ABSTRACT
Operation Canine Lifeline was a tabletop exercise developed by students and faculty of Boston University School of Medicine's Healthcare Emergency Management master's program. The tabletop exercise led to discussion on current protocols for canines working in the field, what occurs if a canine encounters a toxin in the field, and what to do in situations of national security that require working with civilian agencies. This discussion led to the creation of a set of recommendations around providing prehospital veterinary care to government working dogs. The recommendations include a government-run veterinary toxicology hotline for the sole use of the government, issuing handlers deployment kits and preprogrammed smartphones that contain information on the care practices for dogs, and an increased effort for civilian integration, through local emergency medical services, in the emergency care of government canines. (Disaster Med Public Health Preparedness. 2017;11:15-20).
Subject(s)
Emergency Medical Services/standards , Environmental Exposure/adverse effects , Government Employees , Sarin/toxicity , Veterinary Medicine/methods , Animals , Boston , Disaster Planning/methods , Disaster Planning/organization & administration , Disaster Planning/standards , Dogs , Emergency Medical Services/methodsABSTRACT
We evaluated the serological and molecular prevalence of selected organisms in 145 dogs during late spring (May/June) of 2005 and in 88 dogs during winter (February) of 2007 from the Hopi Indian reservation. Additionally, in 2005, 442 ticks attached to dogs were collected and identified as Rhipicephalus sanguineus. Infection with or exposure to at least one organism was detected in 69% and 66% of the dogs in May/June 2005 and February 2007, respectively. Exposure to spotted fever group (SFG) rickettsiae was detected in 66.4% (2005) and 53.4% (2007) of dogs, but rickettsial DNA was not detected using polymerase chain reaction. Active Ehrlichia canis infection (by polymerase chain reaction) was identified in 36.6% (2005) and 36.3% (2007) of the dogs. E. canis infection was associated with SFG rickettsiae seroreactivity (p < 0.001). Anaplasma platys DNA was detected in 8.3% (2005) and 4.5% (2007) of the dogs. Babesia canis and Bartonella vinsonii berkhoffii seroprevalences were 6.7% and 1% in 2005, whereas in 2007 prevalences were 0% and 1.1%, respectively. No Bartonella spp., Ehrlichia chaffeensis, or Ehrlichia ewingii DNA was detected. Dogs on this Hopi Indian reservation were most frequently infected with E. canis or A. platys; however, more than half of the dogs were exposed to a SFG-Rickettsia species.
Subject(s)
Anaplasmosis/epidemiology , Dog Diseases/microbiology , Dog Diseases/parasitology , Ehrlichiosis/veterinary , Anaplasma/isolation & purification , Animals , Arizona/epidemiology , Dog Diseases/epidemiology , Dogs , Ehrlichia/isolation & purification , Ehrlichiosis/epidemiology , Female , Host-Pathogen Interactions , Male , Prevalence , Tick Infestations/epidemiology , Tick Infestations/veterinaryABSTRACT
Shigella flexneri is a gram-negative bacterium that causes bacillary dysentery in humans that is characterized by an acute inflammatory response of the colon. The fate of phagocytes that are infected in vitro with virulent Shigella has been the subject of some investigation and debate. In this study we found that virulent Shigella caused a rapid increase in the cell membrane permeability of infected human monocyte-derived macrophages (HMDM) but not in the cell membrane permeability of monocytes, as demonstrated by the uptake of fluorescent vital dyes. Within 2 h of infection, 59% +/- 6% of the HMDM and =4% of the monocytes were stained with propidium iodide. Treatment of the cells with the inhibitors of caspases YVAD and zVAD, the antioxidants N-acetyl-l-cysteine and butylated hydroxyanisole, or an inhibitor of NADPH oxidase, diphenyleniodonium, did not alter the infection outcome. Importantly, we found that virulent Shigella caused a rapid drop in the ATP level to about 50% in infected HMDM. Furthermore, using a combination of fluorescent vital dyes and mitochondrial membrane potential-sensitive dyes, we observed that cells that exhibited a permeable cell membrane were not stained by the mitochondrion-specific dyes, indicating that the mitochondrial membrane potential was lost in these cells. We also observed infected cells that were not stained with either type of dye, indicating that the loss of the mitochondrial membrane potential preceded the increase in cell membrane permeability. Taken together, our studies showed that virulent Shigella flexneri targets the host cell mitochondria for destruction. This activity may account for the necrotic cell death precipitated by these pathogens.