No abstract

BackgroundThree flaviviruses (equine pegivirus [EPgV]; Theiler's disease–associated virus [TDAV]; non‐primate hepacivirus [NPHV]) and equine parvovirus (EqPV‐H) are present in equine blood products; the TDAV, NPHV, and EqPV‐H have been suggested as potential causes of serum hepatitis.ObjectiveTo determine the prevalence of these viruses in horses with equine serum hepatitis.AnimalsEighteen horses diagnosed with serum hepatitis, enrolled from US referral hospitals.MethodsIn the prospective case study, liver, serum, or both samples were tested for EPgV, TDAV, NPHV, and EqPV‐H by PCR.ResultsBoth liver tissue and serum were tested for 6 cases, serum only for 8 cases, and liver only for 4 cases. Twelve horses received tetanus antitoxin (TAT) 4‐12.7 weeks (median = 8 weeks), 3 horses received commercial equine plasma 6‐8.6 weeks, and 3 horses received allogenic stem cells 6.4‐7.6 weeks before the onset of hepatic failure. All samples were TDAV negative. Two of 14 serum samples were NPHV‐positive. Six of 14 serum samples were EPgV‐positive. All liver samples were NPHV‐negative and EPgV‐negative. EqPV‐H was detected in the serum (N = 8), liver (N = 4), or both samples (N = 6) of all 18 cases. The TAT of the same lot number was available for virologic testing in 10 of 12 TAT‐associated cases, and all 10 samples were EqPV‐H positive.Conclusions and Clinical ImportanceWe demonstrated EqPV‐H in 18 consecutive cases of serum hepatitis. EPgV, TDAV, and NPHV were not consistently present. This information should encourage blood product manufacturers to test for EqPV‐H and eliminate EqPV‐H–infected horses from their donor herds.

Classes of antibody bound to erythrocytes were determined using direct immunofluorescence (DIF) flow cytometry in 3 horses and 12 dogs with immune-mediated hemolytic anemia (IMHA). Background levels of antibody binding were determined in samples from 12 horses and 12 dogs that were free of clinical disease. The range of nonspecific binding of a fluorescein isothiocyanate (FITC)-conjugated goat anti-equine immunoglobulin G (IgG) was 19.9-36.7%, but was eliminated by the use of the F(abЈ) 2 fragment of FITC-conjugated goat anti-equine IgG. Background binding by other class-specific antibodies to equine and canine erythrocytes was negligible. The DIF results were compared to the direct antiglobulin (Coombs') test in 5 horses and 20 dogs with anemia. The former assay was more sensitive in dogs with IMHA than was the Coombs' test (100% versus 58%). In contrast, the Coombs' test had better specificity than the DIF assay (100% versus 87.5%, respectively). Using clinical parameters or response to therapy as the comparison, the positive and negative predictive values for the DIF test were 92% and 100% compared to the values of the Coombs' test of 100% and 62%. The DIF assay detected low levels of cells bound with antibody (Ͻ30%) in 5 dogs that were Coombs' test-negative. For both species, performance of the DIF test was independent of the prozone effect. Five dogs with IMHA had IgG and IgM on erythrocytes, 5 had IgG, and 2 had IgM. Three horses had surface-bound IgG, including a horse with suspected penicillin-induced IMHA, a foal with neonatal isoerythrolysis, and a foal with clostridial septicemia. The DIF method was valuable in monitoring the response to therapy in the foal with neonatal isoerythrolysis.Key words: Antibody classes; Coombs' test; Direct immunofluorescence; Erythrocyte antibody; Flow cytometry. Immune-mediated hemolytic anemia (IMHA) is an immunohematologic disorder in which destruction of red blood cells is accelerated by the attachment of antibody, with or without complement, to the erythrocyte membrane. Antibodies may be directed against unaltered red blood cells (primary or idiopathic) or against erythrocytes that have been antigenically altered through interaction with secondary causes, including drugs, neoplasia, and infectious diseases.1-6 The relative frequencies of primary and secondary IMHA in dogs are 43% and 57%, respectively. 7The diagnosis is confirmed by the presence of spherocytosis, autoagglutination, or by a positive direct antiglobulin (Coombs') test that has been validated for use in the species of interest. [8][9][10][11][12] The Coombs' test is based on detection of agglutination or clumping of erythrocytes after addition of an anti-species polyvalent mixture of antibody to immunoglobulin M (IgM), IgG, and complement protein C 3 . Serial dilutions of the polyvalent Coombs' reagent are prepared and tested against patient erythrocytes to provide the proper concentration equivalence between antiglobulin and the antibody-coated erythrocytes at which agglutination occurs. Because of the...

