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- Author or Editor: Emma Hooijberg x
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African Horse Sickness (AHS) is a vector-borne disease endemic to sub-Saharan Africa caused by African Horse Sickness Virus (AHVS). Infections in naïve horses have high morbidity and mortality rates. AHS pathogenesis is not well understood; neither the hematologic changes nor acute phase response occurring during infection has been fully evaluated. The study’s objective was to characterize the hematologic changes and acute phase response during experimental infection with AHSV.
4 horses negative for AHSV group-specific antibodies.
In this prospective, longitudinal study conducted between November 23 and December 2, 2020, horses were experimentally infected with AHSV, and blood samples were obtained before inoculation and then every 12 hours until euthanasia. Hematologic changes and changes for serum amyloid A (SAA) and iron concentration were evaluated over time using a general linear model including natural logarithm of sampling time.
All horses were humanely euthanized due to severe clinical signs typical of AHS. Median Hct increased significantly, and the median WBC count, monocyte count, eosinophil count, and myeloperoxidase index changed significantly in all horses over time. Horses developed marked thrombocytopenia (median, 48 X 103 cells/µL; range, 21 X 103 to 58 X 103 cells/µL) while markers of platelet activation also changed significantly. Median SAA increased and serum iron concentration decreased significantly over time.
Results indicated severe thrombocytopenia with platelet activation occurs during infection with AHSV. Changes in acute phase reactants SAA and iron, while significant, were unexpectedly mild and might not be useful clinical markers.
To compare the serum cobalamin concentrations in canine parvovirus (CPV)–infected dogs with those of healthy control dogs.
45 dogs with CPV enteritis and 17 healthy age-matched control dogs.
Infection was confirmed by visualization of CPV-2 through fecal electron microscopy. All dogs received supportive care. Serum samples taken at admission were used to determine cobalamin, C-reactive protein, and albumin concentrations.
Serum cobalamin concentrations were significantly lower in the CPV-infected group (median [interquartile range], 173 pmol/L [< 111 to 722 pmol/L]) than in healthy control dogs (379 pmol/L [193 to > 738 pmol/L). There was no association between cobalamin concentration and C-reactive protein or albumin concentration.
While hypocobalaminemia was common in CPV-infected dogs, the clinical relevance of this finding remains to be determined. Studies assessing markers of cellular cobalamin deficiency in dogs with CPV infection appear warranted.