The role of indigenous wild, semidomestic, and exotic birds in the epizootiology of velogenic viscerotropic Newcastle disease in southern California, 1972-1973.

During an epornitic of velogenic viscerotropic Newcastle disease (VVND) in southern California, free-flying wild birds, captive and free-ranging semidomestic birds, and exotic birds were collected from the quarantine area to determine their role in the epizootiology of the disease. The VVND virus was isolated from 0.04% of 9,446 free-flying wild birds, 0.76% of 4,367 semidomestic birds, and 1.01% of 3,780 exotic birds examined. Three house sparrows and 1 crow directly associated with infected poultry flocks were the only free-flying wild birds from which VVND virus was isolated. Among semidomestic species, ducks, quail, chukars, pheasants, peafowl, pigeons, and doves were found to be infected. Psttacines, pittas, and toucans accounted for 92% of the VVND virus isolations from exotic birds. In addition, domestic Newcastle disease virus (NDV) was isolated from 0.29% of the free-flying wild birds, from 1.65% of the semidomestic birds, and from 0.19% of the exotic birds collected. Hemagglutination-inhibition against domestic NDV was demonstrated in 0.24% of 3,796 wild bird serums, 8.28% of 2,004 semidomestic bird serums, and 3.90% of 231 exotic bird serums tested. Although few free-flying wild birds were infected with VVND virus in this epornitic, the isolation of domestic NDV strains from free-flying wild ducks and mourning doves suggests the potential for transportation of NDV over long distances by migratory birds.     

Methods of spread of velogenic viscerotropic Newcastle disease virus in the southern Californian epidemic of 1971-1973.

Data collected during the velogenic viscerotropic Newcastle disease (VVND) epidemic that occurred in southern California from 1971 to 1973 were analyzed to determine the methods of spread of the disease. Spread between chicken flocks was extensive and due mainly to the movement of live birds and mechanical transport of virus by man, especially by vaccination and poultry service crews. Spread to exotic birds was from contact with infected imported stock. Spread to other species was most probably through contact with infected chickens. Infection persisted in commercial chicken flocks because of intensive vaccination programs, heavy traffic and contact between layer operations, and the maintenance of multi-age flocks. These foci of infection probably led to spread of the disease to areas from which VVND had been eradicated several months before. There was no evidence of significant wind-borne spread of virus between flocks.     

Failure to demonstrate viscerotropic velogenic Newcastle disease in psittacine birds in the Republic of the Philippines

Birds on the islands of Luzon, Mindanao, and Palawan in the Republic of the Philippines were surveyed for viscerotropic velogenic Newcastle disease (VVND). Virus isolation was attempted on 728 cloacal samples from native and exotic psittacine birds, non-psittacine birds, and domestic chickens and ducks. A VVND virus isolate was obtained from a single domestic chicken that had exhibited ocular discharge and diarrhea 3 days before sampling. All other birds were negative for VVND.     

Blackhead disease in turkeys: direct transmission of Histomonas meleagridis from bird to bird in a laboratory model

The spread of Histomonas meleagridis infections through groups of turkeys in the absence of the cecal worm vector (Heterakis gallinarum) was studied in a battery cage model. Battery-reared poults were exposed at 2 wk of age by commingling with infected birds into cages that had the floor lined with paper. One treatment received no exposure, whereas other birds were commingled with two, three, or four birds/cage (25%, 37.5%, or 50%) inoculated per cloaca with cultured H. meleagridis (200,000/bird). Inoculated birds died at 7-13 days postinoculation (DPI) showing typical liver and cecal lesions of histomoniasis. By 14 DPI, 87.5% of the directly inoculated birds died or had severe lesions of histomoniasis. Turkeys commingled with two, three, or four infected birds became infected at the rate of 72%, 80%, or 75%, respectively. In another experiment, two birds/cage (25%) were inoculated with Histomonas from culture and allowed to commingle with other birds for 1, 2, 3, or 4 days. Two of 12 (16.7%) birds had minor cecal lesions after contact with inoculated birds for 1 day, but 87.5%-100% became infected if inoculated birds remained in the cage for 2-4 days. Contemporaneous inoculation with cecal coccidia (Eimeria adenoeides) as a predisposing factor in blackhead infections was studied using the model. Turkey poults directly inoculated with Histomonas were allowed to commingle for 5 days with uninoculated birds that had received inoculation with 0, 10(3), or 10(4) sporulated oocysts. The coccidian infection appeared to interfere with transmission of blackhead infection by 7 DPI, as suggested by lessened severity of cecal lesions and a lower percentage of infected birds. These studies confirm that histomoniasis is transmitted readily from directly exposed young turkeys to others in the absence of the cecal worm vector, and that this phenomenon can be reproduced in battery cages as an experimental model.     

