Environmental Lead and Wild Birds: A Review.

Lead is a persistent inorganic environmental pollutant that affects humans and animals worldwide. Avian species are especially susceptible to lead exposure through consumption of lead ammunition, lead fishing tackle, and other contaminated food sources such as aquatic species ingesting lead contaminated sediments in mining areas. Even with government regulations on the use of lead ammunition in many countries, including the United States, terrestrial, aquatic, predatory, and scavenger avian species are still at risk of exposure to potentially lethal concentrations of lead. The toxicities seen in these avian species include increased oxidative stress and decreased anti-oxidant enzymes in hepatic and renal tissue. The avian immune system is also a target of lead and displays a number of altered functions suggestive of immune suppression; however, studies in wildlife and laboratory species remain too limited for definitive statements with regard to population risk. In contrast, lead clearly inhibits reproductive capabilities in adult birds, and alters growth and development of hatchlings. Environmental remediation for lead removal, which would lower toxic exposure in wildlife, presently is a monumental and prohibitively expensive effort. Wildlife exposure will therefore continue in contaminated areas, necessitating development of new remediation practices. These plans should aim toward limiting more widespread or heavier contamination of wildlife habitats. This chapter reviews presently available information of lead toxicity in wild bird species, and suggests continued monitoring and reduction strategies to reduce lead exposure for at-risk avian populations.

The route of inoculation dictates the replication patterns of the infectious laryngotracheitis virus (ILTV) pathogenic strain and chicken embryo origin (CEO) vaccine.

Infectious laryngotracheitis virus (ILTV) has a high proclivity to replicate in the larynx and trachea of chickens causing severe lesions. There is a lack of knowledge on the ability of ILTV to replicate in other respiratory associated tissues apart from in the trachea. The objective of this study was to investigate how tissues that first encounter the virus dictate further sites of viral replication during the lytic stage of infection. Replication patterns of the pathogenic strain 63140 and the chicken embryo origin (CEO) vaccine in the conjunctiva, the Harderian gland, nasal cavity and trachea were evaluated after ocular, oral, intranasal or intratracheal inoculation of specific pathogen-free chickens. Viral replication was assessed by detection of microscopic cytolytic lesions, detection of viral antigen and viral genome load. The route of viral entry greatly influenced virus replication of both strain 63140 and CEO vaccine in the conjunctiva and trachea, while replication in the nasal cavity was not affected. In the Harderian gland, independently of the route of viral entry, microscopic lesions characteristic of lytic replication were absent, whereas viral antigen and viral genomes for either virus were detected, suggesting that the Harderian gland may be a key site of antigen uptake. Findings from this study suggest that interactions of the virus with the epithelial-lymphoid tissues of the nasal cavity, conjunctiva and the Harderian gland dictate patterns of ILTV lytic replication.

Ingestion of a Single 2.3 mm Lead Pellet by Laying Roller Pigeon Hens Reduces Egg Size and Adversely Affects F1 Generation Hatchlings.

Many aquatic and terrestrial avian species inadvertently ingest lead (Pb) in the form of spent or fragmented ammunition, mistaking it for food or grit. Previous studies in our laboratory have shown that ingestion of even a single 45-mg pellet can significantly increase blood-Pb levels and significantly inhibit the enzyme delta aminolevulinic-acid dehydratase (δ-ALAD) for a period of greater than 4 weeks. In the current study, proven breeder pairs of domestic Roller pigeons were housed in individual cages. The hens were orally gavaged with dH2O vehicle, a single #9 Pb pellet (2.0 mm/45 mg) or a single #7.5 Pb pellet (2.3 mm/95 mg), placed back with the cock bird and allowed to mate for two consecutive clutches. The eggs were monitored for fertilization, shell damage, egg weight, and length during the 16- to 18-day incubation period. Hatchlings remained with the hen and cock through the weaning period (28-35 days post hatch) and were monitored for weight, development, and mortality. Weanling blood was collected for blood-Pb levels, δ-ALAD activity, red blood cell counts, total protein, and packed cell volume. Following euthanasia, weanling liver, spleen, kidney, sciatic nerve, thymus, and brain were collected for histopathology. Egg weight and length were significantly decreased in the #7.5 Pb pellet treatment group for the first clutch, and hatchling weight 7 days post hatch also was significantly less in the #7.5 Pb pellet treatment group during the first clutch. Histopathologic analysis showed increased lesions in liver, kidney, spleen, and thymus of the Pb-treated weanlings, during both the first and second clutch compared with the non-Pb-treated weanlings. These data suggest that maternal consumption of a single 95-mg Pb pellet can adversely impact egg size and hatchling organ development.

