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Marek's disease virus (MDV) is a highly pathogenic and oncogenic herpesvirus of chickens. MDV encodes a basic leucine zipper (bZIP) protein, Meq (MDV EcoQ). The bZIP domain of Meq shares homology with Jun/Fos, whereas the transactivation/repressor domain is entirely different. Increasing evidence suggests that Meq is the oncoprotein of MDV. Direct evidence that Meq transforms chicken cells and the underlying mechanism, however, remain completely unknown. Taking advantage of the DF-1 chicken embryo fibroblast transformation system, a well established model for studying avian sarcoma and leukemia oncogenes, we probed the transformation properties and pathways of Meq. We found that Meq transforms DF-1, with a cell morphology akin to v-Jun and v-Ski transformed cells, and protects DF-1 from apoptosis, and the transformed cells are tumorigenic in chorioallantoic membrane assay. Significantly, using microarray and RT-PCR analyses, we have identified up-regulated genes such as JTAP-1, JAC, and HB-EGF, which belong to the v-Jun transforming pathway. In addition, c-Jun was found to form stable dimers with Meq and colocalize with it in the transformed cells. RNA interference to Meq and c-Jun down-modulated the expression of these genes and reduced the growth of the transformed DF-1, suggesting that Meq transforms chicken cells by pirating the Jun pathway. These data suggest that avian herpesvirus and retrovirus oncogenes use a similar strategy in transformation and oncogenesis.

A defect in the pupil shape ofrosecomb bantam chickens was noticed by a breeder. The pupil in affected birds appeared to be elongated at the lower margin and consistent with a coloboma of the iris. Upon examination of all birds in the flock, the defect was found in 26% of females and 9% of males. Examination of breeders older than 1 yr led to the discovery ofcolobomas, although there were not enough birds to accurately determine the prevalence of the problem for previous generations. Affected birds were examined for other lesions, and none were found. Specific-pathogen-free (SPF) eggs were incubated and hatched with eggs from the affected flock as sentinels. No SPF chicks developed colobomas of the iris, while 37% of the bantams in the same hatch were affected. This experiment eliminated many possible infectious agents and incubator or brooder malfunction as causes of this eye lesion. An analysis of the flock pedigree suggested that the defect might be inherited and might be related either to feather color or to gender. No statistically significant correlation could be made between feather color and the iris colobomas. However, the trait was twice as likely to occur in females as in males, which suggests that it is a sex-influenced trait. Based on the determination that this was an inherited trait, a breeding strategy to reduce the prevalence of the lesion in which affected birds were removed from the breeding flock was developed and followed for 2 yr. The prevalence of colobomas was 22% in females and 2.9% in males after the first year and 7.8% and 0.8% in females and males, respectively, after the second year.

A homologue of interleukin-8, viral interleukin-8 (vIL-8) has been identified in the genome of Marek's disease virus (MDV). This protein attracts peripheral blood mononuclear cells in vitro although its role in the pathogenesis of Marek's disease (MD) is not known. P chickens, genetically susceptible to MD, and N chickens, genetically resistant to the disease, were inoculated with either RB1B MDVor RB1BvIL-8smGFP, a vIL8 knockout RB1B MDV, to assess the role of vIL8 in the pathogenesis of MD. The tumor incidence was highest in the P birds given the RBIB virus, where the incidence was 100%. Tumor incidence in N birds given RB1B was 41.5%. Thirty-one percent of the P birds given RB1BvIL-8smGFP developed tumors, and no N bird given RB1BvIL-8smGFP developed tumors. Histologically, the tumors from RB1B-inoculated birds were larger and more invasive and had a more homogeneous cellular composition than those from RB1BvIL-8smGFP-inoculated birds, which were best described as microtumors. These microtumors did not obliterate the normal architecture of the tissues, and in contrast to the RBIB tumors, moderate numbers of heterophils were admixed with the proliferating lymphocytes. Susceptible birds receiving RB1B had the highest viral titers throughout the study, followed by the resistant birds inoculated with RB1B. P and N birds receiving RB1BvIL-8smGFP virus had consistently lower levels of viremia than their RB1B-inoculated counterparts although virus could be recovered from the birds during all stages of MD. In addition, the RB1BvIL-8smGFP virus was detected in birds held in contact with the inoculated group, although no tumors developed in contact control birds. This result indicates that RB1BvIL-8smGFP replicates in vivo but not as well as RB1B and that vIL8 is not essential for the completion of the pathogenesis of MD.