The pathogenicity of four avian influenza viruses for fowls, turkeys and ducks

Groups of 10 two-week-old chicks, turkey poults and ducklings were each infected by the intranasal route with one of four avian influenza viruses: a/fowl/Germany/34 (Hav 1N))--Rostock, A/FPV/Dutch/27 (Hav 1 Neq 1)--Dutch, A/fowl/Victoria/75 (Hav 1 Neq 1)--Australian, and A/parrot/Ulster/73 (Hav 1 N1)--Ulster. Eight hours after infection 10 birds of the same age and species were placed in contact with each group and allowed to mix. The clinical signs of disease and onset of sickness and death were recorded. Ulster virus was completely avirulent for all birds. Rostock, Dutch and Australian viruses were virulent for fowls and turkeys causing death in all birds with the exception of 3/10 in contact fowls from the Rostock virus group and 2/10 in contact fowls from the Australian virus group. Only Rostock virus caused sicked sickness or death in ducks, 9/10 intranasally infected and 6/7 in contact birds showed clinical signs and 2/10 intranasally infected and 3/7 in contact ducks died. Intranasal and in contact pathogenicity indices were calculated for each virus in each bird species and indicated quantitatively the differences in virulence of the four virus strains. Virus isolation and immune response studies indicated that surviving in contact fowls in the Rostock virus group had never been infected but that surviving Australian virus in contact fowls had recovered from infection. Infection was not established in Ulster virus in contact fowls and Australian virus intranasally infected and in contact ducks. The birds in all other groups showed positive virus isolations and a high incidence of positive immune response. The last virus isolation was made at 22 days after intranasal infection of ducks with Ulster virus.     

Viremia, virus shedding, and antibody response during natural avian polyomavirus infection in parrots

OBJECTIVE: To determine rapidity of spread and onset and duration of viremia, virus shedding, and antibody production in parrots naturally infected with avian polyomavirus (APV). DESIGN: Case series. ANIMALS: 92 parrots in 2 aviaries. PROCEDURE: Blood samples were obtained from parrots naturally exposed to APV during a 3- to 4-month period for determination of serum virus neutralizing antibody and detection of viral DNA. Nestlings from the next year's hatch were monitored for APV infection. RESULTS: The first indication of inapparent infection was viremia, which developed simultaneously with or was followed within 1 week by cloacal virus shedding and antibody production. Cloacal virus shedding continued after viremia ceased. During viremia, viral DNA was detected continuously in blood samples. Viral DNA was detected in serial cloacal swab specimens in most birds, but it was detected inconsistently in 6 birds and not detected in 3 birds, even though these birds were viremic. Duration of cloacal virus shedding was < or = 4.5 months. In 1 aviary, prevalence of infection was 88% and dissemination of virus through the 3-room building required 4.5 months. In the second aviary, a single-room nursery, prevalence of infection was > or = 90%. For all affected birds, infection could be detected 18 days after the first death. CONCLUSIONS AND CLINICAL RELEVANCE: If a single sampling is used for polymerase chain reaction detection of viral DNA, blood and cloacal swab specimens are required. In nestling nonbudgerigar parrots, cloacal virus shedding may persist for 4.5 months. Management protocols alone are sufficient to prevent introduction of APV into a nursery.     

Experimental West Nile virus infection in Eastern Screech Owls (Megascops asio)

Eastern Screech Owls (EASOs) were experimentally infected with the pathogenic New York 1999 strain of West Nile virus (WNV) by subcutaneous injection or per os. Two of nine subcutaneously inoculated birds died or were euthanatized on 8 or 9 days postinfection (DPI) after <24 hr of lethargy and recumbency. All subcutaneously inoculated birds developed levels of viremia that are likely infectious to mosquitoes, with peak viremia levels ranging from 10(5.0) to 10(9.6) plaque-forming units/ml. Despite the viremia, the remaining seven birds did not display signs of illness. All birds alive beyond 5 DPI seroconverted, although the morbid birds demonstrated significantly lower antibody titers than the clinically normal birds. Cagemates of infected birds did not become infected. One of five orally exposed EASOs became viremic and seroconverted, whereas WNV infection in the remaining four birds was not evident. All infected birds shed virus via the oral and cloacal route. Early during infection, WNV targeted skin, spleen, esophagus, and skeletal muscle. The two morbid owls had myocardial and skeletal muscle necrosis and mild encephalitis and nephritis, whereas some of the clinically healthy birds that were sacrificed on 14 DPI had myocardial arteritis and renal phlebitis. WNV is a significant pathogen of EASOs, causing pathologic lesions with varying clinical outcomes.     