The Helicobacter pylori CZB Cytoplasmic Chemoreceptor TlpD Forms an Autonomous Polar Chemotaxis Signaling Complex That Mediates a Tactic Response to Oxidative Stress.

UNLABELLED: Cytoplasmic chemoreceptors are widespread among prokaryotes but are far less understood than transmembrane chemoreceptors, despite being implicated in many processes. One such cytoplasmic chemoreceptor is Helicobacter pylori TlpD, which is required for stomach colonization and drives a chemotaxis response to cellular energy levels. Neither the signals sensed by TlpD nor its molecular mechanisms of action are known. We report here that TlpD functions independently of the other chemoreceptors. When TlpD is the sole chemoreceptor, it is able to localize to the pole and recruits CheW, CheA, and at least two CheV proteins to this location. It loses the normal membrane association that appears to be driven by interactions with other chemoreceptors and with CheW, CheV1, and CheA. These results suggest that TlpD can form an autonomous signaling unit. We further determined that TlpD mediates a repellent chemotaxis response to conditions that promote oxidative stress, including being in the presence of iron, hydrogen peroxide, paraquat, and metronidazole. Last, we found that all tested H. pylori strains express TlpD, whereas other chemoreceptors were present to various degrees. Our data suggest a model in which TlpD coordinates a signaling complex that responds to oxidative stress and may allow H. pylori to avoid areas of the stomach with high concentrations of reactive oxygen species. IMPORTANCE: Helicobacter pylori senses its environment with proteins called chemoreceptors. Chemoreceptors integrate this sensory information to affect flagellum-based motility in a process called chemotaxis. Chemotaxis is employed during infection and presumably aids H. pylori in encountering and colonizing preferred niches. A cytoplasmic chemoreceptor named TlpD is particularly important in this process, and we report here that this chemoreceptor is able to operate independently of other chemoreceptors to organize a chemotaxis signaling complex and mediate a repellent response to oxidative stress conditions. H. pylori encounters and must cope with oxidative stress during infection due to oxygen and reactive oxygen species produced by host cells. TlpD's repellent response may allow the bacteria to escape niches experiencing inflammation and elevated reactive oxygen species (ROS) production.

Serial passage in ducks of a low-pathogenic avian influenza virus isolated from a chicken reveals a high mutation rate in the hemagglutinin that is likely due to selection in the host.

A comparative study of the ability of three low-pathogenic avian influenza virus (LPAIV) isolates to be transmitted from duck to duck was performed. Pekin ducks were inoculated with two LPAIV isolates from chickens (A/Ck/PA/13609/93 [H5N2], H5N2-Ck; A/Ck/TX/167280-4/02 [H5N3], H5N3-Ck) and one isolate from a wild bird (A/Mute Swan/ MI/451072/06 [H5N1], H5N1-WB). During the establishment of the passage model, only two viruses (H5N1, H5N2) were able to be transmitted from duck to duck. Transmission of these isolates was dependent on the inoculation dose and route of infection. Analysis of swab samples taken from ducks revealed that the wild-bird isolate, H5N1-WB, was primarily shed via the cloacal route. The chicken isolate, H5N2-Ck, was isolated from cloacal as well as oro-pharyngeal swabs. Analysis of the amino acid sequences of the viral surface glycoproteins showed that the hemagglutinin (HA) of the H5N2-Ck isolate was under a stronger evolutionary pressure than the HA of the H5N1-WB isolate, as indicated by the presence of a larger number of amino acid changes observed during passage. The neuraminidase (NA) of both viruses showed either no (in the case of H5N1-WB) or very few amino acid changes.

