The potential for transport and dissemination of certain pathogenic microorganisms by migratory birds is of concern. Migratory birds might be involved in dispersal of microorganisms as their biological carriers, mechanical carriers, or as carriers of infected hematophagous ecto- parasites (e.g., ixodid ticks). Many species of microorganisms pathogenic to homeothermic ver- tebrates including humans have been associated with free-living migratory birds. Migratory birds of diverse species can play significant roles in the ecology and circulation of some arboviruses (e.g., eastern and western equine encephalomyelitis and Sindbis alphaviruses, West Nile and St. Louis encephalitis flaviviruses), influenza A virus, Newcastle disease virus, duck plague herpes- virus, Chlamydophila psittaci, Anaplasma phagocytophilum, Borrelia burgdorferi sensu lato, Campylobacter jejuni, Salmonella enterica, Pasteurella multocida, Mycobacterium avium, Candida spp., and avian hematozoans. The efficiency of dispersal of pathogenic microorganisms depends on a wide variety of biotic and abiotic factors affecting the survival of the agent in, or disap- pearance from, a habitat or ecosystem in a new geographic area.

https://bioone.org/journals/journal-of-wildlife-diseases/volume-40/issue-4/0090-3558-40.4.639/AN-ANNOTATED-CHECKLIST-OF-PATHOGENIC-MICROORGANISMS-ASSOCIATED-WITH-MIGRATORY-BIRDS/10.7589/0090-3558-40.4.639.pdf

An annotated checklist of pathogenic microorganisms associated with migratory birds

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.

Partial E1 envelope glycoprotein gene sequences and complete structural polyprotein sequences were used to compare divergence and construct phylogenetic trees for the genus Alphavirus. Tree topologies indicated that the mosquito-borne alphaviruses could have arisen in either the Old or the New World, with at least two transoceanic introductions to account for their current distribution. The time frame for alphavirus diversification could not be estimated because maximum-likelihood analyses indicated that the nucleotide substitution rate varies considerably across sites within the genome. While most trees showed evolutionary relationships consistent with current antigenic complexes and species, several changes to the current classification are proposed. The recently identified fish alphaviruses salmon pancreas disease virus and sleeping disease virus appear to be variants or subtypes of a new alphavirus species. Southern elephant seal virus is also a new alphavirus distantly related to all of the others analyzed. Tonate virus and Venezuelan equine encephalitis virus strain 78V3531 also appear to be distinct alphavirus species based on genetic, antigenic, and ecological criteria. Trocara virus, isolated from mosquitoes in Brazil and Peru, also represents a new species and probably a new alphavirus complex.

Evolutionary Relationships and Systematics of the Alphaviruses

Venezuelan equine encephalitis (VEE) is an emerging infectious disease in Latin America. Outbreaks have been recorded for decades in countries with enzootic circulation, and the recent implementation of surveillance systems has allowed the detection of additional human cases in countries and areas with previously unknown VEE activity. Clinically, VEE is indistinguishable from dengue and other arboviral diseases and confirmatory diagnosis requires the use of specialized laboratory tests that are difficult to afford in resource-limited regions. Thus, the disease burden of endemic VEE in developing countries remains largely unknown, but recent surveillance suggests that it may represent up to 10% of the dengue burden in neotropical cities, or tens-of-thousands of cases per year throughout Latin America. The potential emergence of epizootic viruses from enzootic progenitors further highlights the need to strengthen surveillance activities, identify mosquito vectors and reservoirs and develop effective strategies to control the disease. In this article, we provide an overview of the current status of endemic VEE that results from spillover of the enzootic cycles, and we discuss public health measures for disease control as well as future avenues for VEE research.

/pdf/endemic-venezuelan-equine-encephalitis-in-the-americas-290anhqlup.pdf

Endemic Venezuelan equine encephalitis in the Americas: hidden under the dengue umbrella.

Venezuelan equine encephalitis (VEE) epidemics and equine epizootics occurred periodically in the Americas from the 1920s until the early 1970s, when the causative viruses, subtypes IAB and IC, were postulated to have become extinct. Recent outbreaks in Columbia and Venezuela have renewed interest in the source of epidemic/epizootic viruses and their mechanism of interepizootic maintenance. We performed phylogenetic analyses of VEE virus isolates spanning the entire temporal and geographic range of strains available, using 857-nucleotide reverse transcription-PCR products including the E3 and E2 genes. Analyses indicated that epidemic/epizootic viruses are closely related to four distinct, enzootic subtype ID-like lineages. One of these lineages, which occurs in Columbia, Peru, and Venezuela, also included all of the epidemic/epizootic isolates; the remaining three ID-like lineages, which occur in Panama, Peru, Florida, coastal Ecuador, and southwestern Columbia, were apparently not associated with epizootic VEE emergence. Within the Columbia/Peru/Venezuela lineage, three distinct monophyletic groups of epidemic/epizootic viruses were delineated, indicating that VEE emergence has occurred independently at least three times (convergent evolution). Representative, complete E2 amino acid sequences were compared to identify potential determinants of equine virulence and epizootic emergence. Amino acids implicated previously in laboratory mouse attenuation generally did not vary among the natural isolates that we examined, indicating that they probably are not involved in equine virulence changes associated with VEE emergence. Most informative amino acids correlated with phylogenetic relationships rather than phenotypic characteristics, suggesting that VEE emergence has resulted from several distinct combinations of mutations that generate viruses with similar antigenic and equine virulence phenotypes.

Repeated emergence of epidemic/epizootic Venezuelan equine encephalitis from a single genotype of enzootic subtype ID virus.

A second virus with distinct biological, serological, and physiochemical properties was detected as a minority viral subpopulation in specimens of Cliff Swallow nest bugs (Oeciacus vicarius) and nestling bird sera containing Fort Morgan (FM) virus. The second virus, detected by a breakthrough neutralization test employing FM antiserum, was present in 5 of 11 FM virus-positive pools of nest bugs and in 4 of 38 birds from Colorado and South Dakota. The concentration of the second virus was 10-fold to 1,000-fold lower than that of FM virus. The second virus, which was provisionally named "Bijou Bridge" (BB) virus was shown by conventional serological tests to be a member of the Venezuelan equine encephalomyelitis (VEE) complex, and by tests employing antisera to the E2 viral glycoprotein to be identical with Tonate virus, previously isolated from birds and mosquitoes only in French Guiana. Experimental infection of House Sparrows and Cliff Swallows showed that they develop brief BB viremias and antibodies. Oe. vicarius bugs were resistant to oral infection with BB virus. The epidemiological significance of recovery of Tonate virus in North American is discussed.

Recovery of Tonate virus ("Bijou Bridge" strain), a member of the Venezuelan equine encephalomyelitis virus complex, from cliff swallow nest bugs (Oeciacus vicarius) and nestling birds in North America.

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Recovery of Tonate virus ("Bijou Bridge" strain), a member of the Venezuelan equine encephalomyelitis virus complex, from cliff swallow nest bugs (Oeciacus vicarius) and nestling birds in North America.