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Marfin, A. A., Petersen, L. R., Eidson, M., Miller, J., Hadler, J., Farello, C., et al. (2001). Widespread West Nile virus activity, eastern United States, 2000. Emerg Infect Dis, 7(4), 730–735.
Abstract: In 1999, the U.S. West Nile (WN) virus epidemic was preceded by widespread reports of avian deaths. In 2000, ArboNET, a cooperative WN virus surveillance system, was implemented to monitor the sentinel epizootic that precedes human infection. This report summarizes 2000 surveillance data, documents widespread virus activity in 2000, and demonstrates the utility of monitoring virus activity in animals to identify human risk for infection.
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Dargatz, D. A., & Traub-Dargatz, J. L. (2004). Multidrug-resistant Salmonella and nosocomial infections. Vet Clin North Am Equine Pract, 20(3), 587–600.
Abstract: Nosocomial infections are a serious threat to optimum patient care. In addition, nosocomial infections can have far-reaching consequences for the hospital personnel and the financial aspects of the hospital. Nosocomial infections with Salmonella spp have been described among hospitalized equine populations more frequently than any other agent. Salmonella spp associated with hospitalized equids often possess more antimicrobial resistance determinants than do Salmonella spp isolated from healthy horses in the general population. There is little evidence to suggest that resistant salmonellae are more virulent than nonresistant forms. MDR forms of Salmonella complicate the selection of appropriate antimicrobials when they are indicated, however. Furthermore, the use of some antimicrobials may apply selection pressure toward enhanced ability of MDR Salmonella to colonize equine patients. Further research should help to elucidate the risky uses of antimicrobials in the hospital setting and define the role of disinfectants and treatments such as NSAIDs in the ecology of MDR forms of nosocomial infections, including Salmonella. In the meantime, thoughtful selection of when and how to use antimicrobials in equine patients, together with deliberate selection of which antimicrobials to use based on monitoring data and other factors, such as safety and spectrum, is advised.
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Cilnis, M. J., Kang, W., & Weaver, S. C. (1996). Genetic conservation of Highlands J viruses. Virology, 218(2), 343–351.
Abstract: We studied molecular evolution of the mosquito-borne alphavirus Highlands J (HJ) virus by sequencing PCR products generated from 19 strains isolated between 1952 and 1994. Sequences of 1200 nucleotides including portions of the E1 gene and the 3' untranslated region revealed a relatively slow evolutionary rate estimated at 0.9-1.6 x 10(-4) substitutions per nucleotide per year. Phylogenetic trees indicated that all HJ viruses descended from a common ancestor and suggested the presence of one dominant lineage in North America. However, two or more minor lineages probably circulated simultaneously for periods of years to a few decades. Strains isolated from a horse suffering encephalitis, and implicated in a recent turkey outbreak, were not phylogenetically distinct from strains isolated in other locations during the same time periods. Our findings are remarkably similar to those we obtained previously for another North American alphavirus, eastern equine encephalomyelitis virus, with which Highlands J shares primary mosquito and avian hosts, geographical distribution, and ecology. These results support the hypotheses that the duration of the transmission season affects arboviral evolutionary rates and vertebrate host mobility influences genetic diversity.
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Dauphin, G., Zientara, S., Zeller, H., & Murgue, B. (2004). West Nile: worldwide current situation in animals and humans. Comp Immunol Microbiol Infect Dis, 27(5), 343–355.
Abstract: West Nile (WN) virus is a mosquito-borne flavivirus that is native to Africa, Europe, and Western Asia. It mainly circulates among birds, but can infect many species of mammals, as well as amphibians and reptiles. Epidemics can occur in rural as well as urban areas. Transmission of WN virus, sometimes involving significant mortality in humans and horses, has been documented at erratic intervals in many countries, but never in the New World until it appeared in New York City in 1999. During the next four summers it spread with incredible speed to large portions of 46 US states, and to Canada, Mexico, Central America and the Caribbean. In many respects, WN virus is an outstanding example of a zoonotic pathogen that has leaped geographical barriers and can cause severe disease in human and equine. In Europe, in the past two decades there have been a number of significant outbreaks in several countries. However, very little is known of the ecology and natural history of WN virus transmission in Europe and most WN outbreaks in humans and animals remain unpredictable and difficult to control.
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Munoz-Sanz, A. (2006). [Christopher Columbus flu. A hypothesis for an ecological catastrophe]. Enferm Infecc Microbiol Clin, 24(5), 326–334.
Abstract: When Christopher Columbus and his men embarked on the second Colombian expedition to the New World (1493), the crew suffered from fever, respiratory symptoms and malaise. It is generally accepted that the disease was influenza. Pigs, horses and hens acquired in Gomera (Canary Islands) traveled in the same ship. The pigs may well have been the origin of the flu and the intermediary hosts for genetic recombination of other viral subtypes. The Caribbean archipelago had a large population of birds, the natural reservoir of the avian influenza virus. In this ecological scenario there was a concurrence of several biological elements that had never before coexisted in the New World: pigs, horses, the influenza virus and humans. We propose that birds are likely to have played an important role in the epidemiology of the flu occurring on the second Colombian trip, which caused a fatal demographic catastrophe, with an estimated mortality of 90% among the natives.
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