The infection of turkey poults with Histomonas meleagridis by contact with infected birds or contaminated cages

The conditions under which infection with Histomonas meleagridis could spread from directly inoculated turkey poults to uninoculated poults without the aid of invertebrate hosts or vectors was investigated in several experiments. In three experiments in battery cages, uninoculated poults were commingled with directly infected birds on pine-shaving litter. Directly exposed birds were inoculated per cloaca with H. meleagridis by means of a plastic pipette tip attached to a 10-ml syringe or orally gavaged with fresh cecal droppings from donor turkeys 4 days postinoculation (PI). Of the cloacally inoculated controls in these experiments, 31 of 44 (70.5%) birds had severe lesions ofhistomoniasis at 14 days PI, whereas none of the orally gavaged birds became infected. Histomoniasis developed in 11 of 36 (30.5%) birds allowed to commingle with inoculated birds. In other treatments, poults were allowed only contact with droppings from directly inoculated birds after the infected birds were removed from the cages. This was done for a single period of 1 hr or repeated five times. Four of 32 birds (12.5%) became infected in this way after the single exposure, whereas only four of 44 birds (9.1%) exposed five times developed lesions. In a comparison of floor materials, 35 of 35 control birds inoculated per cloaca developed severe liver and cecal lesions, irrespective of litter. Uninoculated birds allowed to commingle with infected birds on paper or pine shavings became severely infected in all cases (12/12 and 12/12 birds, respectively), whereas only 33% of those on wire-floored cages became infected (4/12). These results suggest that transmission of infection is more likely to occur as a result of direct contact between birds than from contact with litter or fecal material.     

Effect of reticuloendotheliosis virus on the response of chickens to Salmonella typhimurium infection

Groups of 25 chickens free of maternal antibody to reticuloendotheliosis virus (REV) were inoculated with either third or seventh passage REV at either one or seven days of age. Some of the birds inoculated at day 1 with REV were inoculated with Salmonella typhimurium either concurrently or six or 13 days later while some of those inoculated with REV at day 7 were inoculated concurrently with S typhimurium. At day old, infection with S typhimurium alone caused the death of 12 of 25 chicks whereas in the dual infection, using the third passage REV, 18 of 25 birds died. Similarly no seven or 14 day old chickens died when challenged with S typhimurium alone, but previous day-old infection with REV caused a respective mortality of eight of 25 and five of 25 birds. With the seventh passage REV a similar pattern was seen. At day old S typhimurium infection alone killed seven of 25 birds whereas combined with virus the mortality was 14 of 25 and while S typhimurium alone killed none of 25 chicks infected at seven days old, the mortality in birds also infected with REV was 14 of 25. Combined virus and bacterial infections did not increase the proportion of feathering defects in birds surviving S typhimurium infections. There was a significantly higher proportion of feathering defects in birds infected with third passage virus compared with seventh passage virus. Although a higher proportion of birds had antibody responses to REV in the seventh than in the third passage group, there was no discernible difference in the effect the different viruses had on chickens' susceptibility to S typhimurium.     

Experimental aerosol infection of cattle (Bos taurus) with ovine herpesvirus 2 using nasal secretions from infected sheep

Infection of clinically susceptible ruminants, including domesticated cattle and American bison, with ovine herpesvirus 2 (OvHV-2) can result in the fatal lymphoproliferative and vasculitis syndrome known as malignant catarrhal fever (MCF). A reliable experimental infection model is needed to study the pathogenesis of MCF and to develop effective vaccination strategies to control the disease. An experimental aerosol infection model using sheep, the natural carriers of OvHV-2, has been developed (Taus et al., 2005). Using the protocol and OvHV-2 inoculum established in the previous study, eight calves were nebulized with four different doses of OvHV-2 in nasal secretions from infected sheep. Two control calves were nebulized with nasal secretions from uninfected sheep. Infection status of all calves was monitored using competitive inhibition ELISA, PCR and clinical parameters. Six of eight nebulized calves became infected with OvHV-2. One calf receiving the highest dose of virus developed typical clinical, gross and histological changes of MCF. This study showed that nasal secretions collected from sheep experiencing OvHV-2 shedding episodes were infectious for cattle and capable of inducing MCF. The data also indicate that cattle are relatively resistant to disease following infection. The use of more susceptible species as experimental animal models, such as bison and selected cervid species should be examined.     

