SARS

Introduction to SARS Infectious atypical pneumonia (SARS) is a special infectious pneumonia caused by SARS-CoV (SARS-CoV) that is contagious and can affect multiple organ systems. World Health Organization (WHO) It is named as severe acute respiratory syndrome (SARS). It is clinically characterized by fever, fatigue, headache, muscle and joint pain and other respiratory symptoms such as dry cough, chest tightness and dyspnea. Some cases may have diarrhea, etc. Gastrointestinal symptoms; chest X-ray examination showed pulmonary inflammatory infiltration, laboratory examination of peripheral blood leukocyte counts normal or decreased, antibacterial drug treatment is an important feature. Severe cases show significant dyspnea and can rapidly develop into acute respiratory distress syndrome (ARDS). As of August 7, 2003, the cumulative number of cases worldwide was 8422, and the average case fatality rate based on reported cases reached 9.3%. basic knowledge The proportion of sickness: 0.00001% Susceptible people: no special people. Mode of infection: respiratory transmission Complications: shock, sepsis, gastrointestinal bleeding, disseminated intravascular coagulation

SARS cause

(1) Epidemiology

Classical coronavirus infection mainly occurs in winter and spring, and is widely distributed throughout the world. The virus includes three groups. The first and second groups are mainly mammalian coronavirus, the third group mainly includes avian coronavirus, and the human coronavirus has two. A bloody type (HCo-229E, HCoV-OC43) is an important pathogen of human respiratory infection. 20% of human common cold is caused by coronavirus. Coronavirus is also one of the important causes of acute exacerbation of chronic bronchitis in adults. Genomics The results show that the SARS-CoV gene is different from the known three classical coronaviruses. The first group of virus sera can react with SARS-CoV, while the SARS patients' serum cannot react with the known coronavirus. Therefore, As a new coronavirus, SARS-CoV can be classified as the fourth group.

(2) Morphological structure

SARS-CoV belongs to the genus Coronavirus of the Coronavirus family. It is an enveloped virus with a diameter of 60-120 nm. It has petal-like or cilia-like protrusions on the envelope. It is about 20 nm long or longer. The base is narrow and looks like a crown. Similar to the classic coronavirus, the morphogenesis of the virus is long and complex. The mature virus is spherical, elliptical, and the mature and immature virions vary greatly in size and morphology. Many strange things can occur. Morphology, such as kidney shape, drumstick shape, horseshoe shape, bell shape, etc., is easily confused with organelles. In size, the virus particles are reduced from the initial 400nm to the late mature stage of 60-120nm, and also in the patient's autopsy specimens. A variety of viral particles can be seen.

(3) Biological characteristics

The virus proliferates in the cytoplasm, and the polymerase encoded by the RNA gene utilizes cellular material for RNA replication and protein synthesis, assembles into a new virus, and buds are secreted outside the cell. Unlike the coronavirus previously discovered, Vero-E6 or Vero (green monkey) is used. The kidney cells are easy to isolate and culture the SARS-CoV. The virus grows well at 37 °C. The cells can be infected within 24 hours after infection. The virus can be titrated with plaques. The culture titer of the early isolates is generally up to 1 ×106pfu/ml or so, can be cultured on RD (human striated muscle tumor cells), MDCK (dog kidney cells), 293 (human embryonic kidney cells), 2BS (human embryo lung cells) and other cell lines, but the titer is low. .

The virus can survive for at least 10 days in the urine at room temperature of 24 ° C, survive for more than 5 days in the sputum and feces of diarrhea patients, and survive for 15 days in the blood, in plastic, glass, mosaic, metal, cloth, copy A variety of objects such as paper can survive for 2-3 days.

The virus is sensitive to temperature and has a decreased resistance with increasing temperature. It can survive for 4 days at 37 ° C, 90 minutes at 56 ° C, and 30 minutes at 75 ° C to inactivate the virus. UV irradiation for 60 minutes can kill the virus.

The virus is sensitive to organic solvents. The effect of the ether at 4 ° C for 24 hours can completely inactivate the virus, 75% ethanol for 5 minutes can make the virus lose its vitality, and the chlorine-containing disinfectant can inactivate the virus for 5 minutes.