Infectious bronchitis virus (IBV) produces six subgenomic (sg) mRNAs, each containing a 64 nucleotide (nt) leader sequence, derived from the 5' end of the genome by a discontinuous process. Several putative functional domains such as a papain-like proteinase (PL(pro)), main protease (M(pro)), RNA-dependent RNA polymerase (RdRp), and RNA helicase encoded by the replicase gene are important for virus replication. We have sequenced four regions of the replicase genes corresponding to the 5'-terminal sequence, PL(pro), M(pro), and RdRp domains from 20 heterologous IBV strains, and compared them with previously published coronavirus sequences. All the coronavirus 5'-termini and PL(pro) domains were divergent, unlike the M(pro) and the RdRp domains that were highly conserved with 28% and 48% conserved residues, respectively. Among IBV strains, the 5' untranslated region including the leader sequence was highly conserved (94% identical); whereas, the N-terminal coding region and the PL(pro) domains were highly variable ranging from 84.6% to 100%, and 77.6% to 100% identity, respectively. The IBV M(pro) and RdRp domains were highly conserved with 82.7% and 92.7% conserved residues, respectively. The BJ strain was the most different from other IBVs in all four regions of the replicase. Phylogeny-based clustering based on replicase genes was identical to the antigen-based classification of coronaviruses into three groups. However, the IBV strain classification based on replicase gene domains did not correlate with that of the type-specific antigenic groups. The replicase gene sequences of many IBVs recovered from infected chickens were identical to those of vaccine viruses irrespective of serotype, suggesting that either there has been an exchange of genetic material among vaccine and field isolates or that there is a convergent evolution to a specific replicase genotype. There was no correlation between the genotype of any region of the replicase gene and pathotype, suggesting that the replicase is not the sole determinant of IBV pathogenicity.

The judicious use of medications is a part of any balanced management program. Even so, disease outbreaks should be considered failures of nutrition, management, biosecurity, cleaning and disinfection, or vaccination programs. Preventative measures most effectively limit the adverse effects of disease but when they fail, medication can, and should be used to end the clinical signs of disease and return the flock to its normal balance. Medications should never be applied to flocks without also addressing the management failures that led to the outbreak (see Diseases of the Chicken, Chapter 27).

Free-ranging local chicken flocks are important for the livelihood of resource-poor rural farmers in Tanzania, as they provide a critical source of animal protein and a ready source of income through the sale of chickens and eggs. An occurrence of highly pathogenic avian influenza (HPAI) in the village setting of Tanzania would result in a disastrous loss of livelihood. This paper attempts to offer an alternative method for preventing and controlling HPAI in village settings of Tanzania through community-based approaches.

The specific-pathogen-free (SPF) flocks of chickens maintained by the Department of Microbiology and Immunology at Cornell University became infected, inadvertently, with chicken anaemia virus (CAV), as demonstrated by seroconversion. Chickens from five flocks representing three different strains were examined for the presence of CAV using nested PCR. Virus was detected in ovaries, infundibula, vas deferentia, testes and spleens. Ovaries were positive in 38 to 72% of the hens in four flocks with 13 to 56 birds examined per flock. Interestingly, the ovaries were often the only positive tissues, while a few hens had only positive spleens. In roosters, the vas deferens was positive in 30 to 79% of the birds with 5 to 19 birds examined per flock; the vas deferens was the only positive tissue in 20 to 37%. Individual cells in the theca externa and rare epithelial cells in the infundibular epithelium were positive for CAV by in situ PCR. Positive cells were not detected in testes or vas deferentia. The SH-1 strain of CAV was isolated from these tissues and partially sequenced. Only minor sequence differences were found compared to CIA-1 and Cux-1. Embryos from matings between persistently infected dams and sire had CAV-positive cells in mesenchyme near the developing vertebral column. The data show that CAV persists in the reproductive tissues far longer than previously thought, and that it can be vertically transmitted from persistently infected birds.

