Chickens, turkeys, and other poultry in a production environment can be exposed to stressors and infectious diseases that impair innate and acquired immunity, erode general health and welfare, and diminish genetic and nutritional potential for efficient production. Innate immunity can be affected by stressful physiologic events related to hatching and to environmental factors during the first week of life. Exposure to environmental ammonia, foodborne mycotoxins, and suboptimal nutrition can diminish innate immunity. Infectious bursal disease (IBD), chicken infectious anemia (CIA), and Marek's disease (MD) are major infectious diseases that increase susceptibility to viral, bacterial, and parasitic diseases and interfere with acquired vaccinal immunity. A shared feature is lymphocytolytic infection capable of suppressing both humoral and cell-mediated immune functions. Enteric viral infections can be accompanied by atrophic and depleted lymphoid organs, but the immunosuppressive features are modestly characterized. Some reoviruses cause atrophy of lymphoid organs and replicate in blood monocytes. Enteric parvoviruses of chickens and turkeys merit further study for immunosuppression. Hemorrhagic enteritis of turkeys has immunosuppressive features similar to IBD. Other virulent fowl adenoviruses have immunosuppressive capabilities. Newcastle disease can damage lymphoid tissues and macrophages. Avian pneumovirus infections impair the mucociliary functions of the upper respiratory tract and augment deeper bacterial infections. Recognition of immunosuppression involves detection of specific diseases using diagnostic tests such as serology, etiologic agent detection, and pathology. Broader measurements of immunosuppression by combined noninfectious and infectious causes have not found general application. Microarray technology to detect genetic expression of immunologic mediators and receptors offers potential advances but is currently at the developmental state. Control methods for immunosuppressive diseases rely largely on minimizing stress, reducing exposure to infectious agents through biosecurity, and increasing host resistance to infectious immunosuppressive diseases by vaccination. A longer term approach involves genetic selection for resistance to immunosuppressive diseases, which has shown promising results for MD but equivocal results for IBD and CIA.

Abbreviations: BF = bursa of Fabricius; CAV = chicken anemia virus; CIA = chicken infectious anemia; FAV = fowl adenovirus; HE = hemorrhagic enteritis; HEV = hemorrhagic enteritis virus; HVT = turkey herpesvirus; IBD = infectious bursal disease; IBDV = infectious bursal disease virus; IBV = infectious bronchitis virus; MD = Marek's disease; MDV = Marek's disease virus; MHC = major histocompatibility complex; NDV = Newcastle disease virus; ORT = Ornithobacterium rhinotracheale; PEMS = poultry enteritis and mortality syndrome; REV = reticuloendotheliosis virus; RSS = runting stunting syndrome; SE = Salmonella enterica serovar Enteritidis; ST = Salmonella Typhimurium

Turkey astrovirus type-2 (TAstV-2), turkey rotavirus (TRotV), and turkey reovirus (TReoV) have been implicated as possible causes of enteric diseases and poor production in turkeys; however, numerous studies with each individual virus have failed to reproduce the disease as observed in the field. Therefore, in this study we evaluated the pathogenesis of all possible combinations of one, two, or three viruses in comparison to sham inoculates in 3-day-old turkey poults. Body weights were recorded at 2, 4, 7, 10, and 14 days postinoculation (PI) and were decreased in virus-infected turkeys throughout the experiment as compared to sham inoculates. Although not significantly different from the other virus-exposed groups, the poults exposed to all three viruses had the lowest body weights throughout the experiment. Clinical signs, including huddling, diarrhea, and agitation, were only observed in groups exposed to TAstV-2 and/or TRotV. At 4 days PI, birds from each treatment group were necropsied, and pale intestines with watery contents and undigested feed were observed in the groups that were exposed to TRotV TReoV or TRotV TAstV-2 and the group exposed to all three viruses. Minimal microscopic lesions were observed in the intestines of turkeys infected with TAstV-2, TReoV, or a combination of both. In the turkeys infected with TRotV, either alone or in combination with other viruses, mild microscopic lesions were found in all sections of the small intestine and viral antigen was identified by immunohistochemical staining in mature enterocytes. No or very mild lesions were observed in other organs with the exception of the bursa of Fabricius, where mild to severe atrophy was observed in all virus-infected poults examined. Cloacal shedding of TAstV-2 and TRotV was evaluated by reverse-transcription PCR testing of cloacal swabs and minimal differences were observed among the treatment groups.