Evaluation of efficacy of Vero cell-adapted,thermostable Newcastle disease vaccine in broilers

The main theme of this project was to develop a Vero cell-adapted, thermostable NDV I-2 vaccine and evaluate its efficacy against challenge infection. For this purpose, serial passages of virus were done in Vero cell line up to 13 times and after each passage samples were subjected to heat treatment at 56°C for 40 min. After 13 passages, the virus was completely adapted on Vero cell line and cytopathic effects were observed, including syncytial formation, rounding, degeneration, and detachment of cells. Hemagglutination and infectivity titers showed that the virus was thermostable after each passages in Vero cell line. One-day-old broiler chicks (Group 1) were vaccinated orally with thermostable NDV I-2 vaccine. A commercially available thermolabile NDV LaSota was used in Group 2 used as positive control. NDV I-2 vaccine produced maximum % inhibition migration at d 6 (50%) as compared with LaSota ND vaccine (i.e., 32%). On encounter with virulent NDV I-2, 100% safety was accomplished in group 1 and 60% in case of group 2. All the birds in the control negative group had died. This study led to the conclusion that thermostable Vero cell adapted I-2 strain vaccine resulted in better immunization in broiler birds than obtained by the use of commercially available thermolabile vaccines.     

Outbreak of duck plague (duck herpesvirus enteritis) in numerous species of captive ducks and geese in temporal conjunction with enforced biosecurity (in-house keeping) due to the threat of avian influenza A virus of the subtype Asia H5N1

The continuing westward spread of avian influenza A virus of the subtype H5N1 in free-living and domestic birds forced the European Union and the German federal government to enhance all biosecurity measures including in-house keeping of all captive birds from October 20 to December 15, 2005. Movement of captive ducks and geese of many different species from a free-range system to tight enclosures and maintenance for prolonged times in such overcrowded sheds resulted in pronounced disturbance of natural behaviour, interruption of mating and breeding activities and possibly additional stress. Under these conditions the birds developed signs of severe disease and enhanced mortality twentyfour days later. A total of 17 out of 124 (14%) adult birds and 149 out of 184 year-old birds (81 %) died during the outbreak. A herpesvirus was isolated from many organs of succumbed ducks and geese that was identified as a duck plague herpesvirus by cross neutralization test using known antisera against duck plague virus. The published host range of duck plague comprises 34 species within the order Anseriformes. We report here on additional 14 species of this order that were found to be susceptible to duck plague virus. The exact source of the herpesvirus could not identified. However, low antibody titres in some ducks at day of vaccination indicate that at least some of the birds were latently infected with a duck plague herpesvirus. The remaining healthy appearing birds were subcutaneously vaccinated with a modified live duck plague vaccine (Intervet, Boxmeer, NL) that stopped losses and resulted in seroconversion in most of the vaccinated birds.     

Reproduction of inclusion body hepatitis in conventionally raised chickens inoculated with a New Zealand isolate of avian adenovirus

Conventionally raised chickens were inoculated with a local isolate of serotype 8 of avian adenovirus by an oral or intraperitoneal route, or were exposed to the infection by contact. Fatal hepatitis, resembling inclusion body hepatitis, occurred in 30% and 45% of the birds inoculated by the oral and intraperitoneal routes respectively, and severe growth depression was recorded in survivors and in birds in contact. Birds which had maternally derived virus neutralising antibody titres of 64 or greater at the time of viral exposure did not succumb to fatal infection, but their growth rates were significantly depressed.     

Experimental infection of rosellas (Platycercus eximius) with velogenic viscerotropic Newcastle disease virus (VVNDV)

Plaque-purified and non-plaque-purified velogenic viscerotropic Newcastle disease viruses (VVNDVs) were inoculated into golden-mantled rosellas (Platycercus eximius). VVNDV produced acute clinical disease in this species: all birds died within 6 days postexposure. There was no difference between the two inoculation groups in clinical signs. Seven tissues and five tissue swabs were collected from each of 15 birds. The VVNDV concentration in each specimen was titrated, and the concentrations were compared. The lung and trachea had the highest concentrations of virus in both the tissue suspensions and the swab suspensions. The average virus concentrations of the lung were 10(5.9) 50% embryo lethal doses (ELD50) per 0.1 ml for the tissue suspension and 10(4.9) for the swab. The average virus concentrations of the trachea were 10(5.6) ELD50 per 0.1 ml of tissue suspension and 10(4.6) for the swab.     

