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1
Beddard, Frank E. "Notes on the Visceral Anatomy of Birds.-No. II. On the Respiratory Organs in certain Diving Birds." Proceedings of the Zoological Society of London 56, no. 1 (August 20, 2009): 252–58. http://dx.doi.org/10.1111/j.1469-7998.1888.tb06705.x.
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Sergeev, A. A., O. V. P’Yankov, O. K. Demina, A. N. Shikov, Al A. Sergeev, L. N. Shishkina, A. S. Safatov, A. P. Agafonov, and A. N. Sergeev. "Studies of Sensitivity to Avian Flu Virus A/H5N1 in Chickens." Problems of Particularly Dangerous Infections, no. 3(113) (June 20, 2012): 71–73. http://dx.doi.org/10.21055/0370-1069-2012-3-71-73.
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) appear to be highly virulent for chickens. The chance of AFV infection of chickens in case of intranasal challenge is 20 times as great as in the case of peroral one, and 300 times as great as in the case of intragastral one, which bears evidence to higher sensitivity to AFV of the tissues of avian respiratory organs, in comparison with the tissues of gastro-intestinal tract. Therewith, primary target organ for virus in intranasal infected birds is their respiratory channel (mucous membrane of the nasal cavity in particular). Registered is the possibility of existence of fecal-nasal AFV transfer mechanism in chickens.
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Farooq, Saba. "Biological Characterization of Locally Circulating Mycoplasma gallisepticum in Poultry." Pakistan Veterinary Journal 41, no. 01 (March 1, 2021): 112–16. http://dx.doi.org/10.29261/pakvetj/2020.079.
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Mycoplasma gallisepticum (MG) is a pathogen of concern for poultry. Present study was conducted to determine the biological characteristics of a field isolate of MG, recovered from an MG-affected flock. This isolation was made through conventional method of MG cultivation, using modified Frey’s media after confirming the isolate by polymerase chain reaction (PCR). A total of 48 birds were segregated into experimental group (32 birds) and the control group (16 birds). To appraise primary site of infection, MG broth propagated culture containing 1x106 CFU/ml was inoculated intratracheally to each bird in the experimental group, whereas the control group was sham inoculated by uninoculated broth. The clinical signs and symptoms were recorded daily from day 1 to 21 post-infection (p.i.). Seroconversion monitoring was carried out, at day 5, 10, 15, 20 p.i. by Serum Plate Agglutination test (SPA) and Enzyme Linked Immunosorbent Assay (ELISA). To determine the dissemination pattern of MG, birds were sacrificed according to plan, swabbed from various organs and subjected to MG-specific PCR. Tracheal lesions and air sac lesions were scored after necropsy. Clinically, mild signs of respiratory discomfort were observed on day 5 p.i., which intensified on day 9 to 21 p.i. in the experimental group. PCR of tracheal swab samples was positive from day 7 to 21 p.i., and the swabs collected from lungs were positive for MG from day 9 to 21 p.i. The study concluded that, MG isolate from field showed limited dissemination pattern and is restricted to respiratory tract.
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Ali, A., G. Elmowalid, M. Abdel-Glil, T. Sharafeldin, F. Abdallah, S. Mansour, A. Nagy, B. Ahmed, and M. Abdelmoneim. "Etiology and pathology of epidemic outbreaks of avian influenza H5N1 infection in Egyptian chicken farms." Polish Journal of Veterinary Sciences 18, no. 4 (December 1, 2015): 779–86. http://dx.doi.org/10.1515/pjvs-2015-0101.
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AbstractEpidemic outbreaks of avian influenza (AI) virus H5N1 have been frequently reported in Egypt during the last nine years. Here we investigate the involvement of AI H5N1 in outbreaks of acute respiratory disease that occurred in several commercial chicken farms in Egypt in 2011, and we describe to the pathology caused by the virus in the course of the outbreak.Twenty-one chicken farms with history of acute respiratory symptoms and high mortalities were screened for AI H5N1. Virus identification was based on hemagglutination inhibition test, and PCR detection and sequencing of the hemagglutinin and neuraminidase genes. Virus distribution was determined by immunohistochemical staining of AI antigens in organs of infected birds. Standard H&E staining was performed for histological examination of affected organs.Eighty-one % of the examined birds, representing 100% of the screened farms, were positive for AI H5N1 virus. Phylogenetic analysis of the hemagglutinin and neuraminidase genes of the isolated virus reveals its affiliation to clade 2.2.1. Viral antigens were localized in the endothelial cells of the heart, liver, lungs and skin, where pathological lesions including congestion, hemorrhages, multifocal inflammation and necrosis were concurrently observed. According to the pattern of the viral antigen and lesion distribution in the visceral organs, we suggest cardiovascular and circulatory failures as the probable cause of death during these outbreaks. In conclusion, the present study further confirms the epidemic status of AI H5N1 virus in Egypt and reveals the highly pathogenic nature of the local isolates.
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Fotina, H. A., and Y. M. Opanasenko. "Effect of fluoroquinolones on the male chicken reproductive organs." Scientific Messenger of LNU of Veterinary Medicine and Biotechnologies 21, no. 96 (December 14, 2019): 86–89. http://dx.doi.org/10.32718/nvlvet9615.
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The using of antibiotics in poultry has some disadvantages. The problem of antibiotic resistance of microorganisms is recognized globally and is currently one of the strategic goals worldwide. Fluoroquinolones are an important and large group of synthetic antimicrobials that have great importance in the treatment of infectious-inflammatory poultry diseases of different etiologies. Fluoroquinolones have high bactericidal activity against a number of bacterial pathogens that infect poultry including E. coli, Hebsiell spp., Pseudomonas spp., Staphylococoeus spp. and Chlamydia spp. Enrofloxacin (ENR) is an antimicrobial agent belonging to the group of third-generation fluoroquinolones. ENR has been historically used as veterinary medicine for treatment of gastrointestinal and respiratory infections in several animal species, including poultrys cursing diseases caused by gram-positive and negative bacteria. Enrofloxacin presents 1,4-dihydro-1-cyclopropyl-7-(4-ethyl-1-piperazinyl)-6-fluoro-4-oxo-3-quinoli;3-quinoline carboxylic acid. A further synthesis allowed the reaching of active substances of cyclopropyl, as an antibacterial action to get further extension. A crystalline active substance with faint yellow color that was obtained to develop in high purity, is hardly soluble in water at pH 7, but as the molecule contains acidic and basic groups, it is easily dissolved at both alkaline and acid pH. The goal of the work. The purpose of our study was to investigate the sperm of male chicken after the use of enrofloxacin and to identify metabolites. Materials and methods of research. The researches were conducted in the conditions of vivarium clinics of the veterinary faculty and laboratories of the department of epizootology and parasitology of Sumy National Agrarian University. 80 male chickens were placed for research, which were kept in metal cages for 5–6 individuals. The use, care and transportation of birds for toxicological research were with all applicable animal welfare laws. All reasonable steps were taken to avoid or minimize discomfort, distress or pain of birds. Results of research and discussion. The differences between normal motility and defect sperm in control and enrofloxacin treated birds were not founded. Weight of testes, wattles and combs was not affected by drug. Ascorbic acid, total protein, testosterone and cholesterol concentration were similar in control and enrofloxacin treated groups. It is suggested that enrofloxacin at doses used were safe for male chicken. The administration of the drug “Enzin 10%” to the male chicken did not affect the concentration of ascorbic acid in the testicles, total protein and cholesterol. These indicators are actively involved in spermatogenesis. Thus, it can be concluded that the use of the drug “Enzin 10%” at therapeutic doses for 10 days had no negative effect on spermatogenesis of the male chicken.
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Jezdimirović, Nemanja, Branislav Kureljušić, Vojin Ivetić, Dejan Krnjaić, Oliver Radanović, Jadranka Žutić, Ljiljana Spalević, and Milijan Jovanović. "Comparative Pathomorphological, Mycological and Molecular Examination of Turkey Poults with Different Immunological Status Experimentally Infected with Aspergillus fumigatus." Acta Veterinaria 69, no. 2 (June 1, 2019): 201–17. http://dx.doi.org/10.2478/acve-2019-0016.
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Abstract The aim of this study was to determine the pathological, mycological and molecular findings in turkey poults with different immunological status experimentally infected with Aspergillus fumigatus. The investigation was carried out 1, 3, 7, 14 and 21 days after intratracheal inoculation of 5.056×107 spores of A. fumigatus to 14-day-old turkey poults in group G-1, as well as to turkey poults in group G-2 which were treated prior to infection with dexamethasone. A. fumigatus was isolated on day 1 p.i. in both groups, but the number of positive samples was bigger in group G-1. A. fumigatus was isolated from the respiratory organs of group G-1as early as on day 1 and 3 p.i. in 4 out of 12 examined specimens (33%). On day 7 p.i. A. fumigatus was possible to isolate from the respiratory organs of 50% of infected birds, on day 14 in 83.33% and on day 21 p.i. A. fumigatus was isolated in 6 out of 6 sacrificed turkey poults (100%). In dexamethasone-treated group A. fumigatus isolates from the respiratory organs on day 1 and 3 p.i. were same as in group G-1, whereas on days 7 and 14 p.i. the number of turkey poults positive to A. fumigatus increased in comparison with the untreated G-1 group. The histopathological lesions in turkey poults treated with dexamethasone developed earlier, were more intensive and extensive. The mycological and nested PCR results revealed a higher number of samples positive for the presence of A. fumigatus DNA in the group G-2, pretreated with dexamethasone.
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Butler, P. J., D. L. Turner, A. Al-Wassia, and R. M. Bevan. "Regional distribution of blood flow during swimming in the tufted duck (Aythya fuligula)." Journal of Experimental Biology 135, no. 1 (March 1, 1988): 461–72. http://dx.doi.org/10.1242/jeb.135.1.461.
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The distribution of blood flow to a number of organs and tissues of the tufted duck was determined (by the microsphere technique) before and while the birds were swimming at close to their maximum sustainable velocity (i.e. at 0.69 +/− 0.01 ms-1). During swimming, oxygen uptake was twice the pre-exercise value. Cardiac output increased by 70%, there was no significant change in arterial blood pressure and total systemic conductance increased by 44%. There were no significant changes in blood flow to the brain, liver, adrenal glands, spleen and respiratory muscles. Not surprisingly, there were increases in blood flow to the heart (30% increase) and to the muscles of the hindlimbs (to 3.1 times the pre-exercise value). Significant reductions in flow occurred to various parts of the gastrointestinal tract (although not to the gastrointestinal tract as a whole), to the pancreas and to the pectoralis muscles. In the case of the flight musculature as a whole, the reduction was to approximately 40% of the values in the ducks before exercise. Thus, despite the fact that cardiac output was some three times lower than it would have been during flight, there was a clear redistribution of blood away from some visceral organs and inactive muscles during surface swimming in the tufted duck. This lends support to the suggestion that blood is selectively directed to the legs, as well as to the brain and central nervous system (CNS) and away from the visceral organs and inactive muscles during voluntary diving in these birds.