A/Chicken/Beijing/1/94 (Ck/BJ/1/94) avian influenza virus (AIV), a prototype of the H9N2 subtype, is phylogenetically similar in its hemagglutinin (HA) and neuraminidase (NA) genes to A/Chicken/Shanghai/F/98 (Ck/SH/F/98; H9N2) AIV, a natural reassortant between different sublineages. To understand the role of HA and NA genes in the airborne transmission of H9N2 AIV, we compared the transmission route and the relative replication efficiency of these strains in specific-pathogen-free chickens. Three recombinant viruses were generated by reverse genetics, containing the HA and NA genes (or both) from A/Chicken/Guangdong/SS/94 (Ck/GD/SS/94), in a background of internal genes derived from Ck/SH/F/98. Inoculated chickens were kept in either direct or indirect contact with uninoculated chickens, and viral shedding and titers were monitored. The results showed that Ck/GD/SS/94 lacks the ability to be transmitted through indirect contact, while Ck/SH/F/98 could be transmitted indirectly. Recombinant virus (RF/SSHA), containing the internal genes of Ck/SH/F/98 and the HA gene of Ck/GD/SS/94, resulted in decreased viral titers in lung tissue as compared to the parental strain. Interestingly, substituting the NA gene, or both the NA and HA genes, of Ck/SH/F/98 with that of Ck/GD/SS/94 completely abolished the airborne transmission of the recombinant RF/SSNA and RF/SSHA/SSNA. In conclusion, Ck/SH/F/98 acquired the ability of airborne transmission and replicated with a higher efficiency in the respiratory tract of the chickens. Our data indicated that the NA gene of Ck/SH/F/98 can affect virus replication and, therefore, indirectly affect the transmission for the gene constellations of these viruses.

Nifurtimox (NFX), a compound with known antiprotozoal activity, was evaluated for potential use in the prevention or treatment of histomoniasis in turkeys. A test of NFX in vitro showed that the compound was progressively active at concentrations of 12.5–200 ppm. Lower concentrations appeared only to delay growth of histomonads, while a concentration of 200 ppm was completely inhibitory. A series of tests in turkey poults showed that NFX had significant (P < 0.05) efficacy at 300–400 ppm when given in the feed throughout a 14-day experimental infection period. The beneficial effect was most prominent in the reduction of mortality and the suppression of liver lesions. Cecal lesions appeared less affected. Treatment with 400 ppm for a 3-day period after inoculation of turkeys was partially effective. In all tests, liver lesions were suppressed more effectively than cecal lesions, indicating that the concentration of the compound in the liver during metabolic excretion was important in the observed efficacy of this compound. Lack of any effect on growth or feed consumption in uninfected turkeys during a medication period of 16 days indicated that this compound was well tolerated by turkeys at 400 ppm in the feed and might be of benefit in the prevention or treatment of histomoniasis in turkeys.

Several lytic bacteriophages effective at destroying a genetically diverse population of Clostridium perfringens were isolated from the environment, extensively characterized, and used to formulate a multivalent bacteriophage cocktail designated “INT-401.” Two in vivo studies were conducted to determine the cocktail's efficacy in controlling necrotic enteritis (NE) caused by C. perfringens. The first study investigated the efficacy of INT-401 and a bacteriophage-derived, toxoid-type vaccine in controlling NE in C. perfringens–challenged broiler chickens. The study was designed as a proof-of-concept battery cage study with birds reared until 28 days old. Compared with the mortality observed with the C. perfringens–challenged but untreated chickens, oral administration of INT-401 significantly (P < 0.05) reduced the mortality of the C. perfringens–challenged birds by 92%. Overall, INT-401 was more effective than the toxoid vaccine in controlling active C. perfringens infection. The second study was conducted to investigate the effectiveness of the cocktail when administered via oral gavage, feed, or drinking water. The study was conducted in floor pens, with birds reared to 42 days old. INT-401 administered by all three methods significantly (P < 0.05) reduced mortality. Weight gain and feed conversion ratios were significantly better in the C. perfringens–challenged chickens treated with INT-401 than in the C. perfringens–challenged, phage-untreated control birds. The data indicate that delivering INT-401 to broiler chickens via their drinking water or feed may be an effective means for controlling NE caused by C. perfringens and may improve weight gain and feed conversion ratios in birds with clinical or subclinical NE.

