LEPTOSPIRA ANTIBODIES DETECTED IN WILDLIFE IN THE USA AND THE US VIRGIN ISLANDS.

From 2011 to 2017, 4,534 serum samples from 13 wildlife species collected across the US and in one territory (US Virgin Islands) were tested for exposure to Leptospira serovars Bratislava, Canicola, Grippotyphosa, Hardjo, Icterohaemorrhagiae, and Pomona. Of 1,759 canids, 1,043 cervids, 23 small Indian mongooses ( Herpestes auropunctatus), 1,704 raccoons ( Procyon lotor), and five striped skunks ( Mephitis mephitis), 27.0, 44.4, 30.4, 40.8, and 60%, respectively, were antibody positive for any of the six serovars. The most commonly detected serovars across all species were Bratislava and Grippotyphosa. Our results indicate that Leptospira titers are very common in a wide variety of wildlife species. These species may act as important reservoirs in the epidemiological cycle of the pathogen. Additional studies to determine the relationship between serologic evidence and shedding of the pathogen by wildlife are necessary to better understand the risk.

LIMITED ANTIBODY EVIDENCE OF EXPOSURE TO MYCOBACTERIUM BOVIS IN FERAL SWINE (SUS SCROFA) IN THE USA.

Bovine tuberculosis is a chronic disease of cattle ( Bos taurus ) caused by the bacterium Mycobacterium bovis . Efforts have been made in the US to eradicate the disease in cattle, but spillover into wildlife and subsequent spillback have impeded progress in some states. In particular, infection in white-tailed deer ( Odocoileus virginianus ) has been followed by infection in cattle in some Midwestern states. Infection has also been documented in feral swine ( Sus scrofa ) on the Hawaiian island of Molokai and in various European countries, but no large-scale survey of antibody exposure to the bacteria has been conducted in feral swine in the US. We tested 488 sera from feral swine collected near previously documented outbreaks of bovine tuberculosis in cattle and captive cervids, in addition to 2,237 feral swine sera collected across the US from 1 October 2013 to 30 September 2014. While all but one of the samples were antibody negative, the results are important for establishing baseline negative data since feral swine are capable reservoirs and could be implicated in future outbreaks of the disease.

Molecular surveillance of low pathogenic avian influenza viruses in wild birds across the United States: inferences from the hemagglutinin gene.

A United States interagency avian influenza surveillance plan was initiated in 2006 for early detection of highly pathogenic avian influenza viruses (HPAIV) in wild birds. The plan included a variety of wild bird sampling strategies including the testing of fecal samples from aquatic areas throughout the United States from April 2006 through December 2007. Although HPAIV was not detected through this surveillance effort we were able to obtain 759 fecal samples that were positive for low pathogenic avian influenza virus (LPAIV). We used 136 DNA sequences obtained from these samples along with samples from a public influenza sequence database for a phylogenetic assessment of hemagglutinin (HA) diversity in the United States. We analyzed sequences from all HA subtypes except H5, H7, H14 and H15 to examine genetic variation, exchange between Eurasia and North America, and geographic distribution of LPAIV in wild birds in the United States. This study confirms intercontinental exchange of some HA subtypes (including a newly documented H9 exchange event), as well as identifies subtypes that do not regularly experience intercontinental gene flow but have been circulating and evolving in North America for at least the past 20 years. These HA subtypes have high levels of genetic diversity with many lineages co-circulating within the wild birds of North America. The surveillance effort that provided these samples demonstrates that such efforts, albeit labor-intensive, provide important information about the ecology of LPAIV circulating in North America.

Shedding and serologic responses following primary and secondary inoculation of house sparrows (Passer domesticus) and European starlings (Sturnus vulgaris) with low-pathogenicity avian influenza virus.

Waterfowl and shorebirds are well-recognized natural reservoirs of low-pathogenicity avian influenza viruses (LPAIV); however, little is known about the role of passerines in avian influenza virus ecology. Passerines are abundant, widespread, and commonly come into contact with free-ranging birds as well as captive game birds and poultry. We inoculated and subsequently challenged house sparrows (Passer domesticus) and European starlings (Sturnus vulgaris) with wild-bird origin LPAIV H3N8 to evaluate their potential role in transmission. Oropharyngeal shedding was short lived, and was detected in more starlings (97.2%) than sparrows (47.2%; n=36 of each). Cloacal shedding was rare in both species (8.3%; n=36 of each) and no cage-mate transmission occurred. Infectious LPAIV was cultured from oropharyngeal and cloacal swabs and gastrointestinal and respiratory tissues from both species. Seroconversion was detected as early as 3 days post inoculation (d.p.i.) (16.7% of sparrows and 0% of starlings; n=6 each); 50% of these individuals seroconverted by 5 d.p.i., and nearly all birds (97%; n=35) seroconverted by 28 d.p.i. In general, pre-existing homologous immunity led to reduced shedding and increased antibody levels within 7 days of challenge. Limited shedding and lack of cage-mate transmission suggest that passerines are not significant reservoirs of LPAIV, although species differences apparently exist. Passerines readily and consistently seroconverted to LPAIV, and therefore inclusion of passerines in epidemiological studies of influenza outbreaks in wildlife and domestic animals may provide further insight into the potential involvement of passerines in avian influenza virus transmission ecology.

Increased detection of influenza A H16 in the United States.

As a result of an US interagency avian influenza surveillance effort in wild birds, four isolates of influenza A viruses were initially identified as H7 by hemagglutination inhibition (HI) but subsequently identified as H16 through genetic sequence analysis. We report the development of internal primers for amplification and cycle-sequencing of the full-length H16 gene, increased detection of H16 within the US, and possible steric inhibition or cross-reaction between H7 and H16 antigens during the conventional HI assay. The latter could have critical implications for poultry operations if H16 viruses are detected and mistakenly reported as H7 viruses.