(4) Characteristics of molecular biology

The viral genome is a single-stranded positive-stranded RNA consisting of approximately 30,000 nucleotides, which is only about 60% homologous to the classical coronavirus, but the genome is organized similarly to other coronaviruses, with the genome from 5 to 3 :5'-Polymerase-SEMN-3, with a methylated cap structure at the 5'-end, followed by a 72-nucleotide leader sequence, and approximately 2/3 of the genomic RNA is the Open Journalist Framework (ORF) 1a/1b, encoding RNA polymerase (Rep), which directly translates from genomic RNA to form a polyprotein precursor, which is further cleaved by the major protease 3CLpro, which is responsible for transcription and replication of the virus. There are 4 ORFs downstream of Rep, encoding S, respectively. E, M and N four structural proteins, which are translated from subgenomic mRNA, subgenomic mRNA is synthesized by a mechanism of discontinuous transcription, transcription is initiated by transcriptional regulatory sequence (TRS), and the conserved sequence of the latter is AAACGAAC, genome The 3 end has a polyA tail.

The viral envelope is a bilayer lipid membrane, and the outer membrane proteins include glycoprotein S, M and vesicle E protein. M glycoprotein is different from other coronavirus glycoproteins, and only the short amino terminal domain is exposed to the viral envelope. Outside, the long and curved spiral nucleocapsid structure consists of a single molecule of genomic RNA, a multi-molecular basic N protein, and the carboxy terminus of the M protein. The simulated structure of the virus is shown in Figure 1. The S protein is responsible for cell adhesion. , membrane fusion and induction of neutralizing antibodies, relative molecular mass of about 150,000-180000, including extracellular domain, transmembrane domain and short carboxy terminal cytoplasmic domain, in classical coronavirus, E protein and M protein may have the smallest composition In the assembly unit, the E protein plays a key role in the assembly of the virus. The M protein plays an important role in the stability of the virus core. Unlike other coronaviruses, between S and E (X1-274aa, X2-154aa) and M and Potential coding sequences for polypeptides with more than 50 amino acids between N (X3-63aa, X4-122aa, X5-84aa), and potential coding sequences for polypeptides with less than 50 amino acids between M and N, homology search result Ming, these potential polypeptide with any other protein sequence have no similarity.

At present, domestic and foreign scientists have reported the genome-wide sequence of several SARS-CoVs, and found that the degree of variation is not high. There are 4 strains from Singapore, 1 strain in Canada, 1 strain in the United States, 2 strains in Hong Kong, 4 strains in Beijing and 1 strain in Guangdong. A total of 129 mutations were found in 13 strains. According to its phylogenetic tree, the current epidemic strains can be divided into two genomes: one group includes four strains of Beijing (BJ01-BJ04), and one strain of Guangzhou (GZ01). One strain (CUHK) measured by the Chinese University of Hong Kong and other strains belong to another group. Analysis of the variability of the virus may provide clues for tracking the source of the virus.

(5) Immunological characteristics

In most cases, when SARS-CoV is infected, the human immune system can stimulate humoral and cellular immune responses and gradually control infection and clear the virus. There is a lot of evidence that the human immune system can stimulate humoral immunity and cells when SARS-CoV is infected. The immune response gradually controls the infection and clears the virus. There is a lot of evidence that SARS-CoV can directly invade the immune system, leading to lymphocytes, leukopenia and pathological damage of peripheral lymphoid tissues. The majority of SARS patients have normal or decreased peripheral blood leukocyte counts. CD3+, CD4+, CD8+, T lymphocytes were significantly lower than normal people. The more severe the disease, the more obvious the decrease of T lymphocyte count. After the recovery of SARS patients, the number and function of T lymphocytes gradually returned to normal. SARS-CoV nucleic acids were generally 5 days after the onset of clinical symptoms, it can be detected from the patient's nasopharyngeal extract, peaking around the 10th day, and then starting to decrease; 21 days, 47% of patients with nasopharyngeal extract is positive, 67% of stool specimens are positive, 21 % urine sample is positive, N protein can induce strong immune response, so it can be used for antibody detection Test, the detection of antibodies showed that 1 week after the onset of the disease, IgM began to occur in the patient, which lasted for up to 3 months; IgG started to be produced around 7-10 days, then gradually increased, and the antibody titer reached a peak around 1 month. And all positive conversion, until the patient recovered 6 months still high level positive, SARS is a new disease, the population is generally susceptible, epidemiological data show that SARS-CoV mainly causes dominant infection, there is still no subclinical Evidence of infection, after the SARS epidemic, did not form an immune protective barrier in the population, the population is still generally susceptible, detection of serum SARS-VoV-specific antibodies in patients with clinical diagnosis.