The matrix 1 (M1) gene, present in all subtypes of avian influenza virus (AIV), was cloned and expressed in Escherichia coli. Reactivity of the expressed protein was confirmed by western blot. Subsequently, the M1 gene expression product was purified and used as the antigen to develop a latex agglutination test (LAT) for detecting antibodies against these conventional subtypes of AIV including AIV H3, H5, H7, and H9 from chicken sera. The LAT is specific for AIV, and no cross-reaction was shown with chicken antisera against other avian viruses. Compared with the hemagglutination inhibition test, the corresponding specificity, sensitivity, and correlation were 95.7%, 88.7%, and 89.0%, respectively, in detecting 491 serum samples from vaccinated chickens.

Cornell University maintains two genetic lines of specific-pathogen-free chickens in a filtered-air, positive-pressure house as a closed colony. Offspring from each generation are maintained in the same house as the parents without clean-out between successive generations. The two lines have been persistently infected with chicken infectious anemia virus (CIAV) since the mid-1990s. All flocks were monitored from 1999 to 2008 for the presence of CIAV antibodies two to four times over the 65-wk life span of each flock, starting at approximately 15 wk of age. The serologic data were modeled using the logistic mixed model for seroprevalence and the Poisson generalized linear mixed model for seroconversion. We defined seroprevalence as the percentage of seropositive birds on a sampling date; seroconversion was defined as the difference in the percentage of seropositive birds between two subsequent bleeding dates. Seroprevalence varied between flocks from 1% to 95% but was never zero. Strain and gender in general did not influence seroprevalence or seroconversion rates, but sires of the P2a line had a significantly higher seroprevalence than all other groups. There are at least two different explanations possible for the extreme variation in seroconversion. The first one is that a low level of continuous horizontal infection from seropositive to seronegative birds occurs in the facility. The second explanation is based on the concept of latency of infection, with reactivation occurring during and after sexual maturity. Latency may occur in both seropositive and seronegative chickens. Our data are compatible with reactivation from latency, perhaps followed by limited horizontal spread as well as with a low level of continuous horizontal transmission. Although the fitted Poisson model supports both options, we propose that the reactivation from latency is the likely explanation for the observed data.

The hemagglutinin-neuraminidase (HN) protein of Newcastle disease virus (NDV) plays an important role in the pathogenesis of Newcastle disease (ND). Recombinant HN (rHN) protein, produced either by direct injection of recombinant viruses containing HN gene or baculovirus expression systems, has been used to elicit immunity against NDV in chickens. In the present study, a 60.4-kDa rHN was expressed by a prokaryotic expression system and formulated into ND vaccines. Inclusion of rHN (10 µg/ml) into conventional, inactivated ND vaccines significantly (P < 0.05) increased the titer of serum hemagglutination-inhibition Ab in specific-pathogen-free or commercial chickens. Furthermore, when the rHN protein was formulated into ND IC (infectious coryza) bivalent or ND IC FC (fowl cholera) multivalent vaccines, the protection rate of immunized chickens increased from ∼80%–90% to 100% after being challenged by a velogenic strain of NDV. Our data indicated that inclusion of rHN protein produced by an economical prokaryotic expression system could enhance the immunogenicity of traditional and multivalent inactivated ND vaccines. This approach may be adapted to improve the efficacy of ND vaccines currently used in the poultry industry.

Avian metapneumovirus (AMPV) causes an upper respiratory tract infection in turkeys leading to serious economic losses to the turkey industry. The G glycoprotein of AMPV is known to be associated with viral attachment and pathogenesis. In this study, we determined the role of the G glycoprotein in the pathogenicity and immunogenicity of AMPV strain Colorado (AMPV/CO). Recombinant AMPV/CO lacking the G protein (rAMPV/CO-ΔG) was generated using a reverse-genetics system. The recovered rAMPV/CO-ΔG replicated slightly better than did wild-type AMPV in Vero cells. However, deletion of the G gene in AMPV resulted in attenuation of the virus in turkeys. The mutant virus induced less-severe clinical signs and a weaker immune response in turkeys than did the wild-type AMPV. Our results suggest that the G glycoprotein is an important determinant for the pathogenicity and immunogenicity of AMPV.

