VECTOR/PATHOGEN/HOST INTERACTION Grasshoppers (Orthoptera: Acrididae) Could Serve as Reservoirs and Vectors of Vesicular Stomatitis Virus RICHARD A. NUNAMAKER, 1 JEFFREY A. LOCKWOOD, 2 CHARLES E. STITH, COREY L. CAMPBELL, SCOTT P. SCHELL, 2 BARBARA S. DROLET, WILLIAM C. WILSON, DAVID M. WHITE, AND GEOFFREY J. LETCHWORTH 3 USDAÐARS, Arthropod-borne Animal Diseases Research Laboratory, P.O. Box 3965, Laramie, WY 82071 J. Med. Entomol. 40(6): 957Ð963 (2003) ABSTRACT Vesicular stomatitis (VS) is an economically devastating disease of livestock in the Americas. Despite strong circumstantial evidence for the role of arthropods in epizootics, no hema- tophagous vector explains the Þeld evidence. Based on the spatiotemporal association of grasshopper outbreaks and VS epizootics, we investigated the potential role of these insects as vectors and reservoirs of the disease. The critical steps in the grasshopperÐ bovine transmission cycle were demonstrated, including 1) 62% of grasshoppers [Melanoplus sanguinipes (F.)] fed vesicular stomatitis virus (VSV) from cell culture became infected, with titers reaching 40,000 times the inoculative dose; 2) 40% of grasshoppers that cannibalized VSV-infected grasshopper cadavers became infected, amplifying virus up to 1,000-fold; 3) one of three cattle consuming VSV-infected grasshopper cadavers contracted typical VS and shed virus in saliva; and 4) 15% of grasshoppers became infected when fed saliva from this infected cow. The ecological conditions and biological processes necessary for these transmissions to occur are present throughout much of the Americas. Field studies will be required to show these Þndings are relevant to the natural epidemiology of VSV. KEY WORDS vesicular stomatitis virus, VSV, grasshopper, bovine, Melanoplus sanguinipes VESICULAR STOMATITIS (VS) IS an economically devas- tating disease of horses, cows, and pigs, but it also affects many wildlife species, as well as humans. In the United States, two vesicular stomatitis virus (VSV) serotypes, NJ and Indiana, cause disease. The disease is enzootic from Mexico to Colombia and periodically spreads into temperate regions. Northern movements originating in southern Mexico (Rodriguez et al. 2000) may develop into epizootics in the western United States, occasionally spreading as far north as Canada. Each outbreak of VS in the United States provokes quarantines designed to slow the spread of the disease and allow time to distinguish it from foot-and-mouth disease (FMD), which causes similar vesicular lesions of the mouth, teats, and coronary bands of cattle, sheep, and pigs. Unlike FMD, VSV can spread to live- stock owners and veterinarians, causing a short-lived but debilitating disease (Hanson and Karstad 1958, Fields and Hawkins 1967, Johnson et al. 1969, Tesh et al. 1969, Reif et al. 1987). Infection of people in rural Central America is relatively common (Tesh et al. 1969). VS spreads quickly within a herd of animals by direct contact and fomites contaminated with virus shed in saliva and vesicular exudates (Fig. 1, step 1). However, this does not explain the onset of wide- spread epizootics or the rapid long-distance spread during VS outbreaks. Field observations and circum- stantial evidence strongly suggest VSV is spread by one or more arthropod species. The pathogen has even been proposed as a well-adapted insect virus that inadvertently spreads to vertebrates (Tesh and Chani- otis 1975). In tropical and subtropical zones, VS is most common at the end of the rainy season or early in the dry season when many insect species are most abun- dant (Mason et al. 1976, Orrego et al. 1987, Rodriguez et al. 1990). Similarly, in temperate regions VS is as- sociated with periods of insect activity, occurring in the summer, usually disappearing after the Þrst hard frost, and often sparing horses that are protected from insects (Hanson 1981, Carver 1984, Webb et al. 1987). Outbreaks seem to follow terrestrial features such as rivers or distinct ecological features such as open woodlands or savannas (Acree et al. 1964, Hanson et al. 1968, Hanson 1981). The 1982 VS outbreak in the western Unites States seemed to spread long distances in a windward direction (Sellers and Maarouf 1990). The transmission of VSV only by hematophagous vectors and fomites is not consistent with the ecolog- ical evidence. Experimentally infected hematopha- 1 Current address: 640 Leon St., Delta, CO 81416. 2 Entomology Section, Department of Renewable Resources, Uni- versity of Wyoming, Laramie, WY 82071. 3 E-mail: gjl3@uwyo.edu. Downloaded from https://academic.oup.com/jme/article/40/6/957/837806 by guest on 20 November 2021