Most low pathogenicity avian influenza (LPAI) viruses cause no or mild diseases in avian species. The H9N2 subtype are commonly detected LPAI viruses that have crossed the species barrier to infect humans, unlike most other LPAI viruses. We report in this study that chicken macrophages are susceptible to infection with H9N2 and H6N2 viruses and infection led to apoptosis. Additionally, in H9N2 virus-infected macrophages, major histocompatibility complex (MHC) antigens, class II in particular, were downregulated, which also occurred in the lungs of H9N2 infected chickens. Pro-inflammatory cytokines and chemokines were differentially regulated in both infected macrophages and lungs. Among the regulated genes, IL-4, IL-4R, and CD74 were downregulated, all of which are pivotal in the activation of CD4+ helper T cells and humoral immunity. Remarkably, in H9N2 virus-infected chickens the antibody response was largely suppressed. This is in contrast to what was observed in those infected with H6N2 virus. This finding suggests that the pathogenesis of H9N2 infection in chickens may involve humoral immune suppression. Modulation of MHC antigens and the subsequent impact on the immune responses in mammals infected with avian influenza viruses is largely unclear. These findings raise questions about how some LPAI viruses regulate avian immune responses and if they have similar effects on mammalian immune function.

Waterfowl from northwestern Minnesota were sampled by cloacal swabbing for Avian Influenza Virus (AIV) from July – October in 2007 and 2008. AIV was detected in 222 (9.1%) of 2,441 ducks in 2007 and in 438 (17.9%) of 2,452 ducks in 2008. Prevalence of AIV peaked in late summer. We detected 27 AIV subtypes during 2007 and 31 during 2008. Ten hemagglutinin (HA) subtypes were detected each year (i.e., H1, 3–8, and 10–12 during 2007; H1-8, 10 and 11 during 2008). All neuraminidase (NA) subtypes were detected during each year of the study. Subtype diversity varied between years and increased with prevalence into September. Predominant subtypes during 2007 (comprising ≥5% of subtype diversity) included H1N1, H3N6, H3N8, H4N6, H7N3, H10N7, and H11N9. Predominant subtypes during 2008 included H3N6, H3N8, H4N6, H4N8, H6N1, and H10N7. Additionally, within each HA subtype, the same predominant HA/NA subtype combinations were detected each year and included H1N1, H3N8, H4N6, H5N2, H6N1, H7N3, H8N4, H10N7, and H11N9. The H2N3 and H12N5 viruses also predominated within the H2 and H12 subtypes, respectively, but only were detected during a single year (H2 and H12 viruses were not detected during 2007 and 2008, respectively). Mallards were the predominant species sampled (63.7% of the total), and 531 AIV were isolated from this species (80.5% of the total isolates). Mallard data collected during both years adequately described the observed temporal and spatial prevalence from the total sample and also adequately represented subtype diversity. Juvenile mallards also were adequate in describing the temporal and spatial prevalence of AIV as well as subtype diversity.

An unidentified, pleomorphic, gram-negative rod (PGNR) bacterium has been isolated from domestic fowl with respiratory disease. The PGNR was isolated in 5% of turkey accessions and 3% of chicken accessions, primarily from the respiratory tract. Preliminary characterization of this organism included reviewing accession records, conducting cultural and biochemical tests, and analyzing cellular fatty acids. The PGNR was also compared with other bacteria capable of inhabiting the avian respiratory system. Biochemical and cellular fatty acid analysis failed to identify the organism, however all 14 isolates were similar.

