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Sin Nombre virus (SNV) is the principal cause of hantavirus pulmonary syndrome (HPS) in the United States and deer mice ( Peromyscus maniculatus) are its principal rodent host, and thus the natural cycle of the virus is related to the occurrence of HPS. Prevalence of rodent infection appears to be associated with fluctuations in deer mouse populations and, indirectly, with timing and amount of precipitation, a complex of biologic events. Given that rodent population abundances fluctuate, often acutely, it is not unreasonable to assume a direct correlation between the numbers of infected rodents and the number of human infections, unless confounding factors are involved. During a 13-year longitudinal study at a site in southwestern Colorado, we accumulated data regarding deer mice and antibody to SNV and therefore had the opportunity to compare dynamics of deer mouse populations, seroprevalence of antibody to SNV in the rodents, and numbers of HPS cases in Durango and in the State of Colorado as a whole. If abundances of deer mouse populations are directly correlated with occurrence of HPS, it is reasonable to assume that low densities of deer mice and low prevalences of antibody to SNV would lead to fewer human cases than would high densities and high prevalences. Our results substantiate such an assumption and suggest that the risk of acquisition of HPS is likely related to both high numbers of infected deer mice and human activities, rather than being strictly related to prevalence of SNV in the host rodent. [ABSTRACT FROM AUTHOR]

Presents a study that reported the first isolations of West Nile virus (WNV) from a sick person and from a pool of Culex quinquefasciatus mosquitoes and described their phylogenetic relationship to other representative WNV strains from the U.S. and Mexico. Methods used in the study; Summary of mosquitoes collected in Nuevo Leon, Mexico, during the summer of 2003 and tested for WNV; Conclusions.

Discusses the ecology and evolutionary history of Hantavirus Pulmonary Syndrome (H.P.S.) Focus on the outbreak in the U.S. Southwest in 1993; Consideration of the coevolution of Western Hemisphere rodents and hantaviruses; Characteristics of the Sin Nombre virus as an evolved human disease; Speculation about the ecological causes for the H.P.S. outbreak; Role of El Niño in the trophic cascade hypothesis.

From 1995 to 1999, we conducted longitudinal studies of white- throated woodrats (Neotoma albigula) in southeastern Colorado. Forty-five (42.9%) of 105 female and 15 (26.8%) of 56 male N. albigula had antibodies against Whitewater Arroyo virus (WWAV). Sixteen female and three male N. albigula seroconverted during the study period, most of them during July-November, when population densities are highest. Analyses of longevity data, minimum numbers alive and infected, movements, and weight data suggest that the dominant mode of WWAV transmission among white-throated woodrats in Colorado is direct contact. WWAV was recently reported to cause fatal infection in humans. Our findings will lead to better assessment of the public health threat posed by infected woodrats and may be useful in predicting periods of increased risk for human infection. [ABSTRACT FROM AUTHOR]

A mark-recapture longitudinal study of immunoglobulin G (IgG) antibody to Sin Nombre virus (SNV) in rodent populations in western Colorado (1994-results summarized to October 1997) indicates the presence of SNV or a closely related hantavirus at two sites. Most rodents (principally deer mice, Peromyscus maniculatus, and pinyon mice, P. truei) did not persist on the trapping webs much beyond 1 month after first capture. Some persisted more than 1 year, which suggests that even a few infected deer mice could serve as transseasonal reservoirs and mechanisms for over-winter virus maintenance. A positive association between wounds and SNV antibody in adult animals at both sites suggests that when infected rodents in certain populations fight with uninfected rodents, virus amplification occurs. At both sites, male rodents comprised a larger percentage of seropositive mice than recaptured mice, which suggests that male mice contribute more to the SNV epizootic cycle than female mice. In deer mice, IgG antibody prevalence fluctuations were positively associated with population fluctuations. The rates of seroconversion, which in deer mice at both sites occurred mostly during late summer and midwinter, were higher than the seroprevalence, which suggests that the longer deer mice live, the greater the probability they will become infected with SNV. [ABSTRACT FROM AUTHOR]

