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WS/T 562-2017 English PDF

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WS/T 562-2017: (Diagnosis of gram-ya disease)
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WS/T 562-2017English629 Add to Cart 5 days [Need to translate] (Diagnosis of gram-ya disease) Valid WS/T 562-2017
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Basic data

Standard ID WS/T 562-2017 (WS/T562-2017)
Description (Translated English) (Diagnosis of gram-ya disease)
Sector / Industry Health Industry Standard (Recommended)
Classification of Chinese Standard C59
Word Count Estimation 25,254
Date of Issue 2017-07-24
Date of Implementation 2018-02-01
Regulation (derived from) State-Health-Communication (2017) 7
Issuing agency(ies) National Health and Family Planning Commission of the People's Republic of China

WS/T 562-2017: (Diagnosis of gram-ya disease)

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Diagnosis for Creutzfeldt-Jakob disease ICS 11.020 C 59 WS People's Republic of China Health Industry Standard Creutzfeldt-Jakob disease diagnosis 2017-07-24 released 2018-02-01 implementation Issued by the National Health and Family Planning Commission of the People's Republic of China

Table of contents

Foreword...II 1 Scope...1 2 Terms and definitions...1 3 Abbreviations...3 4 Principles of Diagnosis...3 5 Diagnosis basis...3 6 Differential diagnosis...5 Appendix A (Normative Appendix) Western blot detection of 14-3-3 protein in cerebrospinal fluid...6 Appendix B (Normative Appendix) Brain Histopathology Test...7 Appendix C (Normative Appendix) Immunohistochemical Detection of PrPSc in Brain Tissue...9 Appendix D (Normative Appendix) Western blot detection of PrPSc in brain tissue...11 Appendix E (Normative Appendix) Western blot detection of PrPSc in the tonsils of vCJD patients...13 Appendix F (Normative Appendix) Immunohistochemical detection of PrPSc in the tonsils of vCJD patients...13 Appendix G (Normative Appendix) PRNP gene sequence, 129 and 219 amino acid polymorphism detection...15 Appendix H (informative appendix) genetic or familial human prion disease PRNP gene mutation site...19 Appendix I (informative appendix) Differential diagnosis of Creutzfeldt-Jakob disease...20 References...22

Foreword

This standard was drafted in accordance with the rules given in GB/T 1.1-2009. Drafting organizations of this standard. China Center for Disease Control and Prevention, Viral Disease Prevention and Control Institute, Beijing Friendship Hospital, Guangzhou Zhongshan Hospital, Henan Provincial Center for Disease Control and Prevention, Beijing Municipal Center for Disease Control and Prevention. The main drafters of this standard. Dong Xiaoping, Han Jun, Chen Cao, Shi Qi, Wang Dexin, Gao Chen, Tian Chan, Xia Shengli, Li Xunhua, Zhang Xiuchun. Creutzfeldt-Jakob disease diagnosis

1 Scope

This standard specifies Creutzfeldt-Jakob disease and genetic or familial human prion disease (including genetic or familial Creutzfeldt-Jakob disease, Gistman-Straw The diagnosis principle, diagnosis basis, diagnosis classification and differential diagnosis of Sisi syndrome, fatal familial insomnia). This standard is applicable to the treatment of Creutzfeldt-Jakob disease and genetic or familial human prion disease by medical and health institutions and their medical staff at all levels and (Including genetic or familial Creutzfeldt-Jakob disease, Gistmann-Strauss syndrome, fatal familial insomnia) diagnosis.