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Dankovych, R., and V. Tumanov. "ПАТОМОРФОЛОГІЧНІ ЗМІНИ ЗА СПОНТАННОГО ОТРУЄННЯ ГОЛУБІВ ДІАЗИНОНОМ." Scientific Messenger of LNU of Veterinary Medicine and Biotechnology 18, no. 3(70) (September 4, 2016): 74–78. http://dx.doi.org/10.15421/nvlvet7017.
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Organophosphate pesticides, including diazinon, often used for illegal poisoning wild or domestic birds. The loss of a significant quantity of animals often become the subject of investigation in civil or criminal cases. For an objective diagnosis in such cases it is necessary to complete pathological–anatomical and chemical–toxicological studies. This article describes the structural changes that develop in the digestive system, cardiovascular system, respiratory, urinary, skin and central nervous system by spontaneous poisoning pigeons of diazinon. When conducted pathological–anatomical studies revealed pronounced dyscirculatory processes: congestive hyperemia (especially in the vessels of the skin in the neck and ox), and in the internal organs, stasis, perivascular edema and hemorrhage. Also registered alteration changes (protein degeneration and necrosis) of hepatocytes, cardiomyocytes, cells of nefron and neuron of cerebrum. Revealed changes suggest alternative development of irreversible processes in parenchymal cells of the liver, kidneys, myocardium and cerebrum. When autopsy selected material (feed the masses crop of birds) for chemical–toxicological research. As a result the research the extract of selected content crop of birds by thin layer chromatography paper manifestation of iodine bismuth quality received positive reaction on the compound diazinon.
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Mase, Masaji, Tadao Imada, Yasuyuki Sanada, Mariko Etoh, Naoko Sanada, Kenji Tsukamoto, Yoshihiro Kawaoka, and Shigeo Yamaguchi. "Imported Parakeets Harbor H9N2 Influenza A Viruses That Are Genetically Closely Related to Those Transmitted to Humans in Hong Kong." Journal of Virology 75, no. 7 (April 1, 2001): 3490–94. http://dx.doi.org/10.1128/jvi.75.7.3490-3494.2001.
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ABSTRACT In 1997 and 1998, H9N2 influenza A viruses were isolated from the respiratory organs of Indian ring-necked parakeets (Psittacula Krameri manillensis) that had been imported from Pakistan to Japan. The two isolates were closely related to each other (>99% as determined by nucleotide analysis of eight RNA segments), indicating that H9N2 viruses of the same lineage were maintained in these birds for at least 1 year. The hemagglutinins and neuraminidases of both isolates showed >97% nucleotide identity with those of H9N2 viruses isolated from humans in Hong Kong in 1999, while the six genes encoding internal proteins were >99% identical to the corresponding genes of H5N1 viruses recovered during the 1997 outbreak in Hong Kong. These results suggest that the H9N2 parakeet viruses originating in Pakistan share an immediate ancestor with the H9N2 human viruses. Thus, influenza A viruses with the potential to be transmitted directly to humans may be circulating in captive birds worldwide.
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Sturm-Ramirez, Katharine M., Trevor Ellis, Barry Bousfield, Lucy Bissett, Kitman Dyrting, Jerold E. Rehg, Leo Poon, Yi Guan, Malik Peiris, and Robert G. Webster. "Reemerging H5N1 Influenza Viruses in Hong Kong in 2002 Are Highly Pathogenic to Ducks." Journal of Virology 78, no. 9 (May 1, 2004): 4892–901. http://dx.doi.org/10.1128/jvi.78.9.4892-4901.2004.
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ABSTRACT Waterfowl are the natural reservoir of all influenza A viruses, which are usually nonpathogenic in wild aquatic birds. However, in late 2002, outbreaks of highly pathogenic H5N1 influenza virus caused deaths among wild migratory birds and resident waterfowl, including ducks, in two Hong Kong parks. In February 2003, an avian H5N1 virus closely related to one of these viruses was isolated from two humans with acute respiratory distress, one of whom died. Antigenic analysis of the new avian isolates showed a reactivity pattern different from that of H5N1 viruses isolated in 1997 and 2001. This finding suggests that significant antigenic variation has recently occurred among H5N1 viruses. We inoculated mallards with antigenically different H5N1 influenza viruses isolated between 1997 and 2003. The new 2002 avian isolates caused systemic infection in the ducks, with high virus titers and pathology in multiple organs, particularly the brain. Ducks developed acute disease, including severe neurological dysfunction and death. Virus was also isolated at high titers from the birds' drinking water and from contact birds, demonstrating efficient transmission. In contrast, H5N1 isolates from 1997 and 2001 were not consistently transmitted efficiently among ducks and did not cause significant disease. Despite a high level of genomic homology, the human isolate showed striking biological differences from its avian homologue in a duck model. This is the first reported case of lethal influenza virus infection in wild aquatic birds since 1961.
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Stoimenov, G., G. Goujgoulova, and K. Hristov. "Analysis of a highly pathogenic avian influenza (H5N1) virus causing the first outbreak in domestic poultry in Bulgaria in January 2015." Veterinární Medicína 65, No. 10 (October 29, 2020): 435–44. http://dx.doi.org/10.17221/148/2019-vetmed.
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This study documents the clinical signs, necropsy findings and viral antigen distribution of the highly pathogenic avian influenza (HPAI) H5N1 virus infection in domestic poultry (a backyard farm) and the phylogenetic analysis of the virus. On January 29, 2015, an outbreak of HPAI H5N1 in domestic poultry was reported on a backyard farm in Bulgaria. Out of the twenty-two chickens with clinical signs, twenty died while the remaining two were destroyed. The morbidity was 100%, whereas the overall mortality and lethality were 90.91%. The clinical observations made were sudden death, high mortality, weakness, and recumbency. Although multisystemic lesions were observed occasionally, the main pathologic findings were observed in the nervous, circulatory, respiratory, and gastrointestinal systems. An influenza virus nucleocapsid protein was identified by an immunohistochemical analysis in all the analysed organs: brain 3/3, trachea 3/3, lung 3/3, intestine 3/3, heart 3/3, which confirmed the systemic infection. The phylogenetic analyses of the virus showed a close genetic relationship with the H5N1 viruses of Asian origin, isolated in 2012 and 2013, belonging to the clade 2.3.2.1c. The HA-gene genetically clusters with HPAI H5N1 viruses isolated from wild pelicans in Romania and Bulgaria, thereby demonstrating the link between wild and domestic birds in the epidemiology of avian influenza. The contact between the affected chickens and migrating water birds over Bulgaria’s territory was suspected as a reason for the outbreak in the backyard farm. In addition, the detection of the virus in wild bird populations in Bulgaria three days earlier strongly supports the hypothesis of migrating wild birds spreading HPAI H5N1.
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ANDREOPOULOU (Μ. ΑΝΔΡΕΟΠΟΥΛΟΥ), M., V. TSIOURIS (Β. ΤΣΙΟΥΡΗΣ), I. GEORGOPOULOU (Ι. ΓΕΩΡΓΟΠΟΥΛΟΥ), and E. PAPADOPOULOS (Η.ΠΑΠΑΔΟΠΟΥΛΟΣ). "Case of syngamosis in partridges of a backyard farm." Journal of the Hellenic Veterinary Medical Society 62, no. 4 (November 13, 2017): 327. http://dx.doi.org/10.12681/jhvms.14863.
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Sick and dead 2-months-old partridges (Alectoris chukar) were presented to the unit of Avian Medicine, Faculty of Veterinary Medicine, Aristotle University of Thessaloniki, Greece. The birds were reared at a specially constructed wire cage, which covered 600 m2 of the ground, including self-growing flora, in the region of Diavata, in the countryside of Thessaloniki. The farm consisted of young partridges, adult pheasants and wild passerines. Two months after placing the birds, 5 partridges were found dead. During the clinical examination of the submitted sick partridges, severe respiratory distress was observed, while some birds had anemic combs and others were breathing with open beaks and had their necks stretched. The necropsy revealed the presence of numerous gapeworms in the lumen of the trachea, forming the typical " Y" shape, since male and female Syngamus trachea are locked in copulation. The mucosa of trachea was, also, thickened, irritated and congested. No lesions to other organs were observed and the microbiological examination of liver, spleen and air-sacs samples was negative. Meanwhile, faecal samples were collected from the farm for parasitological examination. A sedimentation method was used and eggs of S. trachea were found. Syngamosis was determined to be the cause of the partridges' death. The gapeworms are considered potentially dangerous, especially for backyard, game-birds and free-living birds, while the control of the disease is complicated. This fact, along with the selective appearance of the clinical signs and the mortality only in the partridges of the farm are the remarkable points discussed in this article.
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Dolka, I., R. Sapierzyński, W. Bielecki, E. Malicka, A. Żbikowski, and P. Szeleszczuk. "Histopathology in diagnosis of broiler chicken and layer diseases – review of cases 1999-2010." Polish Journal of Veterinary Sciences 15, no. 4 (December 1, 2012): 773–79. http://dx.doi.org/10.2478/v10181-012-0117-0.
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Abstract The aim of this study was to estimate the prevalence of histopathological lesions in the different organs in relation to the commercial-type and the age of birds (i.e. broiler chickens and layers). During the period 1999-2010 a total of 189 cases was submitted to the Division of Animal Pathomorphology, Department of Pathology and Veterinary Diagnostics at WULS. Most cases were found in broiler chickens (66.7%). The majority of the histopathological lesions were detected in the liver and lymphoid organs. In of 29% cases of hepatic injury pathognomonic lesions associated with inclusion body hepatitis (IBH) were found. The mean age of birds was 23 days. Among IBH cases proventriculitis (58%) was more often found than gizzard lesions (25.8%). Interestingly, we noted some intranuclear inclusions in the epithelial cells within the proventriculus. A low percentage of histopathological evidence of infectious bursal disease (IBD) was reported in chickens. The gastrointestinal tract was the second most frequent predilection site for histopathological lesions. Histopathological findings within the heart and lungs were less common and were more often seen in the upper respiratory tract. Cases of infectious laryngotracheitis (ILT) were registered in broiler chickens (3.2%, mean age 37 days) and in layers (4.8%; mean age 196 days). Lesions associated with Marek’s disease, avian leukosis and fowl pox were recognized only in layers, respectively in 3.2% (mean age 176 days), 1.6% (mean age 205 days) and 1.1% (mean age 196 days) of all cases. Avian encephalomyelitis (AE) was noted only in 0.5% of all cases.
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Baloch, Abdul latif. "Prevalence of Multiple Drug Resistance among Avian Pathogenic E. coli Isolates from Commercial Poultry." Pak-Euro Journal of Medical and Life Sciences 2, no. 4 (April 3, 2020): 83–88. http://dx.doi.org/10.31580/pjmls.v2i4.1168.