SARS is a new infectious disease caused by SARS-CoV. The understanding of its pathogenesis is still unclear. Some of the clues obtained are mainly from autopsy data of SARS deaths, ultrastructural studies, and SARS at the nucleic acid level. Many aspects of CoV detection and clinical data of patients with SARS are still speculated and inevitably affected by treatment measures.

SARS-CoV enters the human body through the respiratory tract and replicates in the mucosal epithelium of the respiratory tract, further causing viremia. The cells infected by the virus include tracheal bronchial epithelial cells, alveolar epithelial cells, vascular endothelial cells, macrophages, intestinal epithelial cells, Renal distal ductal epithelium and lymphocytes, alveolar epithelial cells and pulmonary vascular endothelial cells can damage the integrity of the respiratory membrane blood gas barrier, accompanied by inflammatory hyperemia, causing massive exudation of serum and fibrinogen, exudation Fibrinogen aggregates into cellulose, which in turn forms a transparent membrane with necrotic alveolar epithelial debris.

The body's response to SARS-CoV infection can be manifested by macrophage and lymphocyte exudation in the interstitial lung. Activated macrophages and lymphocytes release cytokines and free radicals, further increasing the permeability of alveolar capillaries. And induced fibroblast proliferation, damaged alveolar epithelial cells fall into the alveolar cavity can form desquamative alveolitis, and the alveolar cavity contains a large number of macrophages, proliferative shedding of alveolar epithelial cells and macrophages can form giant Cells, in terms of giant cell phenotype, are mainly alveolar epithelial cell sources (AE1/AE3 positive), and a few are macrophage sources (CD68 positive). The formation of giant cells may be related to SARS-CoV infection, because in vitro experiments It is proved that SARS-CoV infection can fuse Vero cells to form syncytial cells. The above changes in lungs are consistent with the change of exudation period of diffuse alveolar damage (DAD). The proliferative phase of DAD is followed by patients with severe or poor recovery. And fibroblasts, and produce type I and type III collagen fibers, intestinal epithelial cells and kidney distal segmental epithelial cells are infected by SARS-CoV, on the one hand Gastrointestinal symptoms in patients with clinical part, it also may have some significance in terms of transmission of the disease,

Due to decreased blood oxygen saturation caused by DAD and diffuse lung changes, and endovascular intravascular coagulation caused by factors such as vascular endothelial cell injury, multiple organ failure often results in death of the patient.

The peripheral blood lymphocytes of SARS patients are reduced, especially the number of CD4+ cells is reduced, and there is evidence that SARS-CoV directly infects lymphocytes, which may be related to the cytotoxicity of SARS-CoV and the induction of apoptosis. The humoral immune response of patients with kjqdSARS It seems normal, but SARS-CoV infection will affect the humoral immune response to varying degrees from the perspective of SARS patients' recovery serum. SARS-CoV affects cellular and humoral immune responses in the development of SARS. Certainly, at least means that patients with cellular and humoral immune damage have a poor prognosis.

The materials related to SARS biopsy and autopsy are limited, so the understanding of pathological changes is still limited. Based on current autopsy materials and a small amount of bronchial biopsy, SARS mainly involves lung and immune organs such as spleen and lymph nodes, other organs such as heart and liver. Kidney, adrenal gland, brain, etc. can also be seen with varying degrees of damage,

Lung: generally bulging, swelling, weight increase, except for secondary infection, the pleura is generally smooth, dark red or dark gray-brown, no or a small amount of fluid in the chest, the lung tissue section is more uniform It can affect the whole lung and other leaves, like the hepatic metamorphosis of lobar pneumonia, color reddish brown or dark purple, secondary infection can have the formation of abscesses of different sizes, thrombus can be seen in the pulmonary blood vessels, some cases can appear local Pulmonary infarction in the area, hilar lymphadenopathy can be seen in some cases.

