ABSTRACT
Boletim com o objetivo de demonstrar o perfil epidemiológico dos casos que foram notificados entre 2019 a 2023, apresentando os indicadores epidemiológicos e operacionais de relevância do estado, para fins de tomada de decisão em relação às ações do Programa para Eliminação das Hepatites Virais até 2030. Trata-se de uma análise de dados secundários obtidos do Sistema de Informação de Agravos de Notificações (SINAN), referentes aos casos diagnosticados e notificados, por município de residência entre 2019 e 2023 pelos serviços de saúde do Estado de Goiás
Bulletin with the aim of demonstrating the epidemiological profile of cases that were reported between 2019 and 2023, presenting epidemiological and operational indicators of relevance to the state, for decision-making purposes in relation to the actions of the Program for the Elimination of Viral Hepatitis by 2030. This is an analysis of secondary data obtained from the Notifiable Diseases Information System (SINAN), referring to cases diagnosed and notified, by municipality of residence between 2019 and 2023 by the health services of the State of Goiás
Subject(s)
Humans , Hepatitis/epidemiology , Hepatitis C/diagnosis , Hepatitis C/mortality , Hepatitis C/epidemiology , Hepatitis B/diagnosis , Hepatitis B/mortality , Hepatitis B/epidemiologyABSTRACT
Immunotherapy with immune checkpoint inhibitors (ICIs) has revolutionized advanced cancer management. Nevertheless, the generalized use of these medications has led to an increase in the incidence of adverse immune-mediated events and the liver is one of the most frequently affected organs. Liver involvement associated with the administration of immunotherapy is known as immune-mediated hepatitis (IMH), whose incidence and clinical characteristics have been described by different authors. It often presents as mild elevations of amino transferase levels, seen in routine blood tests, that spontaneously return to normal, but it can also manifest as severe transaminitis, possibly leading to the permanent discontinuation of treatment. The aim of the following review was to describe the most up-to-date concepts regarding the epidemiology, diagnosis, risk factors, and progression of IMH, as well as its incidence in different types of common cancers, including hepatocellular carcinoma. Treatment recommendations according to the most current guidelines are also provided.
Subject(s)
Carcinoma, Hepatocellular , Hepatitis A , Hepatitis , Liver Neoplasms , Humans , Hepatitis/epidemiology , Hepatitis/etiology , Hepatitis/therapy , Carcinoma, Hepatocellular/etiology , Immunotherapy/adverse effects , Liver Neoplasms/complicationsABSTRACT
INTRODUCTION: Severe acute hepatitis (SAH) is defined by a severe inflammation of hepatocytes in the liver parenchyma which can lead to an acute liver failure, a clinical condition with high mortality rate that can be triggered by several factors but is usually associated to hepatotropic viruses' infection. In 2022, cases of children with severe acute hepatitis of unknown origin hospitalized in Glasgow, Scotland, were reported. Possible causes of this condition include, but are not limited to, undiagnosed viral (and non-viral) infections, autoimmune hepatitis, drug and/or chemical toxicity, mitochondrial chain respiratory and metabolic disorders. AREAS COVERED: Herpesviruses can cause severe acute hepatitis, but little is known about the role and the mechanisms of herpesviruses as a causative agent of this type of hepatitis. We review the role of herpesviruses as causative agent of SAH in children and other possible mechanisms involved in this disease. EXPERT OPINION: Differential diagnosis for herpesvirus in SAH should be implemented in all settings. Alternative fluids, such as saliva and dried blood, could be used in the diagnosis to overwhelm the availability of biological specimens at sufficient volume. In the future, genetic studies could also be added to increase the knowledge about severe acute hepatitis in children.