The effects of feeding diets containing grains naturally contaminated with Fusarium mycotoxins on intestinal histology were studied in chickens raised to 10 wk of age in the absence or presence of coccidial challenge. Experimental diets included the following: controls, diets containing grains naturally contaminated with Fusarium mycotoxins, and diets containing contaminated grains 0.2% polymeric glucomannan mycotoxin adsorbent. Contaminated diets contained up to 3.8 µg/g deoxynivalenol (DON), 0.3 µg/g 15-acetyl DON, and 0.2 µg/g zearalenone. An optimized mixture (inducing lesions without mortality) of Eimeria acervulina, Eimeria maxima, and Eimeria tenella was used to challenge birds at 8 wk of age. Intestinal tissues were collected from duodenum, jejunum, and ileum prior to challenge; at the end of the challenge period (7 days postinfection; PI); and at the end of the recovery period (14 days PI). Mean villus height (VH) in the duodenum of birds fed the contaminated diets in the absence of coccidial challenge was significantly lower than that of the controls. Mean VH in the jejunum and ileum of the same birds was significantly higher compared to controls, indicating a compensatory mechanism. Fusarium mycotoxins retarded duodenal recovery from coccidial lesions, as indicated by lower duodenal VH and apparent villus surface area comparing challenged birds fed the contaminated diets to challenged controls of the same age. Increased VH was frequently associated with cryptal hyperplasia and increased numbers of mitotic figures in crypts. It was concluded that diets contaminated with Fusarium mycotoxins below levels that negatively affect performance could alter intestinal morphology and interfere with intestinal recovery from an enteric coccidial infection.

In 2007, an inclusion body hepatitis (IBH) outbreak affected several broiler farms in Mississippi. Results of logistic regression analyses showed significant associations between IBH occurrence and high enzyme-linked immunosorbent assay geometric mean titers for infectious bursal disease virus. However, there was no association between IBH occurrence and chicken infectious anemia virus status. Results of linear regression model analyses showed significant associations between IBH occurrence with average weight and with cost deviation. Broiler meat production cost was $0.0058/kg more expensive to produce when IBH occurred. Although feed conversion was higher with IBH occurrence, the association was not significant. IBH onset in the first farms affected occurred between 19 and 30 days of age, whereas in the last farms affected, IBH onset occurred as early as 10 days.

Natural infections with different subtypes of low pathogenicity avian influenza viruses (LPAIVs) are very common in wild duck populations. Recent outbreaks of high pathogenicity avian influenza virus (HPAIV) H5N1 in Eurasian and African countries stimulated monitoring activities in aquatic wild bird populations. Surveillance mainly focused on virus detection. Only a few serologic investigations have been conducted so far, although such data may retrospectively elucidate epidemiologic patterns of different AIV subtypes in the populations under study. To better understand the immunologic and serologic reactions of mallards after infection with LPAIV, we investigated the AIV type- and subtype-specific antibody dynamics in mallards after different LPAIV infections by hemagglutination inhibition, competitive enzyme-linked immunosorbent assay, and western blot analysis, as appropriate. Four groups of mallard ducks were used: 1) naturally infected birds, 2) birds that were experimentally infected with LPAIV, 3) birds that were immunized with inactivated virus preparations, and 4) negative control birds. Ducks were monitored for up to 15 mo, and serum samples were investigated every 1–4 wk. It could be shown that infection with LPAIV in mallards can be traced serologically over prolonged periods of time.

The role of maternal antibodies in the lag phase of Campylobacter positivity, widely observed in commercial broiler flocks, was investigated. The results indicate that 3-wk-old birds derived from a commercial flock are more susceptible to colonization with Campylobacter jejuni than 1-to-2-wk-old birds. This increasing susceptibility parallels the loss of maternally derived, circulating, anti-Campylobacter, immunoglobulin Y antibodies as detected by enzyme-linked immunosorbent assay. The role of these antibodies in resistance to colonization was further investigated using progeny from breeder flocks of known Campylobacter status. These results confirmed that maternal antibodies confer partial protection against Campylobacter colonization on young chickens (1–2 wk old). This protection was directed against challenge with both homologous and heterologous strains of C. jejuni and even against strains with a high colonization potential. However, evidence presented indicates that newly hatched chicks, with the highest levels of maternal antibodies, were as susceptible to Campylobacter challenge as 3-wk-old birds. This conundrum was investigated further, and an increase in resistance was detected from 1 to 3 days of age. The reasons for this are, as yet, unknown, but the observation validates the use of newly hatched chicks in models of Campylobacter colonization. Moreover, this high susceptibility in the first few days of life may explain the occasional early flock colonization observed, especially when environmental exposure to Campylobacter is high, for example, in free-range birds.