Light microscopy: The lesions of the lungs are usually milder, involving almost all the lungs, mainly manifested as changes in the temperature-induced alveolar damage. According to the different stages of the disease, the following manifestations can be made: the cases with a course of about 10 days are mainly pulmonary edema, fibers. Exudation, formation of transparent membrane, accumulation of macrophage in the alveolar cavity and proliferation of type II alveolar epithelial cells fall into the alveolar formation of desquamable pneumonia and focal pulmonary hemorrhage, which is not only visible in autopsy specimens, but also In the fiberoptic bronchoscopy lung biopsy material, there is also the same lesion change. The partially proliferating alveolar epithelium is fused to each other and is a combined multinucleated giant cell. The virus is visible in the cytoplasm of the proliferating alveolar epithelium and exuded monocytes. Inclusion bodies, as the lesion progresses, the pathogenesis of alveolar exudate is often seen in cases with a disease duration of more than 3 weeks. The mechanization of the transparent membrane and the fibroblast proliferation of the alveolar septum are continuously fused, eventually forming alveoli. Occlusion and atrophy, resulting in consolidation of the whole lung, only some cases have obvious fibrosis, leading to pulmonary fibrosis and even hardening, small blood vessels in the lung are often visible Fibrinous microthrombus, the above lesions can be very different in different patients, even in the same patient's lung can also be seen in different periods of the disease, some cases, especially long-term treatment of patients, often seen scattered lobular Pneumonia and even a large area of fungal infection, of which Aspergillus infection is the most common, secondary infection can involve the pleura, causing pleural effusion, pleural adhesions, and even pleural occlusion.

Lymph nodes (abdominal lymph nodes and hilar lymph nodes): In some cases, lymphadenopathy is seen. Under the microscope, almost all lymph nodes in the lymph nodes have atrophy or disappearance. The lymphocyte distribution is sparse, the number is reduced, and the blood vessels and lymphatic sinuses are obvious. Dilated and hyperemia, sinus tissue cells are obviously proliferating, and some diseases can show bleeding and necrosis.

SARS prevention

Prevention of SARS:

1. The air supply system should be ensured for safe air supply and sufficient fresh air input should be ensured. All exhaust air should be discharged directly to the outside. The return air passage should be closed when the air conditioner is not in use.

2. Regularly disinfect the surface of the ground, walls, elevators, etc. Spray disinfection should be carried out in the order of first, then, then, and then left and right. Spray disinfection can be sprayed with a 0.1% to 0.2% peroxyacetic acid solution or an effective bromine solution of 500 mg/L to 1000 mg/L dibromohydantoin or a chlorine-containing disinfectant solution having an effective chlorine content of 500 mg/L to 1000 mg/L. Dosage: The soil wall absorbs 150 mg/m2 to 300 ml/m2, and the cement wall, wooden wall and lime wall are 100 ml/m2. The amount of ground disinfection spray is 200ml/m2300ml/m2, spray disinfection from inside to outside, the action time should be no less than 60 minutes.

3. Regularly disinfect items and food drinks that are frequently used or touched. For counters, tables, chairs, door handles, faucets, etc. with a lot of human contact, spray or wipe disinfection with 0.2% to 0.5% peroxyacetic acid solution or chlorine-containing disinfectant with effective chlorine of 1000mg/L to 2000mg/L. 30 minutes. Food and drink can be sterilized by circulating steam for 20min (temperature is 100 °C); boiled and disinfected for 15 to 30 minutes; use far infrared ray disinfection cupboard, the temperature reaches 125 °C, maintain for 15 minutes, the temperature after disinfection should be reduced to below 40 °C. . Chemical disinfection can be applied to units that do not have thermal disinfection or food and drink that cannot be used for thermal disinfection. For example, a chlorine-containing disinfectant with an effective chlorine content of 250 mg/L-500 mg/L, a dibromohydantoin solution with an effective bromine content of 250-500 mg/L, a solution of 200 mg/L chlorine dioxide, and 0.5% peroxyacetic acid. Soak the solution for 30 min. After disinfection, rinse with water, empty and dry for future use.