2 Terms and definitions

The following terms and definitions apply to this document. 2.1 Creutzfeldt-Jakob disease German scientists and a rare central nervous system disease first reported in 1922, It was later confirmed to be human prion diseases, including sporadic, genetic or familial, iatrogenic and variant types. Among them, sporadic forms account for the total number of cases The genetic or familial type accounts for about 10% to 15% of the total number of cases, and the iatrogenic type accounts for about 1% of the total number of cases. 2.2 Prion disease A class of transmissible and degenerative diseases of the central nervous system of humans and animals caused by prions. The disease has a long incubation period and the case fatality rate 100%. Prion-related diseases and transmissible spongiform encephalopathy are also proper terms for such diseases. 2.3 Prion The infectious agent of prion disease, also known as sheep pruritus factor-like or amyloid prion protein (abnormal prion protein). It is currently considered to be a kind of self-replicating Capable infectious protein particles, an abnormal form transformed from the normal prion protein on the cell surface, which is infectious and resistant to proteases Hydrolysis (protease resistance) is also called prions and prions. 2.4 Prion protein A normal cellular protein, also known as cellular prion protein, in the central nervous system (brain And spinal cord tissue) neuronal cells and glial cells, and in other tissues of the body, including peripheral tissues, lymphoid tissues and other cells. There is expression. 2.5 Sporadic Creutzfeldt-Jakob disease Most cases of Creutzfeldt-Jakob disease are sporadic, without geographical clustering, and no obvious transmission between patients. The cause is now clear, so it is called sporadic Creutzfeldt-Jakob disease. The age of onset of such diseases is between 14 and 92 years old, with an average of 65 years old. The incidence rate is 1 to 2 persons/per million persons/year, and the ratio of male to female patients is consistent with the gender ratio of the entire population and has nothing to do with socioeconomic status. 2.6 Iatrogenic Creutzfeldt-Jakob disease Treatment with prion contaminated surgical instruments, corneal and dura mater transplantation, or pituitary gland extract, growth hormone and gonadotropin Infect recipient patients, causing iatrogenic Creutzfeldt-Jakob disease. 2.7 Genetic or familial human prion disease Genetic or familial human prion diseases include genetic or familial Creutzfeldt-Jakob disease, Gistman-Strauss syndrome, and fatal familial Insomnia. The incidence rate accounts for about 10% to 15% of all human prion disease cases. 2.8 Genetic or familial Creutzfeldt-Jakob disease It is a type of genetic or familial human prion disease, which is a dominant characteristic genetic disease. When the human prion gene appears at a specific point Mutations and repeated insertions or deletions of specific octapeptides can cause such diseases. Clinical manifestations of such patients and sporadic Creutzfeldt-Jakob disease Similar, but depending on the mutation site and type, the age of onset, clinical course, clinical auxiliary examination, laboratory testing and pathological changes There are differences. 2.9 Gistmann-Strauss syndrome The specific point mutations and octapeptide insertions in the prion protein coding genes of such patients are related to heredity or family in clinical manifestations and pathological features. Type Creutzfeldt-Jakob disease is obviously different. The clinical manifestation is progressive cerebellar ataxia, and characteristic amyloid plaque deposits can be seen in neuropathology. 2.10 Fatal familial insomnia When the 129th codon of the human prion gene is methionine homozygous, the 178th amino acid is mutated from aspartic acid (D) to day With paraffin (N), these patients have severe sleep disturbances. Pathologically manifested as significant loss of thalamic neurons and glial hyperplasia, very Little or no spongy degeneration. 2.11 Variant Creutzfeldt-Jakob disease The new variant of Creutzfeldt-Jakob disease first discovered in the UK in.1996, mostly occurs in young people, and its clinical symptoms and pathological changes are similar to sporadic Creutzfeldt-Jakob disease is different. The brain and cerebellum of such patients show extensive vacuolation and "petal-like" abnormal prion protein plaque deposition. Variant Creutzfeldt-Jakob disease has been confirmed to be associated with bovine spongiform encephalopathy that broke out in the UK and Europe in the mid-1980s.

3 Abbreviations

The following abbreviations apply to this document.

4 Principles of diagnosis

Comprehensive judgment based on the patient's epidemiological history, clinical symptoms, clinical auxiliary examinations, laboratory and genetic testing. Diagnosis results are divided into Suspected diagnosis, clinical diagnosis and confirmed diagnosis, among which the confirmed diagnosis of the case depends on the detection of protease-resistant protease in the brain tissue of the patient And/or spongiform degeneration and/or specific PRNP gene mutations.

