
age. Plasma IgG concentrations were determined by
radial immunodiffusion assay. Neutrophil function
was assessed by a flow cytometry assay providing
simultaneous measurement of bacteria-induced
phagocytosis and oxidative burst. The opsonic capacity
of kitten plasma was determined in an
opsonophagocytosis assay with bacteria incubated in
untreated or heat-inactivated plasma.
Results—Among treatment groups, there were no
significant differences in neutrophil phagocytic and
oxidative burst responses to bacteria or opsonic
capacity of plasma. In all samples of plasma, inactivation
of complement and other heat-labile opsonins
significantly reduced the opsonic capacity. Plasma
IgG concentrations in kittens did not correlate with
neutrophil function or plasma opsonic capacity before
or after inactivation of complement.
Conclusions and Clinical Relevance—The plasma
opsonic capacity and neutrophil phagocytic and oxidative
burst responses in vitro of kittens receiving passive
transfer of IgG via colostrum intake or IgG supplementation
and those deprived of colostrum were similar.
The alternate complement pathway or other heat-labile
opsonins may be more important than IgG in bacterial
opsonization and phagocytosis. ( Am J Vet Res
Objective—To evaluate the effect of acepromazine maleate administered IV on platelet function assessed in healthy dogs by use of a modified thromboelastography assay.
Animals—6 healthy adult mixed-breed dogs.
Procedures—Dogs received each of 3 treatments (saline [0.9% NaCl] solution [1 to 2 mL, IV] and acepromazine maleate [0.05 and 0.1 mg/kg, IV]) in a randomized crossover study with a minimum 3-day washout period between treatments. From each dog, blood samples were collected via jugular venipuncture immediately before and 30 and 240 minutes after administration of each treatment. A modified thromboelastography assay, consisting of citrated kaolin–activated (baseline assessment), reptilase-ADP–activated (ADP-activated), and reptilase-arachidonic acid (AA)–activated (AA-activated) thromboelastography, was performed for each sample. Platelet inhibition was evaluated by assessing the percentage change in maximum amplitude for ADP-activated or AA-activated samples, compared with baseline values. Percentage change in maximum amplitude was analyzed by use of Skillings-Mack tests with significance accepted at a family-wise error rate of P < 0.05 by use of Bonferroni corrections for multiple comparisons.
Results—No significant differences were found in the percentage change of maximum amplitude from baseline for ADP-activated or AA-activated samples among treatments at any time.
Conclusions and Clinical Relevance—Platelet function in dogs, as assessed by use of a modified thromboelastography assay, was not inhibited by acepromazine at doses of 0.05 or 0.1 mg/kg, IV. This was in contrast to previous reports in which it was suggested that acepromazine may alter platelet function via inhibition of ADP and AA.
Objective—To determine whether thromboelastography is more accurate than conventional methods of evaluating hemostasis for the prediction of clinical bleeding in thrombocytopenic dogs following total body irradiation (TBI) and bone marrow transplantation (BMT).
Animals—10 client-owned thrombocytopenic dogs with multicentric lymphoma.
Procedures—Results of a kaolin-activated thromboelastography assay, platelet count, and buccal mucosal bleeding time were evaluated for correlation to clinical bleeding.
Results—Maximum amplitude, derived via thromboelastography, was the only hemostatic variable with significant correlation to clinical bleeding. Buccal mucosal bleeding time had a high sensitivity but poor specificity for identifying dogs with clinical bleeding.
Conclusions and Clinical Relevance—Compared with buccal mucosal bleeding time and platelet count, thromboelastography was more reliable at identifying thrombocytopenic dogs with a low risk of bleeding and could be considered to help guide the use of transfusion products in dogs undergoing TBI and BMT.