4, wash, diligent clothes and bedding, etc., can also use sterile sterilization detergent and detergent to wash clothes.

5, the bathroom, kitchen and living room should be cleaned frequently, sanitary ware can be soaked and wiped with chlorine disinfectant with effective chlorine content of 500mgL for 30 minutes.

SARS complications Complications, shock, gastrointestinal bleeding, disseminated intravascular coagulation

Shock, heart rate disorder or cardiac insufficiency, renal dysfunction, liver damage, DIC, sepsis, gastrointestinal bleeding.

SARS symptoms Common symptoms Persistent fever, dyspnea, dry cough, chills, fatigue, high fever

Clinical manifestation

1. Incubation period

The incubation period of SARS is usually limited to 2 weeks, usually about 2 to 10 days.

2, clinical symptoms

Acute onset, from the date of onset, within 2 to 3 weeks, the condition can be in progress, mainly the following three types of symptoms.

(1) fever and related symptoms

Frequently with fever as the first and main symptoms, body temperature is generally higher than 38 ° C, often persistent high fever, may be accompanied by chills, muscle soreness, joint pain, headache, fatigue, in the early stage, the use of antipyretics can be effective; In the meantime, it is often difficult to control hyperthermia with antipyretics, and glucocorticoids can interfere with the heat type.

(2) respiratory symptoms

There may be cough, mostly dry cough, less phlegm, a small number of patients with sore throat, often no symptoms of upper respiratory catarrh, may have chest tightness, severe breathing gradually accelerate, shortness of breath, even respiratory distress, dyspnea and hypoxemia Symptoms are more common after 6 to 12 days of onset.

(3) Other symptoms

Some patients have gastrointestinal symptoms such as diarrhea, nausea and vomiting.

3, signs

The lung signs of patients with SARS are often not obvious. Some patients may smell a little wet rales, or have signs of lung consolidation, occasional local turbidity, decreased respiratory sounds and other signs of pleural effusion.

Other organ changes:

Heart: The hypertrophy of the heart of SARS patients is more common, generally characterized by thickening of left and right heart, thickening of myocardial interstitial edema, interstitial infiltration of lymphocytes and monocytes, and vacuolar degeneration of cardiomyocytes in some cases. Focal myocarditis changes or myocardial small necrosis, severe secondary infections such as fungal infections can also affect the heart.

Liver: In most cases, glomerular glomerular congestion and renal tubular epithelial cell degeneration are observed. In some cases, extensive fibrinous thrombosis can be seen in the capillaries of the glomerulus. In some cases, small focal necrosis and lymphocyte and monocyte infiltration in the medulla are observed. Renal interstitial vasodilatation and hyperemia, some cases can be seen due to secondary infection caused by small pus, occasionally vasculitis.

Adrenal gland: Adrenal medullary focal hemorrhage, necrosis, lymphocytic infiltration, vacuolar degeneration of cortical bundle cells and/or decreased lipid content may be seen in some cases.

Brain: There are different degrees of edema in the brain tissue. In some cases, scattered neurons can be seen in the brain. In severe cases, brain tissue necrosis can be seen, and some nerve fibers can be demyelinated.

Bone marrow: The number of cells in the granulocyte and megakaryocyte system in the hematopoietic tissues of most patients is relatively reduced. In some cases, the erythroid cells show small focal lesions.

Gastrointestinal tract: The submucosal lymphoid tissue in the stomach, small intestine and colon is reduced, lymphocytes are sparse, interstitial edema, and in some cases, superficial erosion or ulceration can be seen in the stomach.

Pancreas: interstitial vascular congestion, some cases have mild fibrous tissue hyperplasia and lymphocytic infiltration, exocrine glands atrophy, zymogen particles decreased, and some islet cells degeneration.

Gallbladder: No obvious lesions were seen.

Testicles: In some cases, spermatogenic cells are degenerated, spermatogenesis is reduced, and interstitial vasodilatation and hemorrhage are seen.

Prostate, uterus, ovary and fallopian tubes: no obvious lesions.