of three techniques for detecting bovine herpesvirus type 1 (BHV1) in naturally and experimentally contaminated bovine semen. Zuchthygiene 23:1-9. 3. Darcel CLQ, Coulter GH: 1976, IBR neutralizing substance in bull seminal fluid and its removal prior to attempts at virus isolation from semen. Can Vet J 17:317-343. 4. Kahrs RF, Johnson ME, Bender GM: 1977, Studies on the detection of infectious bovine rhinotracheitis (IBR) virus in bovine semen. Proc Annu Meet Am Assoc Vet Lab Diagn 20:187-208. 5. Kahrs RF, Littell RC: 1980, Detection of viruses in bovine semen. Influence of preparative centrifugation on isolation of IBR virus. Proc Annu Meet Am Assoc Vet Lab Diagn 23:251-262. 6. Loewen KG, Darcel CLQ: 1985, A comparison of two methods for the isolation of bovine herpesvirus 1 (BHV-1) from extended bovine semen. Theriogenology 23:935-939. 7. Moorthy ARS: 1985, Outbreak of balanoposthitis in breeding bulls. Vet Rec 116:98. 8. Schultz RD, Sheffy BE: 1980, Current status of viral infection of bovine genital tract with emphasis on IBR/IPV virus. In: Current therapy in theriogenology, ed. Morrow DA, pp. 503-509. W. B. Saunders Co., Philadelphia, PA. 9. Snowdow WA: 1965, The IBR/IPV virus reaction to infection and intermittent recovery of the virus from experimentally inoculated cattle. Aust Vet J 41:135-142.

Avian influenza virus (AIV) H9N2 subtype has circulated in wild birds and domestic poultry, has successfully crossed the species boundary to transmit to and infect humans and have contributed to the generation of highly pathogenic H5N1 viruses. Little is known about host responses to H9N2 viruses in human airway respiratory epithelium. We used apically differentiated primary human tracheobronchial epithelial (hTBE) cultures to study host antiviral and apoptotic responses to an H9N2 virus strain. Compared to the immortalized bronchial epithelial cells HBE1, differentiated hTBE were less susceptible to the H9N2 virus. Among the antiviral cytokines, IFN-β was the prominent antiviral component in primary cultures. We found that IL-6, TNF-α, IP10 and CCL5 seemed to play important roles in proinflammatory responses while IL-1β and CCL5 were downregulated in primary hTBE cells. The AIV H9N2 virus caused apoptosis in both HBE1 and primary hTBE cultures. In addition to the extrinsic apoptotic pathway, we found that the mitochondria-mediated intrinsic cascade participated in H9N2-induced apoptosis, demonstrated by the cytosolic presence of active caspase 9 and cytochrome c. Further, our data indicated that FLIP and Bcl-2 family members Bax and Bcl-Xs appeared to be involved in the apoptotic regulation. The findings will further our understanding on host defense mechanisms and pathogenesis in human respiratory epithelium infected with AIV H9N2 virus.

The emergence of highly pathogenic avian influenza (HPAI) H5N1 has elevated concerns about wild birds as virus hosts; however, little is known about the ecological and epidemiological factors of transmission by shorebirds. Here we summarize results for 2,773 shorebirds that were live-trapped on the Pacific coast of the United States during 2006-2007 and tested for avian influenza virus using real-time reverse transcriptase-polymerase chain reaction (RT-PCR) and virus isolation. As was the case throughout North America, HPAI H5N1 was not detected in shorebirds during this interval. Contrary to other wild bird groups, most notably waterfowl, the prevalence of even low pathogenicity virus among shorebirds in our study areas in California, Washington, and Alaska was extremely low (0.5%). Virus was detected by RT-PCR from four different species, including, Dunlin (Calidris alpina; N = 3), Western Sandpiper (C. mauri; N = 8), Long-billed Dowitcher (Limnodromus scolopaceus; N = 1), and American Avocet (...

Ulcerative enteritis is a disease that typically responds well to medication. An outbreak of ulcerative enteritis that was persistent and unresponsive to treatment is described. The outbreak started in semimature birds and progressively spread to younger birds. Confounding factors leading to this persistence were a significant coccidosis problem, a feed mixing error, and suspected antibiotic resistance. Although Clostridium colinum was never isolated, a bacitracin-resistant Clostridium perfringens was cultured from affected birds. Only the combined treatment of the flocks with an anticoccidial and tylosin was effective in controlling clinical disease. Numerous other management and treatment strategies were unsuccessful in lowering the severe mortality.