5 Diagnosis basis

5.1 Sporadic Creutzfeldt-Jakob disease 5.1.1 Medical history and epidemiological history The medical history and epidemiological history are as follows. a) Have symptoms of progressive dementia; b) Clinical course of disease < 2 years; c) Routine testing to exclude other diseases; d) No clear history of iatrogenic exposure. 5.1.2 Clinical manifestations The clinical manifestations are as follows. a) Myoclonus; b) Visual impairment or cerebellar ataxia; c) Abnormal function of the pyramidal/extrapyramidal system; d) Inactive silence. 5.1.3 Clinical examination The characteristic clinical examination results are as follows. a) Periodic three-phase waves appear in the EEG during the course of the disease; b) MRI imaging of the head shows abnormally high signal in the putamen/caudate nucleus, or the diffusion-weighted image shows symmetrical gray matter "ribbon" Levy". 5.1.4 Laboratory testing The characteristic laboratory test results are as follows. a) The cerebrospinal fluid 14-3-3 protein test is positive (see Appendix A); b) Brain histopathological examination showed typical/standard neuropathological changes, that is, spongiform degeneration (see Appendix B); c) Brain tissue immunohistochemical detection of the deposition of protease-resistant PrPSc (see Appendix C); d) Western blotting of brain tissue detects the presence of protease-resistant PrPSc (see Appendix D). 5.1.5 Diagnosis classification The diagnosis classification mainly includes the following three types. a) Suspected diagnosis. meet any two of 5.1.1 plus 5.1.2; b) Clinical diagnosis. on the basis of suspected diagnosis, meet any of 5.1.3 or 5.1.4 a); c) Confirmed diagnosis. On the basis of suspected diagnosis, any one of b), c), and d) in 5.1.4 is met. 5.2 Iatrogenic Creutzfeldt-Jakob disease 5.2.1 Medical history and main clinical manifestations Similar to sporadic Creutzfeldt-Jakob disease. 5.2.2 Diagnosis classification The diagnostic classification is only a confirmed diagnosis. Based on the confirmed diagnosis of sporadic Creutzfeldt-Jakob disease, meet any of the following. a) Progressive cerebellar syndrome occurs in patients receiving pituitary hormone therapy extracted from human brain; b) Determined exposure risk, such as having received dural transplantation, corneal transplantation and other operations from CJD patients. 5.3 Variant Creutzfeldt-Jakob disease 5.3.1 Medical history and epidemiological history The medical history and epidemiological history are as follows. a) Progressive neuropsychiatric disorder; b) Course of disease ≥ 6 months; c) Routine examination does not indicate the presence of other diseases; d) No clear history of iatrogenic exposure; e) Exclude genetic or familial human prion diseases. 5.3.2 Clinical manifestations The clinical manifestations are as follows. a) Early mental symptoms (depression, anxiety, indifference, withdrawal, delusion); b) Persistent pain (pain and/or paresthesia); c) Ataxia; d) Myoclonus, chorea, dystonia; e) Dementia. 5.3.3 Clinical testing The characteristic clinical test results are as follows. a) There is no typical three-phase wave in the early EEG (three-phase wave may appear in the late period); b) MRI. Diffusion-weighted imaging and fluid attenuation inversion recovery imaging showed high signal intensity in both thalamus occipital (posterior nodules). 5.3.4 Laboratory testing The characteristic laboratory test results are as follows. a) Western blotting of tonsils to detect the presence of protease-resistant PrPSc (see Appendix E) or immunohistochemical detection of tonsils to confirm With PrPSc deposition (see Appendix F); b) Histopathological examination of the brain showed extensive vacuolation of the brain and cerebellum (see Appendix B); c) The brain tissue immunohistochemical test confirmed that there are "petal-like" protease-resistant PrPSc plaque deposits (see Appendix C); d) Western blotting of brain tissue detects the presence of protease-resistant PrPSc (see Appendix D). 5.3.5 Diagnosis classification The diagnostic classification includes the following three types. a) Suspected diagnosis. meet any 4 items in 5.3.1 plus 5.3.2 plus 5.3.3a); b) Clinical diagnosis. meet 5.3.3b) on the basis of suspected diagnosis; or 5.3.1 plus 5.3.4a); c) Confirmed diagnosis. any one of b), c), d) in 5.3.1 plus 5.3.4. 5.4 Genetic or familial human prion disease 5.4.1 Medical history and epidemiological history There are confirmed cases of genetic or familial human prion disease in first-degree relatives. 5.4.2 Diagnosis classification The diagnostic classification includes the following two types. a) Suspected diagnosis. Add 5.4.1 on the basis of meeting the sCJD suspected diagnosis criteria or the appearance of progressive neuropsychiatric symptoms. b) Confirmed diagnosis. On the basis of suspected diagnosis, the patient's PRNP gene sequence test (see Appendix G) confirms that the patient has a specific gene Mutations (see Appendix H).

6 Differential diagnosis

The diagnosis of Creutzfeldt-Jakob disease should be related to viral encephalitis, Hashimoto’s encephalopathy, mitochondrial encephalopathy, Alzheimer’s disease, vascular dementia, and central nervous system. Systemic lymphoma and other brain tumors, cortical vein thrombosis, and paraneoplastic subacute cerebellar degeneration are differentiated (see Appendix I).