In addition, in some cases, pulmonary, heart, liver, kidney, brain, adrenal gland, striated muscle, etc. can be seen as small vasculitis mainly caused by small veins, which are characterized by vascular wall and perivascular edema, vascular endothelial cell swelling and Apoptosis, fibrinoid necrosis of the vessel wall, infiltration of monocytes and lymphocytes in the vessel wall and around the blood vessels.

Clinical stage

(a) early

Generally 1-7 days of the onset of illness, acute onset, fever as the first symptom, general temperature >38 ° C, more than half of the patients with headache, joint muscle soreness, fatigue and other symptoms, some patients may have dry cough, chest pain, diarrhea Other symptoms; but there are few upper respiratory catarrh symptoms, lung signs are not obvious, some patients can smell a little wet rales, X-ray chest lung shadows can appear on the second day of onset, on average 4 days More than 95% of patients had a positive change within 7 days of the disease.

(2) Progress period

Most occur in the course of 8 to 14 days, individual patients can be longer, in this period, fever and infection symptoms continue to exist, lung lesions progressively worse, manifested as chest tightness, shortness of breath, difficulty breathing, especially after the event X-ray chest X-ray examination of lung shadow development is rapid, and often multi-leaf disease, a small number of patients (10% to 15%) with ARDS and life-threatening.

(3) Recovery period

After the progress period, the body temperature gradually decreased, the clinical symptoms were relieved, and the lung lesions began to be absorbed. Most patients recovered after 2 weeks, and the discharge standard was reached. The absorption of lung shadows took a long time, and a few critically ill patients may be quite Restrictive ventilatory dysfunction and decreased lung function were left over a long period of time, but most of them gradually recovered within 2-3 months after discharge.

SARS check

First, general laboratory inspection

1. Peripheral blood

White blood cell counts are generally normal or decreased; often lymphocyte counts are reduced [if the lymphocyte count is <0.9×109/L, the significance of the diagnosis is greater; if the lymphocyte count is between (0.9~1.2)×109/L, The diagnosis is only suspicious]; some patients have thrombocytopenia.

2, T lymphocyte subset count

In the early stage of the disease, CD4+ and CD8+ cell counts are reduced, and the ratio is normal or decreased.

Second, chest imaging

In the early stage of the lesion, different degrees of flaky, patchy ground glass density appeared in the lungs, and a few were lung solid shadows. Shadows often change frequently or/and bilaterally, and progress in the course of the disease. Some cases progress rapidly and merge into large-scale shadows in the short term.

X-ray films may be difficult to detect when lung lesions are at an early stage with small or thin shadows or where their location coincides with shadows and/or large blood vessels. Therefore, if the early chest X-ray is negative, the first 1 to 2 days of dynamic review is still needed. If available, a chest CT scan can be arranged to help detect early mild lesions or lesions that coincide with the heart and/or large blood vessels.

Chest X-ray imaging review must be performed regularly to observe changes in arteries in the lung lesions.

Third, specific pathogen detection

1, SARS-CoV serum specific antibody detection

After 10 days of onset, IFA can be used to detect specific antibodies to SARS-CoV in patients' serum (if ELISA is used, 21 days after onset). From the advanced phase to the recovery phase, the antibody positive or antibody titer is increased by 4 times or more, which has the significance of pathogenic diagnosis. The first serum specimen should be collected as soon as possible.

2. SARS-CoV RNA detection

Accurate SARS-CoV RNA detection has early diagnostic implications. Using RT-PCR method to detect SARS-CoV RNA from human secretions such as respiratory secretions, blood or feces, especially for multiple, multiple specimens and multiple kits. SARS-CoV RNA is positive and has important support for pathogenic diagnosis.

3. Other early diagnosis methods

Detection of SARS-CoV-specific structural proteins in nasopharyngeal or airway exfoliated cells by immunofluorescence antibody assay, as well as detection methods such as gene chip technology, remains to be further studied.

SARS diagnosis

1, differential diagnosis project

In the early diagnosis of SARS, detection of influenza virus (A, B, C), parainfluenza virus, respiratory syncytial virus (RSV), adenovirus, pneumococcal bacteria, Mycoplasma pneumoniae, Chlamydia pneumoniae and respiratory bacteria Differential diagnosis of SARS.