This is a comparative study on seroconversion to chicken infectious anemia virus (CIAV) in a closed flock of specific-pathogen-free chickens undergoing a natural outbreak and after vaccination of some of these flocks with a commercial, live vaccine. The N2a strain (B21B21 haplotype) had the highest seroconversion after natural infection (94%) or vaccination (100%), followed by the P2a strain (B19B19) at 75%-82% seroconversion after natural infection and 85% seroconversion after vaccination. The S13 (B13B13) chickens were 26% seropositive after natural infection and 75% seropositive after vaccination. N2a chickens with polymerase chain reaction (PCR)-positive tissues were 97% seropositive compared to 80%-83% PCR-positive and seropositive for the P2a chickens and only 8% seropositive and PCR-positive for the S13 chickens. Seroconversion occurred at or near sexual maturity after natural infection in seven flocks studied.

Chicken infectious anemia virus (CIAV) is known to infect and replicate in various Marek's disease chicken cell lines (MDCCs) derived from Marek's disease (MD) tumors. One line, MDCC-MSB1, has been the substrate used in most studies. We compared a total of 26 MDCCs, including two sublines of MDCC-MSB1, MSB1 (L) and MSB1 (S), four other MD tumor-derived lines, and 20 lines derived from MD virus-induced local lesions, for susceptibility to the Cux-1 and CIA-1 strains of CIAV. The cell lines represented six phenotypic groups of T cells based on the expression of CD4, CD8, and TCR-2 and -3 surface markers. Susceptibility was measured by the number of cells positive for viral antigen in immunofluorescence (IF) tests at 3-10 days postinfection. No clear-cut differences were found in susceptibility related to phenotype, although CD4-/8+ lines and CD4-/8- lines might be more susceptible than CD4+/8- lines. However, several individual lines were more susceptible to Cux-1 than the two MSB1 sublines tested. Contrary to an earlier report, cells of MDCC-CU147, a CD8+, TCR3+, local-lesion derived line, were found to be susceptible to CIA-1. In fact, CU147 was distinguished by very high susceptibility to both CIAV strains. In direct comparisons with MSB1, CU147 detected approximately 10-fold lower doses of virus. Also, virus spread was faster (P < 0.05) in CU147 than in MSB1 and other lines. Results from polymerase chain reaction (PCR) tests to detect infection in titrations were in general agreement with IF test results although PCR detected infection in a few terminal dilution cultures that were negative by IF.

Hemorrhagic enteritis (HE) is an economically important disease of turkeys caused by a type II aviadenovirus, hemorrhagic enteritis virus (HEV). The vaccines currently available to the commercial poultry producer are highly effective in preventing disease outbreaks; however, they are immunosuppressive. A recombinant fowl poxvirus (rFPV) expressing the native hexon of HEV has been shown to induce an anti-HEV humoral immune response in turkeys. In this study, the rFPV expressing the native hexon of HEV was compared with a commercial HEV vaccine (vxHEV) for its ability to protect turkeys from virulent HEV challenge. Complete protection from the enteritis of HE was achieved in experimental groups vaccinated with either the rFPV or the vxHEV. Lymphocyte stimulation was measured in turkeys inoculated with rFPV, vxHEV, or a sublethal dose of HEV or not inoculated. No statistically significant immunodepression was observed in turkeys receiving the rFPV.

Severe cephalic swelling and facial cellulitis in turkeys associated with fowl cholera were present in seven accessions submitted to two laboratories in a 2-year period. Flocks ranged in age from 6 to 18 weeks and included both toms and hens. Interestingly, turkeys with facial cellulitis had no gross internal lesions of fowl cholera, whereas birds with gross lung, liver, and air-sac lesions did not have swollen heads. Histologically, the facial cellulitis was characterized by extensive fibrinonecrotic inflammation of the deep dermis with heterophilic perivasculitis and thrombosis. Additional characterization of Pasteurella multocida isolates from these cases was conducted retrospectively from lyophilized cultures. Serogrouping, serotyping, and an enzyme-linked immunosorbent assay (ELISA) for dermonecrotic factor were performed. All isolates were serogroup A or unencapsulated. Serotype 1 was the most prevalent serotype isolated in association with facial cellulitis. ELISA results for dermonecrotic toxin were inconclusive.

