Increased Survival In Puppies Affected By Canine Parvovirus Type II Using An Immunomodulator As A Therapeutic Aid

Abstract Background: The canine parvoviral enteritis (CPE) promotes sepsis and systemic inflammatory response syndrome (SIRS). Mortality in this disease is usually registered within 48–72 h post-hospitalization, the critical period of the disease. It has been recently described that the use of an immunomodulator whose major component is monomeric ubiquitin (mUb) without the last two glycine residues (Ub∆GG) in pediatric patients with sepsis improves survival. It is known that CXCR4 is the cell receptor of extracellular ubiquitin in humans. The aim of this work was to explore the effect of one immunomodulator (hDLE) as a therapeutic auxiliary in CPE puppies with sepsis and SIRS. Results: We studied two groups of puppies with CPE confirmed by polymerase chain reaction. The first group received conventional treatment (CT) and vehicle (V), while the second group received CT plus an immunomodulator (I). In both groups, we assessed the survival, clinical condition, number of erythrocytes, neutrophils, and lymphocytes, and values of hematocrit, hemoglobin, plasma proteins, cortisol, and norepinephrine epinephrine, and serotonin, during hospitalization.Puppies treated with CT+I showed 81% survival and milder clinical signs and a significant decrease in circulating neutrophils and lymphocytes in the critical period of the treatment. In contrast, the CT+V group presented a survival of 42%, severe clinical status, and no improvement of the parameters evaluated in the critical period of the disease. We determined in silico that human Ub∆GG can stimulate dog CXCR4. Conclusions: The administration of an immunomodulator (5 mg/day x 5 days) to puppies with CPE under 6 months of age reduces the severity of clinical signs, increases survival, and modulates inflammatory cell parameters. Further studies are necessary to take full advantage of these clinical findings which might be mediated by the human Ub∆GG to canine CXCR4 interaction.