White stork (Ciconia ciconia) chicks have previously been suggested to be particularly susceptible to environmental conditions such as climatic changes during their first 3 wk of life. However, limited data are available on causes of mortality in free-ranging birds prior to fledging in general. One hundred and one white stork chicks found dead in 2007 and 2008 were examined and the causes of death identified. Of these, 44.6% had fungal granulomatous pneumonia resulting in obstruction and compression of airways. Of note, 94.1% of pulmonary infections occurred in white stork chicks below 23 days of age. PCR amplification and sequencing of the fungal internal transcribed spacer region 1 identified Aspergillus fumigatus and various zygomycetes as primary causative agents. Thermomyces lanuginosus, previously unknown to cause pulmonary infections, was identified in one chick. The findings suggest that fungal pneumonia plays a major role in the loss of white stork chicks of up to 3 wk of age and represents a major threat, similar to the threat posed to young poultry.

Commercial chickens with a high level of maternal antibodies for Newcastle disease were vaccinated when newly hatched with Queensland V4 or Ulster 2C Newcastle disease virus (NDV) strains by nebulization. The exposure time to a fine aerosol of vaccine produced with an ultrasonic nebulizer was 60 sec. The chickens were challenged oculonasally with virulent NDV strain Texas GB in weekly intervals up to the 49th day of life. Although protected for several weeks by maternal antibody, they were sufficiently protected thereafter by active immune response to the vaccines. Vaccinal reactions were not observed. Queensland V4 produced higher titers than Ulster 2C and provided better protection to challenge.

Infectious bronchitis viruses (IBVs) in Taiwan have been divided into two genogroups, Taiwan group I (TW-I) and Taiwan group II (TW-II). Heterologous Mass-type strains are widely used as vaccines in the field. This work reports on a rapid and reliable multiplex reverse transcriptase–polymerase chain reaction (mRT-PCR) assay for the genotyping of IBVs. Multiplex primer sets were designed to amplify the region covering hypervariable regions 1 and 2 of the S1 glycoprotein gene. Several local strains and commercially available vaccines were used for evaluating the viral genotyping assay, and a number of field isolates were examined for clinical application. The results showed that all of the examined IBVs were accurately genotyped by identifying the corresponding bands on agarose gels (TW-I: 322 bp, TW-II: 161 bp, Mass type: 256 bp) after the mRT-PCR, in agreement with the viral genome sequence data. The mRT-PCR assay was able to detect viral RNA copies as low as 10³, 10⁵, and 10³ for the TW-I, TW-II, and Mass-type strains, respectively. The mRT-PCR assay accurately detected and discriminated vaccine viruses from wild-type strains in the field. This assay may be beneficial for virus identification and differentiation in routine disease surveillance.

Avian influenza virus (AIV) monitoring in migratory birds has been performed in Taiwan since 1998. From 1998 to 2007, 29,287 samples were collected from wild ducks, shorebirds, and other wild birds in the four wetlands around Taiwan and at two outside islets, Penghu and Kinmen. Virus isolation was performed for all collected samples by inoculating chicken embryos. The AIV in the allantoic fluid was identified using hemagglutination and reverse transcription PCR. The AIV prevalence from those samples was 0.81% (237/29,287). The peak prevalence reached 1.06% (186/17,493) from September to December, during which time migrating ducks came from the North. The prevalence from January to April was 0.51%. However, no virus was isolated from May to August. The partial HA genes of 28 H4 AIVs were sequenced and analyzed. The phylogenetic tree showed that a correlation existed between the isolation years and the evolutional distances. The pathogenicity of the isolated H5 and H7 AIVs was determined by intravenous pathogenicity index (IVPI) testing in specific-pathogen-free chickens and by HA cleavage sequencing. Using the IVPI test and the HA cleavage sequences, all of the H5 or H7 AIVs isolated were determined to be low pathogenicity AIVs.