SUMMARY. Three birds from a flock of 125 Cochin bantam chickens were true hermaphrodites, having both ovarian and testicular tissues. These birds were recognizable by their intermediate comb size, intermediate plumage, and spur development. At necropsy, the left gonad of all three birds was an ovotestis and the right gonad was a testis. Microscopically, both ovarian follicles and seminiferous tubules were present within the ovotestes. Chromosomal analysis of lymphocytes from the whole blood of the third bird revealed triploid ZZW sex chromosomes. This high incidence (2.4%) of hermaphrodism suggests that there may be a hereditary predisposition for genetic intersex. RESUMEN. Reporte de Caso-Hermafroditas verdaderos en una parvada de pollos miniatura.

SUMMARY. Monensin was given via gavage to 5- and 6-week-old broad-breasted white turkeys. The birds were allotted into four groups-three groups given monensin and one group of controls-in two experimental trials. Treated turkeys in Trial 1 received one dose of monensin per day for 4 days at 4.7 mg monensin/kg body weight, 8.8 mg/kg, or 17.6 mg/ kg. Treated turkeys in Trial 2 received one dose of monensin per day for 5 days at 1.93 mg/ kg, 4.7 mg/kg, or 8.8 mg/kg. Turkeys receiving the lowest dose showed no clinical signs of myopathy. Birds receiving 4.7 mg monensin/kg developed ataxia after the third dose and rear limb paresis and paralysis after the fifth dose. Turkeys receiving 8.8 mg/kg were ataxic after the second dose and paretic or paralyzed after the fourth dose. Turkeys receiving 17.6 mg/kg were ataxic 3 hours after the first dose and paretic or paralyzed 8 hours after the first dose. Histologically, a necrotizing skeletal myopathy was present in the muscles of the rear limbs. A dose-related response was observed in the percentage of myofibers damaged in birds that survived until the end of the trials. Intrafiber edema and vacuolation were observed in histologic sections from myocardium of turkeys from the two highest dose groups.

Two unrelated flocks of chicks experienced elevated mortality from 4 to 10 days of age. Clinical signs in affected birds included a full range of neurological disorders. Livers and spleens were grossly enlarged at necropsy. Enterococcus durans was isolated from multiple organs, including brains. Histologically, there were multifocal coagulative necrosis in the liver, areas of malacia in brain stem, and cerebellar white matter. Inoculation of 1-day-old chicks with a suspension of E. durans resulted in bacteremia but did not produce the lesions observed in field cases.

Two 5-week-old bronze turkeys were submitted with crooked necks that could not be straightened. Both birds were serologically and culturally positive for Mycoplasma meleagridis (MM). Histologically, there were lymphoid follicles in the cranial thoracic and cervicoclavicular air sacs, and inflammatory changes in the cartilage of some cervical vertebrae. This appeared to be a case of MM-associated wry necks.

Intranuclear inclusions were observed with light microscopy in tissues from necropsy cases from three different species of birds. Because of the nature of these inclusions, the species affected, or their distribution, the inclusions were considered of unknown pathogenic significance. The inclusions were examined ultrastructurally. Parvovirus-like particles were observed in the intranuclear inclusions of pigeon hepatocytes and duodenal stromal cells from a quail. Finely granular eosinophilic intranuclear inclusion bodies from two unrelated pigeon cases were found to be composed of loosely organized filaments. One liver sample from a 16-week-old laying chicken had prominent eosinophilic hepatocellular intranuclear inclusions composed of electron-dense coarsely granular amorphous material.

A necrotizing skeletal myopathy of rear limbs was diagnosed in 17 flocks of commercial turkeys. The mean mortality attributed to the myopathy was 2.29% (range = 0.13-9.7%) over a mean period of 9.6 days (range = 6-14 days). The mean age of the birds at the time of onset was 7.4 weeks (range = 4-10.5 weeks). Clinically, birds experienced an episode of watery droppings and high-pitched crying, followed by rear-limb paresis or paralysis. Creatine kinase and aspartate aminotransferase were markedly elevated in birds with the myopathy. Grossly, a few birds had pale streaking in the muscles of the thighs and legs. Histologically, acute and subacute degeneration was present in myofibers of the legs, abdomen, thighs, back, and tail. The subacute lesion was characterized by marked sarcolemmal cell proliferation. Feed analyses ruled out selenium deficiency and the presence of mycotoxins as etiologies. Monensin was present in approved usage or only slightly elevated levels. A known potentiating antibiotic was being used concurrently with monensin in only one flock.