Appendix A

(Normative appendix) Western blot detection of 14-3-3 protein in cerebrospinal fluid A.1 Principle The content of 14-3-3 protein in the cerebrospinal fluid of CJD patients tends to increase. After SDS-PAGE electrophoresis and electroporation of cerebrospinal fluid, 14-3-3 protein and The specific antibody reacts, and a protein band of about 30 KD appears after color development. A.2 The main instruments of the experiment Protein electrophoresis and electroporation device. A.3 Experimental procedure Proceed as follows. A.4 Judgment of results The positive control uses sheep brain tissue homogenate or 14-3-3 positive cerebrospinal fluid; a protein band appears at 30 KD after color development, and In the positive control, the protein bands move at the same position, which can be judged to be 14-3-3 positive in the cerebrospinal fluid.

Appendix B

(Normative appendix) Brain tissue pathology examination B.1 Central nervous tissue partition collection Central nervous tissue partition collection includes the following five steps. a) Remove the dura mater and weigh. b) The central nervous system is fixed with formalin, and the best time for fixation is 10 to 21 days. c) Brain tissue. Conventional methods and methods are used to cut brains, obtain materials in different regions, record and mark separately. d) Spinal cord. Cut the dura mater of the spinal cord and record and mark the tissue blocks of the cervical, thoracic, and lumbar spinal cords. Then collect the spinal nerve root ganglion. e) Infectious removal of specimens. Before further testing, all fixed tissues should be immersed in more than 96% formic acid solution to 1 h less. It should be noted that the interaction of denaturants can produce chemical reactions, and any tissue that has been treated with phenol in advance will No more than 96% formic acid treatment, so these tissues are still infectious. B.2 Dehydration and wax immersion of specimens B.3 Production The production mainly includes the following four steps. a) The trimming, sectioning and preparation of wax blocks of tissue specimens shall be carried out in accordance with conventional pathological methods; b) If the tissue wax block is not treated with 96% formic acid, the operator should wear metal mesh gloves for protection to avoid injury; c) The thickness of the brain tissue slice used for routine pathological examination and immunohistochemical examination is 5 µm; d) After collecting waste tissues, wax blocks, fragments, etc., autoclave at 134 ℃ for 1 h or incinerate. B.4 HE staining HE staining was performed according to conventional pathological methods. B.5 Judgment of results B.5.1 sCJD, gCJD or fCJD, iCJD Spongy lesions appear in the brain, cerebellar cortex, and subcortical gray matter. B.5.2 vCJD A large number of astrocytes proliferate in the posterior part of the thalamus, and neurons are lost, that is, spongiform degeneration with a large amount of PrPSc deposits, especially in the large The gray matter of the brain and cerebellar cortex is surrounded by a circle of spongy vacuoles (petal-like) around amyloid plaques. B.5.3 GSS There is little or no spongy degeneration. B.5.4 FFI There is significant loss of thalamic neurons and gliosis, with little or no spongiform degeneration.

Appendix C

(Normative appendix) Immunohistochemical detection of PrPSc in brain tissue C.1 Principle C.2 Main experimental equipment Optical microscope. C.3 Experimental procedure The experiment operation is carried out in the following order. a) Tissue sections are baked at 56 ℃ for 24 hours, and routinely deparaffinized to water; b) After taking it out, soak it in water for 5 minutes, soak in saturated picric acid for 15 minutes to remove formalin pigment; c) Wash 3 times, 5 min each time, to remove picric acid; d) 3% hydrogen peroxide/methanol blocking for 15 min to 20 min (blocking endogenous peroxidase); e) Wash 3 times, 5 min each time; f) High-pressure hydrolysis (121 ℃, double distilled water) for 10 min, or microwave oven (high power switch, double distilled water) 3 times, 5 min each time; g) Cool down at room temperature after taking it out; h) Soak in formic acid with a content of not less than 96% for 5 min to 10 min (specimen not treated with formic acid before paraffin embedding); i) Wash with water 3 times (wash with water slowly); j) 4 mol/L guanidine isothiocyanate soaked for 2 h (4 ℃); k) Wash thoroughly; l) Serum blocking normal goat serum/phosphate buffered saline (PBS) diluted 1.100 for 20 min; m) Discard the blocking solution, add the primary antibody (diluted with 1.100 normal goat serum/PBS) and incubate overnight, the prion protein specific monoclonal antibody Body (such as 3F4), the dilution is 1.500～1.1 000; n) Wash with PBS 3 times, 5 min each time; o) Add the secondary antibody (diluted with 1.100 normal goat serum/PBS) and incubate for 30 min, horseradish peroxidase (HRP) labeled Anti-rabbit antibody diluted 1.200 for polyclonal antibody detection; or HRP-labeled anti-mouse antibody diluted 1.200 for single Clonal antibody detection; C.4 Observation of results Sc protein positive staining is brown, and the distribution can be scattered, plaque and mixed, and the nucleus is light blue. C.5 Judgment of results C.5.1 sCJD, iCJD, gCJD or fCJD With PrPSc deposition (plaque type, diffuse synaptic type, plaque/vacuum peripheral type). C.5.2 vCJD PrPSc plaques with no clear shape appear around the cells and blood vessels, especially in the cerebellum. C.5.3 GSS Visible characteristic amyloid plaque deposits. C.5.4 FFI Little or no deposition of PrPSc.