This study was conducted to compare oropharyngeal (OP) and cloacal samples of wild birds (n  =  137) for the detection and isolation of avian influenza virus (AIV). A total of 39 (28.5%) cloacal and 85 (62.0%) OP samples were positive for AIV by real-time reverse transcription–PCR (RRT-PCR). The AIV nucleic acid was detected in both cloacal and OP samples from 27 (19.7%) birds, in cloacal samples only from 12 (8.8%) birds, and in OP samples only from 58 (42.3%) birds. Thus, a total of 97 (70.8%) birds were AIV positive by RRT-PCR. The cycle threshold values for the cloacal samples ranged from 16.6 to 36.9 (mean 31.5), and those for OP samples ranged from 18 to 38.9 (mean 34.9). Of the cloacal samples, 12 were positive for H5 subtype influenza virus by RRT-PCR, with one being low pathogenic H5N1. In contrast, five of the OP samples were H5 positive, but none was H5N1. None of the cloacal or OP samples was H7 positive. Eight cloacal samples yielded AIV on inoculation in embryonated chicken eggs, while only one isolate was obtained from OP samples. Thus, from testing of 137 birds, only nine (6.6%) AIV isolates were obtained. The isolates from cloacal samples were subtyped as H6N1 (n  =  5), H3N8 (n  =  2), and H4N8 (n  =  1), and the isolate from OP sample was subtyped as H6N1. No virus was isolated from the corresponding cloacal sample of the bird whose OP sample yielded AIV on virus isolation. These results suggest that surveillance programs for detection of AIV by RRT-PCR may include both sample types (cloacal and OP) to obtain a better picture of AIV prevalence, and OP samples may yield additional isolates of AIV when tested in conjunction with cloacal samples.

Low pathogenic avian influenza H6N2 viruses were biologically characterized by infecting chickens and ducks in order to compare adaptation of these viruses in these species. We examined the clinical signs, virus shedding, and immune response to infection in 4-wk-old white leghorn chickens and in 2-wk-old Pekin ducks. Five H6N2 viruses isolated between 2000 and 2004 from chickens in California, and one H6N2 virus isolated from chickens in New York in 1998, were given intrachoanally at a dose of 1 × 10⁶ 50% embryo infectious dose per bird. Oral–pharyngeal and cloacal swabs were taken at 2, 4, and 7 days postinoculation (PI) and tested by real-time reverse-transcriptase polymerase chain reaction for presence of virus. Serum was collected at 7, 14, and 21 days PI and examined for avian influenza virus antibodies by commercial enzyme-linked immunosorbent assay (ELISA) and hemagglutination inhibition (HI) testing. Virus shedding for all of the viruses was detected in the oral–pharyngeal swabs from chickens at 2 and 4 days PI, but only three of the five viruses were detected at 7 days PI. Only two viruses were detected in the cloacal swabs from the chickens. Virus shedding for four of the five viruses was detected in the oral–pharyngeal cavity of the ducks, and fecal shedding was detected for three of the viruses (including the virus not shed by the oral–pharyngeal route) in ducks at 4 and 7 days PI. All other fecal swabs from the ducks were negative. Fewer ducks shed virus compared to chickens. Both the chickens and the ducks developed antibodies, as evidenced by HI and ELISA titers. The data indicate that the H6N2 viruses can infect both chickens and ducks, but based on the number of birds shedding virus and on histopathology, the viruses appear to be more adapted to chickens. Virus shedding, which could go unnoticed in the absence of clinical signs in commercial chickens, can lead to transmission of the virus among poultry. However, the viruses isolated in 2004 did not appear to replicate or cause more disease than earlier virus isolates.

The QT35 cell line was established in 1977 from methylcholanthrene-induced tumors in Japanese quail. It was later shown that at least some of the QT35 cell lines were latently infected with Marek's disease (MD) virus (MDV). An MDV-like herpesvirus, named quail MDV (QMDV), was isolated from QT35 cells in 2000 by Yamaguchi et al. To determine the pathogenicity of QMDV, we inoculated 10-day-old specific-pathogen-free chickens with QMDV JM (virulent), RB-1B (very virulent), or 584A (very virulent plus). In addition, we inoculated 5-day-old Japanese quail with QMDV, JM, or RB-1B. QMDV is pathogenic in chickens with a tumor incidence comparable to JM. QMDV also caused MD in three out of 18 infected Japanese quail. In conclusion, QMDV is a virulent MDV, and its presence in QT35 cells has implications for the use of QT35 cells for vaccine production.