An outbreak of diarrhea and neurological disease in California racing pigeons caused by avian paramyxovirus type 1 (PMV-1) is documented. Predominant clinical signs were polydipsia, ataxia, poor balance, torticollis, head tremors, inability to fly, and diarrhea that was unresponsive to therapy. Gross pathologic findings were often unremarkable or non-specific. The predominant histologic lesions were interstitial nephritis, chronic tubular necrosis, lymphoplasmacytic infiltration within the kidney, liver, and pancreas, and focal non-suppurative encephalitis. Pigeons from 20 submissions demonstrated characteristic clinical signs of PMV-1 infection. Pigeons from 17 submissions exhibited typical histopathology. Serologic evidence of PMV-1 infection was present in pigeons from 13 submissions, and PMV-1 was isolated from pigeons received in six submissions. None of these pigeons had been vaccinated against PMV-1.

A social strategy was tested for implementing Newcastle disease (ND) vaccination and biosecurity improvements among free-ranging chicken at village level in Tanzania. In addition to training the local poultry vaccinators, data recorders and poultry-keepers, the strategy involved training and empowering leaders at the district, ward and village level. The trainings covered poultry health, management, and marketing of village chickens, with an emphasis on ND vaccination and improving biosecurity against avian influenza (AI), The study sites included villages in one ward in each of three each three districts (Iringa, Mtwara-Mikindani, and Mvomero) of mainland Tanzania. Ninety-six local leaders at district level and 101 leaders at ward levels were trained. In addition, 196 farmers (households) were trained, as well as 86 vaccinators and 26 data recorders. Data recorders were also trained as poultry first aid workers. ND vaccination was conducted by the vaccinators, supervised by their local leaders with technical assistance from veterinarians. A total of 158,343 village chickens were vaccinated in three rounds of vaccination three months apart. The training and empowerment of local leaders and local implementers was the key element for success as it fostered the feeling of local ownership of the program and prevented conflicts with other development activities within the villages. We conclude that most animal health programs will increase their odds of success by involving local leaders and by addressing the current challenges facing the farmers. Further assessment on the usefulness of this approach is needed.

Many theories about the modes of avian influenza virus (AIV) transmission have been proposed, but few have been quantified, and none within a flock or live bird market (LBM) setting where birds are often kept in stacked cages. We describe a novel experimental design and the results collected for the purpose of estimating transmission rates specific to the potential modes of AIV transmission within an LBM. Chickens of the strains and ages found in California LBMs were inoculated with low pathogenicity AIV H6N2. Aerosol exposure was found to be the most important route of transmission for this H6N2 AIV. The handling of infectious chickens resulted in the transmission of H6N2 AIV, though the virus was not detectible by rRT-PCR. Chickens with fecal exposure to infected birds (median=8.0 DPI) had detectable virus earlier than in those with aerosol exposure only (median=10.0 DPI). Changes in the hemagglutinin sequence were not found to be associated with oropharyngeal or cloacal shedding in this study.

Since the end of March 2013, avian a influenza viruses of the H7N9 subtype have caused more than 130 human cases of infection in China, many of which were severe, resulting in 43 fatalities. Although this A(H7N9) virus outbreak is now under control, the virus (or one with similar properties) could reemerge as winter approaches. To better assess the pandemic threat posed by A(H7N9) viruses, NIAID/NIH Centers of Excellence in Influenza Research and Surveillance (CEIRS) investigators and other expert laboratories in China and elsewhere have characterized the wild-type avian A(H7N9) viruses in terms of host range, virulence, and transmission, and are evaluating the effectiveness of antiviral drugs and vaccine candidates. However, to fully assess the potential risk associated with these novel viruses, there is a need for additional research including experiments that may be classified as “gain-of-function” (GOF). Here, we outline the aspects of the current situation that most urgently require additional research, our proposed studies, and risk-mitigation strategies.