Subject(s)
Hepatitis , Herpesviridae , Virus Diseases , Child , Humans , Diagnosis, Differential , Acute DiseaseABSTRACT
BACKGROUND: Bone marrow transplantation (BMT) is a standard treatment for several haematologic conditions. Following BMT, patients may develop hepatobiliary complications that impact morbidity and mortality. The differential diagnosis may include drug-induced liver injury (DILI), sepsis-associated liver injury (SALI), sinusoidal obstruction syndrome (SOS), graft-versus-host disease (GVHD), viral hepatitis, ischaemic hepatitis, and fulminant hepatitis. AIMS: To evaluate the frequency, clinical characteristics, and outcomes of patients with hepatobiliary alterations associated with BMT in a tertiary referral centre. METHODS: This was a cross-sectional study with data collected from the medical records of patients undergoing BMT between January 2017 and June 2022. We diagnosed hepatobiliary complications based on established criteria. RESULTS: We included 377 patients; 55.7% had hepatobiliary complications. Female gender, pre-BMT hepatobiliary alteration, and haploidentical allogeneic transplantation were associated with increased risk with odds ratios (OR) of 1.8 (p = 0.005), 1.72 (p = 0.013) and 3.25 (p = 0.003), respectively. Patients with hepatobiliary complications spent longer in the hospital than those without (27.7 × 19.3 days, respectively; p < 0.001). Among 210 patients with hepatobiliary complications, 28 died compared to 5 of 167 without complications (OR 4.98; p = 0.001). CONCLUSIONS: Hepatobiliary complications are frequent in patients undergoing BMT. There is a greater risk of their occurrence in women, people with pre-BMT liver alterations, and in haploidentical transplants. The occurrence of these complications increases the length of stay and is associated with a higher risk of death.
Subject(s)
Graft vs Host Disease , Hepatitis , Humans , Female , Bone Marrow Transplantation/adverse effects , Cross-Sectional Studies , Bone Marrow , Transplantation, Homologous/adverse effects , Graft vs Host Disease/diagnosis , Graft vs Host Disease/etiology , Hepatitis/complicationsABSTRACT
Se estima que 1,3 millones de personas murieron a causa de hepatitis viral B y C crónica en 2022, es decir, 3 500 muertes por día; se calcula que 254 millones de personas viven con hepatitis B, 50 millones de personas viven con hepatitis C en todo el mundo y 6 000 personas se infectaron con hepatitis viral cada día. En numerosos países, muchas personas siguen sin ser diagnosticadas e incluso cuando se diagnostica la hepatitis, el número de personas que reciben tratamiento sigue siendo increíblemente bajo (1). A nivel mundial la incidencia del virus de la hepatitis B se calcula en 16 casos por 100 000 habitantes, de los cuales el 13,4 % viven con el virus de la hepatitis B crónico diagnosticado y el 2,6 % viven con el virus crónico tratado. La incidencia del virus de la hepatitis C se calcula en 13 casos por 100 000 habitantes, de los cuales el 36,4 % viven con el virus crónico diagnosticado y el 20 % viven con el virus crónico tratado (1, 2) En china se reportan diagnósticos y tratamiento del virus de la hepatitis B de 22 % y 15 %, respectivamente.
An estimated 1.3 million people died from viral hepatitis B and chronic C in 2022, that is, 3,500 deaths per day; It is estimated that 254 million people live with hepatitis B, 50 million people live with hepatitis C worldwide and 6,000 people were infected with hepatitis viral every day. In many countries, many people remain undiagnosed and even when hepatitis is diagnosed, the number of people receiving treatment remains incredibly low (1). Worldwide, the incidence of hepatitis B virus is estimated at 16 cases per 100,000. inhabitants, of which 13.4% live with chronic hepatitis B virus diagnosed and 2.6% live with the chronically treated virus. The incidence of hepatitis C virus is estimated at 13 cases per 100,000 inhabitants, of which of which 36.4% live with the diagnosed chronic virus and 20% live with the chronic virus treated (1, 2) In China, hepatitis B virus diagnoses and treatment are reported to be 22% and 15%, respectively.
Subject(s)
HepatitisABSTRACT
Background: Dengue fever is a mosquito-borne infectious disease endemic in over 100 countries around the world. Among the complications that dengue can cause the Hemophagocytic Lymphohistiocytosis is one of great concern for its severity and complex diagnosis. Case report: Hereby we document a case of this disease expressed on a previously healthy 6-year-old female patient whose dengue infection was so severe that needed intensive care management with vasoactive drugs and diuretics. After a short period of wellness began newly with fever, pancytopenia, hepatitis, and inflammatory response symptoms. Conclusions: A Dengue associated Hemophagocytic Lymphohistiocytosis syndrome was suspected and treated with intravenous corticosteroids on a 3-day scheme at no signs of malignancy with excellent response. The health care professionals must know about this not novel entity in order to reach an efficient diagnosis and treatment mostly, but not only, those in tropical and sub-tropical regions of the word were dengue virus is endemic.
