Presence ofAvibacterium paragallinarumand Histopathologic Lesions Corresponds with Clinical Signs in a Co-infection Model withGallibacterium anatis

Abstract

Recently we demonstrated that co-infection with Avibacterium paragallinarum and Gallibacterium anatis leads to increased severity of clinical signs of infectious coryza in birds. The present study examined the interaction of these two pathogens in chickens by evaluation of histologic lesions in sinus infraorbitalis and nasal turbinates, applying a defined scoring scheme ranging from 0 to 3. Furthermore, for the first time, an in situ hybridization (ISH) technique was applied to detect A. paragallinarum in tissues. The samples were received from vaccinated and nonvaccinated birds that were infected with A. paragallinarum and/or G. anatis. Vaccinated birds were mostly devoid of any histopathologic lesions except a few birds with lesion score 1 at 7 and 14 days postinfection (dpi). Likewise, nonvaccinated birds infected with G. anatis only did not present microscopic changes in the sinus infraorbitalis, except in a single bird at 7 dpi. Interestingly, median lesion scores caused by G. anatis infection were significantly higher in the nasal turbinates of infected birds than in negative control at 7 and 14 dpi. The most prominent histologic changes were recorded from sinus infraorbitalis and nasal turbinates of nonvaccinated birds that were infected either with A. paragallinarum only or together with G. anatis. ISH demonstrated positive signals for A. paragallinarum in exudates present in the lumen or attached to the epithelial layer of investigated tissues. Such signals were mainly detected in tissues from birds with the highest histopathologic lesion scores.

Component Identification and Functional Analysis of Outer Membrane Vesicles Released by Avibacterium paragallinarum

“…The OMVs of Acinetobacter baumannii interact with macrophages to induce the secretion of both pro‐ and anti-inflammatory cytokines, leading to uncontrolled chronic inflammation ( Ahmad et al, 2019 ). It has been suggested that A. paragallinarum may have an immunomodulatory potential that influences host defense and inflammation ( Paudel et al, 2017 ). Our results suggest that it is possible that the OMVs of A. paragallinarum involved in such influence on host responses.…”

Etiology, epidemiology, pathology, and advances in diagnosis, vaccine development, and treatment ofGallibacterium anatisinfection in poultry: a review

“…In the lungs, bronchial goblet cell hyperplasia and hyperplasia of the bronchial lymphoid nodules were reported (Zepeda et al 2010). In another experimental G. anatis or G. anatis -A. paragallinarum co-infection study in chickens, histopathological findings in the infraorbital sinus and nasal turbinates observed were infiltration of inflammatory cells, predominated by mononuclear cells and heterophils, increased mucosal thickness, and necrosis and sloughing of epithelium (Paudel, Ruhnau, et al 2017). Few other similar recent experimental G. anatis infections in commercial broiler chickens reported the enhanced activity of goblet cells, hyperplasia of the epithelial lining, and inflammatory cell infiltration in tracheal tissue.…”

“…Flocks co-infected with other bacterial or viral infections and immunosuppressive agents should be protected by adopting appropriate prophylactic, therapeutic and control measures such as timely vaccination, selective antimicrobial therapy and strict biosecurity measures (He-Ping et al 2012;;Paudel et al 2015;Mataried 2016;Paudel, Ruhnau, et al 2017;El-Hamid et al 2018). Any stress that reduces bird resistance to infection must be ameliorated.…”

“…Host-related factors such as stress, immune status, age, and hormones tend to play a significant role in aggravating disease severity. Co-infection with other pathogenic bacteria or viral agents causing respiratory tract damage, or immunosuppression in the target host, and abrupt change in environmental factors like seasonal variations, cold stress, lack of biosecurity, deficient nutrition, poor ventilation, and overcrowding exacerbate this disease (Gilchrist 1963;Kohlert 1968;Matthes et al 1969;Bisgaard 1977;Shaw et al 1990;Mirle et al 1991;Bojesen et al 2004;Verbrugghe et al 2012;Paudel et al 2015;Persson & Bojesen 2015;Paudel, Ruhnau, et al 2017). Coinfection of G. anatis with infectious bronchitis virus (IBV) has been reported to increase the rate of systemic infection by G. anatis (He-ping et al 2012;;Mataried 2016), and mixed infection in association with other bacterial pathogens such as E. coli, A. paragallinarum, and Mycoplasma gallisepticum may aggravate disease severity in chickens, resulting in increased morbidity and mortality (Neubauer et al 2009;Paudel, Ruhnau, et al 2017;El-Hamid et al 2018).…”

RTX Toxins of Animal Pathogens and Their Role as Antigens in Vaccines and Diagnostics

“…Gallibacterium anatis has emerged in the last few years as an important multi-antibiotic resistant pathogen in intensively reared poultry birds causing losses in production. It causes heavy mortality in broiler chickens and a drop in egg production in layer hens by triggering salpingitis, peritonitis, salpingoperitonitis, bacteremia, oophoritis, follicle degeneration, hepatitis, enteritis, and respiratory tract diseases [111][112][113][114]. G. anatis secretes a strongly cytotoxic and hemolytic RTX toxin named GtxA, which has a particularly high molecular mass of 215 kDa and an uncommon domain structure [115].…”