NOVEL DIAGNOSTIC AND THERAPEUTIC APPROACHES TO ELEPHANT ENDOTHELIOTROPIC HERPESVIRUS 1A HEMORRHAGIC DISEASE IN A CAPTIVE JUVENILE ASIAN ELEPHANT (ELEPHAS MAXIMUS).

Novel diagnostic and therapeutic methods were utilized in the successful management of severe elephant endotheliotropic herpesvirus hemorrhagic disease (EEHV-HD) in a 1.9-yr-old captive Asian elephant (Elephas maximus). High levels of EEHV1A viremia were detected for 12 d. In addition to established EEHV treatments, therapies included famciclovir-fortified elephant whole blood and plasma, mesenchymal stem cells harvested from elephant umbilical tissue, and aminocaproic acid. Testing conducted to examine the effects of EEHV infection on hemostasis suggested marked intravascular coagulation with decreased plasminogen activity and increased D-dimer concentrations. Thromboelastography was used to assess the efficacy of aminocaproic acid and demonstrated hypofibrinolysis on samples taken after drug administration, as compared with samples from healthy adult Asian elephants. A serological assay for a novel EEHV1A-specific antibody marker (E52) was developed due to lack of seroconversion to a previously established EEHV1A-specific antibody marker (ORFQ) and showed a sustained increase after EEHV-HD illness.

Elephant endotheliotropic herpesvirus 5, a newly recognized elephant herpesvirus associated with clinical and subclinical infections in captive Asian elephants (Elephas maximus).

Elephant endotheliotropic herpesviruses (EEHVs) can cause acute hemorrhagic disease with high mortality rates in Asian elephants (Elephas maximus). Recently, a new EEHV type known as EEHV5 has been described, but its prevalence and clinical significance remain unknown. In this report, an outbreak of EEHV5 infection in a herd of captive Asian elephants in a zoo was characterized. In February 2011, a 42-yr-old wild-born female Asian elephant presented with bilaterally swollen temporal glands, oral mucosal hyperemia, vesicles on the tongue, and generalized lethargy. The elephant had a leukopenia and thrombocytopenia. She was treated with flunixin meglumine, famciclovir, and fluids. Clinical signs of illness resolved gradually over 2 wk, and the white blood cell count and platelets rebounded to higher-than-normal values. EEHV5 viremia was detectable starting 1 wk before presentation and peaked at the onset of clinical illness. EEHV5 shedding in trunk secretions peaked after viremia resolved and continued for more than 2 mo. EEHV5 trunk shedding from a female herd mate without any detectable viremia was detected prior to onset of clinical disease in the 42-yr-old elephant, indicating reactivation rather than primary infection in this elephant. Subsequent EEHV5 viremia and trunk shedding was documented in the other five elephants in the herd, who remained asymptomatic, except for 1 day of temporal gland swelling in an otherwise-healthy 1-yr-old calf. Unexpectedly, the two elephants most recently introduced into the herd 40 mo previously shed a distinctive EEHV5 strain from that seen in the other five elephants. This is the first report to document the kinetics of EEHV5 infection in captive Asian elephants and to provide evidence that this virus can cause illness in some animals.

Pulmonic Valve Repair in a Patient with Isolated Pulmonic Valve Endocarditis and Sickle Cell Disease.

A 49-year-old woman with sickle cell disease presented with one month of exertional dyspnea, weakness, and fever and was diagnosed with isolated pulmonic valve endocarditis secondary to methicillin-resistant Staphylococcus bacteremia in the setting of a peripherally inserted central venous catheter. Chest computerized tomography showed multiple bilateral pulmonary nodular opacities consistent with septic emboli. Transthoracic and transesophageal echocardiograms revealed a large echodensity on the pulmonic valve requiring vegetation excision and pulmonic valve repair. In conclusion, isolated pulmonic valve endocarditis is a rare cause of infective endocarditis that warrants a high index of clinical suspicion. Furthermore the management of patients with sickle cell disease and endocarditis requires special consideration.