Infection of Broilers with Two Virulent Strains of Infectious Laryngotracheitis Virus: Criteria for Evaluation of Experimental Infections.

Infectious laryngotracheitis (ILT) is a highly contagious disease of chickens and is responsible for significant economic losses in the poultry industry worldwide; it is caused by Gallid herpesvirus-1 (GaHV-1), commonly known as infectious laryngotracheitis virus (ILTV). Experimental evaluation of ILTV strains is fundamental to identify changes in virulence that can contribute to the severity and spread of outbreaks and consequently influence the efficacy of vaccination. Several criteria had been utilized to determine the degree of virulence associated with ILTV strains. The objectives of this study were to compare the levels of virulence of the standard United States Department of Agriculture (USDA) challenge strain with a contemporary outbreak-related strain (63140) and to evaluate the efficacy of individual criteria to identify changes in virulence. Broilers were inoculated with increasing infectious doses of each strain. The criteria utilized to evaluate virulence were clinical signs of the disease, mortality, microscopic tracheal lesions, trachea genome viral loads, and antibody titers. Clinical signs scores were a useful parameter to define the peak of clinical disease but did not reveal differences in virulence between strains. Similarly, trachea microscopic lesion scores or levels of serum antibody titers were parameters that did not reveal obvious differences in virulence between strains. However, mortalities and increased viral genome loads in trachea of chickens inoculated with lower (log10 1 to 2) infectious doses clearly differentiated 63140 as a more-virulent ILTV strain. This study provides the framework to compare the virulence level of emerging ILTV isolates to the now-characterized USDA and 63140 strains.

Evaluating Protection Against Infectious Bronchitis Virus by Clinical Signs, Ciliostasis, Challenge Virus Detection, and Histopathology.

In this study, we examined the association among clinical signs, ciliostasis, virus detection, and histopathology for evaluating protection of vaccinated chickens against homologous and heterologous infectious bronchitis virus (IBV) challenge. At 5 days following challenge with IBV, we found a good correlation among clinical signs, ciliostasis in the trachea, challenge virus detection, and microscopic lesions in the trachea, with all four criteria being negative in fully protected birds and positive in fully susceptible birds. In partially protected birds we observed clinical signs and detected challenge virus; however, the ciliated epithelium was intact. In a second experiment, we challenged fully protected, partially protected, and fully susceptible birds with IBV, and then at 5 days postchallenge we gave the birds an opportunistic bacterium intranasally. Twenty Bordetella avium colonies were recovered from one of five fully protected birds, and only five colonies were isolated from two of five partially protected birds without ciliostasis, whereas in birds with ciliostasis, numerous colonies were isolated. Obviously, decreasing IBV infection and replication in the upper respiratory tract will decrease transmission and mutations, leading to variant viruses, and herein we demonstrate that protection of the cilia will decrease secondary bacterial infections, which have been shown to lead to condemnations and increased mortality. Thus, it appears that examining both criteria would be important when evaluating IBV vaccine efficacy.

Tribasic copper chloride toxicosis in commercial broiler chicks.

Two broiler chicken houses containing 17,500 chicks each experienced an extreme elevation in chick mortality beginning on day 3 after placement. Clinical signs observed upon farm visit included numerous small chicks for their age; depressed, lethargic, and comatose chicks; and chicks huddling near feed pans and under heaters. Necropsied chicks were markedly pale and had atrophy of the thymus and bursa, swollen and edematous proventriculus, erosions in the koilin and in the proventricular-ventricular junction, pale kidneys, and yellowish to brownish-orange liver often with linear pale areas. The chicks had watery blood and hematocrits measured from 9.5% to 18%. Chicken infectious anemia was initially suspected based on the clinical signs and gross lesions. Histopathology revealed multifocal acute hepatic degeneration and necrosis with golden-brown pigment in the cytoplasm of hepatocytes and Kupffer cells, moderate to severe koilin degeneration and fragmentation, multifocal mild to moderate proventricular necrosis, mild to moderate necrosis and loss of enterocytes, blunting of small intestinal villi, lymphoid depletion in the thymus and bursa, erythrophagocytosis in the liver and spleen, and acute renal tubular degeneration and necrosis. Special stains revealed mild to abundant accumulation of copper pigment in the cytoplasm of hepatocytes and iron pigment in the cytoplasm of Kupffer cells. Feed analysis revealed 2140 to 2393 parts per million of copper in the starter ration, and heavy metal analysis detected markedly elevated copper levels in formalin-fixed samples of the liver. Excessive amounts of tribasic copper chloride in the starter ration caused copper toxicosis in these chicks. Similar clinical signs and lesions were reproduced when the suspect feed was used in an experimental pen trial.

