RESUMO
The highly pathogenic Avian Influenza virus (HPAIV) H5N1 has caused a global outbreak affecting both wild and domestic animals, predominantly avian species. To date, cases of the HPAIV H5 Clade 2.3.4.4b in penguins have exclusively been reported in African Penguins. In Chile, the virus was confirmed in pelicans in December 2022 and subsequently spread across the country, affecting several species, including Humboldt penguins. This study aims to provide an overview of the incidents involving stranded and deceased Humboldt penguins and establish a connection between these events and HPAIV H5N1. Historical data about strandings between 2009 and 2023 was collected, and samples from suspected cases in 2023 were obtained to confirm the presence of HPAIV H5N1. Between January and August 2023, 2,788 cases of stranded and deceased penguins were recorded. Out of these, a total of 2,712 penguins deceased, evidencing a significative increase in mortality starting in early 2023 coinciding with the introduction and spreading of HPAIV H5N1 in the country. Thirty-seven events were categorized as mass mortality events, with the number of deceased penguins varying from 11 to 98. Most cases (97â¯%) were observed in the North of Chile. One hundred and eighty-one specimens were subjected to HPAIV diagnosis, four of which tested positive for HPAIV H5N1. Spatial analysis validates the correlation between mass mortality events and outbreaks of HPAIV in Chile. However, the limited rate of HPAIV H5N1 detection, which can be attributed to the type and quality of the samples, requiring further exploration.
Assuntos
Surtos de Doenças , Virus da Influenza A Subtipo H5N1 , Influenza Aviária , Spheniscidae , Animais , Spheniscidae/virologia , Chile/epidemiologia , Surtos de Doenças/veterinária , Influenza Aviária/epidemiologia , Influenza Aviária/virologia , Influenza Aviária/mortalidadeRESUMO
We describe the evolution of the outbreak of Highly Pathogenic Avian Influenza (HPAI) A(H5N1) in sea lions (Otaria flavescens) of South America. At least 24,000 sea lions died in Peru, Chile, Argentina, Uruguay, and Brazil between January-October 2023. The most plausible route of infection is cohabiting with or foraging on infected birds. However, we urge a detailed evaluation of the sea lions actual source of infection given that the concomitant massive wild bird mortalities registered in the Pacific Ocean did not occur in the Atlantic Ocean.
Assuntos
Virus da Influenza A Subtipo H5N1 , Leões-Marinhos , Animais , América do Sul/epidemiologia , Surtos de Doenças , Influenza Aviária/mortalidade , Influenza Aviária/epidemiologia , Influenza Aviária/virologia , Oceano Atlântico , Oceano Pacífico , Infecções por Orthomyxoviridae/veterinária , Infecções por Orthomyxoviridae/mortalidade , Infecções por Orthomyxoviridae/virologia , Infecções por Orthomyxoviridae/epidemiologia , Aves/virologiaRESUMO
La carga de enfermedad por influenza está bien documentada en países de clima templado, pero hasta la fecha en Honduras solo se ha realizado un estudio, siendo este el segundo con respecto a la carga médica asociada a influenza. Objetivo: Estimar el número de hospitalizaciones y defunciones, debidos a la influenza, como causante de las infecciones respiratorias agudas en la población. Material yMétodos: Se realizó un estudio descriptivo retrospectivo. Seutilizó tres fuentes de datos secundarias:registros de todos los egresos hospitalarios, resultados de detección viral por influenza y proyecciones de población por grupos de edad. Se estimó la tasa de incidencia y su intervalo de confianza al 95%, combinando las tres fuentes de datos. Resultados: Las hospitalizaciones en las infecciones respiratorias agudas graves (IRAG) J09-J18 asociadas a influenza en el 2011-2015 son mayores en los menores de cinco años, en donde las hospitalizaciones son mayores en los años 2013 con 68.2 (IC 95%: 64.2-72.1) casos por 100, 000 habitantes. En el periodo 2011-2015. Las tasas de incidencia en las defunciones de IRAG asociadas a influenza1.Doctor(a) en medicina y cirugía.2.Doctor(a) en Pediatría3.Nivel Básico de Epidemiologia de Campo del FETP4.MSc.Epidemiólogo del FETP, coordinador de las enfermedades Transmisibles de la unidad devigilancia de la salud, Secretaria de Salud de HondurasAutor de correspondencia: Hommer