Antecedentes: La fiebre por dengue es una enfermedad infecciosa transmitida por mosquitos, endémica en más de 100 países alrededor del mundo. La Linfohistiocitosis Hemofagocítica, dentro de las complicaciones que puede ocasionar el dengue, es una de las más preocupantes por su complejidad diagnostica y gravedad. Reporte de caso: Femenino de 6 años de edad, previamente sana, cuya infección por dengue fue tan grave que requirió manejo en cuidados intensivos. Después de un breve período de bienestar recrudeció la fiebre, además de pancitopenia, hepatitis y síntomas de respuesta inflamatoria. Conclusiones: Se sospechó síndrome de Linfohistiocitosis Hemofagocítica asociada a Dengue y se trató con corticoides intravenosos en un esquema de 3 días con excelente respuesta. Los profesionales de la salud deben conocer esta entidad no novedosa para poder llegar a un diagnóstico y tratamiento eficaz en su mayoría, pero no solo, en las regiones tropicales y subtropicales del mundo donde el virus del dengue es endémico.
Subject(s)
Dengue , Hepatitis , Lymphohistiocytosis, Hemophagocytic , Female , Humans , Child , Lymphohistiocytosis, Hemophagocytic/etiology , Hepatitis/complications , Dengue/complicationsABSTRACT
Hepatosplenic schistosomiasis (HSS) is a serious complication of chronic schistosomiasis that can result in portal hypertension and variceal bleeding. ß-blockers, a class of medications commonly used to treat hypertension and other cardiovascular conditions, have been investigated for their potential use in preventing variceal bleeding in HSS. Several studies have shown that ß-blockers can reduce portal pressure and prevent variceal bleeding effectively in these patients. However, there are limited data on the long-term efficacy and safety of ß-blockers in this setting, and further research is needed to determine the optimal use of these medications. This review summarizes the evidence supporting current recommendations of ß-blocker use in patients with HSS.
Subject(s)
Esophageal and Gastric Varices , Fascioliasis , Hepatitis , Hypertension, Portal , Schistosomiasis , Splenic Diseases , Humans , Esophageal and Gastric Varices/complications , Gastrointestinal Hemorrhage/etiology , Schistosomiasis/complications , Schistosomiasis/drug therapy , Hypertension, Portal/complications , Hypertension, Portal/drug therapy , Splenic Diseases/drug therapy , Fascioliasis/complicationsABSTRACT
BACKGROUND: Simplexvirus humanalpha1 (HuAHV-1) are common anthropozoonosis reported in marmosets but rare in howler monkeys (Alouatta sp.). METHODS: Necropsy of two brown-howler monkeys (A. caraya) and one red-howler monkey (A. guariba clamitans) from different zoo collections were performed. Fragments of all organs were examined through microscopy. Samples were submitted to IHC for Simplexvirus humanalpha 2 (HuAHV-2) [sin. Herpesvirus simplex type 2] and PCR. RESULTS: Grossly, only the A. guariba showed liver lesions characterized by multifocal, pinpoint white areas corresponding microscopically as random necrotizing herpetic hepatitis and ulcerative glossitis. Both A. caraya showed necrotizing meningoencephalitis with Cowdry A-type body inclusions within neurons and astrocytes. Immunolabeling for HuAHV-1/2 was observed in the tongue, liver, and brain. HuAHV-1 was confirmed in all samples by PCR, Sanger sequencing, and phylogenetic analyses. CONCLUSION: Necrotizing meningoencephalitis was appreciated in 2/3 of animals, and it is associated with neurologic signs. Along with ulcerative glossitis, a hallmark lesion in marmosets, it was present in one animal. Regarding herpetic hepatitis, it is not frequent in monkeys and occurs mainly in immunocompromised animals. HuAHV-1 infection was confirmed corroborating with a human source. This is the second report on captive black-howler monkeys and the first gross, histologic, immunohistochemical, and molecular description of herpetic hepatitis and ulcerative glossitis in red-howler monkeys (A. guariba).
