Search

Avian influenza viruses from wild birds can cause outbreaks in poultry, and occasionally infect humans upon exposure to infected poultry. Identification and characterization of viral reservoirs and transmission routes is important to develop strategies that prevent infection of poultry, and subsequently virus transmission between poultry holdings and to humans. Based on spatial, temporal and phylogenetic analyses of data generated as part of intense and large-scale influenza surveillance programs in wild birds and poultry in the Netherlands from 2006 to 2011, we demonstrate that LPAIV subtype distribution differed between wild birds and poultry, suggestive of host-range restrictions. LPAIV isolated from Dutch poultry were genetically most closely related to LPAIV isolated from wild birds in the Netherlands or occasionally elsewhere in Western Europe. However, a relatively long time interval was observed between the isolations of related viruses from wild birds and poultry. Spatial analyses provided evidence for mallards (Anas platyrhynchos) being more abundant near primary infected poultry farms. Detailed year-round investigation of virus prevalence and wild bird species distribution and behavior near poultry farms should be used to improve risk assessment in relation to avian influenza virus introduction and retarget avian influenza surveillance programs.

Avian influenza virus-infected poultry can release a large amount of virus-contaminated droppings that serve as sources of infection for susceptible birds. Much research so far has focused on virus spread within flocks. However, as fecal material or manure is a major constituent of airborne poultry dust, virus-contaminated particulate matter from infected flocks may be dispersed into the environment. We collected samples of suspended particulate matter, or the inhalable dust fraction, inside, upwind and downwind of buildings holding poultry infected with low-pathogenic avian influenza virus, and tested them for the presence of endotoxins and influenza virus to characterize the potential impact of airborne influenza virus transmission during outbreaks at commercial poultry farms. Influenza viruses were detected by RT-PCR in filter-rinse fluids collected up to 60 meters downwind from the barns, but virus isolation did not yield any isolates. Viral loads in the air samples were low and beyond the limit of RT-PCR quantification except for one in-barn measurement showing a virus concentration of 8.48x104 genome copies/m3. Air samples taken outside poultry barns had endotoxin concentrations of ∼50 EU/m3 that declined with increasing distance from the barn. Atmospheric dispersion modeling of particulate matter, using location-specific meteorological data for the sampling days, demonstrated a positive correlation between endotoxin measurements and modeled particulate matter concentrations, with an R2 varying from 0.59 to 0.88. Our data suggest that areas at high risk for human or animal exposure to airborne influenza viruses can be modeled during an outbreak to allow directed interventions following targeted surveillance.

The recently identified human infections with avian influenza A(H7N9) viruses in China raise important questions regarding possible source and risk to humans. Sequence comparison with an influenza A(H7N7) outbreak in the Netherlands in 2003 and an A(H7N1) epidemic in Italy in 1999-2000 suggests that widespread circulation of A(H7N9) viruses must have occurred in China. The emergence of human adaptation marker PB2 E627K in human A(H7N9) cases parallels that of the fatal A(H7N7) human case in the Netherlands.

Although increasing data have become available that link human adaptation with specific molecular changes in nonhuman influenza viruses, the molecular changes of these viruses during a large highly pathogenic avian influenza virus (HPAI) outbreak in poultry along with avian-to-human transmission have never been documented. By comprehensive virologic analysis of combined veterinary and human samples obtained during a large HPAI A (H7N7) outbreak in the Netherlands in 2003, we mapped the acquisition of human adaptation markers to identify the public health risk associated with an HPAI outbreak in poultry. Full-length hemagglutinin (HA), neuraminidase (NA), and PB2 sequencing of A (H7N7) viruses obtained from 45 human cases showed amino acid variations at different codons in HA (n = 20), NA (n = 23), and PB2 (n = 23). Identification o

Although increasing data have become available that link human adaptation with specific molecular changes in nonhuman influenza viruses, the molecular changes of these viruses during a large highly pathogenic avian influenza virus (HPAI) outbreak in poultry along with avian-to-human transmission have never been documented. By comprehensive virologic analysis of combined veterinary and human samples obtained during a large HPAI A (H7N7) outbreak in the Netherlands in 2003, we mapped the acquisition of human adaptation markers to identify the public health risk associated with an HPAI outbreak in poultry. Full-length hemagglutinin (HA), neuraminidase (NA), and PB2 sequencing of A (H7N7) viruses obtained from 45 human cases showed amino acid variations at different codons in HA (n = 20), NA (n = 23), and PB2 (n = 23). Identification o

Summary: The aim of this study was to identify difficulties and barriers to reporting clinically suspect situations, possibly caused by avian influenza (AI), and to explore possible incentives to reporting such situations, with the ultimate aim of facilitating early detection of AI outbreaks. Focus group sessions were held with policy-makers from the competent authority, representatives of veterinary practitioners and poultry farmers. Personal interviews with a group of poultry farmers and practitioners were held to ascertain the difficulties and barriers they perceived and their proposed solutions. An electronic questionnaire was put on the websites of a poultry farmer union and the Royal Dutch Veterinary Association to investigate perceptions and attitudes concerning AI-suspect situations in the Netherlands. Six themes emerged identifying factors that hinder the reporting of a clinically suspect situation: lack of knowledge and uncertainty about clinical signs of AI; guilt, shame and prejudice; negative opinion of control measures; dissatisfaction with post-reporting procedures; lack of trust in veterinary authorities; lack of transparency in reporting procedures and uncertainty about the notification process. Recommendations to facilitate early detection of AI are discussed.

Highly pathogenic avian influenza A viruses of subtypes H5 and H7 are the causative agents of fowl plague in poultry. Influenza A viruses of subtype H

The bone marrow (BM) is the major production site of B lymphocytes. The newly formed small B lymphocytes migrate, after a maturation period of one or more days, to the peripheral lymphoid organs (spleen, lymph nodes, tonsils, etc.), where they can be activated by antigen (after which they can differentiate into antibody-forming cells) or die. According to this view, most of the immunoglobul in(lg)- and antibodyproducing eel ls are considered to be confined to the peripheral lymphoid organs. However, publications have appeared during the last ninety years presenting evidence that antibody formation can also take place in the BM (Chapter 3). This thesis further investigates this phenomenon with mice as experimental animals. After primary immunization of mice with thymus-dependent (TO) antigens, antibody formation almost exclusively takes place in the peripheral lymphoid organs. However, after secondary immunization with the same antigen, substantial numbers of antibody-producing plaqueforming eel ls (PFC) are found not only in the peripheral lymphoid organs, but also in the BM. The first phase of the secondary response, about 1 week of duration, is characterized by much higher numbers of PFC in the spleen and/or lymph nodes than in the BM. But after this first phase, the PFC response in the BM is much higher than in al 1 other lymphoid organs together