Rodents are the most abundant and diversified order of living mammals in the world. Already since the Middle Ages we know that they can contribute to human disease, as black rats were associated with distribution of plague. However, also in modern times rodents form a threat for public health. In this review article a large number of pathogens that are directly or indirectly transmitted by rodents are described. Moreover, a simplified rodent disease model is discussed.

Rodent-borne diseases and their risks for public health

The effect of temperature on the ability of Aedes aegypti to transmit dengue (DEN) 2 virus to rhesus monkeys was assessed as a possible explanation for the seasonal variation in the incidence of dengue hemorrhagic fever in Bangkok, Thailand. In two laboratory experiments, a Bangkok strain of Ae. aegypti was allowed to feed upon viremic monkeys infected with DEN-2 virus. Blood-engorged mosquitoes were separated into two groups and retained at constant temperatures. Virus infection and transmission rates were determined for Ae. aegypti at intervals ranging from 4 to 7 days during a 25-day incubation period. Results of the first experiment for mosquitoes infected with a low dose of DEN-2 virus and maintained at 20,24,26, and 3O"C, indicated that the infection rate ranged from 25% to 75% depending on the incubation period. However, DEN-2 virus was transmitted to monkeys only by Ae. aegypti retained at 30°C for 25 days. In the second experiment, the infection rate for Ae. aegypti that ingested a higher viral dose, and incubated at 26, 30, 32, and 35°C ranged from 67% to 95%. DEN-2 virus was transmitted to monkeys only by mosquitoes maintained at L 30°C. The extrinsic incubation period was 12 days for mos- quitoes at 3O"C, and was reduced to 7 days for mosquitoes incubated at 32°C and 35°C. These results imply that temperature-induced variations in the vector efficiency of Ae. aegypti may be a significant determinant in the annual cyclic pattern of dengue hemorrhagic fever epidemics in-Bangkok.

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Effect of temperature on the vector efficiency of Aedes aegypti for dengue 2 virus.

Most studies on the ability of insect populations to transmit pathogens consider only constant temperatures and do not account for realistic daily temperature fluctuations that can impact vector–pathogen interactions. Here, we show that diurnal temperature range (DTR) affects two important parameters underlying dengue virus (DENV) transmission by Aedes aegypti. In two independent experiments using different DENV serotypes, mosquitoes were less susceptible to virus infection and died faster under larger DTR around the same mean temperature. Large DTR (20 °C) decreased the probability of midgut infection, but not duration of the virus extrinsic incubation period (EIP), compared with moderate DTR (10 °C) or constant temperature. A thermodynamic model predicted that at mean temperatures 18 °C, larger DTR reduces DENV transmission. The negative impact of DTR on Ae. aegypti survival indicates that large temperature fluctuations will reduce the probability of vector survival through EIP and expectation of infectious life. Seasonal variation in the amplitude of daily temperature fluctuations helps to explain seasonal forcing of DENV transmission at locations where average temperature does not vary seasonally and mosquito abundance is not associated with dengue incidence. Mosquitoes lived longer and were more likely to become infected under moderate temperature fluctuations, which is typical of the high DENV transmission season than under large temperature fluctuations, which is typical of the low DENV transmission season. Our findings reveal the importance of considering short-term temperature variations when studying DENV transmission dynamics.

Impact of daily temperature fluctuations on dengue virus transmission by Aedes aegypti

that exist between the virus, the invertebrate host (vector), and the vertebrate host, each of which is influenced to varying degrees by environmental conditions. These interrela­ tionships have been reviewed elsewhere (17, 60,98, 109, 111, 113, 124) and are not discussed in depth here. Rather, this review focuses on vector competence or vector efficiency. Particular attention is given to recent studies that have contributed to our knowledge of intrinsic factors and mechanisms that control the ability of mosquitoes to vector arboviruses. No attempt is made to review transovarial transmission of arboviruses by ar­ thropods even though this is obviously an important aspect of vector com­ petence in certain arthropod-arbovi rus associations (35, 125, 140,