Subject(s)
Alouatta caraya , Alouatta , Glossitis , Hepatitis , Meningoencephalitis , Humans , Animals , Simplexvirus , Callithrix , PhylogenyABSTRACT
This study described a soluble mediator storm in acute Yellow Fever/YF infection along the kinetics timeline towards convalescent disease. The analyses of the YF Viral RNAnemia, chemokines, cytokines, and growth factors were performed in YF patients at acute/(D1-15) and convalescent/(D16-315) phases. Patients with acute YF infection displayed a trimodal viremia profile spreading along D3, D6, and D8-14. A massive storm of mediators was observed in acute YF. Higher levels of mediators were observed in YF with higher morbidity scores, patients under intensive care, and those progressing to death than in YF patients who progress to late-relapsing hepatitis/L-Hep. A unimodal peak of biomarkers around D4-6 with a progressive decrease towards D181-315 was observed in non-L-Hep patients, while a bimodal pattern with a second peak around D61-90 was associated with L-Hep. This study provided a comprehensive landscape of evidence that distinct immune responses drive pathogenesis, disease progression, and L-Hep in YF patients.
Subject(s)
Hepatitis , Yellow Fever Vaccine , Yellow Fever , Humans , Yellow Fever/pathology , Prognosis , Cytokines , BiomarkersABSTRACT
BACKGROUND: Late-relapsing hepatitis after yellow fever (LHep-YF) during the convalescent phase of the disease has been described during recent yellow fever (YF) outbreaks in Brazil. LHep-YF is marked by a rebound in liver enzymes and nonspecific clinical manifestations around 46-60 days after YF symptom onset. METHODS: Here we have characterized the clinical course and risk factors for LHep-YF using data from a representative cohort of patients who survived YF in Brazil, 2017-2018. A total of 221 YF-positive patients were discharged from the infectious disease reference hospital in Minas Gerais and were followed up at 30, 45, and 60 days post-symptom onset. RESULTS: From 46 to 60 days post-symptom onset, 16% of YF patients (n = 36/221) exhibited a rebound of aminotransferases (aspartate aminotransferase or alanine aminotransferase >500 IU/L), alkaline phosphatase, and total bilirubin levels. Other etiologies of liver inflammation such as infectious hepatitis, autoimmune hepatitis, and metabolic liver disease were ruled out. Jaundice, fatigue, headache, and low platelet levels were associated with LHep-YF. Demographic factors, clinical manifestations, laboratory tests, ultrasound findings, and viral load during the acute phase of YF were not associated with the occurrence of LHep-YF. CONCLUSIONS: These findings provide new data on the clinical course of Late-relapsing hepatitis during the convalescent phase of YF and highlight the need for extended patient follow-up after acute YF.
Subject(s)
Hepatitis A , Hepatitis , Yellow Fever Vaccine , Yellow Fever , Humans , Yellow Fever/complications , Yellow Fever/epidemiology , Disease Outbreaks , Risk Factors , Hepatitis/epidemiology , Hepatitis A/epidemiology , Brazil/epidemiology , Disease ProgressionABSTRACT
OBJECTIVE: To evaluate whether the nature and severity of non-A-E severe acute hepatitis in children noted by the World Health Organization from late 2021 through early 2022 was indeed increased in 2021-2022 compared with prior years. STUDY DESIGN: We performed a single-center, retrospective study to track the etiology and outcomes of children with non-A-E severe acute hepatitis in 2021-2022 compared with the prior 3-year periods (2018-2019, 2019-2020, and 2020-2021). We queried electronic medical records of children ≤16 years of age with alanine or aspartate aminotransferase levels of >500 IU. Data were analyzed for the periods of October 1, 2021, to May 1, 2022, and compared with the same time periods in 2018-2021. RESULTS: Of 107 children meeting entry criteria, 82 cases occurred from October to May of 2018-2022. The average annual case number was 16.3 in 2018-2021 compared with a 2-fold increase (to 33) in 2021-2022 (P = .0054). Analyses of etiologies showed that this increase was associated with a higher number of children who tested positive for viruses (n = 16) when compared with the average of 3.7 for 2018-2021 (P = .018). Adenovirus (26.1%) and severe acute respiratory syndrome coronavirus-2 (10.3%) were the most frequently detected viruses in 2021-2022. Despite evidence of acute liver failure in 37.8% of children in the entire cohort and in 47% of those with viral infection, the overall survival rate was high at 91.4% and 88.9%, respectively. CONCLUSIONS: The number of children with severe acute hepatitis in our center increased from 2021 to May 2022, with a greater frequency of cases associated with adenovirus, yet transplant-free survival remains high.
