Transient flu-like symptoms
Introduction
Introduction Avian influenza is a syndrome of a variety of symptoms ranging from respiratory diseases to severe sepsis in poultry and wild birds caused by influenza A virus. It has occurred in many countries and regions in the world, causing huge economic losses to the poultry industry. This avian influenza virus mainly causes systemic or respiratory diseases of poultry. Poultry and wild birds such as chickens, turkeys, ducks and quails, water birds and seabirds can be infected. The incidence is from acute septic death to asymptomatic. The variety of poisons, etc., depends mainly on the resistance of the diseased body and the type and virulence of the virus. The avian flu virus is different from the SARS virus. The avian flu virus has so far only been transmitted to humans through poultry and cannot be transmitted to humans through humans. The human avian influenza virus H5N1 is a new variant of the virus, not the H5N2 that has been circulating in chickens and ducks for decades. There is no need to talk about the avian flu discoloration. At present, no chickens have been found to cause avian influenza H5N1 infection. They are all in close contact with chickens and may cause infections due to direct inhalation or entry into the mucosa.
Cause
Cause
The cause of transient flu-like symptoms:
Human avian influenza (hereinafter referred to as human avian influenza) is an acute respiratory infection caused by a strain of certain subtypes of avian influenza A virus.
The causative agent of avian influenza (AI) is avian influenza virus (AIV), which belongs to the genus of the Orthomyxoviridae influenza virus.
(1) Characteristics of the Orthomyxoviridae: The viruses of the Orthomyxovirus and Paramyxoviridae have many of the same characteristics, both with neuraminidase (NA) and hemagglutinin (HA), which can agglutinate red blood cells of certain animals. It has pathogenicity to the respiratory system, especially the two viruses have a special affinity for mucopolysaccharides and glycoproteins, especially for sialic acid-containing receptors on the cell surface.
There is only one genus in the Orthomyxovirus family, namely the genus of influenza virus. According to the antigenicity of influenza virus nucleoprotein (NP) and matrix protein (MS), it is divided into three serotypes A, B and C. The difference of antigen between them can be measured by agar diffusion test and complement binding test. Out. In addition to the different antigenicity of their nuclear proteins and matrix proteins, the A, B, and C influenza viruses have the following different biological characteristics.
(2) Influenza A is likely to infect humans, but also infects many other species of animals, such as horses, pigs, poultry, seals, etc., while type B mainly infects humans, but type C can also be isolated from pigs. . The surface glycoprotein of type A flow-infected virus has higher variability than type B and type C. In terms of morphological characteristics and molecular biological characteristics, both type A and type B have eight nucleic acid fragments, while type C has only seven fragments.
According to the difference in the antigenicity of influenza virus hemagglutinin HA and neuraminidase NA, they can be divided into different subtypes. Currently, influenza A viruses have 15 specific HAs and 9 specific NAs.
(3) Avian influenza virus strain classification: The classification of AIV strains is based on HA and NA subtypes. Fifteen hemagglutinin HAs and nine neuraminidase NAs have been discovered, all of which have been identified from avian influenza isolates in different combinations. To identify the HA and NA of the virus, a set of antisera specific for different subtypes was applied and the isolates were subjected to hemagglutination inhibition (HI) and neuraminidase inhibition (NA) assays.
Comparison of the same subtype of virus, commonly used chicken and snow leopard infected serum and monoclonal antibodies. The use of monoclonal antibodies allows for a more detailed comparison of the relevant viruses present in the same or different species of animals, after which the virus is compared by HI, enzyme-linked immunosorbent assay (DLISA) and neutralization assays.
(4) Naming: For the naming of AIV, the standard system for naming influenza viruses was proposed in 1971 and revised in 1980. The name of an influenza virus includes type (A, B or C), host source (except human), geographical origin. The strain number (if any) and the age of the isolate, followed by the antigenicity of HA(H) and (N) in parentheses.
2. Morphology: AIV particles are generally spherical and have a diameter of 80 to 120 nm, but they often have a filamentous shape of the same diameter and vary in length. The surface of the virion is covered with dense nails or fibrils of 10 to 12 nm, and a spiral nucleocapsid is present in the viral envelope. Two differently shaped surface spikes are HA (rod trimer) and NA (mushroom tetramer).