Appendix D

(Normative appendix) Western blot detection of PrPSc in brain tissue D.1 Principle Sc protein is resistant to proteinase K hydrolysis and its molecular weight decreases after proteinase K digestion. Extract brain tissue protein, after egg SDS-PAGE electrophoresis was carried out after the hydrolysis of white enzyme K. The protein electrophoresis strips are charged to nitrocellulose membrane or nylon membrane, and PrP specific monoclonal Antibody response. After the protein band with protease resistance develops color, the position is between 17 KD and 27 KD. D.2 Main experimental equipment Including the following. a) Tissue grinder; b) Centrifuge; c) Protein electrophoresis/electrotransmission device. D.3 Extraction and processing of brain tissue The grinding and extraction of brain tissue should be carried out in a laboratory above the level of biological safety. Operators need to wear protective work clothes, protective masks, Eye protection, double gloves, protective shoe covers, etc. If an oscillator is required, a low-power block should be used; frozen brain tissue should be in biosafety Thaw in the cabinet, cut out a small amount of tissue (< 100 mg = put into the cryotube, and weigh; the specific operations are carried out in the following order. a) Add an appropriate amount of extraction buffer at a ratio of 1.10 (m/V), transfer the tissue to the tissue grinder, and prepare 10% brain tissue Homogenate. After use, the grinder is soaked in 2 mol/L NaOH or 5% NaClO (20 000 µg/g free chlorine) solution for at least 1 hour. b) Transfer the brain tissue homogenate to a cryopreservation tube, centrifuge at 2 000 r/min at 4°C for 10 min. c) Collect the supernatant and store at -20°C. All the test tubes and pipette tips used are immersed in 2 mol/L NaOH or 5% NaClO (20 000 µg/g free chlorine) solution for at least 1 h. D.4 Proteinase K hydrolysis and electrophoresis, electrotransmission Follow the steps below. a) Add proteinase K at a final concentration of 20 µg/mL to the brain tissue homogenate, and let it act at 37 ℃ for 1 h to 2 h. b) Add an equal volume of 2× loading buffer and boil at 100 ℃ for 10 min. c) Routinely prepare 15% separating gel and 5% concentrated gel. Routine sample loading, using concentrated gel 80 V, separation gel 156 V voltage conditions Under electrophoresis for 2 h..200 mA steady flow for 70 min (wet type) or 60 mA for 60 min (semi-dry type) electrotransfer to nitrocellulose membrane. D.5 Western blotting reaction D.6 Results judgment The positive control uses the brain tissue extract of hamsters infected with sheep pruritus virus strain 263K, or the brain tissue extract of confirmed CJD patients. Negative The control is a normal hamster brain tissue extract, or a non-CJD patient brain tissue extract. Treatment of positive and negative controls, proteinase K hydrolysis and Western blotting reaction was carried out according to D.3, D.4, and D.5. After the brain tissue extract is hydrolyzed by proteinase K, there are still multiple (usually three) chromogenic protein bands at positions 17 KD to 27 KD. Compared with the color bands of PrP protein that have not been digested with proteinase K (usually three, the electrophoretic migration position is about 30 KD ~ 35 KD), The migrating position of the protease-treated PrP chromogenic band shifted down significantly. It can be determined that the PrPSc protein in the brain tissue is positive.

Appendix E

(Normative appendix)

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