Response of white leghorn chickens to infection with avian leukosis virus subgroup J and infectious bursal disease virus

The effects of viral-induced immunosuppression on the infectious status (viremia and antibody) and shedding of avian leukosis virus (ALV) were studied. Experimental white leghorn chickens were inoculated with ALV subgroup J (ALV-J) and infectious bursal disease virus (IBDV) at day of hatch with the ALV-J ADOL prototype strain Hcl, the Lukert strain of IBDV, or both. Appropriate groups were exposed a second time with the Lukert strain at 2 wk of age. Serum samples were collected at 2 and 4 wk of age for IBDV antibody detection. Samples for ALV-J viremia, antibody detection, and cloacal shedding were collected at 4, 10, 18, and 30 wk of age. The experiment was terminated at 30 wk of age, and birds were necropsied and examined grossly for tumor development. Neoplasias detected included hemangiomas, bile duct carcinoma, and anaplastic sarcoma of the nerve. Control birds and IBDV-infected birds were negative for ALV-J-induced viremia, antibodies, and cloacal shedding throughout experiment. By 10 wk, ALV-J-infected groups began to develop antibodies to ALV-J. However, at 18 wk the incidence of virus isolation increased in both groups, with a simultaneous decrease in antibody levels. At 30 wk, 97% of birds in the ALV-J group were virus positive and 41% were antibody positive. In the ALV-J/IDBV group, 96% of the birds were virus positive at 30 wk, and 27% had antibodies to ALV-J. In this study, infection with a mild classic strain of IBDV did not influence ALV-J infection or antibody production.     

The effects of avian leukosis virus subgroup J on broiler chicken performance and response to vaccination

The effects of avian leukosis virus subgroup J (ALV-J) infection on meat-type chickens reared in a simulated commercial setting were evaluated. Each of three ALV-J isolates was evaluated with both simulated horizontal transmission (SHT) and simulated vertical transmission (SVT). Mortality, morbidity, disease condemnations, and feed conversions were increased and body weights at processing were decreased in ALV-J infected birds as compared to sham inoculated hatch mates. The adverse effects of ALV-J infection were more severe in birds exposed by SVT than in birds exposed by SHT. At 8 weeks of age response to vaccination for infectious bronchitis virus and Newcastle disease virus or prior exposure to a pathogenic reovirus was assessed in the ALV-J and sham inoculated broiler chickens by challenge studies. Although not statistically significant, an overall trend of decreased protection to challenge after vaccination, or prior exposure, was observed in the ALV-J inoculates as compared to sham inoculated hatch mates. Differences in vaccine response were most evident in groups inoculated with ALV-J by the SVT route.     

Anticoagulant rodenticide exposure and toxicosis in four species of birds of prey presented to a wildlife clinic in Massachusetts, 2006-2010

Mortalities among birds of prey from anticoagulant rodenticide (AR) toxicosis have been documented in several countries. Reports on extent of exposure within regions of the United States are limited. This study investigated AR exposure and toxicosis in four species of birds of prey (red-tailed hawks [Buteo jamaicensis], barred owls [Strix varia], eastern screech owls [Megascops asio] and great horned owls [Bubo virginianus]) presented to a wildlife clinic in Massachusetts. The aims of this study are to document the proportion of these four species that died or were euthanized due to their presenting injuries that had detectable amounts of ARs in liver tissue; to identify and quantify ARs present; to describe clinical, postmortem, and histopathologic signs of toxicosis; to evaluate potential sublethal effects of AR exposure; and to associate liver AR level with toxicosis. Birds included in the study were sampled without regard to signs of AR toxicosis. Postmortem examinations were conducted, and liver samples were analyzed for AR residues. Of 161 birds tested, 86% had AR residues in liver tissue. The second-generation AR (SGAR) brodifacoum was identified in 99% of positive birds. Mortality from AR toxicosis was diagnosed in 6% of birds. No indications of sublethal effects of exposure were found, and no association between liver brodifacoum level and signs of toxicosis was apparent. Given the high proportion of birds in this study exposed to ARs, specifically brodifacoum, continued monitoring is warranted as new U.S. Environmental Protection Agency regulations on the sale and use of SGARs are enacted.