Are anti-ganglioside antibodies associated with proventricular dilatation disease in birds?

The identification of Parrot bornaviruses (PaBV) in psittacine birds with proventricular dilatation disease (PDD) has not been sufficient to explain the pathogenesis of this fatal disease, since not all infected birds develop clinical signs. Although the most accepted theory indicates that PaBV directly triggers an inflammatory response in this disease, another hypothesis suggests the disease is triggered by autoantibodies targeting neuronal gangliosides, and PDD might therefore resemble Guillain-Barré Syndrome (GBS) in its pathogenesis. Experimental inoculation of pure gangliosides and brain-derived ganglioside extracts were used in two different immunization studies. The first study was performed on 17 healthy chickens (Gallus gallus domesticus): 11 chickens were inoculated with a brain ganglioside extract in Freund’s complete adjuvant (FCA) and six chickens inoculated with phosphate-buffered saline. A second study was performed five healthy quaker parrots (Myiopsitta monachus) that were divided into three groups: Two quaker parrots received purified gangliosides in FCA, two received a crude brain extract in FCA, and one control quaker parrot received FCA alone. One chicken developed difficult in walking. Histologically, only a mild perivascular and perineural lymphocytic infiltrate in the proventriculus. Two quaker parrots (one from each treatment group) had mild lymphoplasmacytic encephalitis and myelitis. However, none of the quaker parrots developed myenteric ganglioneuritis, suggesting that autoantibodies against gangliosides in birds are not associated with a condition resembling PDD

In utero ultrafine particulate matter exposure causes offspring pulmonary immunosuppression.

Early life exposure to fine particulate matter (PM) in air is associated with infant respiratory disease and childhood asthma, but limited epidemiological data exist concerning the impacts of ultrafine particles (UFPs) on the etiology of childhood respiratory disease. Specifically, the role of UFPs in amplifying Th2- and/or Th17-driven inflammation (asthma promotion) or suppressing effector T cells (increased susceptibility to respiratory infection) remains unclear. Using a mouse model of in utero UFP exposure, we determined early immunological responses to house dust mite (HDM) allergen in offspring challenged from 0 to 4 wk of age. Two mice strains were exposed throughout gestation: C57BL/6 (sensitive to oxidative stress) and BALB/C (sensitive to allergen exposure). Offspring exposed to UFPs in utero exhibited reduced inflammatory response to HDM. Compared with filtered air (FA)-exposed/HDM-challenged mice, UFP-exposed offspring had lower white blood cell counts in bronchoalveolar lavage fluid and less pronounced peribronchiolar inflammation in both strains, albeit more apparent in C57BL/6 mice. In the C57BL/6 strain, offspring exposed in utero to FA and challenged with HDM exhibited a robust response in inflammatory cytokines IL-13 and Il-17. In contrast, this response was lost in offspring exposed in utero to UFPs. Circulating IL-10 was significantly up-regulated in C57BL/6 offspring exposed to UFPs, suggesting increased regulatory T cell expression and suppressed Th2/Th17 response. Our results reveal that in utero UFP exposure at a level close to the WHO recommended PM guideline suppresses an early immune response to HDM allergen, likely predisposing neonates to respiratory infection and altering long-term pulmonary health

Pathological Aspects and Pathogenesis of Parrot Bornavirus 2 (PaBV-2) Infection in Psittacine Birds

Parrot bornaviruses (PaBVs) are RNA viruses of the Bornaviridae family and the causative agents of proventricular dilatation disease (PDD). PDD has many aspects that remain to be elucidated, including the mechanisms involved in its pathogenesis. The purpose of this work was to investigate different hypotheses linked to the pathogenesis of Parrot bornavirus 2 (PaBV-2) infection in psittacine birds. We first tested the hypothesis of antibodies against gangliosides being involved in the development of PDD in psittacine birds. We analyzed the relationship between the presence of antiganglioside antibodies and microscopic lesions related to PDD in birds. No association between the presence of anti-ganglioside antibodies and the development of lesions resembling PDD was observed in our study, which corroborates with the hypothesis that PDD is not an auto-immune disease as previously speculated. Second, we analyzed the progression of viral antigen and inflammatory lesions after the intramuscular inoculation of PaBV-2 in cockatiels. Histopathological, immunohistochemical and molecular analyses were performed in tissues of cockatiels in a chronological fashion. PaBV-2 was first detected in leukocytes in the inoculation site and adjacent nerves, then reached the brachial plexus, centripetally spread to the thoracic segment of the spinal cord, and subsequently invaded the other spinal segments and brain. PaBV-2 then centrifugally spread out of the central nervous system (CNS) to peripheral ganglia. Our results demonstrate that PaBV-2 first targets the CNS, before migrating to peripheral tissues such as the GI system. Finally, we aimed to evaluate the distribution of inflammatory foci and viral antigen throughout 4 selected levels of brain and 3 segments of spinal cord in cockatiels experimentally infected with PaBV-2. Immunolabeling was first observed in the ventral horns of the thoracic spinal cord. Inflammatory lesions were first identified in the gray matter of the thalamus and brainstem. Encephalitis was more severe in the thalamus and brainstem, while myelitis was equally distributed between all segments of the spinal cord. Our results demonstrate a caudal-rostral viral distribution of PABV-2. Our results reemphasize the role of PaBVs as the causative agents of PDD; the lack of an autoimmune component; and the detection of PaBV-2 in the CNS before peripheral organs

