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No authors listed. (1995). Workshop on the geographic spread of Aedes albopictus in Europe and the concern among public health authorities. Proceedings of a workshop held at the Istituto Superiore di Sanita, Rome, Italy, 19-20 December 1994. In Parassitologia (Vol. 37, pp. 87–90).
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Crans, W. J., McNelly, J., Schulze, T. L., & Main, A. (1986). Isolation of eastern equine encephalitis virus from Aedes sollicitans during an epizootic in southern New Jersey. J Am Mosq Control Assoc, 2(1), 68–72.
Abstract: Eastern equine encephalitis virus (EEE) was isolated from the salt marsh mosquito, Aedes sollicitans, collected from coastal areas of New Jersey on 3 occasions during the late summer and fall of 1982. The isolations were made at a time when local Culiseta melanura were either undergoing a population increase or exhibiting high levels of EEE virus. Although no human cases were reported during the epizootic period, the data lend support to the hypothesis that Ae. sollicitans is capable of functioning as an epidemic vector in the coastal areas of New Jersey where human cases of EEE have been most common.
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Hardy, J. L. (1987). The ecology of western equine encephalomyelitis virus in the Central Valley of California, 1945-1985. Am J Trop Med Hyg, 37(3 Suppl), 18s–32s.
Abstract: Reeves' concept of the summer transmission cycle of western equine encephalomyelitis virus in 1945 was that the virus was amplified in a silent transmission cycle involving mosquitoes, domestic chickens, and possibly wild birds, from which it could be transmitted tangentially to and cause disease in human and equine populations. Extensive field and laboratory studies done since 1945 in the Central Valley of California have more clearly defined the specific invertebrate and vertebrate hosts involved in the basic virus transmission cycle, but the overall concept remains unchanged. The basic transmission cycle involves Culex tarsalis as the primary vector mosquito species and house finches and house sparrows as the primary amplifying hosts. Secondary amplifying hosts, upon which Cx. tarsalis frequently feeds, include other passerine species, chickens, and possibly pheasants in areas where they are abundant. Another transmission cycle that most likely is initiated from the Cx. tarsalis-wild bird cycle involves Aedes melanimon and the blacktail jackrabbit. Like humans and horses, California ground squirrels, western tree squirrels, and a few other wild mammal species become infected tangentially with the virus but do not contribute significantly to virus amplification.
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Fulhorst, C. F., Hardy, J. L., Eldridge, B. F., Chiles, R. E., & Reeves, W. C. (1996). Ecology of Jamestown Canyon virus (Bunyaviridae: California serogroup) in coastal California. Am J Trop Med Hyg, 55(2), 185–189.
Abstract: This paper reports the first isolation of Jamestown Canyon (JC) virus from coastal California and the results of tests for antibody to JC virus in mammals living in coastal California. The virus isolation was made from a pool of 50 Aedes dorsalis females collected as adults from Morro Bay, San Luis Obispo County, California. The virus isolate was identified by two-way plaque reduction-serum dilution neutralization tests done in Vero cell cultures. Sera from the mammals were tested for antibody to JC virus by a plaque-reduction serum dilution neutralization method. A high prevalence of JC virus-specific antibody was found in horses and cattle sampled from Morro Bay. This finding is additional evidence for the presence of a virus antigenically identical or closely related to JC virus in Morro Bay and indicates that the vectors of the virus in Morro Bay feed on large mammals. A high prevalence of virus-specific antibody was also found in horses sampled from Marin and San Diego counties. This finding suggests that viruses antigenically identical or closely related to JC virus are geographically widespread in coastal California.
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Bertram, D. S. (1971). Mosquitoes of British Honduras, with some comments on malaria, and on arbovirus antibodies in man and equines. Trans R Soc Trop Med Hyg, 65(6), 742–762.
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Mellor, P. S. (1993). African horse sickness: transmission and epidemiology. Vet Res, 24(2), 199–212.