Pulsed electric field (PEF) as an intensification pretreatment for greener solvent lipid extraction from microalgae.

Microalgae, with their high lipid content, are a promising feedstock for renewable fuels. Traditionally, human and environmentally toxic solvents have been used to extract these lipids, diminishing the sustainability of this process. Herein, pulsed electric field technology was utilized as a process intensification strategy to enhance lipid extraction from Ankistrodesmus falcatus wet biomass using the green solvent, ethyl acetate. The extraction efficiency for ethyl acetate without PEF was lower (83-88%) than chloroform. In addition, the ethyl acetate exhibited a 2-h induction period, while the chloroform showed no time dependence. Utilizing PEF technology resulted in 90% of the cells being lysed and a significant enhancement in the rate of lipid recovery using ethyl acetate. The increase in lipid recovery was due to the presence of the electric field and not due to temperature effects. The PEF technology uses less energy than other PEF systems reported in the literature.

An in vivo experimental model to determine antigenic variations among infectious bursal disease viruses.

Infectious bursal disease virus (IBDV) is a double-stranded RNA virus causing infectious bursal disease in chickens. IBDV undergoes antigenic drift, so characterizing the antigenicity of IBDV plays an important role for identification and selection of vaccine candidates. In this study, an in vivo experimental model was developed to differentiate a new antigenic variant of IBDV. To this end, a hyper-immune serum to IBDV E/Del-type virus was generated in specific pathogen-free chickens and a standard volume of the hyper-immune serum was serially diluted and injected in specific pathogen-free birds via intravenous, subcutaneous, or intramuscular routes. The chickens were bled at different time points in order to evaluate the dynamics of virus neutralization titres. Based on the results, chickens were injected with different serum dilutions by the subcutaneous route. Twenty-four hours later, chickens were bled and then challenged with 100 median chicken infectious doses of the E/Del virus and a new IBDV variant. Chickens were euthanized at 7 days post infection and the bursa of Fabricius was removed for microscopic evaluation to determine the bursal lesion score. The determined virus neutralization titre along with the bursal lesion score was used to determine the breakthrough titre in the in vivo chicken model. Based on the data obtained, an antigenic subtype of IBDV was identified and determined to be different from E/Del. This model is a sensitive model for determination of IBDV antigenicity of non-tissue culture adapted IBDV.

Evaluation of infectious bronchitis virus Arkansas-type vaccine failure in commercial broilers.

Infectious bronchitis virus (IBV) causes an upper respiratory tract disease in chickens and is highly contagious. Many different types of the virus exist, but only a few types are used as attenuated live vaccines in the commercial poultry industry. Of the vaccine types used, the Arkansas (Ark)-type virus is most frequently reisolated from vaccinated broilers. Previous research has suggested that incomplete clearance of Ark-type vaccine virus plays a role in the inadequate protection observed when vaccinated broilers are challenged with pathogenic Ark virus. In this study, we examine routes of vaccine administration using multiple IBV types including Ark in an effort to understand why Ark vaccines do not provide good protection and persist in commercial broilers. We found that interference between different types of IBV vaccines was not occurring when combined and administered using a commercial hatchery spray cabinet. Also, Ark vaccine virus was not efficacious in 1-day-old broilers when sprayed using a hatchery spray cabinet, but it gave good protection when administrated by eyedrop inoculation. We also found that the amount of Ark vaccine virus was low or undetectable in choanal swabs out to 35 days postvaccination when vaccine was administered by eyedrop or drinking water. Alternatively, a subpopulation of the Ark vaccine isolated from a vaccinated bird, Ark-RI-EP1, showed a peak titer at 7-10 days of age when given by the same routes, suggesting that the Ark-RI-EP1 was more fit with regard to infection, replication in the birds, or both. Moreover, we found that detection of IBV vaccine virus early after administration, regardless of strain or route, correlated with protection against homologous challenge and may thus be a good indicator of vaccine efficacy in the field because humoral antibody titers are typically low or undetectable after vaccination. These experiments provided key findings that can be used to direct efforts for improving the efficacy of IBV Ark-type vaccines given in the hatchery. They also elucidated factors contributing to the persistence of Ark vaccine in the field.