Mejía, homams2003@yahool.comRecibido: Aprobado: (J09-J18) fueron mayores en el año 2014 con 1 caso (IC 95%: 0.4-1.6) por 100 000 habitantes. La circulación por influenza comenzó a incrementarse a partir de agosto del 2011 luego en los años 2012-2015 con picos altos durante los meses de octubre y noviembre. Conclusión: La carga médica asociada a influenza representa un impacto para los servicios de salud de Honduras, siendo los grupos de población en edades extremas, los que más hospitalizaciones y muertes presentaron. Se sugiere promover la vacunación contra influenza con la composición de cepas circulantes en el país y en temporada apropiada, enfatizando en los grupos más vulnerables de la población...(AU)
Assuntos
Humanos , Masculino , Feminino , Pré-Escolar , Criança , Adolescente , Influenza Humana/diagnóstico , Influenza Aviária/mortalidade , Hospitalização/estatística & dados numéricos , Infecções Respiratórias/complicaçõesRESUMO
The most foolproof way to promote survival in epidemics of potentially lethal influenza is to target, not highly mutable viral proteins, but rather intracellular signaling pathways which promote viral propagation or lung inflammation. NF-kappaB, activated in influenza-infected lung epithelial cells and macrophages, is one likely target in this regard, as it plays a role both in viral replication and in the excessive lung inflammation often evoked by influenza infection. Indeed, salicylates, which suppress NF-kappaB activation, have been shown to reduce the lethality of H5N1 avian-type influenza in mice. Another potential target is NADPH oxidase, as this may be a major source of influenza-evoked oxidant stress in lung epithelial cells as well as in phagocytes attracted to lung parenchyma. A number of studies demonstrate that oxidant stress contributes to overexuberant lung inflammation and lethality in influenza-infected mice. The documented utility of N-acetylcysteine, a glutathione precursor, for promoting survival in influenza-infected mice, and diminishing the severity of influenza-like infections in elderly humans, presumably reflects a key role for oxidative stress in influenza. The lethality of influenza is also reduced in mice pretreated with adenovirus carrying the gene for heme oxygenase-1; this benefit may be mediated, at least in part, by the ability of bilirubin to inhibit NADPH oxidase. It may be feasible to replicate this benefit clinically by administering biliverdin or its homolog phycocyanobilin, richly supplied by spirulina. If this latter speculation can be confirmed in rodent studies, a practical and inexpensive regimen consisting of high-dose salicylates, spirulina, and N-acetylcysteine, initiated at the earliest feasible time, may prove to have life-saving efficacy when the next killer influenza pandemic strikes.
Assuntos
Regulação Enzimológica da Expressão Gênica , Influenza Humana/enzimologia , Influenza Humana/mortalidade , NADPH Oxidases/metabolismo , NF-kappa B/metabolismo , Animais , Aves , Surtos de Doenças , Humanos , Inflamação , Influenza Aviária/enzimologia , Influenza Aviária/mortalidade , Pulmão/patologia , Macrófagos/metabolismo , Camundongos , Modelos Teóricos , Ficobilinas/farmacologia , Ficocianina/farmacologia , Transdução de SinaisRESUMO
Se hace referencia a las características virológicas de la influenza aviar, expansión geográfica y migración de las aves en los Continentes, probabilidad de riesgo de pandemia en un futuro cercano, descripción clínica de la patología y terapéutica disponible, así como también a los avances preventivos y recomendaciones. (AU)
Assuntos
Humanos , Animais , Influenza Aviária/tratamento farmacológico , Influenza Aviária/prevenção & controle , Influenza Aviária/transmissão , Influenza Aviária/virologia , Influenza Aviária/diagnóstico , Influenza Aviária/mortalidade , Migração Animal , Surtos de Doenças , Europa (Continente) , América , Vírus da Influenza A , Zoonoses/transmissão , Zoonoses/virologia , Argentina , Saúde GlobalRESUMO
Se hace referencia a las características virológicas de la influenza aviar, expansión geográfica y migración de las aves en los Continentes, probabilidad de riesgo de pandemia en un futuro cercano, descripción clínica de la patología y terapéutica disponible, así como también a los avances preventivos y recomendaciones.