The role of HA is to adsorb virions on cell surface receptors (sialic oligosaccharides) and correlate with the hemagglutination activity of the virus. In the neutralization of viruses and protection against infection, anti-HA antibodies are very important; the activity of NA enzymes is to release new viruses from cells through the action of neuraminic acid in the receptor. Anti-NA antibody pairs Protection is also important.
The three-dimensional structure of hemagglutination H2HA and neuraminic acid N2 and N9NAS has been determined and important antigenic regions or epitopes have been identified.
Both HA and NA, as well as small proteins called M2, are embedded in the lipid membrane of the host cell plasma membrane. The viral envelope is the major structural protein M1, which is located around the RNA molecule, and is responsible for RNA replication and transcription with the molecular protein NP and three large proteins (PB1, PB2 and PA).
The viral genome consists of 8 negative-stranded single-stranded RNA fragments. These 8 fragments encode 10 viral proteins, 8 of which are components of virions (HA, NA, NP, M1, M2, PB1, PB2, and PA). The smallest molecular fragment of RNA encodes two non-structural proteins. NS1 and NS2. NS1 is associated with cytoplasmic inclusion bodies, but the function of NS1 and NS2 is unclear. The entire sequence of several avian subtype HA genes including H3, H5 and H7, as well as partial sequences of all 14 hemagglutinin genes, have now been obtained.
3. Chemical composition: Influenza virions consist of approximately 0.8% to 1.1% RNA, 70% to 75% protein, 20% to 24% lipid and 5% to 8% carbohydrate. Lipids are located in the membrane of the virus, mostly phospholipids, and a small amount of cholesterol and glycolipids. Several carbohydrates include ribose (in RNA), galactose, mannose, fucose, and glucosamine. It is mainly present in the form of glycoproteins or glycolipids in virions. Viral proteins and potential glycosylation sites are viral genome-specific, but the components of the lipid and carbohydrate chains of the glycoprotein or carbohydrate chain of the viral membrane are determined by the host cell.
4. Viral replication: The virus is sucked on the glycoprotein receptor containing sialic acid on the cell surface, and then the virus enters the cell through receptor-mediated endocytosis. This includes exposure to low pH in the nucleus, resulting in a conformational change in HA that mediates membrane fusion. In this way, the nucleocapsid enters the cytosol and moves to the nucleus. The influenza virus transcribes using a unique mechanism. When transcription is initiated, the endonuclease of the virus cleaves the 5' cap structure from the mRNA of the host cell and serves as a primer for transcription of the viral transcriptase. Six single-seven mRNAs were generated and translated into HA, NA, NP and three polymerases (PB1, PB2 and PA). The mRNAs of the NS and M genes were spliced, each producing two mRNAs, which were translated according to different reading frames to produce NS1, NS2, M1 and M2 proteins. HA and NA are glycosylated in the rough endoplasmic reticulum, modified in the Golgi, then transported to the surface and implanted in the cell membrane. HA requires host cell protease to cleave it into HA1 and HA2, but both still use disulfide bonds. Connected, this cleavage produces an infectious virus and emanately excretes cells from the plasma membrane.
5. Antigenic variation: The frequency of antigenic changes in influenza viruses is high, mainly in two ways: drift and transformation. Antigen drift can cause secondary antigenic changes in HA and/or NA, which can cause major antigenic changes in HA and/or NA.
(1) Antigenic drift: Antigenic drift is caused by point mutation of a gene encoding HA and/or NA protein, and is a reaction for screening variants in an immune population, which can cause the emergence of a more pathogenic virus.
(2) Antigenic transformation: The antigenic transformation is when the cells infect two different influenza viruses, the fragment characteristics of the viral genome allow fragment recombination to occur, thereby causing a transformation. It has the potential to produce 256 genetically distinct progeny viruses of varying virulence.
6. Resistance to physical and chemical factors:
Influenza A virus is an envelope virus that is sensitive to the inactivation of lipid solvents such as detergents. Formalin, beta-propiolactone, oxidizing agents, dilute acid, diethyl ether, sodium deoxycholate, hydroxylamine, sodium lauryl sulfate and ammonium ions can rapidly destroy the infectivity. The avian influenza virus does not have exceptional stability, so it is not difficult to inactivate the virus itself. The virus can be inactivated under heating, extreme pH, non-isotonic and dry conditions.
