• As a general rule, platelet counts obtained by automated cell counters are more consistently accurate than counts measured by manual methods.
• In the presence of platelet clumping, there is no way to accurately count the number of platelets. Both automated and manual platelet counts will be affected by clumping, so that review of the blood smear to provide a platelet estimate gives the best indication of the adequacy of platelet numbers.

Typing canine blood for purposes of identifying suitable blood donors can be performed by screening methods (in-clinic commercial blood typing cards), which type only for the canine DEA 1.1 blood group antigen, or by diagnostic reference laboratories that offer the preferred, more comprehensive typing profiles. At Antech Diagnostics, typing is available for the canine blood group antigens DEA 1.1, 1.2 and 7, a more complete but still not ideal typing profile, as well as the most complete profile that types for all known canine blood group antigens. The ideal canine blood donor has the blood type designation DEA 4, and is typed as negative for all known blood group antigens except 4. While the clinically most important canine red blood cell antigens belong to the DEA 1.1, 1.2 and 7 phenotypes, transfusion incompatibilities can arise against the other antigens, especially DEA 3. As veterinary clinics frequently screen greyhounds available from the racing industry to identify potential blood donors, it is important to realize that up to 23% of greyhounds are DEA 3-positive, as opposed to a frequency of ~ 6% in the general dog population. Administration of DEA 3-positive red blood cells to a previously sensitized DEA 3- negative dog results in loss of the transfused red cells within 5 days and can produce severe, acute transfusion reactions. Naturally occurring anti-DEA 3 antibody has been reported in up to 20% of DEA 3-negative dogs, so the risk of mismatched DEA 3 transfusions is relatively high, especially if greyhounds are the source of donor blood. This problem is avoided by selecting only true "universal donor" dogs (i.e., DEA 4).

Reference: Andrews, Schalm's Veterinary Hematology, 5th ed., Lippincott, Williams, Wilkins, 2000, pp. 767-773.

Fifteen fibrosarcomas, surgically excised from presumed sites of injection in dogs, and 10 canine fibrosarcomas excised from sites not used for injection were histologically and immunohistochemically compared with 20 feline post-vaccinal fibrosarcomas. Canine fibrosarcomas from presumed injection sites were of grade I (3), of grade II (4) and grade III (8). Two fibrosarcomas from non-injection sites were of grade I, four of grade II and four of grade III. Feline samples were classified as grade I (2), grade II (4) and grade III (14). All fibrosarcomas from presumed injection sites of both species showed lymphocytic inflammatory infiltration located at the tumor periphery, while two canine fibrosarcomas from non-injection sites showed perivascular inflammatory infiltration within the neoplasm. All tumors were positive for vimentin. Ten canine fibrosarcomas from presumed injection sites and all feline samples contained cells consistent with a myofibroblastic immunophenotype. Aluminium deposits were detected in 8 canine fibrosarcomas from presumed injection sites and 11 feline post-vaccinal fibrosarcomas. The present study identifies distinct similarities between canine fibrosarcomas from presumed injection sites and feline post-vaccinal fibrosarcomas, suggesting that the development of post-injection sarcomas occurs not only in cats, but also in dogs.

Reference: Vascellari et al., J Vet Med A 50: 286-291, 2003.