Canine parvovirus type 2 is the cause of a highly contagious acute enteritis associated with high morbidity and mortality, with very low survival rates in untreated dogs. Although severe clinical disease typically occurs in dogs younger than 6 months of age, adults with insufficient immunity may potentially be affected. In this article, the current state of knowledge is reviewed regarding the diagnostic aspects of parvoviral enteritis, with special emphasis placed on the clinical relevance of the detection of viral antigens in the feces, detection of viral antibodies in the serum, or the polymerase chain reaction-based amplification of the viral DNA in the feces. In addition, the components of the supportive and symptomatic treatment aiming to optimize the outcome of the disease in the clinical setting are thoroughly reviewed. Immunization guidelines for the prevention of the disease are also updated.

Canine monocytic ehrlichiosis (CME) is a tick-borne disease of worldwide distribution. The major causative agent is Ehrlichia canis, a gram-negative, obligate intracellular, pleomorphic bacterium of the genus Ehrlichia, which infects monocytes, macrophages and lymphocytes, forming intracytoplasmic, membrane-bound bacterial aggregates, called morulae. After an incubation period of 8-20 days, the course of E. canis infection, can be sequentially divided into acute, subclinical and chronic phases, although these phases can hardly be distinguished in the clinical setting. Clinical recovery is the typical outcome of acutely infected dogs, entering the subclinical phase, during which they show no or minimal clinical signs and/or mild hematological abnormalities. Immunocompetent dogs may eliminate the infection during the acute or subclinical phases, but an unpredictable proportion of dogs will eventually develop the chronic phase, characterized by aplastic pancytopenia and high mortality, due to septicemia and/or severe bleeding. This article outlines briefly the pathogenesis of CME due to E. canis, and more thoroughly reviews the recent scientific literature pertaining to the diagnosis and treatment of this devastating disease.

The potential impact of preanalytical factors, such as type of anticoagulant, storage temperature, and time, on the formation of macroplatelets and platelet aggregates (platelet clumping) in dogs is largely elusive. The objective of the current study was to assess the effect of anticoagulant, temperature, and blood storage time in the light microscopy-generated macroplatelet percentages and the frequency of visually inspected platelet aggregates in clinically healthy dogs. Giemsa-stained blood smears from 70 healthy dogs were reviewed after exposure to different anticoagulants (ethylenediamine tetra-acetic acid [EDTA] vs. citrate), temperatures (25°C vs. 4°C), and storage times (up to 24 hr postsampling). The mean percentage of macroplatelets (platelets with diameter or length ≥ μm) was higher (P = 0.0006) when EDTA was used as the anticoagulant. For either anticoagulant, the mean percentage of macroplatelets was higher (P < 0.0001) at 25°C than at 4°C. Platelet clumping was 1.9 times (P < 0.0001) more likely to occur when citrate- rather than EDTA-anticoagulated blood was examined; regardless of the anticoagulant used, clumping occurred 3 times (P < 0.0001) more often when samples were preserved at 4°C than when they were preserved at 25°C. Storage time did not significantly influence the macroplatelet percentages or the frequency of platelet clumping. The results of this study indicate that macroplatelet percentages in the canine blood should be interpreted in relation to anticoagulant- and temperature-specific reference intervals and that future studies are warranted in order to investigate the clinical relevance of this calculation. In addition, the significant association of citrate with the formation of platelet aggregates may preclude its use for platelet enumeration in the dog.