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Infections associated with Avian Pathogenic E. coli are responsible for huge economic losses for poultry industry worldwide. Particularly, its association with colibacillosis, a complex syndrome which is characterized by lesions of multiple organs i.e. peritonitis, pericarditis, air Sacculitis, osteomyelitis, salpingitis and yolk sac infections is responsible for high mortality and morbidity. Moreover, it causes respiratory tract infections among poultry birds, followed by septicaemia. Liver samples were collected from commercial poultry birds from the various retail shops located in Peshawar City. Bacteria were identified by biochemical and molecular methods. Out of all the tested isolates n=85, 98% were identified as Avian Pathogenic E. coli (APEC). Identified APEC samples were further tested against 23 different antibiotics including amoxicillin (89.40%), levofloxacin (62.40%), ciprofloxacin (71.80%), tobramycin (14.10%), gentamycin (34.10%),neomycin (53.00%), streptomycin (81.00%), tigecyclines (0.00%), oxytetracyclines (96.50%), doxycycline (61.20%), nitrofurantoin (1.00%), chloramphenicol (63.50%), cefixime (7%), cefepime (4.70%), ceftazidime (8.30%), cefotaxime (8.00%), cephalothin (43.50%), trimethoprim, sulfamethoxazole (77.60%), lincomycin (100%), augmentin (4.70%), carbapenem (4%) and polymyxin B (15%). Out of all n=85 isolates 99.9% were multi-drug resistant. Furthermore, ESBL encoding TEM, OXA, SHV were detected in following percentages 53.60%, 19.50%, 9.70% respectively genes.
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Zitzow, Lois A., Thomas Rowe, Timothy Morken, Wun-Ju Shieh, Sherif Zaki, and Jacqueline M. Katz. "Pathogenesis of Avian Influenza A (H5N1) Viruses in Ferrets." Journal of Virology 76, no. 9 (May 1, 2002): 4420–29. http://dx.doi.org/10.1128/jvi.76.9.4420-4429.2002.
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ABSTRACT Highly pathogenic avian influenza A H5N1 viruses caused outbreaks of disease in domestic poultry and humans in Hong Kong in 1997. Direct transmission of the H5N1 viruses from birds to humans resulted in 18 documented cases of respiratory illness, including six deaths. Here we evaluated two of the avian H5N1 viruses isolated from humans for their ability to replicate and cause disease in outbred ferrets. A/Hong Kong/483/97 virus was isolated from a fatal case and was highly pathogenic in the BALB/c mouse model, whereas A/Hong Kong/486/97 virus was isolated from a case with mild illness and exhibited a low-pathogenicity phenotype in mice. Ferrets infected intranasally with 107 50% egg infectious doses (EID50) of either H5N1 virus exhibited severe lethargy, fever, weight loss, transient lymphopenia, and replication in the upper and lower respiratory tract, as well as multiple systemic organs, including the brain. Gastrointestinal symptoms were seen in some animals. In contrast, weight loss and severe lethargy were not noted in ferrets infected with 107 EID50 of two recent human H3N2 viruses, although these viruses were also isolated from the brains, but not other extrapulmonary organs, of infected animals. The results demonstrate that both H5N1 viruses were highly virulent in the outbred ferret model, unlike the differential pathogenicity documented in inbred BALB/c mice. We propose the ferret as an alternative model system for the study of these highly pathogenic avian viruses.
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Chen, Hualan, Yanbing Li, Zejun Li, Jianzhong Shi, Kyoko Shinya, Guohua Deng, Qiaoling Qi, et al. "Properties and Dissemination of H5N1 Viruses Isolated during an Influenza Outbreak in Migratory Waterfowl in Western China." Journal of Virology 80, no. 12 (June 15, 2006): 5976–83. http://dx.doi.org/10.1128/jvi.00110-06.
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ABSTRACT H5N1 influenza A viruses are widely distributed among poultry in Asia, but until recently, only a limited number of wild birds were affected. During late April through June 2005, an outbreak of H5N1 virus infection occurred among wild birds at Qinghai Lake in China. Here, we describe the features of this outbreak. First identified in bar-headed geese, the disease soon spread to other avian species populating the lake. Sequence analysis of 15 viruses representing six avian species and collected at different times during the outbreak revealed four different H5N1 genotypes. Most of the isolates possessed lysine at position 627 in the PB2 protein, a residue known to be associated with virulence in mice and adaptation to humans. However, neither of the two index viruses possessed this residue. All of the viruses tested were pathogenic in mice, with the exception of one index virus. We also tested the replication of two viruses isolated during the Qinghai Lake outbreak and one unrelated duck H5N1 virus in rhesus macaques. The Qinghai Lake viruses did not replicate efficiently in these animals, producing no evidence of disease other than transient fever, while the duck virus replicated in multiple organs and caused symptoms of respiratory illness. Importantly, H5N1 viruses isolated in Mongolia, Russia, Inner Mongolia, and the Liaoning Province of China after August 2005 were genetically closely related to one of the genotypes isolated during the Qinghai outbreak, suggesting the dominant nature of this genotype and underscoring the need for worldwide intensive surveillance to minimize its devastating consequences.
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Al Rawashdeh, M. S. M. "Immunohistochemical and clinical changes in the respiratory tract of chickens, naturally infected with the fowlpox virus." Regulatory Mechanisms in Biosystems 8, no. 2 (April 23, 2017): 271–76. http://dx.doi.org/10.15421/021742.
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It is clear that currently the question of study of the pathological changes in the respiratory tract of chickens due to the impact of the fowlpox virus remains relevant, as the pathogenesis of nutritional deficiency, the presence of mycotoxins or the papilloma virus are characterized by the same clinical manifestations. We analyzed 88 chickens, naturally infected with the fowlpox virus, using clinical and immunohistochemical methods of investigation. Among all species of birds, we studied only chickens, data on which were collected for five years from veterinary clinics. The investigation revealed lesions basically characterized by the presence of changes in the typical structure of the chicken’s respiratory tract. As a result, we found clear criteria for the pathological process in the respiratory tract of chickens, which are typical for fowlpox. Thus, we discovered respiratory tract obstruction, as well as many intracytoplasmic pale eosinophilic inclusions in hyperplastic cells. We found an accumulation of mononuclear cells consisting mainly of macrophages, lymphocytes, plasma and mononuclear cells inside the mucous and muscle membranes. Bronchial lumens were blocked by necrotic and desquamated epithelial cells, red blood cells, bacterial colonies and amorphous eosinophilic material. We found accumulations of lymphocytes and macrophages in the parenchyma of the lungs. The hyperplastic epithelial cells reacted immunohistochemically with antibodies against the fowlpox virus in the respiratory tract. Immunoreaction occurred mainly in the cytoplasm of infected cells, inclusions, and necrotic and desquamated cells. The study proved immunohistochemical methods of investigation can be a useful additional tool for establishing a final diagnosis, especially in acute and subacute phases of the disease. The following respiratory signs were observed in severe cases of fowlpox: damage to the lungs in 33 cases (46.5%), parabronchium – 20 (28.2%), parabronchial connective tissue – 8 (11.3%), and mucous membrane of the larynx and trachea – 10 (14.1%). In mild and moderate cases of fowlpox, the following respiratory signs were observed: hyperemia and thickening of the mucous membrane of the trachea – 14 (82.4%), as well as hyperemia in the nasal conchae and paranasal sinuses – 3 (17.7%). In the future, it will be necessary to conduct deeper studies to detect pathological manifestations of this disease, not only in the respiratory tract, but also in other organs and systems of chickens.
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Dancovych, R. S., and I. S. Kolyada. "Патоморфологія аспергільозу полярних сов (Bubo scandiacus)." Scientific Messenger of LNU of Veterinary Medicine and Biotechnologies 19, no. 73 (February 3, 2017): 50–54. http://dx.doi.org/10.15421/nvlvet7311.
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This article describes pathomorphological changes developing on the conditions of aspergillosis polar owls. Research Proven to 6 polar sovah (Bubo scandiacus), which are kept at home. Dissection of birds that died were carried out by Shor. Internal organs were removed only Organocomplexes, keeping their anatomical and physiological relationships. When opening the selected material for histological examination. Fixation of the pieces performed in 10% neutral formalin solution. Histozrizy sleigh made using microtome, stained with hematoxylin-eosin, methylene green and pironinom by brush. The diagnosis is established complex, based on history, clinical signs of the analysis, the results of postmortem (including histological) study. During the autopsy the most pronounced structural changes found in respiratory organs. In the pneumatic bags and lungs vizualizuvalys multiple granulomas white and yellow compacted consistency. Form asperhiloznyh preferably concentric lesions, hudzykopodibna. Some granulomas in its center containing necrotic mass. Often found conglomerates asperhiloznyh knots. Affected pneumatic bags are thick, dense (because of diffuse proliferation of connective tissue), delayed on the surface of fibrin. Often asperhilozni granuloma located on the thick connective tissue stem. For histological examination revealed that the center was located granulomas significant number of sero-fibrinous fluid that infiltrated abundant histiocytes, poorly lymphoid elements. On the periphery vizualizuvalys lymphocytes, and plasma cells psevdoeozynofily, fibroblasts. In the center of «mature» asperhiloznyh granulomas develop pronounced necrotic changes. Around hyperemic vessels developed peryvazalni pronounced swelling. In addition, the bags found povitryanosnyh sclerotic changes (increase of fibroblast proliferation and connective tissue), and in the lungs - perifocal sero-fibrinous pneumonia. In the small intestine recorded acute catarrhal or hemorrhagic inflammation. Also showed signs of intoxication (dystrophic and necrotic changes in hepatocytes and nefrotsytiv), general anemia, cardiovascular and pulmonary disease.
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Lazar, Veronica, and Petronela Ancuta. "SARS-CoV-2 - SYNOPTIC CHART OF THE MAIN CHARACTERISTICS OF VIRUS, PATHOGENESIS, IMMUNE RESPONSE, IMMUNOPROPHYLAXIS." Romanian Archives of Microbiology and Immunology 80, no. 1 (March 30, 2021): 51–80. http://dx.doi.org/10.54044/rami.2021.01.07.