Abstract: African horse sickness (AHS) virus causes a non-contagious, infectious, arthropod-borne disease of equines and occasionally of dogs. The virus is widely distributed across sub-Saharan African where it is transmitted between susceptible vertebrate hosts by the vectors. These are usually considered to be species of Culicoides biting midges but mosquitoes and/or ticks may also be involved to a greater or lesser extent. Periodically the virus makes excursions beyond its sub-Saharan enzootic zones but until recently does not appear to have been able to maintain itself outside these areas for more than 2-3 consecutive years at most. This is probably due to a number of factors including the apparent absence of a long term vertebrate reservoir, the prevalence and seasonal incidence of the vectors and the efficiency of control measures (vaccination and vector abatement). The recent AHS epizootics in Iberia and N Africa spanning as they do, 5 or more yr, seem to have established a new pattern in AHS virus persistence. This is probably linked to the continuous presence of adult C imicola in the area. Culicoides imicola is basically an Afro-Asiatic insect and prefers warm climates. Therefore its continuous adult presence in parts of Iberia and N Africa may be due to some recent moderations of the climate in these areas.
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Nelson, G. S. (1970). Onchocerciasis. Adv Parasitol, 8, 173–224.
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Bourdin, P., & Laurent, A. (1974). [Ecology of African horsesickness]. Rev Elev Med Vet Pays Trop, 27(2), 163–168.
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Venter, G. J., Koekemoer, J. J. O., & Paweska, J. T. (2006). Investigations on outbreaks of African horse sickness in the surveillance zone in South Africa. Rev Sci Tech, 25(3), 1097–1109.
Abstract: Confirmed outbreaks of African horse sickness (AHS) occurred in the surveillance zone of the Western Cape in 1999 and 2004, both of which led to a two-year suspension on the export of horses. Light trap surveys in the outbreak areas showed that known vector competent Culicoides species, notably C. imicola, were abundant and present in numbers equal to those in the traditional AHS endemic areas. Isolations of AHS virus serotypes 1 and 7, equine encephalosis virus, and bluetongue virus from field-collected C. imicola in the surveillance zone demonstrated that this species was highly competent and could transmit viruses belonging to different serogroups of the Orbivirus genus. Molecular identification of recovered virus isolates indicated that at least two incursions of AHS into the surveillance zone had taken place in 2004. The designation of an AHS-free zone in the Western Cape remains controversial since it can be easily compromised, as evidenced by the two recent outbreaks. In light of the results reported in the present study, the policy of maintaining a large population of unvaccinated horses in the surveillance zone should be reconsidered, as it leaves them vulnerable to infection with AHS virus, which is the most pathogenic of all equine viruses.
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Sinclair, M., Buhrmann, G., & Gummow, B. (2006). An epidemiological investigation of the African horsesickness outbreak in the Western Cape Province of South Africa in 2004 and its relevance to the current equine export protocol. J S Afr Vet Assoc, 77(4), 191–196.
Abstract: African Horsesickness (AHS) is a controlled disease in South Africa. The country is divided into an infected area and a control area. An outbreak of AHS in the control area can result in a ban of exports for at least 2 years. A retrospective epidemiological study was carried out on data collected during the 2004 AHS outbreak in the surveillance zone of the AHS control area in the Western Cape Province. The objective of this study was to describe the 2004 outbreak and compare it with the 1999 AHS outbreak in the same area. As part of the investigation, a questionnaire survey was conducted in the 30 km radius surrounding the index case. Spatial, temporal and population patterns for the outbreak are described. The investigation found that the outbreak occurred before any significant rainfall and that the main AHS vector (Culicoides imicola) was present in abundance during the outbreak. Furthermore, 63% of cases occurred at temperatures < or = 15 degrees C, the Eerste River Valley was a high risk area, only 17% of owners used vector protection as a control measure and 70% of horses in the outbreak area were protected by means of vaccination at the start of the outbreak. The study revealed that the current AHS control measures do not function optimally because of the high percentage of vaccinated horses in the surveillance zone, which results in insufficient sentinel animals and the consequent failure of the early warning system. Alternative options for control that allow continued export are discussed in the paper.
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