Assuntos
Humanos , Animais , Influenza Aviária/diagnóstico , Influenza Aviária/mortalidade , Influenza Aviária/prevenção & controle , Influenza Aviária/tratamento farmacológico , Influenza Aviária/transmissão , Influenza Aviária/virologia , América , Argentina , Surtos de Doenças , Europa (Continente) , Migração Animal , Saúde Global , Vírus da Influenza A , Zoonoses/transmissão , Zoonoses/virologiaRESUMO
Durante el año 2005, se notificaron 7.410 casos clínicos de influenza. La tasa nacional global corresponde a 634 casos por 100.000 hab., inferior en un 40 por ciento a lo observado a igual fecha del año 2004 (1.071 por 100.000 hab., y levemente superior a la tasa global de 2003 (513 por 100.000 hab.). Para el año 2005, el número de casos proyectados fue de 102.142 casos, mientras que la misma fecha de 2004 era de 170.885 casos. El incremento estacional se observó a partir de la semana 21, llegando a su máximo en la semana 25 (correspondiente a la tercera semana de junio), con una tasa de notificación de 60 casos por 100.000 hab., coincidiendo con el máximo de la detección viral. Este aumento duró 11 semanas, considerando las semanas con tasas superiores a 15 x 100.000 hab., disminuyendo con algunas oscilaciones a una tasa inferior a 3 x 100.000 hab., a fines de año. En el año 2004 el máximo de la notificación fue más precoz (semana 22), con una tasa de notificación semanal de 92 por 100.000 hab.
Assuntos
Humanos , Masculino , Feminino , Influenza Aviária/epidemiologia , Influenza Aviária/mortalidade , Influenza Humana/epidemiologia , Vírus da Influenza B , Chile , Notificação de Abuso , Monitoramento EpidemiológicoRESUMO
To determine the association between specific structural changes in the hemagglutinin gene and pathogenicity of avian influenza viruses (AIVs), groups of 4-week-old White Plymouth Rock chickens were inoculated intravenously or intranasally with AIVs of varying pathogenicities isolated from chickens in central Mexico during 1994-1995. Mildly pathogenic (MP) viruses had a common hemagglutinin-connecting peptide sequence of Pro-Gln-Arg-Glu-Thr-Arg decreases Gly and had restricted capability for replication and production of lesions in tissues. The principle targets for virus replication or lesion production were the lungs, lymphoid organs, and visceral organs containing epithelial cells, such as kidney and pancreas. Death was associated with respiratory and/or renal failure. By contrast, highly pathogenic (HP) AIVs had one substitution and the addition of two basic amino acids in the hemagglutinin connecting peptide, for a sequence of Pro-Gln-Arg-Lys-Arg-Lys-Thr-Arg decreases Gly. The HP AIVs were pantropic in virus replication and lesion production ability. However, the most severe histologic lesions were produced in the brain, heart, adrenal glands, and pancreas, and failure of multiple critical organs was responsible for disease pathogenesis and death. No differences in lesion distribution patterns or in sites of AIV replication were evident to explain the variation in mortality rates for different HP AIVs, but HP AIVs that produced the highest mortality rates had more severe necrosis in heart and pancreas. The ability of individual HP AIVs to produce low or high mortality rates could not be explained by changes in sequence of the hemagglutinin-connecting peptide alone, but probably required the addition of other undetermined genomic changes.