Intrinsic Factors Affecting Vector Competence of Mosquitoes for Arboviruses

Venezuelan equine encephalitis virus (VEEV) remains a naturally emerging disease threat as well as a highly developed biological weapon. Recently, progress has been made in understanding the complex ecological and viral genetic mechanisms that coincide in time and space to generate outbreaks. Enzootic, equine avirulent, serotype ID VEEV strains appear to alter their serotype to IAB or IC, and their vertebrate and mosquito host range, to mediate repeated VEE emergence via mutations in the E2 envelope glycoprotein that represent convergent evolution. Adaptation to equines results in highly efficient amplification, which results in human disease. Although epizootic VEEV strains are opportunistic in their use of mosquito vectors, the most widespread outbreaks appear to involve specific adaptation to Ochlerotatus taeniorhynchus, the most common vector in many coastal areas. In contrast, enzootic VEEV strains are highly specialized and appear to utilize vectors exclusively in the Spissipes section of the Culex (Melanoconion) subgenus.

Venezuelan equine encephalitis.

Mechanism of Transmission of Viruses by Mosquitoes

A major epidemic of Venezuelan equine encephalitis occurred in south Texas in the summer of 1971. More than 1500 equines died of VEE in Texas, and 110 human cases with no deaths were reported. Vector studies in south Texas and northern Tamaulipas revealed that the overall mosquito infection rates during the peak of the epidemic were about 1:100, one of the highest rates observed for a major epidemic. Mosquito infection rates of this magnitude could easily explain the intensity of VEE outbreaks in both equines and man. A total of 943 VEE virus isolations were made from mosquitoes. Eight of the 12 mosquito species found infected were implicated in the epidemic cycle of VEE for the first time. Sufficient laboratory and field evidence is available to prove that Psorophora confinnis was one of the primary vectors of VEE. The lack of laboratory evidence necessitates the use of the term "probable" primary vectors for other species apparently equally as involved on the basis of field infections; these include Aedes sollicitans, Aedes thelcter and Psorophora discolor. Eight other species from which less than 10 VEE virus isolations were made were considered auxiliary vectors. Mosquitoes of some species were tested individually; such tests showed 2-4% of the probable primary vectors to be infected. The first isolation of VEE virus of the epidemic was made from P. confinnis on June 28, 1971. Highest mosquito infection rates occurred during the week of July 5. Mosquito infection rates declined precipitously in the last 3 weeks of July 1971, signaling the end of the epidemic in the study area. One explanation for the decline was that equines, the principal epidemic hosts, were eliminated as a source of virus by death or by acquisition of natural or induced immunity. Mosquito control appeared to be effective in reducing the infected mosquito population while the immunization of equines with TC 83 VEE vaccine was accomplished. Quarantines appeared to be effective in restricting the VEE virus activity to south Texas. Undoubtedly all of the control measures contributed to stopping the epidemic. Continued VEE surveillance by various government and other agencies failed to reveal any further epidemic VEE activity in the US in 1972. Other arboviruses isolated during the VEE studies in south Texas included St. Louis encephalitis virus, and San Angelo subtype of the California Group. A virus of the Bunyamwera Group was also isolated from Palo Blanco, Tamaulipas.

Epidemic venezuelan equine encephalitis in north america in 1971: vector studies

The Effects of Temperature upon the extrinsic Incubation of Eastern Equine Encephalitis in Mosquitoes.

Arbovirus studies in south florida, with emphasis on venezuelan equine encephalomyelitis virus

Venezuelan equine encephalitis virus was isolated three times from the Culex (Melanoconion) species of mosquitoes collected in south Florida in June, July, and October, 1963. Specific antibody was present in 16 of 28 Peromyscus gossypinus (cotton mice) and 3 of 16 Sigmodon hispidus (cotton rats) sampled from one of the infected sites in January 1964.

https://science.sciencemag.org/content/sci/145/3629/272.full.pdf

W. D. Sudia

Papers

Mechanism of Transmission of Viruses by Mosquitoes

Epidemic venezuelan equine encephalitis in north america in 1971: vector studies

The Effects of Temperature upon the extrinsic Incubation of Eastern Equine Encephalitis in Mosquitoes.

Arbovirus studies in south florida, with emphasis on venezuelan equine encephalomyelitis virus

Venezuelan Equine Encephalitis Virus from South Florida