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Coronaviruses (CoVs) are viruses of zoonotic origin, transmitted from person to person mainly via the respiratory tract. Seven types of CoVs have succeeded in making the leap from animals to humans. Among them, four produce the common cold, while the other three, more recently emerged CoVs, cause the Severe Acute Respiratory Syndrome (SARS) and exhibit a high epidemic/pandemic potential: SARS-CoV, Middle East Respiratory Syndrome (MERS)-CoV, and SARS-CoV-2. The new SARS-CoV-2 is the etiological agent of the current and unprecedented pandemic, associated with a unique pathology named Corona-virus Disease 2019 (COVID-19). These viruses belong to the Coronaviridae family - classified by ICTV (International Committee for Taxonomy of Viruses) in the fourth Class, that of enveloped viruses with a positive-strand RNA genome, infectious for both birds and mammals. As an airborne pathogen, its high infectivity is intensified by the widespread expression of its specific entry receptors (ACE-2, TMPRSS2) in various human organs and tissues, SARS-CoV-2 has spread rapidly from China throughout the whole world, causing numerous infections (approximately 128 million), with a relatively high lethality (approximately 2.8 million). The particular feature of the severe evolution of the SARS-CoV-2 infection is its association with Respiratory Distress Syndrome (ARDS) and Systemic Inflammatory Response Syndrome (SIRS), mainly in older patients or those with comorbidities. In the absence of a standard therapeutic protocol, the medical systems worldwide have been challenged to continuously improve the COVID-19 treatment, based on emerging data from rapidly initiated clinical trials. At the same time, specialists in virology, immunology, and vaccinology have collaborated at an unprecedented pace to design and implement effective SARS-CoV-2 vaccines. In this review we highlight the most important advances made in understanding the characteristics of SARS-CoV-2, including the viral replication cycle, as well as COVID-19 pathogenesis, immune responses mounted by the host following natural infection (with various forms, from moderate to severe and lethal ones) and vaccines.
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Skovgaard, Nini, and Kenneth R. Olson. "Hydrogen sulfide mediates hypoxic vasoconstriction through a production of mitochondrial ROS in trout gills." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 303, no. 5 (September 1, 2012): R487—R494. http://dx.doi.org/10.1152/ajpregu.00151.2012.
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Hypoxic pulmonary vasoconstriction (HPV) is an adaptive response that diverts pulmonary blood flow from poorly ventilated and hypoxic areas of the lung to more well-ventilated parts. This response is important for the local matching of blood perfusion to ventilation and improves pulmonary gas exchange efficiency. HPV is an ancient and highly conserved response, expressed in the respiratory organs of all vertebrates, including lungs of mammals, birds, and reptiles; amphibian skin; and fish gills. The mechanism underlying HPV and how cells sense low Po2 remains elusive. In perfused trout gills ( Oncorhynchus mykiss), acute hypoxia, as well as H2S, caused an initial and transient constriction of the vasculature. Inhibition of the enzymes cystathionine-β-synthase and cystathionine-γ-lyase, which blocks H2S production, abolished the hypoxic response. Individually blocking the four complexes in the electron transport chain abolished both the hypoxic and the H2S-mediated constriction. Glutathione, an antioxidant and scavenger of superoxide, attenuated the vasoconstriction in response to hypoxia and H2S. Furthermore, diethyldithiocarbamate, an inhibitor of superoxide dismutase, attenuated the hypoxic and H2S constriction. This strongly suggests that H2S mediates the hypoxic vasoconstriction in trout gills. H2S may stimulate the mitochondrial production of superoxide, which is then converted to hydrogen peroxide (H2O2). Thus, H2O2 may act as the “downstream” signaling molecule in hypoxic vasoconstriction.
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Tumanov, V. "Діазинон. Основні аспекти біологічної дії, токсикологічні властивості та патоморфологія отруєнь." Scientific Messenger of LNU of Veterinary Medicine and Biotechnologies 19, no. 77 (March 5, 2017): 131–36. http://dx.doi.org/10.15421/nvlvet7729.
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The article represents data on chemical properties and main aspects of the biological action of the diazinon - organophosphate pesticide that is widely used as a drug with marked acaricidal and insecticidal properties. Analyzed published data on metabolism, diazinon accumulation in various organs and systems, and ways of removing from the body. The article shows the median lethal dose (LD50) diazinon for various kinds of animals. The special features of the pathogenesis of poisoning, the main mechanism of action of toxic organophosphorus pesticides is the phosphorylation and inhibition of acetylcholinesterase, resulting in a marked accumulation of acetylcholine in the cholinergic synapses, excessive stimulation of nerves and muscles, disruption passage of nerve impulses. The article detailed the clinical signs of acute poisoning by organophosphate compounds. These data indicate that the effects on the body organophosphorus pesticides includes muscarinic effects (sialorrhea and excessive secretion of sweat glands, bronchorrhea, increased motility of the gastrointestinal tract, accompanied by spastic contractions of the intestinal wall, vomiting and gastroenteritis), nicotine action (miofibrillation, rigidity pectoral muscles, paralysis of respiratory muscles with the development of sudden hypoxemia) and central effects (arising from the impact of the central nervous system and are accompanied by violation of its function). The analysis pathmorphology of poisoning of the organophosphate pesticide. These data indicate that structural changes diazinon poisoning is less specific than clinical signs and characterized by: the development of the circulatory disorders (acute congestive hyperemia recorded and hemorrhage), the appearance of dystrophic and necrotic changes parenchymal elements of the brain and spinal cord, liver, kidneys and so on. Also recorded alterations changes ganglion cells and spinal cord autonomic ganglion, proliferation of glial cells, and for subacute and chronic poisoning – disintegration of the myelin and nerve fibers axial cylinder. Described diazinon influence on organs of the immune system and ability to induce endocrine disorders. There are published data on the potential mutagenic, carcinogenic and teratogenic effects of the diazinon. The range of problems researd structural changes by the origin and development of clinical evidence for the effect of different doses diazinon and certain aspects of forensic veterinary diagnostic poisoning mammals and birds of organophosphate pesticides.
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Edenborough, Kathryn M., Suzanne Lowther, Karen Laurie, Manabu Yamada, Fenella Long, John Bingham, Jean Payne, et al. "Predicting Disease Severity and Viral Spread of H5N1 Influenza Virus in Ferrets in the Context of Natural Exposure Routes." Journal of Virology 90, no. 4 (December 9, 2015): 1888–97. http://dx.doi.org/10.1128/jvi.01878-15.
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ABSTRACTAlthough avian H5N1 influenza virus has yet to develop the capacity for human-to-human spread, the severity of the rare cases of human infection has warranted intensive follow-up of potentially exposed individuals that may require antiviral prophylaxis. For countries where antiviral drugs are limited, the World Health Organization (WHO) has developed a risk categorization for different levels of exposure to environmental, poultry, or human sources of infection. While these take into account the infection source, they do not account for the likely mode of virus entry that the individual may have experienced from that source and how this could affect the disease outcome. Knowledge of the kinetics and spread of virus after natural routes of exposure may further inform the risk of infection, as well as the likely disease severity. Using the ferret model of H5N1 infection, we compared the commonly used but artificial inoculation method that saturates the total respiratory tract (TRT) with virus to upper respiratory tract (URT) and oral routes of delivery, those likely to be encountered by humans in nature. We show that there was no statistically significant difference in survival rate with the different routes of infection, but the disease characteristics were somewhat different. Following URT infection, viral spread to systemic organs was comparatively delayed and more focal than after TRT infection. By both routes, severe disease was associated with early viremia and central nervous system infection. After oral exposure to the virus, mild infections were common suggesting consumption of virus-contaminated liquids may be associated with seroconversion in the absence of severe disease.IMPORTANCERisks for human H5N1 infection include direct contact with infected birds and frequenting contaminated environments. We used H5N1 ferret infection models to show that breathing in the virus was more likely to produce clinical infection than swallowing contaminated liquid. We also showed that virus could spread from the respiratory tract to the brain, which was associated with end-stage disease, and very early viremia provided a marker for this. With upper respiratory tract exposure, infection of the brain was common but hard to detect, suggesting that human neurological infections might be typically undetected at autopsy. However, viral spread to systemic sites was slower after exposure to virus by this route than when virus was additionally delivered to the lungs, providing a better therapeutic window. In addition to exposure history, early parameters of infection, such as viremia, could help prioritize antiviral treatments for patients most at risk of succumbing to infection.
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Mumford, Elizabeth, Jennifer Bishop, Saskia Hendrickx, Peter Ben Embarek, and Michael Perdue. "Avian Influenza H5N1: Risks at the Human–Animal Interface." Food and Nutrition Bulletin 28, no. 2_suppl2 (June 2007): S357—S363. http://dx.doi.org/10.1177/15648265070282s215.
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Background Great concern has arisen over the continued infection of humans with highly pathogenic avian influenza (HPAI) of the H5N1 subtype. Ongoing human exposure potentially increases the risk that a pandemic virus strain will emerge that is easily transmissible among humans. Although the pathogenicity of a pandemic strain cannot be predicted, the high mortality seen in documented H5N1 human infections thus far has raised the level of concern. Objectives To define the three types of influenza that can affect humans, discuss potential exposure risks at the human–animal interface, and suggest ways to reduce exposure and help prevent development of a pandemic virus. Methods This review is based on data and guidelines available from the World Health Organization, the scientific literature, and official governmental reports. Results Epidemiological data on human exposure risk are generally incomplete. Transmission of HPAI to humans is thought to occur through contact with respiratory secretions, feces, contaminated feathers, organs, and blood from live or dead infected birds and possibly from contaminated surfaces. Consumption of properly cooked poultry and eggs is not thought to pose a risk. Use of antiviral containment and vaccination may protect against development of a pandemic. Conclusions To most effectively decrease the risk of a pandemic, the public health and animal health sectors—those which are responsible for protecting and improving the health of humans and animals, respectively—must collaborate to decrease human exposure to HPAI virus, both by controlling virus circulation among poultry and by assessing the risks of human exposure to avian influenza virus at the human—animal interface from primary production through consumption of poultry and poultry products, and implementing risk-based mitigation measures.
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Gao, Peng, Shinji Watanabe, Toshihiro Ito, Hideo Goto, Krisna Wells, Martha McGregor, A. James Cooley, and Yoshihiro Kawaoka. "Biological Heterogeneity, Including Systemic Replication in Mice, of H5N1 Influenza A Virus Isolates from Humans in Hong Kong." Journal of Virology 73, no. 4 (April 1, 1999): 3184–89. http://dx.doi.org/10.1128/jvi.73.4.3184-3189.1999.
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ABSTRACT An H5N1 avian influenza A virus was transmitted to humans in Hong Kong in 1997. Although the virus causes systemic infection and is highly lethal in chickens because of the susceptibility of the hemagglutinin to furin and PC6 proteases, it is not known whether it also causes systemic infection in humans. The clinical outcomes of infection in Hong Kong residents ranged widely, from mild respiratory disease to multiple organ failure leading to death. Therefore, to understand the pathogenesis of influenza due to these H5N1 isolates, we investigated their virulence in mice. The results identified two distinct groups of viruses: group 1, for which the dose lethal for 50% of mice (MLD50) was between 0.3 and 11 PFU, and group 2, for which the MLD50 was more than 103 PFU. One day after intranasal inoculation of mice with 100 PFU of group 1 viruses, the virus titer in lungs was 107 PFU/g or 3 log units higher than that for group 2 viruses. Both types of viruses had replicated to high titers (>106 PFU/g) in the lungs by day 3 and maintained these titers through day 6. More importantly, only the group 1 viruses caused systemic infection, replicating in nonrespiratory organs, including the brain. Immunohistochemical analysis demonstrated the replication of a group 1 virus in brain neurons and glial cells and in cardiac myofibers. Phylogenetic analysis of all viral genes showed that both groups of Hong Kong H5N1 viruses had formed a lineage distinct from those of other viruses and that genetic reassortment between H5N1 and H1 or H3 human viruses had not occurred. Since mice and humans harbor both the furin and the PC6 proteases, we suggest that the virulence mechanism responsible for the lethality of influenza viruses in birds also operates in mammalian hosts. The failure of some H5N1 viruses to produce systemic infection in our model indicates that multiple, still-to-be-identified, factors contribute to the severity of H5N1 infection in mammals. In addition, the ability of these viruses to produce systemic infection in mice and the clear differences in pathogenicity among the isolates studied here indicate that this system provides a useful model for studying the pathogenesis of avian influenza virus infection in mammals.