No abstract

No abstract

Recent years have witnessed a surge in interest directed at innate immune mechanisms. Proper conceptualization of the key elements of innate immunity, however, is still a work in progress, because most research in immunology traditionally has been focused on components of the acquired immune response. The question of why an animal stays healthy in a world filled with many dangers is perhaps as interesting as why it sometimes surrenders to disease. Consequently, studies with an increased focus on inborn mechanisms of animal host defense may help further the development of appropriate preventative and therapeutic measures in veterinary medicine. Host defense peptides (HDPs) are central effector molecules of innate immunity, and are produced by virtually all living species throughout the plant and animal kingdoms. These gene-encoded peptides play a central role in multiple, clinically relevant disease processes. Imbalances in the expression of HDPs can lead to overt pathology in different organ systems and cell types in all species studied. In addition, HDPs are an ancient group of innate chemical protectors, which are now evaluated as model molecules for the development of novel natural antibiotics and immunoregulatory compounds. This review provides an overview of HDPs and is aimed at veterinary practitioners as well as basic researchers with an interest in comparative immunology involving small and large animal species.

A 4-year-old Paint mare was examined because of respiratory tract infection, dermatitis, and weight loss of 2 months' duration. Initial examination revealed generalized pruritic dermatitis, ocular and nasal discharges, and stranguria. Laboratory abnormalities included leukopenia and hypoalbuminemia. Further examination of the respiratory tract revealed grade III of IV pharyngitis and pyogranulomatous pneumonia. Endoscopic examination of the bladder revealed a prolific mass at the junction of the bladder and urethra. Hypoproteinemia was suspected to be caused by protein-losing enteropathy. On histologic examination, skin, rectal, pharyngeal, and urethral biopsy specimens were characterized by infiltration of eosinophils and lymphocytes, and a diagnosis of multisystemic eosinophilic epitheliotropic disease was made. The horse improved following treatment with dexamethasone, trimethoprim-sulfamethoxazole, and an antihistamine and was discharged after 19 days of hospitalization. Treatment with dexamethasone was continued for 4 weeks after hospitalization but was then discontinued. Eight months after discharge, the horse was performing as a pleasure horse and did not require any medical treatment. Multisystemic eosinophilic epitheliotropic disease is typically associated with a poor prognosis in horses. The dermatitis, protein-losing enteropathy, and lower respiratory tract disease in this horse were consistent with previous reports; however, pharyngitis and urethritis have not, to our knowledge, been previously reported in horses with this disease.

The objective of the study was to assess the pharmacokinetics of terbinafine administered orally to horses and Greyhound dogs. A secondary objective was to assess terbinafine metabolites. Six healthy horses and six healthy Greyhound dogs were included in the pharmacokinetic data. The targeted dose of terbinafine was 20 and 30 mg/kg for horses and dogs, respectively. Blood was obtained at predetermined intervals for the determination of terbinafine concentrations with liquid chromatography and mass spectrometry. The half-life (geometric mean) was 8.1 and 8.6 hours for horses and Greyhounds, respectively. The mean maximum plasma concentration was 0.31 and 4.01 μg/mL for horses and Greyhounds, respectively. The area under the curve (to infinity) was 1.793 hr*μg/mL for horses and 17.253 hr*μg/mL for Greyhounds. Adverse effects observed in one study horse included pawing at the ground, curling lips, head shaking, anxiety and circling, but these resolved spontaneously within 30 minutes of onset. No adverse effects were noted in the dogs. Ions consistent with carboxyterbinafine, n-desmethylterbinafine, hydroxyterbinafine and desmethylhydroxyterbinafine were identified in horse and Greyhound plasma after terbinafine administration. Further studies are needed assessing the safety and efficacy of terbinafine in horses and dogs.