2, experimental methods

The current experimental methods mainly include rapid diagnosis, serological diagnosis, detection of molecular biology and separation of viruses (chlamydia, bacteria).

(1) Rapid diagnosis: The enzyme-specific immunoassay (EIA) and indirect immunofluorescence method are usually used to determine the specific antigen or antibody of the pathogen. The operation is simple and rapid, and the result is accurate and reliable.

(2) Serological diagnosis: complement fixation test, metabolic inhibition test, indirect hemagglutination test and indirect immunofluorescence test can be used. Double serum test is used, and antibody titer is increased by 4 times or more. It is generally used for popularization. Disease investigation.

(3) Molecular biological testing: Currently, gene probes and PCR methods are used. Although the gene nucleic acid hybridization technology has high sensitivity and specificity, it has radioactive contamination due to gene probes and isotope labeling, and has high equipment requirements and cumbersome operations, and is generally difficult to promote. PCR technology is simple, rapid, sensitive, and specific, and easy to promote, but the standardization of the laboratory needs to be resolved.

(4) Isolation of virus (chlamydia, bacteria): human nasopharyngeal secretions are used to inoculate human embryonic lung cells or monkey kidney cells, virus and chlamydia are isolated, and antigens are identified by complement binding or neutralization test, IFA or ELISA. However, the positive rate of cell culture is not high enough. In addition, due to the complicated technical operation and high requirements of experimental equipment, the general hospital does not have the conditions, and the sensitivity is affected by the collection, transportation and preservation of the specimen. The experimental method is not suitable for routine detection, and is mostly used for the identification of scientific research and difficult cases.

It is recommended that rapid diagnosis be preferred in the differential diagnosis of SARS.

3. Clinical significance

Bacterial infection can occur directly or after viral infection, with hemolytic streptococcus being more common, followed by Haemophilus influenzae, Streptococcus pneumoniae and Staphylococcus, occasionally Gram-negative bacilli. The main pneumonia pathogens in infants and children are viruses, mainly RSV, adenovirus, parainfluenza virus, influenza A and B viruses. These pathogens can also cause pneumonia in adults. The most common cause of adult pneumonia is bacteria, of which Streptococcus pneumoniae is the most common. Other pathogens include anaerobic bacteria, Staphylococcus aureus, Haemophilus influenzae, catarrhal bacteria, Klebsiella pneumoniae and other Gram-negative bacilli. Etc. Influenza A can also cause respiratory infections in adults. Mycoplasma pneumoniae is a bacterial-like microbe that is a particularly common cause of pneumonia in older children and young adults.

At the end of 2002, in SARS in Guangdong, China, the pathogen SARS-CoV can cause serious respiratory symptoms after being infected with human body, but these symptoms are not unique to SARS. Due to many pathogens that can cause small airway diseases, such as influenza virus (type A, type B), parainfluenza virus (type 1, 2, 3), adenovirus, RSV, Mycoplasma pneumoniae and Chlamydia pneumoniae, Legionella, etc. can cause Respiratory diseases, and currently there is no effective specificity index for laboratory diagnosis in SARS. Therefore, it is very important to add some exclusion experiments in laboratory tests to assist clinical diagnosis. At present, the above-mentioned detection of pathogens can be carried out as an exclusion diagnosis test for SARS. However, in the analysis of the results, it is necessary to consider the possibility of SARS patients with the above pathogen infection.

During hospitalization for SARS patients, approximately 20% of patients may have a secondary lower respiratory tract and/or pulmonary infection. Pathogens include Gram-negative bacilli (non-fermenting bacteria, P. pneumoniae, Acinetobacter baumannii), Gram-positive cocci (anti-methicillin-resistant Staphylococcus), fungi (Candida albicans, Aspergillus) and Mycobacterium tuberculosis Wait. The correct laboratory diagnosis of pathogens is the key to enabling targeted treatment and reducing mortality.