Presumed Spontaneous Astrocytoma in a Domestic Backyard Chicken.

A cerebral tumor was identified in an adult female domestic chicken (Gallus domesticus). On gross examination, the cut surface of the cerebrum revealed a poorly circumscribed, pale tan soft mass within the thalamus and midbrain. On histologic examination, there was an unencapsulated, multilobulated neoplasm composed of spindle cells on a loose fibrovascular stroma. Neoplastic cells had variably distinct cell borders, abundant fibrillar eosinophilic cytoplasm, oval nuclei with finely stippled chromatin, and 1-2 distinct nucleoli. There was moderate anisocytosis and anisokaryosis with <1 mitoses per 2.37 mm2. The morphologic features of the neoplastic cells were consistent with an astrocytic neoplasm. PCR was performed on formalin-fixed paraffin-embedded sections of brain tissue, which was negative for subgroup A avian leukosis virus. Based on these findings, the tumor was diagnosed as a presumed spontaneous astrocytoma.

Reporte de caso - Presunto astrocitoma espontáneo en un pollo doméstico de traspatio. Se identificó un tumor cerebral en una gallina doméstica adulta (Gallus domesticus). En el examen macroscópico, la superficie de corte del cerebro reveló una masa blanda de color canela pálido mal delimitada dentro del tálamo y el mesencéfalo. En el examen histológico, había una neoplasia multilobulada no encapsulada compuesta de células fusiformes sobre un estroma fibrovascular laxo. Las células neoplásicas tenían bordes celulares diferenciados de forma variable, abundante citoplasma eosinofílico fibrilar, núcleos ovalados con cromatina finamente punteada y 1 o 2 nucléolos distintos. Había anisocitosis moderada y anisocariosis con <1 mitosis por 2.37 mm2. Las características morfológicas de las células neoplásicas eran compatibles con una neoplasia astrocítica. Se realizó una PCR en secciones de tejido cerebral incluidas en parafina y fijadas con formalina, que resultó negativa para el virus de la leucosis aviar del subgrupo A. Con base en estos hallazgos, el tumor se diagnosticó como un presunto astrocitoma espontáneo.

Investigation into the aetiology of runting and stunting syndrome in chickens.

Currently, the aetiology of runting and stunting syndrome (RSS) in chickens is unknown. The impact of RSS on weight gain and microscopic lesions in immunological organs and the duodenum, was investigated in 1-day-old commercial broilers at 12 days following exposure to RSS-contaminated litter. Furthermore, the presence of the viral nucleic acids of three astroviruses and one parvovirus was analysed by in situ hybridization from days 1 through 5 post exposure. A 70% decrease in weight was observed in the RSS-exposed group at the end of the experiments when compared with the unexposed controls. Lesions in the bursa of Fabricius and thymus were present in both groups but were significantly higher at the end of the study in the RSS-exposed group. In contrast, no significant difference in Harderian gland lesions was observed between the groups. Histological lesions in the duodenum were already present 24 h after exposure in the RSS-exposed group only, peaked at day 4 and declined until the end of the study. Results of the in situ hybridization studies clearly indicate replication of three astroviruses (chicken astrovirus, avian nephritis virus [ANV]-1, ANV-2) in the duodenum but not in other organs evaluated. Chicken astrovirus nucleic acids were detected on days 1 and 2 post exposure, while ANV-1 and ANV-2 nucleic acids were observed on several days during the period investigated. Surprisingly, no viral nucleic acid specific for the chicken parvovirus was observed. The results indicate that astroviruses probably play an important role during RSS due to the concurrence of viral RNA detection and lesions in the duodenum.