Abstract: Adult mosquitoes were previously collected and tested for West Nile virus during an intense WNV outbreak in 2003–2004 along the Cache la Poudre River in Colorado, USA. A subset of these mosquitoes was also tested for infection with trypanosomatids using nested PCR to amplify 18S rRNA. Of the 69 pools of Culex pipiens that were screened for both pathogens, 4.3% were positive for WNV and 11.6% tested positive for trypanosomes; no pools were found to be co-infected with both pathogens. One hundred and forty-three pools of Culex tarsalis, considered to be the principal WNV vector in this area, were tested in the same manner. 7.7% were positive for WNV and 20.3% of these pools tested positive for trypanosomes. Five pools of C. tarsalis were found to be co-infected with both pathogens, which was approximately 2.2 times more frequent than would be expected if these pathogens are independent of each other. Sequencing and maximum parsimony analysis of 18S rRNA revealed that four of the isolates arise in or near clades of described avian trypanosomes, likely indicating that these are vectored pathogens between birds and mosquitoes. Unexpectedly, the majority (24/28, 86%) of our positive samples form their own separate clade within the order Trypanosomatida with 100% bootstrap support. We have identified a potential new clade of trypanosomatids that exist within important mosquito vectors and discuss the potential ecological connections between these trypanosomes, arboviruses and mosquitoes. [Copyright &y& Elsevier]

Host migration and emerging pathogens are strongly associated, especially with regard to zoonotic diseases. West Nile virus (WNV), a mosquitoborne pathogen capable of causing severe, sometimes fatal, neuroinvasive disease in humans, is maintained in highly mobile avian hosts. Using phylogeographic approaches, we investigated the relationship between WNV circulation in the United States and the flight paths of terrestrial birds. We demonstrated southward migration of WNV in the eastern flyway and northward migration in the central flyway, which is consistent with the looped flight paths of many terrestrial birds. We also identified 3 optimal locations for targeted WNV surveillance campaigns in the United States-Illinois, New York, and Texas. These results illustrate the value of multidisciplinary approaches to surveillance of infectious diseases, especially zoonotic diseases.

Serosurveys were conducted to obtain flavivirus and West Nile virus (WNV) seroprevalence data from mammals. Sera from 513 small- and medium-sized mammals collected during late summer and fall 2003 from Colorado, Louisiana, New York, Ohio, and Pennsylvania were screened for flavivirus-specific antibodies. Sera samples containing antibody to flaviviruses were screened for WNV-specific antibodies by epitope-blocking enzyme-linked immunosorbent assays and confirmed with plaque reduction neutralization tests. Prevalence of WNV antibodies among study sites ranged from 0% to 42.8% among the mammal communities sampled. High prevalence rates for WNV were noted among raccoons (100%, with a very small sample size, N = 2), Virginia opossums (50.0%), fox squirrels (49.1%), and eastern gray squirrels (48.3%). The high WNV antibody prevalence noted for tree squirrels, the peri-domestic tendencies of several of these species, and their ease of observation could make these species useful sentinels for monitoring WNV activity within urban communities.

Aedes aegypti from 24 collections in Mexico and the United States were challenged orally with dengue 2 virus JAM1409 (DEN-2 JAM1409). The vector competence (VC) of the populations ranged from 24% to 83%. Mosquito populations from the Yucatan exhibited greater VC than those from other areas of Mexico. The presence or absence of a midgut infection barrier (MIB) and a midgut escape barrier (MEB) was determined for mosquitoes in each population. The percentage of mosquitoes exhibiting an MIB ranged from 14% to 59%, and those exhibiting an MEB ranged from 4% to 43% in the collections. The MIB and MEB were not completely independent as determined by regression analysis. Midgut infection rates were dose dependent.