In the wild, influenza viruses are often excreted from the nasal secretions and feces of infected birds, and the virus is greatly protected against inactivation by the protection of these organisms. In addition, influenza viruses can survive for a long time in the natural environment, especially in cool and humid conditions. The infectivity of the virus in feces can be maintained for up to 30 to 50 days at 4 ° C and 7 days at 20 ° C.
7. Pathogenicity and virulence of avian influenza virus:
The pathogenicity of avian influenza viruses varies widely. Diseases caused by influenza virus infection may be inconspicuous or mild transient syndromes, even diseases with 100% morbidity and/or mortality. Symptoms of the disease may manifest in the respiratory, intestinal, or reproductive systems and vary with virus type, animal species, age, concurrent infection, surrounding environment, and host immune status. The virulence of avian influenza virus is mainly determined by the replication rate of virions and the amino acid composition near the hemagglutinin cleavage site.
At present, the virulence is generally determined according to the European Community's intravenous inoculation disease index (IVPI). When the IVPI is >1.2, it is considered to be a highly pathogenic strain.
Examine
an examination
Related inspection
Influenza virus antibody chest MRI
Most people with avian influenza have lower white blood cell levels than normal, and lymphocyte levels are not high or even lower. If the platelet level is reduced, it is necessary to consider whether there is diffuse intravascular coagulation due to severe infection, and should be combined with coagulation analysis, fibrinogen levels and other results. Blood biochemical tests mostly increased creatine kinase, lactate dehydrogenase, aspartate aminotransferase, alanine aminotransferase, elevated C-reactive protein, and elevated myoglobin.
Imaging studies revealed a flaky shadow in the lungs of patients with pneumonia. In severe cases, the lesion progresses rapidly, and there are multiple hairy glass shadows and lung consolidation images in the lungs, which can be combined with a small amount of pleural effusion. When ARDS occurs, the lesions are widely distributed.
The most reliable is still the pathogen test. Before the antiviral treatment, the conditional medical unit collects the respiratory specimens for examination (such as nasopharyngeal secretions, oral sputum, tracheal aspirate or respiratory epithelial cells) for viral nucleic acid detection (real-time fluorescent PCR detection) and virus. Separation.
In addition to avian influenza virus infection, human infection with avian influenza often combines or secondary bacterial infections at an early stage. After long-term or large doses of antibacterial drugs and inappropriate use of glucocorticoids, fungal infections may also be combined. Therefore, clinically, sputum culture, respiratory tract culture should be carried out several times to check the type of bacteria and/or fungi, and the type of sensitivity or drug resistance, so as to rationally select antibiotics and guide clinical treatment.
Diagnosis
Differential diagnosis
Symptoms of transient flu-like symptoms that are confusing:
Clinical attention should be paid to the differential diagnosis of diseases such as influenza, common cold, bacterial pneumonia, infectious atypical pneumonia (SARS), infectious mononucleosis, cytomegalovirus infection, chlamydia pneumonia, and mycoplasmal pneumonia.
Identification with influenza:
Influenza is generally divided into three types, namely, type A, type B and type C. Types B and C are generally transmitted only in the crowd and rarely transmitted to other animals. Most of the influenza A is avian flu, and the avian flu virus is rarely ill. Avian flu is mainly transmitted among birds, and can even be infected to humans. Its clinical manifestations are similar to those of human influenza, but human avian flu has serious symptoms and complications, which is different from ordinary flu.
Clinical manifestations:
1. Incubation period: generally 1 to 3 days, usually within 7 days.
2, clinical symptoms of acute onset, early performance similar to the common type of influenza. Mainly for fever, body temperature mostly lasts above 39 °C, heat course 1 to 7 days, usually 3 to 4 days, may be associated with salivation, nasal congestion, cough, sore throat, headache and general malaise. Some patients may have gastrointestinal symptoms such as nausea, abdominal pain, diarrhea, and watery stools. Severe patients develop rapidly, and can have various complications such as pneumonia, acute respiratory distress syndrome, pulmonary hemorrhage, pleural effusion, whole blood cell reduction, renal failure, sepsis, shock and Reye syndrome.
3, physical signs: critically ill patients may have physical signs of the lungs and so on.
