Migratory birds and spread of West Nile virus in the Western Hemisphere. (25/871)

West Nile virus, an Old World flavivirus related to St. Louis encephalitis virus, was first recorded in the New World during August 1999 in the borough of Queens, New York City. Through October 1999, 62 patients, 7 of whom died, had confirmed infections with the virus. Ornithophilic mosquitoes are the principal vectors of West Nile virus in the Old World, and birds of several species, chiefly migrants, appear to be the major introductory or amplifying hosts. If transovarial transmission or survival in overwintering mosquitoes were the principal means for its persistence, West Nile virus might not become established in the New World because of aggressive mosquito suppression campaigns conducted in the New York area. However, the pattern of outbreaks in southern Europe suggests that viremic migratory birds may also contribute to movement of the virus. If so, West Nile virus has the potential to cause outbreaks throughout both temperate and tropical regions of the Western Hemisphere.  (+info)

Compendium of measures to control Chlamydia psittaci infection among humans (psittacosis) and pet birds (avian chlamydiosis), 2000. Centers for Disease Control and Prevention. (26/871)

Psittacosis--also known as parrot fever and ornithosis--is spread by a bacterial infection of birds that can cause severe pneumonia and other serious health problems among humans. From 1988 through 1998, 813 cases of psittacosis (infection with Chlamydia psittaci) were reported to CDC, and most resulted from exposure to infected pet birds, usually cockatiels, parakeets, parrots, and macaws. In birds, C. psittaci infection is referred to as avian chlamydiosis (AC). Infected birds shed the bacteria through feces and nasal discharges, and humans become infected from exposure to these materials. This compendium provides information about psittacosis and AC to public health officials, physicians, veterinarians, the pet bird industry, and others concerned about controlling these diseases and protecting public health. The recommendations in this compendium provide standardized procedures for controlling AC in birds, a vital step to protecting human health.  (+info)

Chlamydophila abortus in a Brown skua (Catharacta antarctica lonnbergi) from a subantarctic island. (27/871)

On Bird Island, South Georgia, a new strain of Chlamydophila abortus was detected in one Brown skua out of 37 specimens from six different seabird species. Phylogenetic analysis of the rnpB and omp1 genes indicated the strain to be more closely related to C. abortus than to 6BC, the type strain of Chlamydophila psittaci.  (+info)

Avian-to-human transmission of H9N2 subtype influenza A viruses: relationship between H9N2 and H5N1 human isolates. (28/871)

In 1997, 18 cases of influenza in Hong Kong (bird flu) caused by a novel H5N1 (chicken) virus resulted in the deaths of six individuals and once again raised the specter of a potentially devastating influenza pandemic. Slaughter of the poultry in the live bird markets removed the source of infection and no further human cases of H5N1 infection have occurred. In March 1999, however, a new pandemic threat appeared when influenza A H9N2 viruses infected two children in Hong Kong. These two virus isolates are similar to an H9N2 virus isolated from a quail in Hong Kong in late 1997. Although differing in their surface hemagglutinin and neuraminidase components, a notable feature of these H9N2 viruses is that the six genes encoding the internal components of the virus are similar to those of the 1997 H5N1 human and avian isolates. This common feature emphasizes the apparent propensity of avian viruses with this genetic complement to infect humans and highlights the potential for the emergence of a novel human pathogen.  (+info)

Recovery and identification of West Nile virus from a hawk in winter. (29/871)

West Nile virus was recovered from the brain of a red-tailed hawk that died in Westchester County, N.Y., in February 2000. Multiple foci of glial cells, lymphocytes, and a few pyknotic nuclei were observed in the brain. Three to 4 days after inoculation of Vero cells with brain homogenates, cytopathic changes were detected. The presence of West Nile virus antigen in fixed cells or cell lysates was revealed by fluorescent antibody testing or enzyme-linked immunosorbent assay, respectively. Furthermore, Reverse transcriptase-PCR with primers specific for the NS3 gene of West Nile virus resulted in an amplicon of the expected size (470 bp). Electron microscopy of thin sections of infected Vero cells revealed the presence of viral particles approximately 40 nm in diameter, within cytoplasmic vesicles. The demonstration of infection with the West Nile virus in the dead of the winter, long after mosquitoes ceased to be active, is significant in that it testifies to the survival of the virus in the region beyond mosquito season and suggests another route of transmission: in this case, prey to predator.  (+info)

West Nile virus activity--New York and New Jersey, 2000. (30/871)

In late August 1999, an outbreak of encephalitis caused by West Nile virus (WNV) was detected in New York City and subsequently identified in neighboring counties (1). In response, an extensive mosquito-control and risk-reduction campaign was initiated, including aerial and ground applications of mosquito adulticides throughout the affected areas. No human WNV infections were found in New York City with an onset date after the campaign was completed. Cases continued to occur among humans in surrounding counties that did not undertake mosquito-control efforts until later, suggesting that the campaign may have reduced human risk. In May 2000, CDC issued guidelines to direct national surveillance, prevention, and control efforts (2) and provided funds to support these efforts in 19 state and local health departments where WNV transmission had occurred or where transmission would probably occur based on known bird migration patterns. This report presents the findings of surveillance activities.  (+info)

Update: West Nile virus activity--Northeastern United States, January-August 7, 2000. (31/871)

Surveillance programs initiated in response to the 1999 West Nile virus (WNV) outbreak have detected increased transmission in the northeastern United States (1). Seventeen states along the Atlantic and gulf coasts, New York City (NYC), and Washington, D.C., have conducted WNV surveillance and are reporting to CDC (1). Surveillance for WNV infection includes monitoring of mosquitoes, sentinel chicken flocks, wild birds, and potentially susceptible mammals (e.g., horses and humans) (2). This report summarizes findings of this surveillance system through August 7, 2000.  (+info)

Hygiene at winter bird feeders in a southwestern Ontario city. (32/871)

To further understand the source of the epidemic of salmonellosis in some species of birds using bird feeders in southern Ontario in the winter of 1997-1998, 124 bird feeder stations were examined for their state of hygiene and for Salmonella on 5 occasions during the winter of 1999 in a city of 100,000 people in southwestern Ontario. No Salmonella were isolated from feed contaminated with feces recovered from the feeders. Squirrel-proof feeders were significantly less contaminated with feces than were other feeder types (hopper, platform, silo), which did not differ significantly in their hygiene scores. Contamination of squirrel-proof feeders increased significantly through the course of the study, but other feeder types showed no significant change. Hygiene was poorer if feeders were maintained equally by both male and female household members, particularly as they grew older, but no age or gender effect was observed if only one person was largely responsible for maintaining the feeders. We concluded that winter bird feeder stations in a southern Ontario city were not contaminated with Salmonella but that bird feeder stations could be designed better to reduce fecal contamination of feed.  (+info)