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Govorkova, Elena A., Jerold E. Rehg, Scott Krauss, Hui-Ling Yen, Yi Guan, Malik Peiris, Tien D. Nguyen, et al. "Lethality to Ferrets of H5N1 Influenza Viruses Isolated from Humans and Poultry in 2004." Journal of Virology 79, no. 4 (February 15, 2005): 2191–98. http://dx.doi.org/10.1128/jvi.79.4.2191-2198.2005.
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ABSTRACT The 2004 outbreaks of H5N1 influenza viruses in Vietnam and Thailand were highly lethal to humans and to poultry; therefore, newly emerging avian influenza A viruses pose a continued threat, not only to avian species but also to humans. We studied the pathogenicity of four human and nine avian H5N1/04 influenza viruses in ferrets (an excellent model for influenza studies). All four human isolates were fatal to intranasally inoculated ferrets. The human isolate A/Vietnam/1203/04 (H5N1) was the most pathogenic isolate; the severity of disease was associated with a broad tissue tropism and high virus titers in multiple organs, including the brain. High fever, weight loss, anorexia, extreme lethargy, and diarrhea were observed. Two avian H5N1/04 isolates were as pathogenic as the human viruses, causing lethal systemic infections in ferrets. Seven of nine H5N1/04 viruses isolated from avian species caused mild infections, with virus replication restricted to the upper respiratory tract. All chicken isolates were nonlethal to ferrets. A sequence analysis revealed polybasic amino acids in the hemagglutinin connecting peptides of all H5N1/04 viruses, indicating that multiple molecular differences in other genes are important for a high level of virulence. Interestingly, the human A/Vietnam/1203/04 isolate had a lysine substitution at position 627 of PB2 and had one to eight amino acid changes in all gene products except that of the M1 gene, unlike the A/chicken/Vietnam/C58/04 and A/quail/Vietnam/36/04 viruses. Our results indicate that viruses that are lethal to mammals are circulating among birds in Asia and suggest that pathogenicity in ferrets, and perhaps humans, reflects a complex combination of different residues rather than a single amino acid difference.
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Lee, Chang-Won, David L. Suarez, Terrence M. Tumpey, Haan-Woo Sung, Yong-Kuk Kwon, Youn-Jeong Lee, Jun-Gu Choi, et al. "Characterization of Highly Pathogenic H5N1 Avian Influenza A Viruses Isolated from South Korea." Journal of Virology 79, no. 6 (March 15, 2005): 3692–702. http://dx.doi.org/10.1128/jvi.79.6.3692-3702.2005.
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ABSTRACT An unprecedented outbreak of H5N1 highly pathogenic avian influenza (HPAI) has been reported for poultry in eight different Asian countries, including South Korea, since December 2003. A phylogenetic analysis of the eight viral genes showed that the H5N1 poultry isolates from South Korea were of avian origin and contained the hemagglutinin and neuraminidase genes of the A/goose/Guangdong/1/96 (Gs/Gd) lineage. The current H5N1 strains in Asia, including the Korean isolates, share a gene constellation similar to that of the Penfold Park, Hong Kong, isolates from late 2002 and contain some molecular markers that seem to have been fixed in the Gs/Gd lineage virus since 2001. However, despite genetic similarities among recent H5N1 isolates, the topology of the phylogenetic tree clearly differentiates the Korean isolates from the Vietnamese and Thai isolates which have been reported to infect humans. A representative Korean isolate was inoculated into mice, with no mortality and no virus being isolated from the brain, although high titers of virus were observed in the lungs. The same isolate, however, caused systemic infections in chickens and quail and killed all of the birds within 2 and 4 days of intranasal inoculation, respectively. This isolate also replicated in multiple organs and tissues of ducks and caused some mortality. However, lower virus titers were observed in all corresponding tissues of ducks than in chicken and quail tissues, and the histological lesions were restricted to the respiratory tract. This study characterizes the molecular and biological properties of the H5N1 HPAI viruses from South Korea and emphasizes the need for comparative analyses of the H5N1 isolates from different countries to help elucidate the risk of a human pandemic from the strains of H5N1 HPAI currently circulating in Asia.
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Najimudeen, Shahnas M., Mohamed S. H. Hassan, Dayna Goldsmith, Davor Ojkic, Susan C. Cork, Martine Boulianne, and Mohamed Faizal Abdul-Careem. "Molecular Characterization of 4/91 Infectious Bronchitis Virus Leading to Studies of Pathogenesis and Host Responses in Laying Hens." Pathogens 10, no. 5 (May 19, 2021): 624. http://dx.doi.org/10.3390/pathogens10050624.
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Infectious bronchitis virus (IBV) initially establishes the infection in the respiratory tract and then spreads to other tissues depending on its virulence. During 2011–2018, the 4/91 IBV strain was isolated from poultry flocks affected by decreased egg production and quality in Eastern Canada. One of the Canadian 4/91 IBV isolates, IBV/Ck/Can/17-038913, was propagated in embryonated chicken eggs and molecularly characterized using whole genome sequencing. An in vivo study in laying hens was conducted to observe if IBV/Ck/Can/17-038913 isolate affects the egg production and quality. Hens were infected with IBV/Ck/Can/17-038913 isolate during the peak of egg lay, using a standard dose and routes maintaining uninfected controls. Oropharyngeal and cloacal swabs were collected at predetermined time points for the quantification of IBV genome loads. At 6 and 10 days post-infection, hens were euthanized to observe the lesions in various organs and collect blood and tissue samples for the quantification of antibody response and IBV genome loads, respectively. Egg production was not impacted during the first 10 days following infection. No gross lesions were observed in the tissues of the infected birds. The IBV genome was quantified in swabs, trachea, lung, proventriculus, cecal tonsils, kidney, and reproductive tissues. The serum antibody response against IBV was quantified in infected hens. In addition, histological changes, and recruitment of immune cells, such as macrophages and T cell subsets in kidney tissues, were measured. Overall, data show that IBV/Ck/Can/17-038913 isolate is not associated with egg production issues in laying hens infected at the peak of lay, while it demonstrates various tissue tropism, including kidney, where histopathological lesions and immune cell recruitments were evident.
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Pulit-Penaloza, Joanna A., Xiangjie Sun, Hannah M. Creager, Hui Zeng, Jessica A. Belser, Taronna R. Maines, and Terrence M. Tumpey. "Pathogenesis and Transmission of Novel Highly Pathogenic Avian Influenza H5N2 and H5N8 Viruses in Ferrets and Mice." Journal of Virology 89, no. 20 (July 29, 2015): 10286–93. http://dx.doi.org/10.1128/jvi.01438-15.
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ABSTRACTA novel highly pathogenic avian influenza (HPAI) H5N8 virus, first detected in January 2014 in poultry and wild birds in South Korea, has spread throughout Asia and Europe and caused outbreaks in Canada and the United States by the end of the year. The spread of H5N8 and the novel reassortant viruses, H5N2 and H5N1 (H5Nx), in domestic poultry across multiple states in the United States pose a potential public health risk. To evaluate the potential of cross-species infection, we determined the pathogenicity and transmissibility of two Asian-origin H5Nx viruses in mammalian animal models. The newly isolated H5N2 and H5N8 viruses were able to cause severe disease in mice only at high doses. Both viruses replicated efficiently in the upper and lower respiratory tracts of ferrets; however, the clinical symptoms were generally mild, and there was no evidence of systemic dissemination of virus to multiple organs. Moreover, these influenza H5Nx viruses lacked the ability to transmit between ferrets in a direct contact setting. We further assessed viral replication kinetics of the novel H5Nx viruses in a human bronchial epithelium cell line, Calu-3. Both H5Nx viruses replicated to a level comparable to a human seasonal H1N1 virus, but significantly lower than a virulent Asian-lineage H5N1 HPAI virus. Although the recently isolated H5N2 and H5N8 viruses displayed moderate pathogenicity in mammalian models, their ability to rapidly spread among avian species, reassort, and generate novel strains underscores the need for continued risk assessment in mammals.IMPORTANCEIn 2015, highly pathogenic avian influenza (HPAI) H5 viruses have caused outbreaks in domestic poultry in multiple U.S. states. The economic losses incurred with H5N8 and H5N2 subtype virus infection have raised serious concerns for the poultry industry and the general public due to the potential risk of human infection. This recent outbreak underscores the need to better understand the pathogenesis and transmission of these viruses in mammals, which is an essential component of pandemic risk assessment. This study demonstrates that the newly isolated H5N2 and H5N8 viruses lacked the ability to transmit between ferrets and exhibited low to moderate virulence in mammals. In human bronchial epithelial (Calu-3) cells, both H5N8 and H5N2 viruses replicated to a level comparable to a human seasonal virus, but significantly lower than a virulent Asian-lineage H5N1 (A/Thailand/16/2004) virus. The results of this study are important for the evaluation of public health risk.
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Suthers, Roderick, Franz Goller, and Carolyn Pytte. "The neuromuscular control of birdsong." Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences 354, no. 1385 (May 29, 1999): 927–39. http://dx.doi.org/10.1098/rstb.1999.0444.
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Birdsong requires complex learned motor skills involving the coordination of respiratory, vocal organ and craniomandibular muscle groups. Recent studies have added to our understanding of how these vocal subsystems function and interact during song production. The respiratory rhythm determines the temporal pattern of song. Sound is produced during expiration and each syllable is typically followed by a small inspiration, except at the highest syllable repetition rates when a pattern of pulsatile expiration is used. Both expiration and inspiration are active processes. The oscine vocal organ, the syrinx, contains two separate sound sources at the cranial end of each bronchus, each with independent motor control. Dorsal syringeal muscles regulate the timing of phonation by adducting the sound–generating labia into the air stream. Ventral syringeal muscles have an important role in determining the fundamental frequency of the sound. Different species use the two sides of their vocal organ in different ways to achieve the particular acoustic properties of their song. Reversible paralysis of the vocal organ during song learning in young birds reveals that motor practice is particularly important in late plastic song around the time of song crystallization in order for normal adult song to develop. Even in adult crystallized song, expiratory muscles use sensory feedback to make compensatory adjustments to perturbations of respiratory pressure. The stereotyped beak movements that accompany song appear to have a role in suppressing harmonics, particularly at low frequencies.
