Fibropapillomatosis is a neoplastic disease of marine turtles, with green turtles (Chelonia mydas) being the most affected species. Fibropapillomatosis causes debilitating tumor growths on soft tissues and internal organs, often with lethal consequences. Disease incidence has been increasing in the last few decades and the reason is still uncertain. The potential viral infectious agent of Fibropapillomatosis, chelonid herpesvirus 5, has been co-evolving with its sea turtle host for millions of years and no major mutation linked with increased disease occurrence has been detected. Hence, frequent outbreaks in recent decades are likely attributable to external drivers such as large-scale anthropogenic changes in the green turtle coastal marine ecosystem. This study found that variations in sea surface temperature, salinity, and nutrient effluent discharge from nearby rivers were correlated with an increased incidence of the disease, substantiating that these may be among the significant environmental drivers impacting Fibropapillomatosis prevalence. This study offers data and insight on the need to establish a baseline of environmental factors which may drive Fibropapillomatosis and its clinical exacerbation. We highlight the multifactorial nature of this disease and support the inclusion of interdisciplinary work in future Fibropapillomatosis research efforts.

Emerging infectious diseases of wildlife have markedly increased in the last few decades. Unsustainable, continuous, and rapid alterations within and between coupled human and natural systems have significantly disrupted wildlife disease dynamics. Direct and indirect anthropogenic effects, such as climate change, pollution, encroachment, urbanization, travel, and trade, can promote outbreaks of infectious diseases in wildlife. We constructed a coupled human and natural systems framework identifying three main wildlife disease risk factors behind these anthropogenic effects: (i) immune suppression, (ii) viral spillover, and (iii) disease propagation. Through complex and convoluted dynamics, each of the anthropogenic effects and activities listed in our framework can lead, to some extent, to one or more of the identified risk factors accelerating disease outbreaks in wildlife. In this review, we present a novel framework to study anthropogenic effects within coupled human and natural systems that facilitate the emergence of infectious disease involving wildlife. We demonstrate the utility of the framework by applying it to Fibropapillomatosis disease of marine turtles. We aim to articulate the intricate and complex nature of anthropogenically exacerbated wildlife infectious diseases as multifactorial. This paper supports the adoption of a One Health approach and invites the integration of multiple disciplines for the achievement of effective and long-lasting conservation and the mitigation of wildlife emerging diseases.

During the past three months, a new coronavirus (SARS-CoV-2) epidemic has been growing exponentially, affecting over 100 thousand people worldwide, and causing enormous distress to economies and societies of affected countries. A plethora of analyses based on viral sequences has already been published, in scientific journals as well as through non-peer reviewed channels, to investigate SARS-CoV-2 genetic heterogeneity and spatiotemporal dissemination. We examined all full genome sequences currently available to assess the presence of sufficient information for reliable phylogenetic and phylogeographic studies. Our analysis clearly shows severe limitations in the present data, in light of which any finding should be considered, at the very best, preliminary and hypothesis-generating. Hence the need for avoiding stigmatization based on partial information, and for continuing concerted efforts to increase number and quality of the sequences required for robust tracing of the epidemic.

Each year, SARS-CoV-2 is infecting an increasingly unprecedented number of species. In the present article, we combine mammalian phylogeny with the genetic characteristics of isolates found in mammals to elaborate on the host-range potential of SARS-CoV-2. Infections in nonhuman mammals mirror those of contemporary viral strains circulating in humans, although, in certain species, extensive viral circulation has led to unique genetic signatures. As in other recent studies, we found that the conservation of the ACE2 receptor cannot be considered the sole major determinant of susceptibility. However, we are able to identify major clades and families as candidates for increased surveillance. On the basis of our findings, we argue that the use of the term panzootic could be a more appropriate term than pandemic to describe the ongoing scenario. This term better captures the magnitude of the SARS-CoV-2 host range and would hopefully inspire inclusive policy actions, including systematic screenings, that could better support the management of this worldwide event.

Fibropapillomatosis (FP) is a neoplastic disease most often found in green turtles (Chelonia mydas). Afflicted turtles are burdened with potentially debilitating tumors concentrated externally on the soft tissues, plastron, and eyes and internally on the lungs, kidneys, and the heart. Clinical signs occur at various levels, ranging from mild disease to severe debilitation. Tumors can both progress and regress in affected turtles, with outcomes ranging from death due to the disease to complete regression. Since its official description in the scientific literature in 1938, tumor growth rates have been rarely documented. In addition, FP tumors come in two very different morphologies; yet, to our knowledge, there have been no quantified differences in growth rates between tumor types. FP tumors are often rugose in texture, with a polypoid to papillomatous morphology, and may or may not be pedunculated. In other cases, tumors are smooth, with a skin-like surface texture and little to no papillose structures. In our study, we assessed growth-rate differences between rugose and smooth tumor morphologies in a rehabilitation setting. We measured average biweekly tumor growth over time in green turtles undergoing rehabilitation at the University of Florida Whitney Laboratory Sea Turtle Hospital in St. Augustine, Florida, and compared growth between rugose and smooth tumors. Our results demonstrate that both rugose and smooth tumors follow a similar active growth progression pattern, but rugose tumors grew at significantly faster rates (p = 0.013) than smooth ones. We also documented regression across several examined tumors, ranging from −0.19% up to −10.8% average biweekly negative growth. Our study offers a first-ever assessment of differential growth between tumor morphologies and an additional diagnostic feature that may lead to a more comprehensive understanding and treatment of the disease. We support the importance of tumor morphological categorization (rugose versus smooth) being documented in future FP hospital- and field-based health assessments.