Animals as sentinels of chemical terrorism agents: an evidence-based review.

OBJECTIVES: The goal of this systematic review was to identify evidence that animals could serve as sentinels of an attack with a chemical terrorism agent. METHODS: The biomedical literature was systematically searched for evidence that wild or domestic animals exposed to certain chemical weapons of terrorism had either greater susceptibility, shorter latency period, or increased exposure risk versus humans. Additionally, we searched for documented reports of such animals historically serving as sentinels for chemical warfare agents. RESULTS: For a small number of agents, there was limited evidence that domestic and/or wild animals could provide sentinel information to humans following an airborne attack with chemical agents, usually related to increased potential for environmental exposure. Some of this evidence was based on anecdotal case reports, and in many cases high quality chemical terrorism agent evidence regarding comparative susceptibility, exposure, and latency between humans and sentinel animal species was not found. CONCLUSION: Currently, there is insufficient evidence for routine use of animals as sentinels for airborne chemical warfare agents. At the same time, Poison Center surveillance systems should include animal calls, and greater communication between veterinarians and physicians could help with preparedness for a chemical terrorism attack. Further analysis of comparative chemical warfare agent toxicity between sentinel animal species and humans is needed.

From "us vs. them" to "shared risk": can animals help link environmental factors to human health?

Linking human health risk to environmental factors can be a challenge for clinicians, public health departments, and environmental health researchers. While it is possible that nonhuman animal species could help identify and mitigate such linkages, the fields of animal and human health remain far apart, and the prevailing human health attitude toward disease events in animals is an "us vs. them" paradigm that considers the degree of threat that animals themselves pose to humans. An alternative would be the development of the concepts of animals as models for environmentally induced disease, as well as potential "sentinels" providing early warning of both noninfectious and infectious hazards in the environment. For such concepts to truly develop, critical knowledge gaps need to be addressed using a "shared risk" paradigm based on the comparative biology of environment-host interactions in different species.

Genomic characterization of a novel poxvirus contributing to the decline of the red squirrel (Sciurus vulgaris) in the UK.

The genome of a virulent squirrelpox virus (SQPV) isolate was characterized in order to determine its relationship with other poxviruses. Restriction enzyme analysis suggested a genome length of approximately 158 kb, whilst sequence analysis of the two ends of the genome indicated a G + C composition of approximately 66 %. Two contiguous stretches of 23 and 37 kb at the left-hand and right-hand ends of the genome, respectively, were sequenced allowing the identification of at least 59 genes contained therein. The partial sequence of a further 15 genes was determined by spot sequencing of restriction fragments located across the genome. Phylogenetic analysis of 15 genes conserved in all the recognized genera of the subfamily Chordopoxvirinae confirmed that the SQPV does not group within the family Parapoxvirinae, but instead partitions on its own in a separate clade of the poxviruses. Analysis of serum from British woodland rodents failed to find any evidence of SQPV infection in wood mice or bank voles, but for the first time serum samples from grey squirrels in the USA were found to contain antibody against SQPV.

Limited infection upon human exposure to a recombinant raccoon pox vaccine vector.

A laboratory accident resulted in human exposure to a recombinant raccoon poxvirus (RCN) developed as a vaccine vector for antigens of Yersinia pestis for protection of wild rodents (and other animals) against plague. Within 9 days, the patient developed a small blister that healed within 4 weeks. Raccoon poxvirus was cultured from the lesion, and the patient developed antibody to plague antigen (F1) and RCN. This is the first documented case of human exposure to RCN.