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Singh, Baljit, Chenzhong Fu, and Jahar Bhattacharya. "Vascular expression of the αvβ3-integrin in lung and other organs." American Journal of Physiology-Lung Cellular and Molecular Physiology 278, no. 1 (January 1, 2000): L217—L226. http://dx.doi.org/10.1152/ajplung.2000.278.1.l217.
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The expression of the αvβ3-integrin in nonproliferating vascular beds remains unclear. To determine possible organ-specific differences, we compared αvβ3-integrin expression in the lung and other organs. Paraffin-embedded tissue sections of lung, liver, brain, muscle and skin obtained from rats were processed for immunohistochemistry with a monoclonal (LM609) and a polyclonal antibody (AB1903) against the αvβ3-integrin. Immunogold electron microscopy was used to localize αvβ3-integrin in rat lung microvasculature. With the use of custom-designed primers, lung sections were subjected to in situ PCR in a thermal cycler to amplify αvor β3mRNA. To confirm specific amplification, PCR products were further hybridized in situ with an αvor β3cDNA probe. In the lung, the αvβ3-integrin protein as well as αvand β3mRNAs was extensively evident in the endothelium of extra-alveolar and alveolar microvessels, in vascular smooth muscle, and in large bronchial epithelium but not in the epithelium of alveolar ducts or alveoli. Ultrastructural immunogold labeling showed the presence of the integrin on the luminal and abluminal faces of the lung microvascular endothelium but not on the apical surface of the alveolar epithelium. Staining for the integrin was generally negative in blood vessels of several systemic organs, although weak staining was evident in branches of the hepatic portal vein. The constitutive presence of the αvand β3mRNAs and the αvβ3-integrin in the lung microvascular bed suggests that gene transcription for the integrin is ongoing in lung vessels. Because it binds vitronectin, the lung vascular αvβ3-integrin may play a role in ligation of bloodborne, vitronectin-containing macromolecular complexes formed in inflammation.
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Litvinov, A. S., A. V. Savin, A. A. Kukhtina, and D. A. Sitovskaya. "Pathogenesis of extrapulmonary organ damage in SARS-CоV-2 coronavirus infection (analytical review)." Nephrology (Saint-Petersburg) 25, no. 2 (February 13, 2021): 18–26. http://dx.doi.org/10.36485/1561-6274-2021-25-2-18-26.
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Over the past two decades, coronavirus infection has caused two major pandemics: SARS in 2002 and acute respiratory syndrome (MERS) in the Middle East in 2012. In December 2019, the novel coronavirus (CV) SARS-CoV-2 caused an outbreak of pneumonia in Wuhan, China. Experts from the World Health Organization (WHO) have confirmed the risk of this disease for the public health of the entire planet. SARS-CoV-2 was isolated from epithelial cells of the human respiratory tract. It was found that the genotype KB SARS-CoV-2 is closer to bat-SL-CoVZC45 and bat-SL-CoVZXC21, and the spike glycoprotein (SB) of the virus, which determines the ability to bind to the cellular receptor, is similar to the SARS-CoV coronavirus, which is responsible for the outbreak of severe acute respiratory syndrome (SARS / SARS) in 2002]. Angiotensin-converting enzyme 2 (ACE2) is an endogenous spike protein (spike glycoprotein with the S-domain) SARS-CoV-2, which, as part of the ACE2 + SARS-CoV-2 complex, binds to the ACE2 receptor located on the target cell membrane. The article discusses the mechanisms of infection with SARS-CoV-2, cell-cell interactions, and transmission routes. The issues of the epidemiology of COVID-19 and the prospects for the involvement of organs and systems other than the respiratory one in maintaining the viral load are covered in detail. The problems of the immune defense of the human body during infection with SARS-CoV-2 have been identified. Clinical parallels with progenitor viruses, namely SARS-CoV-1 and MERS-CoV, have been drawn. Highlighted risk factors for SARSCoV-2 infection, which make it possible to predict the nature of the course and probable outcomes of COVID-19.
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Mehmood, Sabba, Shaista Aslam, and Sidra Younis. "Expression Profile and Implications of ACE2; The Receptor for New SARS-CoV-2." Life and Science 1, supplement (December 23, 2020): 5. http://dx.doi.org/10.37185/lns.1.1.154.
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Expansion of novel coronavirus disease 2019 (COVID-19) involves various risk factors including clinical, genetic, demographic and environmental manifestation but they are insufficient to explain disease pathogenesis. With patients ranging from completely asymptomatic to many suffering mild to severe illness, indicates that COVID- 19 should better be studied at genetic level as different genetic backgrounds predispose to variability in infection susceptibility. Recently, it is recognized that severe acute respiratory syndrome coronavirus 2 (SARS- CoV-2) binds and internalized by the host cells through cell surface receptors angiotensin-converting enzyme 2 (ACE2), which is expressed significantly in variety of human tissues particularly in the lower and upper respiratory tract. To scrutinize the expression profiles and clinical implications of ACE2 gene in humans, literature was extensively reviewed. In common, various studies reported that ACE2 receptor protein is highly conserved among different species, the expression pattern is tissue specific mainly observed in cardiovascular system, breast cells, testis, adipose tissue, kidney, lymphocytes and gastrointestinal system other than the upper and lower respiratory tract. This significant expression makes these organs vulnerable to SARS-CoV-2 virus and hence many comorbidities may be observed during the course of infection. The present review on expression profile of ACE2 not only proposes potential clues for COVID-19 pathogenesis but also designate clinical values of ACE2 gene in heterogeneous disorders.
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Lobanova, O. A., D. S. Trusova, E. E. Rudenko, D. D. Protsenko, and E. A. Kogan. "Pathomorphology of a new coronavirus infection COVID-19." Siberian Journal of Clinical and Experimental Medicine 35, no. 3 (October 17, 2020): 47–52. http://dx.doi.org/10.29001/2073-8552-2020-35-3-47-52.
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On March 11, 2020, the World Health Organization declared COVID-19 apandemic. Despite a large number of scientific publications concerning the clinical picture and trea tment methods, data on structural changes of internal organs in COVID-19 is still insufficient. This review presents and analyzes several clinical cases published by research groups in various countries. COVID-19 infection is caused by a SARS-CoV-2 virus that binds to the angiotensin-converting enzyme 2 ACE2 receptor. Interaction with this receptor is the initial stage of pathogenesis. The morphological picture is similar to pneumonia caused by SARS-CoV and MERS-CoV: at the initial stage, a picture of shock lungs develops, later it ends in fibrosis and organizing pneumonia. One of the most severe complications is acute respiratory distress syndrome, which is observed in some clinical cases reviewed. In this article, we collected cases of clinical and morphological studies of patients with COVID-19, published in international peer-reviewed medical literature to date.
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Soto, María Elena, Verónica Guarner-Lans, Elizabeth Soria-Castro, Linaloe Manzano Pech, and Israel Pérez-Torres. "Is Antioxidant Therapy a Useful Complementary Measure for Covid-19 Treatment? An Algorithm for Its Application." Medicina 56, no. 8 (July 31, 2020): 386. http://dx.doi.org/10.3390/medicina56080386.
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Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) causes the corona virus disease-19 which is accompanied by severe pneumonia, pulmonary alveolar collapses and which stops oxygen exchange. Viral transmissibility and pathogenesis depend on recognition by a receptor in the host, protease cleavage of the host membrane and fusion. SARS-CoV-2 binds to the angiotensin converting enzyme 2 receptor. Here, we discuss the general characteristics of the virus, its mechanism of action and the way in which the mechanism correlates with the comorbidities that increase the death rate. We also discuss the currently proposed therapeutic measures and propose the use of antioxidant drugs to help patients infected with the SARS-CoV-2. Oxidizing agents come from phagocytic leukocytes such as neutrophils, monocytes, macrophages and eosinophils that invade tissue. Free radicals promote cytotoxicity thus injuring cells. They also trigger the mechanism of inflammation by mediating the activation of NFkB and inducing the transcription of cytokine production genes. Release of cytokines enhances the inflammatory response. Oxidative stress is elevated during critical illnesses and contributes to organ failure. In corona virus disease-19 there is an intense inflammatory response known as a cytokine storm that could be mediated by oxidative stress. Although antioxidant therapy has not been tested in corona virus disease-19, the consequences of antioxidant therapy in sepsis, acute respiratory distress syndrome and acute lung injury are known. It improves oxygenation rates, glutathione levels and strengthens the immune response. It reduces mechanical ventilation time, the length of stay in the intensive care unit, multiple organ dysfunctions and the length of stay in the hospital and mortality rates in acute lung injury/acute respiratory distress syndrome and could thus help patients with corona virus disease-19.
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Rodrigues, Rui, and Sofia Costa de Oliveira. "The Impact of Angiotensin-Converting Enzyme 2 (ACE2) Expression Levels in Patients with Comorbidities on COVID-19 Severity: A Comprehensive Review." Microorganisms 9, no. 8 (August 9, 2021): 1692. http://dx.doi.org/10.3390/microorganisms9081692.
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Angiotensin-Converting Enzyme 2 (ACE2) has been proved to be the main host cell receptor for the binding of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the virus responsible for the COVID-19 pandemic. The SARS-CoV-2 spike (S) protein binds to ACE2 to initiate the process of replication. This enzyme is widely present in human organ tissues, such as the heart and lung. The pathophysiology of ACE2 in SARS-CoV-2 infection is complex and may be associated with several factors and conditions that are more severe in COVID-19 patients, such as age, male gender, and comorbidities, namely, cardiovascular diseases, chronic respiratory diseases, obesity, and diabetes. Here we present a comprehensive review that aims to correlate the levels of expression of the ACE2 in patients with comorbidities and with a poor outcome in COVID-19 disease. Significantly higher levels of expression of ACE2 were observed in myocardial and lung tissues in heart failure and COPD patients, respectively. An age-dependent increase in SARS2-CoV-2 receptors in the respiratory epithelium may be also responsible for the increased severity of COVID-19 lung disease in elderly people. Although the role of ACE2 is highlighted regarding the damage that can arise upon the SARS-CoV-2 invasion, there was no association observed between renin-angiotensin-aldosterone system (RAAS) inhibitors and the severity of COVID-19.
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Gupta, Ishita, Balsam Rizeq, Eyad Elkord, Semir Vranic, and Ala-Eddin Al Moustafa. "SARS-CoV-2 Infection and Lung Cancer: Potential Therapeutic Modalities." Cancers 12, no. 8 (August 5, 2020): 2186. http://dx.doi.org/10.3390/cancers12082186.