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.

Improved clinicopathologic assessments of acute liver damage due to trauma in Indian ring-necked parakeets (Psittacula krameri manillensis).

Increased activities of certain biochemical enzymes (alanine aminotransferase [ALT], aspartate aminotransferase [AST], lactate dehydrogenase [LDH], alkaline phosphatase [ALP]) have been associated with blunt liver injury in many species. To evaluate changes in plasma hepatic biochemical parameters in acute avian liver disease caused by trauma and to compare biochemical changes with histologic lesions in hepatic parenchyma, 30 healthy fasted Indian ring-necked parakeets (Psittacula krameri manillensis) were divided into 2 groups, and traumatic liver injury was caused by endoscopic liver biopsy (group 1) or by liver biopsy and crushing injury to the hepatic parenchyma with endoscopic forceps (group 2) in anesthetized birds. Blood samples were collected at baseline and at 12, 24, 36, 48, 60, 72, 84, 96, 108, and 120 hours in alternate groups to compare analyte values after injury with those at baseline. Results showed consistently decreased plasma ALP activity (excluding 1 time point) throughout the study, which was thought to be associated with isoflurane administration. Plasma glutamate dehydrogenase activity initially increased but rapidly declined thereafter and was attributed to acute focal hepatocellular injury. In both groups, increases in plasma AST, ALT, and LDH activities was most likely caused by muscle injury because creatine kinase activity was concurrently increased. Compared with baseline values, bile acid concentration and y-glutamyl transferase activity were not affected by liver biopsy or crush injury. Plasma sorbitol dehydrogenase activity was the most specific indicator of liver injury in both groups. Histologic changes correlated poorly with biochemical results, possibly because the small area of hepatic parenchyma that was damaged did not affect enzyme values substantially.

Pathology in Practice.

In collaboration with the American College of Veterinary Pathologists.

Modulation of folliculogenesis in adult laying chickens by bisphenol A and bisphenol S: Perspectives on ovarian morphology and gene expression.

Both bisphenol A (BPA) and its analog bisphenol S (BPS) are industrial chemicals that have been used to make certain plastic products applied in chicken farms, including food and water containers. They are endocrine disrupting chemicals (EDCs) with xenoestrogenic activities and affect reproductive success in many ways. It was hypothesized that BPA and BPS could adversely affect the folliculogenesis in chickens due to their disruption of the estrogen responses, using either genomic or non-genomic mechanisms. This study investigated the deleterious effects of BPA and BPS on the ovaries when adult layer chickens were orally treated with these EDCs at 50 µg/kg body weight, the reference dose for chronic oral exposure of BPA established by the U.S. EPA. The chickens in both BPA and BPS-treated groups showed a decreased number of the preovulatory follicles. BPA-treated chickens showed a significant decrease in the diameter of F1. Additionally, both BPA and BPS treatments increased the infiltrations of lymphocytes and plasma cells in ovaries. Moreover, it was found that the ovaries of BPS-treated chickens weighed the most among the groups. RNA sequencing and subsequent pathway enrichment analysis of differentially expressed genes revealed that both BPA- and BPS-treatment groups showed significant changes in gene expression and pathways related to reproduction, immune function and carcinogenesis. Taken together, both BPA and BPS are potentially carcinogenic and have deleterious effects on the fertility of laying chickens by inducing inflammation, suggesting that BPS may not be a safe replacement for BPA.

Hemorrhagic Hepatopathy in Broiler Breeder Pullets: Gross and Microscopic Pathology and Factors Associated with Incidence.

