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Platelet dysfunction associated with experimental acute canine ehrlichiosis
  1. S. Harrus, DVM1,
  2. T. Waner, BVSc, MSc2,
  3. A. Eldor, MD3,
  4. E. Zwang3 and
  5. H. Bark, BVSc, PhD1
  1. 1 Small Animal Internal Medicine Department, School of Veterinary Medicine, Hebrew University of Jerusalem, PO Box 12, Rehovot, Israel
  2. 2 Life Science Research Israel, Ness Ziona, Israel
  3. 3 Haematology Department, Tel-Aviv Sourasky Medical Centre, Tel-Aviv, Israel

Abstract

To determine whether platelet dysfunction occurs in canine ehrlichiosis, platelet aggregation studies in response to collagen/ epinephrine, thrombin and adenosine diphosphate (ADP) were carried out by the indirect method, using sera from six dogs experimentally infected with Ehrlichia canis. Samples of serum taken before infection and four and 20 days after infection were tested by incubation with platelet-rich plasma from a seronegative healthy dog. Platelet aggregation was significantly inhibited in five of six infected dogs in response to at least one of the agonists used. A significant increase in preaggregation lag time was recorded in response to collagen/ epinephrine in sera taken 20 days after infection from three of five dogs (P<0.05). When compared with the preinfection values, a significant increase of 45 per cent in the mean preaggregation lag time was detected (P<0.05). Maximal relative aggregation responses to ADP decreased significantly in one serum sample taken four days and one taken 20 days after infection (P<0.01) and there was a significantly lower relative slope for one serum sample 20 days after infection (P<0.05). Maximal relative aggregation responses to thrombin were significantly decreased together with their relative slopes in serum samples from two of four dogs four days after infection (P<0.05). The results suggest that platelet dysfunction may occur in the acute stage of canine ehrlichiosis, and may be a contributing factor to the tendency to bleed commonly observed in this disease. Antiplatelet antibodies directed against platelet glycoproteins may play a role in the inhibition of platelet aggregation.

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