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Human coronaviruses, especially SARS-CoV-2, are emerging pandemic infectious diseases with high morbidity and mortality in certain group of patients. In general, SARS-CoV-2 causes symptoms ranging from the common cold to severe conditions accompanied by lung injury, acute respiratory distress syndrome in addition to other organs’ destruction. The main impact upon SARS-CoV-2 infection is damage to alveolar and acute respiratory failure. Thus, lung cancer patients are identified as a particularly high-risk group for SARS-CoV-2 infection and its complications. On the other hand, it has been reported that SARS-CoV-2 spike (S) protein binds to angiotensin-converting enzyme 2 (ACE-2), that promotes cellular entry of this virus in concert with host proteases, principally transmembrane serine protease 2 (TMPRSS2). Today, there are no vaccines and/or effective drugs against the SARS-CoV-2 coronavirus. Thus, manipulation of key entry genes of this virus especially in lung cancer patients could be one of the best approaches to manage SARS-CoV-2 infection in this group of patients. We herein provide a comprehensive and up-to-date overview of the role of ACE-2 and TMPRSS2 genes, as key entry elements as well as therapeutic targets for SARS-CoV-2 infection, which can help to better understand the applications and capacities of various remedial approaches for infected individuals, especially those with lung cancer.
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Bande, Faruku, Siti Suri Arshad, Abdul Rahman Omar, Mohd Hair Bejo, Muhammad Salisu Abubakar, and Yusuf Abba. "Pathogenesis and Diagnostic Approaches of Avian Infectious Bronchitis." Advances in Virology 2016 (2016): 1–11. http://dx.doi.org/10.1155/2016/4621659.
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Infectious bronchitis (IB) is one of the major economically important poultry diseases distributed worldwide. It is caused by infectious bronchitis virus (IBV) and affects both galliform and nongalliform birds. Its economic impact includes decreased egg production and poor egg quality in layers, stunted growth, poor carcass weight, and mortality in broiler chickens. Although primarily affecting the respiratory tract, IBV demonstrates a wide range of tissues tropism, including the renal and reproductive systems. Thus, disease outcome may be influenced by the organ or tissue involved as well as pathotypes or strain of the infecting virus. Knowledge on the epidemiology of the prevalent IBV strains in a particular region is therefore important to guide control and preventions. Meanwhile previous diagnostic methods such as serology and virus isolations are less sensitive and time consuming, respectively; current methods, such as reverse transcription polymerase chain reaction (RT-PCR), Restriction Fragment Length Polymorphism (RFLP), and sequencing, offer highly sensitive, rapid, and accurate diagnostic results, thus enabling the genotyping of new viral strains within the shortest possible time. This review discusses aspects on pathogenesis and diagnostic methods for IBV infection.
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Maina, John N. "Development, structure, and function of a novel respiratory organ, the lung-air sac system of birds: to go where no other vertebrate has gone." Biological Reviews 81, no. 04 (October 12, 2006): 545. http://dx.doi.org/10.1017/s1464793106007111.
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Maina, John N. "Development, structure, and function of a novel respiratory organ, the lung-air sac system of birds: to go where no other vertebrate has gone." Biological Reviews 81, no. 4 (January 10, 2007): 545–79. http://dx.doi.org/10.1111/j.1469-185x.2006.tb00218.x.
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L. Perkins, L. E., and D. E. Swayne. "Pathobiology of A/Chicken/Hong Kong/220/97 (H5N1) Avian Influenza Virus in Seven Gallinaceous Species." Veterinary Pathology 38, no. 2 (March 2001): 149–64. http://dx.doi.org/10.1354/vp.38-2-149.
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Direct bird-to-human transmission, with the production of severe respiratory disease and human mortality, is unique to the Hong Kong-origin H5N1 highly pathogenic avian influenza (HPAI) virus, which was originally isolated from a disease outbreak in chickens. The pathobiology of the A/chicken/Hong Kong/ 220/97 (H5N1) (HK/220) HPAI virus was investigated in chickens, turkeys, Japanese and Bobwhite quail, guinea fowl, pheasants, and partridges, where it produced 75-100% mortality within 10 days. Depression, mucoid diarrhea, and neurologic dysfunction were common clinical manifestations of disease. Grossly, the most severe and consistent lesions included splenomegaly, pulmonary edema and congestion, and hemorrhages in enteric lymphoid areas, on serosal surfaces, and in skeletal muscle. Histologic lesions were observed in multiple organs and were characterized by exudation, hemorrhage, necrosis, inflammation, or a combination of these features. The lung, heart, brain, spleen, and adrenal glands were the most consistently affected, and viral antigen was most often detected by immunohistochemistry in the parenchyma of these organs. The pathogenesis of infection with the HK/220 HPAI virus in these species was twofold. Early mortality occurring at 1-2 days postinoculation (DPI) corresponded to severe pulmonary edema and congestion and virus localization within the vascular endothelium. Mortality occurring after 2 DPI was related to systemic biochemical imbalance, multiorgan failure, or a combination of these factors. The pathobiologic features were analogous to those experimentally induced with other HPAI viruses in domestic poultry.
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Norouzi, Mahnaz, Shaghayegh Norouzi, Alistaire Ruggiero, Mohammad S. Khan, Stephen Myers, Kylie Kavanagh, and Ravichandra Vemuri. "Type-2 Diabetes as a Risk Factor for Severe COVID-19 Infection." Microorganisms 9, no. 6 (June 3, 2021): 1211. http://dx.doi.org/10.3390/microorganisms9061211.
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The current outbreak caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), termed coronavirus disease 2019 (COVID-19), has generated a notable challenge for diabetic patients. Overall, people with diabetes have a higher risk of developing different infectious diseases and demonstrate increased mortality. Type 2 diabetes mellitus (T2DM) is a significant risk factor for COVID-19 progression and its severity, poor prognosis, and increased mortality. How diabetes contributes to COVID-19 severity is unclear; however, it may be correlated with the effects of hyperglycemia on systemic inflammatory responses and immune system dysfunction. Using the envelope spike glycoprotein SARS-CoV-2, COVID-19 binds to angiotensin-converting enzyme 2 (ACE2) receptors, a key protein expressed in metabolic organs and tissues such as pancreatic islets. Therefore, it has been suggested that diabetic patients are more susceptible to severe SARS-CoV-2 infections, as glucose metabolism impairments complicate the pathophysiology of COVID-19 disease in these patients. In this review, we provide insight into the COVID-19 disease complications relevant to diabetes and try to focus on the present data and growing concepts surrounding SARS-CoV-2 infections in T2DM patients.
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Fakhouri, Eddie W., Stephen J. Peterson, Janish Kothari, Ragin Alex, Joseph I. Shapiro, and Nader G. Abraham. "Genetic Polymorphisms Complicate COVID-19 Therapy: Pivotal Role of HO-1 in Cytokine Storm." Antioxidants 9, no. 7 (July 18, 2020): 636. http://dx.doi.org/10.3390/antiox9070636.
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Coronaviruses are very large RNA viruses that originate in animal reservoirs and include severe acute respiratory distress syndrome (SARS) and Middle East respiratory syndrome (MERS) and other inconsequential coronaviruses from human reservoirs like the common cold. SARS-CoV-2, the virus that causes COVID-19 and is believed to originate from bat, quickly spread into a global pandemic. This RNA virus has a special affinity for porphyrins. It invades the cell at the angiotensin converting enzyme-2 (ACE-2) receptor and binds to hemoproteins, resulting in a severe systemic inflammatory response, particularly in high ACE-2 organs like the lungs, heart, and kidney, resulting in systemic disease. The inflammatory response manifested by increased cytokine levels and reactive oxygen species results in inhibition of heme oxygenase (HO-1), with a subsequent loss of cytoprotection. This has been seen in other viral illness like human immunodeficiency virus (HIV), Ebola, and SARS/MERS. There are a number of medications that have been tried with some showing early clinical promise. This illness disproportionately affects patients with obesity, a chronic inflammatory disease with a baseline excess of cytokines. The majority of the medications used in the treatment of COVID-19 are metabolized by cytochrome P450 (CYP) enzymes, primarily CYP2D6. This is further complicated by genetic polymorphisms of CYP2D6, HO-1, ACE, and ACE-2. There is a potential role for HO-1 upregulation to treat/prevent cytokine storm. Current therapy must focus on antivirals and heme oxygenase upregulation. Vaccine development will be the only magic bullet.
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Lee, Jooyeon, Jimin Jang, Sung-Min Park, and Se-Ran Yang. "An Update on the Role of Nrf2 in Respiratory Disease: Molecular Mechanisms and Therapeutic Approaches." International Journal of Molecular Sciences 22, no. 16 (August 5, 2021): 8406. http://dx.doi.org/10.3390/ijms22168406.
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Nuclear factor erythroid 2-related factor (Nrf2) is a transcriptional activator of the cell protection gene that binds to the antioxidant response element (ARE). Therefore, Nrf2 protects cells and tissues from oxidative stress. Normally, Kelch-like ECH-associated protein 1 (Keap1) inhibits the activation of Nrf2 by binding to Nrf2 and contributes to Nrf2 break down by ubiquitin proteasomes. In moderate oxidative stress, Keap1 is inhibited, allowing Nrf2 to be translocated to the nucleus, which acts as an antioxidant. However, under unusually severe oxidative stress, the Keap1-Nrf2 mechanism becomes disrupted and results in cell and tissue damage. Oxide-containing atmospheric environment generally contributes to the development of respiratory diseases, possibly leading to the failure of the Keap1-Nrf2 pathway. Until now, several studies have identified changes in Keap1-Nrf2 signaling in models of respiratory diseases, such as acute respiratory distress syndrome (ARDS)/acute lung injury (ALI), chronic obstructive pulmonary disease (COPD), idiopathic pulmonary fibrosis (IPF), and asthma. These studies have confirmed that several Nrf2 activators can alleviate symptoms of respiratory diseases. Thus, this review describes how the expression of Keap1-Nrf2 functions in different respiratory diseases and explains the protective effects of reversing this expression.
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Elemans, Coen P. H., Riccardo Zaccarelli, and Hanspeter Herzel. "Biomechanics and control of vocalization in a non-songbird." Journal of The Royal Society Interface 5, no. 24 (November 13, 2007): 691–703. http://dx.doi.org/10.1098/rsif.2007.1237.
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The neuromuscular control of vocalization in birds requires complicated and precisely coordinated motor control of the vocal organ (i.e. the syrinx), the respiratory system and upper vocal tract. The biomechanics of the syrinx is very complex and not well understood. In this paper, we aim to unravel the contribution of different control parameters in the coo of the ring dove ( Streptopelia risoria ) at the syrinx level. We designed and implemented a quantitative biomechanical syrinx model that is driven by physiological control parameters and includes a muscle model. Our simple nonlinear model reproduces the coo, including the inspiratory note, with remarkable accuracy and suggests that harmonic content of song can be controlled by the geometry and rest position of the syrinx. Furthermore, by systematically switching off the control parameters, we demonstrate how they affect amplitude and frequency modulations and generate new experimentally testable hypotheses. Our model suggests that independent control of amplitude and frequency seems not to be possible with the simple syringeal morphology of the ring dove. We speculate that songbirds evolved a syrinx design that uncouples the control of different sound parameters and allows for independent control. This evolutionary key innovation provides an additional explanation for the rapid diversification and speciation of the songbirds.