Hemorrhagic hepatopathy is a syndrome reported in layer pullets resulting in mortality and lesions including hepatic, splenic, and intestinal necrosis; hepatic and splenic enlargement; hemorrhages; amyloidosis of the muscle, spleen, and liver; accumulation of noncoagulated hemorrhagic fluid in the coelom; and frequently, granulomatous myositis at bacterin injection sites. The syndrome is characterized in the literature in table egg layer pullets and is thought to be associated with the administration of bacterin vaccines, namely, frequently Salmonella enterica subsp. enterica bacterins. Hemorrhagic hepatopathy is recognized by industry veterinarians as also occurring infrequently in broiler breeder pullets in the United States. As the condition is likely due to an inflammatory process in response to bacterial lipopolysaccharide inoculation, it is important to characterize both the pathologic changes and predisposing factors for the condition in broiler breeds, which are immunologically different from table egg layer breeds. In this study, we characterize the gross and microscopic lesions observed in a series of diagnostic laboratory cases of hemorrhagic hepatopathy in broiler breeder pullets and suggest a possible pathophysiology for the condition. Additionally, we report results from a case survey of the United States broiler industry that suggest that the condition is due to a reaction to bacterin vaccination and that certain bacterin products may predispose pullet flocks to develop the condition. Although further research is indicated, these findings establish hemorrhagic hepatopathy as a pathologic condition of broiler breeder pullets and may aid in the diagnosis and prevention of the syndrome.

Artículo regular­La hepatopatía hemorrágica en pollitas reproductoras pesadas: Patología macroscópica y microscópica y factores asociados con la incidencia La hepatopatía hemorrágica es un síndrome reportado en pollitas ponedoras que resulta en mortalidad y lesiones, incluyendo necrosis hepática, esplénica e intestinal; agrandamiento hepático y esplénico; hemorragias; amiloidosis del músculo, bazo e hígado; acumulación de líquido hemorrágico no coagulado en la cavidad celómica; y con frecuencia, miositis granulomatosa en los lugares de inyección de bacterina. El síndrome se ha caracterizado en la bibliografía en pollitas ponedoras de huevo comercial y se cree que está asociado con la administración de vacunas de bacterianas, con frecuencia bacterinas de Salmonella. Los veterinarios de la industria reconocen que la hepatopatía hemorrágica también ocurre con poca frecuencia en pollitas de reproductoras pesadas en los Estados Unidos. Como es probable que esta condición se deba a un proceso inflamatorio en respuesta a la inoculación de lipopolisacáridos bacterianos, es importante caracterizar tanto los cambios patológicos como los factores predisponentes para la afección en las líneas de pollos de engorde, que son inmunológicamente diferentes de las líneas ponedoras de huevo comercial. En este estudio, se caracterizaron las lesiones macroscópicas y microscópicas observadas en una serie de casos de laboratorio de diagnóstico de hepatopatía hemorrágica en pollitas reproductoras de pollos de engorde y sugerimos una posible fisiopatología de esta condición. Además, se reportan los resultados de una encuesta de casos de la industria de pollos de engorde en los Estados Unidos que sugiere que la condición se debe a una reacción a la vacunación con bacterinas y que ciertos productos de las bacterinas pueden predisponer a las parvadas de pollitas a desarrollar la afección. Aunque se requieren más investigaciones, estos hallazgos establecen la hepatopatía hemorrágica como una condición patológica de las pollitas reproductoras pesadas y pueden ayudar en el diagnóstico y a la prevención del síndrome.

Hunting the eagle killer: A cyanobacterial neurotoxin causes vacuolar myelinopathy.

Vacuolar myelinopathy is a fatal neurological disease that was initially discovered during a mysterious mass mortality of bald eagles in Arkansas in the United States. The cause of this wildlife disease has eluded scientists for decades while its occurrence has continued to spread throughout freshwater reservoirs in the southeastern United States. Recent studies have demonstrated that vacuolar myelinopathy is induced by consumption of the epiphytic cyanobacterial species Aetokthonos hydrillicola growing on aquatic vegetation, primarily the invasive Hydrilla verticillata Here, we describe the identification, biosynthetic gene cluster, and biological activity of aetokthonotoxin, a pentabrominated biindole alkaloid that is produced by the cyanobacterium A. hydrillicola We identify this cyanobacterial neurotoxin as the causal agent of vacuolar myelinopathy and discuss environmental factors-especially bromide availability-that promote toxin production.