This paper reports on two fatal cases of Salmonella Typhimurium phage type DT160 infection in Moluccan cockatoos (Cacatua moluccensis) from a zoological collection in Italy. No previous clinical signs were observed in birds before death, except for anorexia and mild diarrhea in one bird. At post mortem, necrotic foci surrounded by a hyperemic halo were observed in lungs, heart, liver, spleen, kidneys, and intestine. Microscopically, heterophils and macrophages with rare lymphocyte infiltration associated with gram-negative, rod-shaped bacteria aggregates were detected in necrotic foci. Bacteriology confirmed the presence of Salmonella Typhimurium phage type DT160 in the tissues of birds. The source of Salmonella Typhimurium in these birds remains unknown, but the authors emphasize the need to better control salmonella infections in these avian species because they are important zoonotic agents and responsible for disease in animals and humans. This is the first documentation of Salmonella Typhimurium phage type DT160 infection in Moluccan cockatoos.

Forty-one outbreaks of mortality in wild finches were reported in southern Norway, Sweden, and Finland in the second half of 2008 (n  =  40) and in February 2009 (n  =  1). Greenfinches (Carduelis chloris) and occasional chaffinches (Fringilla coelebs) primarily were affected. Forty-eight greenfinches, eight chaffinches, one hawfinch (Coccothraustes coccothraustes), and one blue tit (Parus caeruleus) from 22 incidents were examined postmortem. Birds were in poor nutritional condition and had necrotizing ingluvitis, esophagitis, and/or oropharyngitis. Viable trichomonads with morphology consistent with Trichomonas gallinae were demonstrated successfully in 65% and 71% of fresh carcasses examined by culture and wet mount, respectively. No primary bacterial pathogens were detected. To our knowledge, this is the first report of epizootic trichomoniasis in wild finches in Europe outside of the U.K.

Two weeks after spiking, a decrease in fertility from 96% to 82% was observed in a 48-week-old broiler breeder flock. Hatchability in the flock was about 86%. Necropsy of 25 males revealed severe testicular atrophy in 60% of the birds. Histopathology of the testes demonstrated no spermatogenesis in most of these birds. No evidence of infectious disease was discovered, and no infectious agents were isolated. Further investigation on the farm revealed standing water in the house, due to heavy rains, and wet and caked litter; this resulted in decreased feed consumption, for at least 5 days prior to submission to the diagnostic laboratory, and a corresponding decrease in body weight of the birds. In conclusion, a combination of a recent introduction of replacement (spiking) males, poor environmental conditions, and decreased feed consumption led to the loss of weight, testicular atrophy, and decreased or no spermatogenesis in individual birds, collectively resulting in decreased flock fertility.

Thirteen whooper swans (Cygnus cygnus) affected with schistosomiasis were examined pathologically. Venous hypertrophy, characterized by marked nodular proliferation of medial smooth muscle fibers with frequent obliteration of the vascular lumen, was observed in eight of the 13 whooper swans. Venous hypertrophy was located in the medium-sized veins of the mesentery, the serosa, and the muscular layer of the duodenum, jejunum, ileum, and cecum. In addition, vascular lesions were seen in the capsule and parenchymal interstitia of the liver, spleen, kidney, heart, aorta, air sac, and pleura. In mild lesions, segmental proliferation of medial smooth muscles was observed in the venous medium of the mesentery and serosa. Moderate lesions had a proliferation of smooth muscles in the veins with obliteration of venous lumens. In marked lesions, more severe proliferation of veins extended into the intestinal muscular layers and depressed them. Schistosome parasites were found in the venous lumens of each of the eight whooper swans with vascular lesions. Bile pigments and hemosiderin were observed in the livers of whooper swans. In addition, adult nematodes (Sarconema sp.) were localized in the myocardium of four of the eight whooper swans. The venous hypertrophy may be caused by the proliferation of medial smooth muscle fibers induced by schistosomiasis.

