Clinical characteristics and possible routes of elephant endotheliotropic herpesvirus (EEHV) shedding in Asian elephant (Elephas maximus) herds

Abstract

Elephant Endotheliotropic Herpesvirus (EEHV) is a viral disease that has emerged as a major threat to the conservation of Asian elephants (Elephas maximus) in recent years. EEHV is a member of the Betaherpesvirinae, first reported in 1990 with polymerase chain reaction (PCR) analysis by causing the death in 3 circus juvenile elephants in Switzerland. The virus primarily affects young elephants between the ages of 1 and 8, with a mortality rate of approximately 80-85% from haemorrhagic disease and multiple-organ failure. High evidence of EEHV infected rate is found in range countries, including Thailand. Despite extensive research, the clinical characteristics, and possible routes of viral shedding in EEHV-infected Asian elephant herds are remain not fully understood. The first study complies and examines the clinical characteristic of 103 EEHV patients that were confirmed by PCR in Thailand between 2009 and 2016. The findings demonstrate that the clinical manifestation of EEHV infection is contingent upon the viral strain, clinical signs, age range, husbandry (trained or weaned), and season but is unaffected by gender. Undoubtedly, blood profile abnormalities including severe grade of heterophil toxicity, leukopenia, thrombocytopenia, anemia and hypoproteinemia are observed in badly afflicted elephants, and antiviral medication treatment for this group of animals has a poor success record. In the second study, pre-mortem diagnoses of EEHV with PCR method by using a non-invasive technique collect the biological samples compare from saliva and feces of 5 elephants for over 12 weeks. This work offers the first proof that detectable quantities of EEHV are expelled in feces and will be useful to applied in wild and free-living elephant population epidemiology studies. The third study, we examine the potential for perinatal EEHV transmission via transplacental or colostral. We present the possible evidence of the EEHV pathogen's capacity to reside in the placenta endothelium without endangering fetuses or it might be only the engulfing of antigen into macrophage cytoplasm. The fetuses may develop antibodies or acquire transplacental maternal protection against EEHV, or the viruses may be dormant and not infectious. Hence, no evidence of colostral transmission was found in this study. To confirm perinatal transmission in EEHV, more positive sample studies are needed, along with specific EEHV antibody confirm, additional research on EEHV antibody level, placental pathogenesis and transplacental immunity of the virus. Overall, the data from our investigations provide more insight into the clinical features and transmission of EEHV and are helpful in the detection of viruses, which will aid in the development of preventative and therapeutic measures for the disease in Asian elephant herds, preserving the integrity of this endangered species.