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Hassan, Sk Sarif, Shinjini Ghosh, Diksha Attrish, Pabitra Pal Choudhury, Alaa A. A. Aljabali, Bruce D. Uhal, Kenneth Lundstrom, et al. "Possible Transmission Flow of SARS-CoV-2 Based on ACE2 Features." Molecules 25, no. 24 (December 13, 2020): 5906. http://dx.doi.org/10.3390/molecules25245906.
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Angiotensin-converting enzyme 2 (ACE2) is the cellular receptor for the Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) that is engendering the severe coronavirus disease 2019 (COVID-19) pandemic. The spike (S) protein receptor-binding domain (RBD) of SARS-CoV-2 binds to the three sub-domains viz. amino acids (aa) 22–42, aa 79–84, and aa 330–393 of ACE2 on human cells to initiate entry. It was reported earlier that the receptor utilization capacity of ACE2 proteins from different species, such as cats, chimpanzees, dogs, and cattle, are different. A comprehensive analysis of ACE2 receptors of nineteen species was carried out in this study, and the findings propose a possible SARS-CoV-2 transmission flow across these nineteen species.
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Meacci, Elisabetta, Mercedes Garcia-Gil, and Federica Pierucci. "SARS-CoV-2 Infection: A Role for S1P/S1P Receptor Signaling in the Nervous System?" International Journal of Molecular Sciences 21, no. 18 (September 15, 2020): 6773. http://dx.doi.org/10.3390/ijms21186773.
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The recent coronavirus disease (COVID-19) is still spreading worldwide. The severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), the virus responsible for COVID-19, binds to its receptor angiotensin-converting enzyme 2 (ACE2), and replicates within the cells of the nasal cavity, then spreads along the airway tracts, causing mild clinical manifestations, and, in a majority of patients, a persisting loss of smell. In some individuals, SARS-CoV-2 reaches and infects several organs, including the lung, leading to severe pulmonary disease. SARS-CoV-2 induces neurological symptoms, likely contributing to morbidity and mortality through unknown mechanisms. Sphingosine 1-phosphate (S1P) is a bioactive sphingolipid with pleiotropic properties and functions in many tissues, including the nervous system. S1P regulates neurogenesis and inflammation and it is implicated in multiple sclerosis (MS). Notably, Fingolimod (FTY720), a modulator of S1P receptors, has been approved for the treatment of MS and is being tested for COVID-19. Here, we discuss the putative role of S1P on viral infection and in the modulation of inflammation and survival in the stem cell niche of the olfactory epithelium. This could help to design therapeutic strategies based on S1P-mediated signaling to limit or overcome the host–virus interaction, virus propagation and the pathogenesis and complications involving the nervous system.
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Stegniy, B. T., D. V. Muzyka, S. V. Tkachenko, O. M. Rula, A. B. Stegniy, O. S. Kolesnyk, S. I. Vovk, and O. O. Napnenko. "Commission testing of the test system “A kit for the detection of antibodies to Newcastle disease virus in hemagglutination inhibition test”." Veterinary Medicine: inter-departmental subject scientific collection, no. 105 (August 7, 2019): 26–31. http://dx.doi.org/10.36016/vm-2019-105-5.
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Newcastle disease or pseudo-plague is a highly contagious viral bird disease, characterized by damage to the respiratory and digestive organs, as well as impaired central nervous system function. Since the middle of the last century, this disease has become widespread in many European countries. Newcastle disease is common in all continents and is especially dangerous. The article provides information on conducting a round of commission tests of the components of the test system “A Kit for Detection of Antibodies to Newcastle Disease Virus in Hemagglutination Inhibition Test”. When testing encrypted antigens and sera with previously characterized and referent samples, they were active and specific, meeting the requirements of the technical specifications of Ukraine for the specified drug. Thus, the positive antigen had activity in the hemagglutination test of 1:256, reacted only with positive to the Newcastle disease virus serum, and did not delay agglutination in the presence of referent to avian influenza virus subtypes H5 and H7 sera. In the presence of positive sera to the Newcastle disease virus in encrypted form, the positive antigen of the corresponding virus delayed the agglutination of the cock erythrocytes in dilutions 1:256–1:512. The results obtained allowed to make a positive decision on the registration of this preparation in the territory of Ukraine
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El Khantour, Abderrazak, Abdelmajid Soulaymani, Mohamed Salek, Abdelkarim Filali Maltouf, Sami Darkaoui, Fatiha El Mellouli, Mariette F. Ducatez, and Siham Fellahi. "Molecular characterization of the hemagglutinin gene of H9N2 avian influenza viruses isolated from broiler flocks in Morocco from 2016 to 2018." Veterinarski arhiv 90, no. 5 (October 15, 2020): 477–84. http://dx.doi.org/10.24099/vet.arhiv.0724.
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Avian influenza viruses of the H9N2 subtype continue to spread in wild birds and poultry worldwide. Infection with H9N2 avian influenza virus was detected for the first time in Morocco in January 2016. In this study, a total of 105 organ and tracheal swab samples from 21 broiler farms in Morocco were collected from July 2016 to October 2018 for H9N2 screening. The suspicion of disease was based on severe respiratory signs such as sneezing, coughing, rales and gasping, while H9N2 virus infection was confirmed by real-time RT-PCR. Hemagglutinin (HA) genes of four isolates were amplified by conventional RT-PCR, sequenced, and aligned for phylogenetic analyses. Among the 21 flocks, 48% (10/21) were qRT-PCR positive for H9, with the cycle threshold values ranging from18.6 to 34.8. The maximum similarity in nucleotide and protein sequences (96-98%) was observed between the Moroccan viruses and an H9 virus isolated from broiler chickens in 2017 in Burkina Faso (A/chicken/BurkinaFaso/17RS93-19/2017) and from a layer chicken in the United Arab Emirates in 2015 (A/chicken/Dubai/D2506/2015). The HA genes revealed the close relationship between the four Moroccan viruses, with 97.9%-99.9% nucleotide identity. Phylogenetic analysis showed that the Moroccan viruses belonged to the G1 lineage, and likely originated from the Middle East, as previously reported in 2016.
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Michaud, Veronique, Malavika Deodhar, Meghan Arwood, Sweilem B. Al Rihani, Pamela Dow, and Jacques Turgeon. "ACE2 as a Therapeutic Target for COVID-19; Its Role in Infectious Processes and Regulation by Modulators of the RAAS System." Journal of Clinical Medicine 9, no. 7 (July 3, 2020): 2096. http://dx.doi.org/10.3390/jcm9072096.
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Angiotensin converting enzyme 2 (ACE2) is the recognized host cell receptor responsible for mediating infection by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). ACE2 bound to tissue facilitates infectivity of SARS-CoV-2; thus, one could argue that decreasing ACE2 tissue expression would be beneficial. However, ACE2 catalytic activity towards angiotensin I (Ang I) and II (Ang II) mitigates deleterious effects associated with activation of the renin-angiotensin-aldosterone system (RAAS) on several organs, including a pro-inflammatory status. At the tissue level, SARS-CoV-2 (a) binds to ACE2, leading to its internalization, and (b) favors ACE2 cleavage to form soluble ACE2: these actions result in decreased ACE2 tissue levels. Preserving tissue ACE2 activity while preventing ACE2 shredding is expected to circumvent unrestrained inflammatory response. Concerns have been raised around RAAS modulators and their effects on ACE2 expression or catalytic activity. Various cellular and animal models report conflicting results in various tissues. However, recent data from observational and meta-analysis studies in SARS-CoV-2-infected patients have concluded that RAAS modulators do not increase plasma ACE2 levels or susceptibility to infection and are not associated with more severe diseases. This review presents our current but evolving knowledge of the complex interplay between SARS-CoV-2 infection, ACE2 levels, modulators of RAAS activity and the effects of RAAS modulators on ACE2 expression.
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Gjessing, Mona C., Natalya Yutin, Torstein Tengs, Tania Senkevich, Eugene Koonin, Hans Petter Rønning, Marta Alarcon, et al. "Salmon Gill Poxvirus, the Deepest Representative of the Chordopoxvirinae." Journal of Virology 89, no. 18 (July 1, 2015): 9348–67. http://dx.doi.org/10.1128/jvi.01174-15.
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ABSTRACTPoxviruses are large DNA viruses of vertebrates and insects causing disease in many animal species, including reptiles, birds, and mammals. Although poxvirus-like particles were detected in diseased farmed koi carp, ayu, and Atlantic salmon, their genetic relationships to poxviruses were not established. Here, we provide the first genome sequence of a fish poxvirus, which was isolated from farmed Atlantic salmon. In the present study, we used quantitative PCR and immunohistochemistry to determine aspects of salmon gill poxvirus disease, which are described here. The gill was the main target organ where immature and mature poxvirus particles were detected. The particles were detected in detaching, apoptotic respiratory epithelial cells preceding clinical disease in the form of lethargy, respiratory distress, and mortality. In moribund salmon, blocking of gas exchange would likely be caused by the adherence of respiratory lamellae and epithelial proliferation obstructing respiratory surfaces. The virus was not found in healthy salmon or in control fish with gill disease without apoptotic cells, although transmission remains to be demonstrated. PCR of archival tissue confirmed virus infection in 14 cases with gill apoptosis in Norway starting from 1995. Phylogenomic analyses showed that the fish poxvirus is the deepest available branch of chordopoxviruses. The virus genome encompasses most key chordopoxvirus genes that are required for genome replication and expression, although the gene order is substantially different from that in other chordopoxviruses. Nevertheless, many highly conserved chordopoxvirus genes involved in viral membrane biogenesis or virus-host interactions are missing. Instead, the salmon poxvirus carries numerous genes encoding unknown proteins, many of which have low sequence complexity and contain simple repeats suggestive of intrinsic disorder or distinct protein structures.IMPORTANCEAquaculture is an increasingly important global source of high-quality food. To sustain the growth in aquaculture, disease control in fish farming is essential. Moreover, the spread of disease from farmed fish to wildlife is a concern. Serious poxviral diseases are emerging in aquaculture, but very little is known about the viruses and the diseases that they cause. There is a possibility that viruses with enhanced virulence may spread to new species, as has occurred with the myxoma poxvirus in rabbits. Provision of the first fish poxvirus genome sequence and specific diagnostics for the salmon gill poxvirus in Atlantic salmon may help curb this disease and provide comparative knowledge. Furthermore, because salmon gill poxvirus represents the deepest branch of chordopoxvirus so far discovered, the genome analysis provided substantial insight into the evolution of different functional modules in this important group of viruses.