Avian salmonellosis is a disease caused by bacteria of the genus Salmonella that can cause three distinct diseases in birds: pullorum diseases, fowl typhoid, and paratyphoid infection. Various wildlife species are susceptible to infections by Salmonella, regardless of whether they live in captivity or freely in the wild. The present study verified the presence of Salmonella enterica serovar Enteritidis in three captive specimens of Amazona aestiva. The study involved a total of 103 birds undergoing rehabilitation to prepare for living in the wild, after having been captured from animal traffickers and delivered to the Centrofauna Project of the Floravida Institute in Sao Paulo, Brazil. This is the first report of Salmonella Enteritidis isolation in A. aestiva that originated from capture associated with animal trafficking; Salmonella was detected during the study by the serologic method of rapid serum agglutination on a plate with bacterial isolate. The antimicrobial profile exam of the isolated samples demonstrated sensitivity to ampicillin, cefaclor, ciprofloxacin, and cloranfenicol. The three samples also presented resistance to more than four antibiotics. The presence of the genes invA and spvC was verified by PCR technique and was associated with virulence and absence of class 1 integron, a gene related to antimicrobial resistance. The commercial antigen for pullorum disease was shown to be a useful tool for rapid detection in the screening of Salmonella of serogroup D₁ in Psittaciformes. New studies on Salmonella carriage in birds involved in trafficking must be performed to better understand their participation in the epidemiologic cycle of salmonellosis in humans and other animals.

Cerebellar hypoplasia and hydrocephalus were identified in day old broiler chickens showing nervous signs, impaired mobility, and diarrhea. At postmortem examination, brains of chickens were misshapen and cerebellums were smaller than normal. Microscopically, cerebellar folia were reduced in size and irregularly shaped, and the ventricles were widely distended. Affected cerebellums had focal areas along the base of folia where the internal granular cell layer had been lost, and Purkinje cells were disorganized and located within the molecular layer. Parvovirus DNA was detected by polymerase chain reaction in three of nine brains with oligonucleotide primers designed for amplification of chicken and turkey parvoviruses. On the basis of phylogenetic analyses, the detected virus was most closely related to chicken parvoviruses. These findings suggest that a chicken parvovirus might cause a neurologic disease of young chickens characterized by cerebellar hypoplasia and hydrocephalus; however, its role as the cause of the disease remains to be confirmed.

This case report describes a severe outbreak of airsacculitis caused by Ornithobacterium rhinotracheale (ORT) in a large falcon breeding farm. Forty young falcons hatched from artificially incubated hatching eggs and were raised by hand for 5–8 days after hatch. Afterwards they were placed back with the parents. Three days after being with the parents, the stock breeder observed that the young falcons stopped begging for food, their crops were empty, and approximately 20% of the young demonstrated respiratory distress. However, all adult falcons and the older young birds appeared to be healthy. Two young falcons died and were submitted for laboratory investigations. A postmortem examination on the two dead falcons and ten 4-wk-old cockerels and baby rats used as feed for the falcons was performed. ORT of serotype A was isolated from lungs and air sacs of both falcons. Samples of the cockerels were positive by ORT PCR. Samples of the baby rats were negative. All young falcons were treated with a long-acting tetracycline (100 mg/kg i.m. followed by a second injection 3 days later). The falcons improved within the next 2 days, and only one additional chick died. According to the available literature, this is the first report of ORT in falcons causing severe clinical disease and outbreak in a breeding farm.

A 29-year-old female green-winged macaw (Ara chloropterus) was presented for acute pelvic limb lameness. On physical examination the bird was found to be mildly dehydrated with paraparesis and proprioceptive deficits of the pelvic limbs. Antemortem diagnostics included a complete blood count and plasma biochemistry panel, fecal Gram and Ziehl-Neelsen acid fast stains, plasma heavy metal concentrations, reverse transcriptase (RT)-PCR testing for West Nile virus (WNV) RNA and PCR testing for Chlamydophila psittaci DNA from choanal/cloacal swabs, and survey radiography. Abnormal findings included a heterophilic leukocytosis, elevated kidney and muscle enzyme values, and a positive RT-PCR result for West Nile viral RNA. Although the bird showed some improvement with supportive care, on the fourth day it began having seizures and was euthanatized. There were no abnormal findings detected on gross necropsy; however, histopathology revealed mononuclear inflammatory cell infiltration in multiple organs including brain, heart, and pancreas. WNV antigen and RNA were detected using immunohistochemistry and RT-PCR in various tissues including brain, pancreas, and spleen. WNV was successfully isolated from brain, pancreas, spleen, and liver. To our knowledge, this is the first report characterizing WNV disease in a green-winged macaw and one of few reports of this disease in a psittacine bird.