A variety of pulmonary interstitial and alveolar lesions can appear on the X-ray and CT on the ground glass and lung consolidation images, including common pneumonia, immune function damage patients with pneumonia and some non-infectious diseases, need to be identified with SARS. The dynamic changes of SARS are rapid. In most cases, the small-format images in the early stage of the lesion rapidly develop into multiple, diffuse lesions of the unilateral lung or both lungs. This is relatively rare in other pneumonias. In addition, the SARS manifestation is limited to a single lung lobe or lung segment, and there is no obvious atelectasis. There is no cavity imaging in the early stage of the lesion, and pleural effusion and mediastinal hilar lymphadenopathy are rare. The principle of differential diagnosis of SARS is that imaging performance is closely combined with medical history, clinical manifestations, and laboratory tests. For the identification of general pneumonia, it is necessary to pay attention to the clinical, laboratory examination and imaging characteristics of the disease. In the identification of pneumonia in patients with immune dysfunction, such as Pneumocystis carinii pneumonia and cytomegalovirus pneumonia, it is necessary to pay attention to the relevant medical history and imaging performance. In the identification of non-infectious diseases, such as pulmonary edema, pulmonary hemorrhage or allergic pneumonia, the clinical manifestations of acute infection are the key to differential diagnosis.

The diagnosis of SARS is currently mainly for clinical diagnosis and is to a considerable extent an exclusionary diagnosis. Before making a SARS diagnosis, other diseases that cause similar clinical manifestations need to be excluded.

Common cold, influenza (flu), general bacterial pneumonia, legionellosis pneumonia, mycoplasma pneumonia, chlamydia pneumonia, fungal pneumonia, AIDS and other immunosuppression (post-transplantation, etc.) patients with pulmonary infection, general virus Pneumonia is a key disease that needs to be identified with SARS.

Other diseases that need to be identified include tuberculosis, epidemic hemorrhagic fever, lung cancer, non-infectious interstitial lung disease, pulmonary edema, atelectasis, pulmonary embolism, pulmonary vasculitis, pulmonary eosinophil infiltration, and the like.

For cases with clinical syndromes similar to SARS, if there is no obvious effect after antibacterial treatment, it will help to eliminate bacteria or mycoplasma and chlamydial lung infection.

Attachment: Key points for differential diagnosis of influenza and SARS

Epidemiological characteristics: The flu is high in the winter and spring seasons, spreading rapidly, and spreads through air droplets and exposure to respiratory secretions. The incubation period is 1-3 days, and it is contagious at the end of the incubation period. The infection is the strongest in the first 2-3 days. When an outbreak occurs, there are often characteristics of the first school and the later residential area. Pediatrics and the elderly are prone to pneumonia.

Symptoms and signs: The flu is onset, often with high fever, systemic symptoms and respiratory symptoms are relatively mild, manifested as headache, fatigue, body aches. The body temperature can reach 39-40 ° C, after 2 to 3 days, the body temperature can be resolved, but the symptoms of sputum, nasal congestion and so on, sore throat and cough become significant. Some severe patients may have difficulty breathing and cyanosis. A small number of patients may have mild gastrointestinal symptoms such as nausea, constipation or diarrhea. The examination showed acute illness, flushing of cheeks, mild congestion of the conjunctiva, tenderness of the eyeball, pharyngeal congestion, herpes in the oral mucosa, and a few lush rales in the auscultation of the lungs.

Laboratory examination: The peripheral blood leukocyte count of influenza patients is normal, decreased or slightly increased, and the proportion of lymphocytes can be increased. The etiology of the flu virus helps to confirm the diagnosis.

X-ray image changes in the lungs: Influenza patients may have no change or only the lungs are heavy in texture. In the early stage of pulmonary infection, the inflammatory infiltrates along the lungs are seen at the beginning, and later staged lamellae are often distributed. In the lung field, the fusion can be changed in the later stage, and it is concentrated in the middle zone of the lung field, similar to pulmonary edema.

Administration of oseltamivir within 48 hours of onset helps to alleviate the onset and symptoms.

According to the epidemic situation at the time, the local flu epidemic and the surrounding population, there is no epidemiological basis of SARS, the symptoms of catarrhal are more prominent, the peripheral blood lymphocytes often increase, and the early onset of oseltamivir helps to alleviate the onset and symptoms. A pathogen examination with influenza and SARS can help identify.

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