Subject(s)
Adenoviridae Infections , COVID-19 , Hepatitis , Humans , Child , Adenoviridae , Retrospective Studies , Incidence , Adenoviridae Infections/epidemiologyABSTRACT
El shunt portosistémico congénito es una anomalía vascular venosa que comunica circulación portal y sistémica, por la que se deriva el flujo sanguíneo, salteando el paso hepático. Es una entidad poco frecuente, cuya incidencia varía entre 1/30 000 y 1/50 000 recién nacidos. Puede cursar de forma asintomática o presentarse con complicaciones en la edad pediátrica o, menos frecuente, en la edad neonatal. Ante el diagnóstico, se deberá definir la necesidad de intervención quirúrgica o intravascular para el cierre. Esta decisión depende de las características anatómicas de la malformación, de las manifestaciones clínicas y complicaciones presentes. Se presenta el caso de un paciente de un mes de vida derivado a nuestro centro para estudio de hepatitis colestásica neonatal, con diagnóstico de shunt portosistémico extrahepático. Se realizó cierre intravascular de la lesión con mejoría significativa posterior.
Congenital portosystemic shunt is a venous vascular abnormality that connects portal and systemic circulation, resulting in diversion of the blood flow, bypassing the hepatic passage. It is a rare malformation; its incidence varies from 1:30 000 to 1:50 000 newborns. It may be asymptomatic or present with complications in the pediatric age or, less frequently, in the neonatal age. Upon diagnosis, the need for a surgical or an intravascular intervention for closure should be defined. This decision depends on the malformation anatomical characteristics, clinical manifestations, and complications. We present the case of a 1-month-old patient referred to our center for the study of neonatal cholestatic hepatitis, with a diagnosis of extrahepatic portosystemic shunt. Intravascular closure of the defect was performed with significant subsequent improvement.
Subject(s)
Humans , Male , Infant, Newborn , Portasystemic Shunt, Transjugular Intrahepatic , Vascular Malformations/complications , Endovascular Procedures , Hepatitis/diagnosis , Hepatitis/etiology , Portal Vein/abnormalitiesSubject(s)
COVID-19 Vaccines , COVID-19 , Drug Hypersensitivity Syndrome , Eosinophilia , Hepatitis , Pancreatitis , Humans , COVID-19/prevention & control , COVID-19/complications , COVID-19 Vaccines/adverse effects , Drug Hypersensitivity Syndrome/complications , Eosinophilia/complications , Hepatitis/complications , Pancreatitis/chemically induced , Pancreatitis/complications , VaccinationABSTRACT
BACKGROUND & AIMS: Fibroblast activation protein (FAP) is expressed on activated fibroblast. Its role in fibrosis and desmoplasia is controversial, and data on pharmacological FAP inhibition are lacking. We aimed to better define the role of FAP in liver fibrosis in vivo and in vitro. METHODS: FAP expression was analyzed in mice and patients with fibrotic liver diseases of various etiologies. Fibrotic mice received a specific FAP inhibitor (FAPi) at 2 doses orally for 2 weeks during parenchymal fibrosis progression (6 weeks of carbon tetrachloride) and regression (2 weeks off carbon tetrachloride), and with biliary fibrosis (Mdr2-/-). Recombinant FAP was added to (co-)cultures of hepatic stellate cells (HSC), fibroblasts, and macrophages. Fibrosis- and inflammation-related parameters were determined biochemically, by quantitative immunohistochemistry, polymerase chain reaction, and transcriptomics. RESULTS: FAP+ fibroblasts/HSCs were α-smooth muscle actin (α-SMA)-negative and located at interfaces of fibrotic septa next to macrophages in murine and human livers. In parenchymal fibrosis, FAPi reduced collagen area, liver collagen content, α-SMA+ myofibroblasts, M2-type macrophages, serum alanine transaminase and aspartate aminotransferase, key fibrogenesis-related transcripts, and increased hepatocyte proliferation 10-fold. During regression, FAP was suppressed, and FAPi was ineffective. FAPi less potently inhibited biliary fibrosis. In vitro, FAP small interfering RNA reduced HSC α-SMA expression and collagen production, and FAPi suppressed their activation and proliferation. Compared with untreated macrophages, FAPi regulated macrophage profibrogenic activation and transcriptome, and their conditioned medium attenuated HSC activation, which was increased with addition of recombinant FAP. CONCLUSIONS: Pharmacological FAP inhibition attenuates inflammation-predominant liver fibrosis. FAP is expressed on subsets of activated fibroblasts/HSC and promotes both macrophage and HSC profibrogenic activity in liver fibrosis.
