Spirocercosis and Parvovirus in an Imported Dog: Implications for Biosecurity and Foreign Infectious Disease Risk.

Increased international travel and importation of animals brings with it the potential for spread of infectious diseases. This report details a case in which an 8-month-old male mixed breed dog died shortly after arrival to the United States from complications secondary to spirocercosis, despite having been deemed healthy and approved for international travel. Four weeks following arrival, the dog developed mild tachypnea and diarrhea. Physical examination revealed moderate pyrexia with generalized cerebellar ataxia, moderate anemia, a mature neutrophilia, and severe panhypoproteinemia. Packed red blood cells were administered. The dog was diagnosed with pyothorax and decompensated with septic shock shortly thereafter. Necropsy revealed severe transmural esophagitis with intralesional Spirocerca lupi. Evaluation of the brain revealed cerebellar hypoplasia, and polymerase chain reaction of brain tissue was positive for canine parvovirus. Despite receiving a clean bill of health in its country of origin, this patient ultimately had evidence of 2 different infectious processes that pre-dated its arrival into the United States. While neither of these diseases posed a significant public health risk, this case highlights the role veterinarians play before and after international travel as important barriers against the spread of exotic diseases, and emphasizes that maintaining vigilance is paramount to that task.

Toxoplasma gondii infection in feline renal transplant recipients: 24 cases (1998-2018).

OBJECTIVE: To evaluate the effects of Toxoplasma gondii infection in feline renal transplant recipients with a preoperative seronegative or unknown serostatus (SN-UNK) for T gondii and the efficacy of lifelong prophylactic treatment of T gondii infection in feline renal transplant recipients with a preoperative seropositive serostatus (SP) for T gondii. ANIMALS: 24 cats with various serostatuses for T gondii before undergoing renal transplantation. PROCEDURES: Medical records of cats that had undergone renal transplantation from 1998 through 2018 were reviewed. Two groups of cats were identified. Before renal transplantation, the SN-UNK group cats were seronegative for T gondii (n = 4) or serostatus for T gondii was unknown (4). The SN-UNK group cats received immunosuppressive therapy but were not maintained on prophylactic treatment of T gondii infection. The SP group cats were seropositive for T gondii (n = 16) prior to initiation of immunosuppressive therapy and renal transplantation and were managed after surgery with prophylactic treatment of T gondii infection. RESULTS: All 8 SN-UNK group cats developed T gondii infections after initiation of immunosuppressive therapy and renal transplantation; T gondii infections were fatal in 6 cats. Of 16 SP group cats, 1 developed a nonfatal T gondii infection resulting in an allograft rejection episode. No SP group cats, which were managed postoperatively with prophylactic treatment, developed a fatal T gondii infection. CONCLUSIONS AND CLINICAL RELEVANCE: T gondii infection resulted in morbidity and death in immunosuppressed cats not receiving prophylactic treatment of T gondii infection after renal transplantation. Seropositive cats were acceptable candidates for renal transplantation when lifelong prophylactic treatment of T gondii infection was provided.

Candidate prognostic indicators in cats with histoplasmosis treated with antifungal therapy.

Objectives The aim of this study was to retrospectively identify candidate prognostic indicators in cats with histoplasmosis treated with antifungal therapy. Methods Medical records of cats diagnosed with histoplasmosis were reviewed. Candidate prognostic indicators were assessed for an association with survival to hospital discharge and survival to 1 and 6 months after diagnosis. Potential indicators included easily obtained data at the time of the initial hospital visit derived from cat signalment, historical information, physical examination, laboratory data, form of disease and initial treatment. Results Approximately 88% of cats survived to discharge, with 77% and 67% surviving to 1 and 6 months, respectively. Clinical variables significantly associated with death at more than one outcome time point included the presence of dyspnea, adventitial lung sounds, fungemia, neurologic disease, neutropenia, lymphopenia, multiple cytopenias (anemia, neutropenia, thrombocytopenia), hyperbilirubinemia and increased creatinine kinase activity. Cats that did not survive were more likely to have received corticosteroids, oxygen supplementation and required hospitalization. In addition, cats that did not survive required significantly longer hospitalization. There was no significant difference between initial antifungal drug and survival. Conclusions and relevance Potential prognostic indicators were associated with more severe respiratory, hepatic, hematologic or neurologic disease. Prospective investigation concerning clinical indicators of disease severity of these body systems is indicated.

Use of a Cyclooxygenase-2 Inhibitor Does Not Inhibit Platelet Activation or Growth Factor Release From Platelet-Rich Plasma.

BACKGROUND: It remains unestablished whether use of cyclooxygenase (COX)-2 inhibitors impairs platelet activation and anabolic growth factor release from platelets in platelet-rich plasma (PRP). PURPOSE: The purpose of this study was to assess the effects of a COX-2 inhibitor on platelet activation and anabolic growth factor release from canine PRP when using a clinically applicable PRP activator and to determine whether a 3-day washout would be sufficient to abrogate any COX-2 inhibitor-related impairment on platelet function. STUDY DESIGN: Controlled laboratory study. METHODS: Ten healthy dogs underwent blood collection and PRP preparation. Dogs were then administered a COX-2 inhibitor for 7 days, after which PRP preparation was repeated. The COX-2 inhibitor was continued for 4 more days and PRP preparation performed a third time, 3 days after discontinuation of the COX-2 inhibitor. Immediately after PRP preparation, the PRP was divided into 4 aliquots: 2 unactivated and 2 activated using human γ-thrombin (HGT). One activated and 1 unactivated sample were assessed using flow cytometry for platelet expression of CD62P and platelet-bound fibrinogen using the canine activated platelet-1 (CAP1) antibody. The 2 remaining samples were centrifuged and the supernatant assayed for transforming growth factor-ß1 (TGF-ß1), platelet-derived growth factor-BB (PDGF-BB), and thromboxane B2 (TXB2) concentrations. Differences in platelet activation and TGF-ß1, PDGF-BB, and TXB2 concentrations over the 3 study weeks were evaluated using a 1-way repeated-measures ANOVA, and comparisons between activated and unactivated samples within a study week were assessed with paired t tests. RESULTS: There were no statistically significant ( P > .05) effects of the COX-2 inhibitor on percentage of platelets positive for CD62P or CAP1 or on concentrations of TGF-ß1, PDGF-BB, or TXB2. All unactivated samples had low levels of activation or growth factor concentrations and significantly ( P < .05) greater activation and growth factor concentrations in HGT-activated samples. CONCLUSION: This COX-2 inhibitor did not impair platelet activation, growth factor release, or TXB2 production in this canine PRP when using HGT as an activator. Studies are warranted to determine whether COX-2 inhibitors affect platelet activation and growth factor release from human PRPs. CLINICAL RELEVANCE: These results suggest that there is no need to withhold a COX-2 inhibitor before PRP preparation, particularly if thrombin is going to be used to activate the PRP. This is clinically relevant information because many patients who are candidates for PRP therapy for treatment of musculoskeletal injury are also using COX-2 inhibitors.