Assuntos
Galinhas , Vírus da Influenza A Subtipo H5N2 , Vírus da Influenza A , Influenza Aviária/patologia , Glândulas Suprarrenais/química , Glândulas Suprarrenais/patologia , Glândulas Suprarrenais/virologia , Animais , Encéfalo/patologia , Encéfalo/virologia , Química Encefálica , Hemaglutininas Virais/química , Hemaglutininas Virais/genética , Imuno-Histoquímica , Vírus da Influenza A/genética , Vírus da Influenza A/patogenicidade , Vírus da Influenza A/fisiologia , Influenza Aviária/epidemiologia , Influenza Aviária/mortalidade , Rim/química , Rim/patologia , Rim/virologia , México/epidemiologia , Miocárdio/química , Miocárdio/patologia , Pâncreas/química , Pâncreas/patologia , Pâncreas/virologia , Organismos Livres de Patógenos Específicos , Baço/química , Baço/patologia , Baço/virologia , Proteínas Virais/análise , Proteínas Virais/metabolismo , Replicação ViralRESUMO
Chickens were inoculated with one of five H5N2 Mexican-origin avian influenza virus (AIV) isolates to determine their pathogenicity for chickens and to determine the ability of routine virologic and serologic tests to detect infections. In laboratory infections, three AIVs, H5/94, M5/94, and J12/94, produced sporadic illness and death and were categorized as mildly pathogenic. Q1/95 produced illness and death in all inoculated chickens and was categorized as highly lethal and highly pathogenic (HP). P11/94B commonly produced clinical illness, but deaths were infrequent. During the presence of clinical signs, oropharyngeal swabs were superior for isolation of AIV, but cloacal swabs were more successful after disappearance of clinical signs. Agar gel precipitin (AGP) serologic test was superior for detecting AIV infection during the clinical phase, but AGP and hemagglutinin inhibition tests were equally effective in detecting infections after recovery from clinical illness. Passage of P11/94B parent stock and selected 14-day-embryo-passed AIVs in adult hens resulted in emergence of some HP AIV derivatives. The hemagglutinin of Q1/95 and P11/ 94B parent stock and derivative AIVs had an identical proteolytic cleavage site of.... Pro-Gln-Arg-Lys-Arg-Lys-Thr-Arg-Gly, consistent with AIVs of high pathogenicity. However, no consistent differences were identified in the sequence of the hemagglutinin gene to explain the discrepancy in lethality patterns of the P11/94B AIVs. This suggests that genes other than the hemagglutinin impact the full expression of high lethality of Mexican-origin AIV infections in chickens.
Assuntos
Vírus da Influenza A Subtipo H5N2 , Vírus da Influenza A/patogenicidade , Influenza Aviária/diagnóstico , Animais , Embrião de Galinha , Galinhas , Feminino , Genes Virais , Vírus da Influenza A/classificação , Vírus da Influenza A/genética , Influenza Aviária/mortalidade , Influenza Aviária/fisiopatologia , México , Reprodutibilidade dos Testes , Especificidade da Espécie , VirulênciaRESUMO
In October of 1993, there was decreased egg production and increased mortality among Mexican chickens, in association with serologic evidence of an H5N2 influenza virus. First isolated from chickens in May of 1994, after spreading widely in the country, the virus caused only a mild respiratory syndrome in specific pathogen-free chickens. Because eradication of the virus by destruction of infected birds posed major obstacles to the poultry industry in Mexico, we were able to conduct a "field experiment" to determine the fate of an avirulent virus after repeated cycles of replication in millions of chickens. By the end of 1994, the virus had mutated to contain a highly cleavable hemagglutinin (HA), but remained only mildly pathogenic in chickens. Within months, however, it had become lethal in poultry. Nucleotide sequence analysis of the HA cleavage site of the original avirulent strain revealed R-E-T-R, typical of avirulent viruses and unlike the K-K-K-R sequence characterizing viruses responsible for the 1983 outbreak in poultry in the United States. Both mildly and highly pathogenic isolates contained insertions and a substitution of basic residues in the HA connecting peptide, R-K-R-K-T-R, which made the HA highly cleavable in trypsin-free chicken embryo fibroblasts. Phylogenetic analysis of the HA of H5 avian influenza viruses, including the Mexican isolates, indicated that the epidemic virus had originated from the introduction of a single virus of the North American lineage into Mexican chickens. This sequence of events demonstrates, apparently for the first time, the stepwise acquisition of virulence by an avian influenza virus in nature.