Subject(s)
Hepatitis , Liver Diseases , Humans , Mice , Animals , Carbon Tetrachloride/toxicity , Liver Cirrhosis/metabolism , Inflammation , Fibrosis , Collagen/metabolism , Fibroblasts/metabolism , Macrophages/metabolismABSTRACT
Congenital portosystemic shunt is a venous vascular abnormality that connects portal and systemic circulation, resulting in diversion of the blood flow, bypassing the hepatic passage. It is a rare malformation; its incidence varies from 1:30 000 to 1:50 000 newborns. It may be asymptomatic or present with complications in the pediatric age or, less frequently, in the neonatal age. Upon diagnosis, the need for a surgical or an intravascular intervention for closure should be defined. This decision depends on the malformation anatomical characteristics, clinical manifestations, and complications. We present the case of a 1-month-old patient referred to our center for the study of neonatal cholestatic hepatitis, with a diagnosis of extrahepatic portosystemic shunt. Intravascular closure of the defect was performed with significant subsequent improvement.
El shunt portosistémico congénito es una anomalía vascular venosa que comunica circulación portal y sistémica, por la que se deriva el flujo sanguíneo, salteando el paso hepático. Es una entidad poco frecuente, cuya incidencia varía entre 1/30 000 y 1/50 000 recién nacidos. Puede cursar de forma asintomática o presentarse con complicaciones en la edad pediátrica o, menos frecuente, en la edad neonatal. Ante el diagnóstico, se deberá definir la necesidad de intervención quirúrgica o intravascular para el cierre. Esta decisión depende de las características anatómicas de la malformación, de las manifestaciones clínicas y complicaciones presentes. Se presenta el caso de un paciente de un mes de vida derivado a nuestro centro para estudio de hepatitis colestásica neonatal, con diagnóstico de shunt portosistémico extrahepático. Se realizó cierre intravascular de la lesión con mejoría significativa posterior.
Subject(s)
Endovascular Procedures , Hepatitis , Portasystemic Shunt, Transjugular Intrahepatic , Vascular Malformations , Infant, Newborn , Humans , Child , Infant , Portal Vein/abnormalities , Hepatitis/diagnosis , Hepatitis/etiology , Vascular Malformations/complicationsABSTRACT
Fowl aviadenovirus (FAdV) is an important pathogen in the global poultry industry and the etiology of inclusion body hepatitis-hydropericardium syndrome (HHS) in chickens. Since the 1990s, several outbreaks of HHS have occurred in poultry producing areas, including South America. The coinfection of FAdV and chicken anemia virus (CAV) may markedly impact the incidence of HHS. This study describes an outbreak of HHS in coinfection with CAV in industrial broiler breeders and characterizes the FAdV isolate. The three-week-old male broiler breeders had pale bone marrow, enlarged and yellowish liver, splenomegaly, and atrophied thymus; one chicken was also found with hydropericardium. Virus isolation was performed in SPF chicken embryos of liver and thymus. Tissues of the naturally infected chickens and the inoculated embryos were evaluated by PCR and histopathology. All affected chickens and inoculated embryos were positive for FAdV and CAV. The inoculated embryos had enlarged, greenish and hemorrhagic livers, and 30% died within 7 days of inoculation. Phylogenetic analysis of the FAdV isolate hexon gene partial sequence enabled grouping with E species. The E species has recently become a relevant species in several countries. The association of FAdV with CAV in breeders is of further concern due to both being capable of vertical transmission. Within the last decade, a worldwide upsurge of HHS in broiler breeders owing to failed biosecurity has occurred. In this episode, the failure on biosecurity may have enabled challenge with both FAdV and CAV, with pathological synergism. The CAV-impaired adaptive immunity may have benefited the FAdV infection.