Seeing beyond a Dilated Proventriculus: Diagnostic Tools for Proventricular Dilatation Disease in Psittacine Birds

Proventricular dilatation disease (PDD) is a life-threatening neurological disease caused by parrot bornaviruses (PaBVs) that affects several species worldwide. PDD can be clinically manifested as either a central nervous system condition or a gastrointestinal condition if the nerves and ganglia of the gastrointestinal tract are compromised. We intend to provide a concise review for veterinary clinicians and diagnosticians with focus on the main tools available for PDD diagnosis, including gross and histopathology, immunohistochemistry, molecular techniques and serology. We suggest that a combination of different strategies can increase the success of diagnostic outcomes, as tools such as reverse transcription polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA) can be implemented for identification of bornaviral infections in live patients, and gross pathology, histopathology, immunohistochemistry and RT-PCR can provide reliable results for postmortem diagnosis of PDD

Histomoniasis outbreak in free-range chickens in semiarid Paraíba, Brazil

We describe an outbreak of histomoniasis in free-range chickens (Gallus gallus domesticus) in the semiarid region of Paraíba State, Brazil. Juvenile chickens aged approximately 48 days showed disease over a 15-day period. Seven of 16 chickens showed yellow, watery stool, anorexia, lethargy, and death within 3-5 days of clinical illness. The mortality rate was 43.7%. The chickens were raised in a backyard with 12 adult birds that remained healthy. None of the chickens were vaccinated or dewormed. A necropsy on one deceased bird showed lesions confined to the cecum and liver. The left cecum was distended and had yellow, slightly elevated areas on the serosa. The liver was reddened with centrally depressed areas surrounded by a pale halo, which were distributed throughout the capsular surface and extended deep throughout the parenchyma. Microscopically, typhlitis and pyogranulomatous necrotizing hepatitis associated with numerous intralesional Histomonas trophozoites was observed. The birds were administered metronidazole and albendazole, which effectively controlled the histomoniasis. Although histomoniasis is rare in free-range poultry, it can occur and cause high mortality and significant economic losses

From nerves to brain to gastrointestinal tract: A time-based study of parrot bornavirus 2 (PaBV-2) pathogenesis in cockatiels (<i>Nymphicus hollandicus</i>)

<div><p>Parrot bornaviruses (PaBVs) are the causative agents of proventricular dilatation disease, however key aspects of its pathogenesis, such as route of infection, viral spread and distribution, and target cells remain unclear. Our study aimed to track the viral spread and lesion development at 5, 10, 20, 25, 35, 40, 60, 80, 95 and 114 dpi using histopathology, immunohistochemistry, and RT-PCR. After intramuscular inoculation of parrot bornavirus 2 (PaBV-2) in the pectoral muscle of cockatiels, this virus was first detected in macrophages and lymphocytes in the inoculation site and adjacent nerves, then reached the brachial plexus, centripetally spread to the thoracic segment of the spinal cord, and subsequently invaded the other spinal segments and brain. After reaching the central nervous system (CNS), PaBV-2 centrifugally spread out the CNS to the ganglia in the gastrointestinal (GI) system, adrenal gland, heart, and kidneys. At late points of infection, PaBV-2 was not only detected in nerves and ganglia but widespread in the smooth muscle and/or scattered epithelial cells of tissues such as crop, intestines, proventriculus, kidneys, skin, and vessels. Despite the hallmark lesion of PaBVs infection being the dilation of the proventriculus, our results demonstrate PaBV-2 first targets the CNS, before migrating to peripheral tissues such as the GI system.</p></div

Proventricular dilatation disease (PDD) outbreak in blue-and-gold macaws (Ara ararauna) in the State of Santa Catarina, southern Brazil

ABSTRACT: Proventricular dilatation disease (PDD) is a lethal and important disease of captive psittacine birds, and affects a wide range of species, including endangered ones, and lacks an effective treatment. This report describes PDD in three blue-and-gold macaws (Ara ararauna) in southern Brazil. All three macaws originated from the same aviary and presented similar clinical signs including anorexia, apathy, emaciation and prostration. At necropsy, one of the macaws presented an enlarged proventriculus. Histologically, lymphoplasmacytic infiltrates was observed in the ganglia and nerves of the esophagus, crop, proventriculus, ventriculus, heart, adrenal glands, and adrenal medulla of all three cases. Two macaws had meningoencephalomyelitis and one had myocarditis. Immunohistochemistry identified PaBV antigen in the brain, proventricular, ventricular ganglia, and epicardial ganglia, and cardiomyocytes of all three macaws

Summary of inflammatory lesions, PCR and IHC results observed in 12 sequential timepoints following days post infection.

<p>Summary of inflammatory lesions, PCR and IHC results observed in 12 sequential timepoints following days post infection.</p

Gross findings.

<p>Comparison of proventriculus size (arrowheads) in a control (A) and infected (B) cockatiels of the same timepoint (35 dpi). Note the distention of the proventricular wall in CK19 when compared to a control cockatiel (CK15).</p