Adenovírus aviário (FAdV) é um importante patógeno na indústria avícola global e a etiologia da síndrome da hepatite por corpúsculo de inclusão-hidropericárdio (SHH) em galinhas. Desde a década de 1990, vários surtos de SHH foram descritos em todas as áreas de produção de aves, incluindo na América do Sul, e a coinfecção entre FAdV e vírus da anemia das galinhas (CAV) pode ser agravante para todos os aspectos da SHH. Objetiva-se descrever um surto de SHH em matrizes de frangos corte, caracterizar a estirpe de FAdV envolvida e destacar a coinfecção com CAV. Foram avaliados machos reprodutores de corte com três semanas de idade, com medula óssea pálida, fígado aumentado e amarelado e esplenomegalia, timo atrofiado e um com hidropericárdio. Fígado e timo foram coletados para isolamento do vírus em embriões de galinhas SPF, PCR e histopatologia. Todas as aves acometidas e embriões inoculados foram positivos para FAdV e CAV. Os embriões inoculados tiveram óbito de 30% em até sete dias após a inoculação e alterações hepáticas por fígados esverdeados e aumentados. A análise filogenética de FAdV com base em parte da sequência do gene que codifica a proteína hexon revelou identidade com a espécie E, que se tornou disseminada em vários países. A coinfecção de FAdV e CAV resulta em maior intensidade de lesões, maior morbidade e mortalidade e em reprodutores tem alta relevância epidemiológica, em razão da transmissão vertical de ambos e da ampla distribuição geográfica das progênies infectadas. Na última década, ocorreu um aumento mundial na ocorrência de SHH em frangos de corte relacionado a falhas em biosseguridade, especialmente em reprodutores, condição que pode ter ocorrido neste episódio. A presença de FAdV e CAV em reprodutores é motivo para preocupação por reflexos negativos à imunidade e viabilidade das progênies.
Subject(s)
Animals , Poultry Diseases , Chickens , Aviadenovirus , Heartwater Disease , HepatitisABSTRACT
Las hepatitis virales crónicas B y C son grandes amenazas para la salud pública a nivel mundial, según la Organización Mundial de la Salud (OMS), en 2019 se estimó la cifra de 354 millones de personas con hepatitis B crónica (296 millones) y C (58 millones), registrando más de 1,1 millones de muertes, principalmente por complicaciones como cirrosis y cáncer hepatocelular. En las Américas, para el 2019 se notificó 3,9 millones de personas con hepatitis B crónica; 7,2 millones de personas con hepatitis C crónica y 125.000 muertes registradas a causa de cáncer de hígado y enfermedad hepática (cirrosis). Para lograr los objetivos de la estrategia global en los próximos ocho años, las nuevas infecciones por hepatitis viral B (HVB) y C (VHC) deben reducirse alrededor de 3 millones de casos nuevos en 2020 a 520.000 para 2030 y las muertes por hepatitis viral B y C deben reducirse de 1,1 millones a menos de 500 000 muertes.
Chronic viral hepatitis B and C are major threats to public health worldwide, according to the World Health Organization (WHO), in 2019 the number of 354 million people with hepatitis B was estimated chronic (296 million) and C (58 million), registering more than 1.1 million of deaths, mainly due to complications such as cirrhosis and hepatocellular cancer. In the Americas, by 2019, 3.9 million people with chronic hepatitis B; 7.2 million people with chronic hepatitis C and 125,000 recorded deaths from liver cancer and liver disease liver (cirrhosis). To achieve the objectives of the global strategy in the next eight years, new viral hepatitis B (HVB) and C (HCV) infections should be reduced from around 3 million new cases in 2020 to 520,000 by 2030 and deaths from viral hepatitis B and C must be reduced from 1.1 million to fewer than 500,000 deaths.