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Diagnosis for pulmonary tuberculosis
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Diagnostic criteria for pulmonary tuberculosis
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Basic data
| Standard ID | WS 288-2017 (WS288-2017) |
| Description (Translated English) | Diagnosis for pulmonary tuberculosis |
| Sector / Industry | Health Industry Standard |
| Classification of Chinese Standard | C59 |
| Word Count Estimation | 24,242 |
| Date of Issue | 2017-11-09 |
| Date of Implementation | 2018-05-01 |
| Older Standard (superseded by this standard) | WS 288-2008 |
| Regulation (derived from) | State-Health-Communication (2017) 25 |
| Issuing agency(ies) | National Health and Family Planning Commission of the People's Republic of China |
WS 288-2017: Diagnosis for pulmonary tuberculosis
---This is a DRAFT version for illustration, not a final translation. Full copy of true-PDF in English version (including equations, symbols, images, flow-chart, tables, and figures etc.) will be manually/carefully translated upon your order.
(Pulmonary tuberculosis diagnostic criteria)
ICS 11.020
C 59
WS
People's Republic of China health industry standards
Replace WS 288-2008
Diagnosis of tuberculosis
Diagnosis for pulmonary tuberculosis
2017-11-09 Published
2018-05-01 implementation
People's Republic of China National Health and Family Planning Commission released
Foreword
This standard "Chapter 3 ~ Chapter 5" is a mandatory clause, the rest are recommended terms.
This standard was drafted in accordance with the rules given in GB/T 1.1-2009.
This standard replaces WS 288-2008 "diagnostic criteria for tuberculosis."
This standard compared with WS 288-2008, the main changes are as follows.
- Added fluorescent staining microscopy, liquid culture medium examination, molecular biology examination (see 3.4.1 and 3.4.2);
- Revised conditions for diagnosis of tuberculosis (increase in molecular biology test results) (see 5.3);
- Increase of interferon-gamma release test (see 3.4.4.2);
- increased bronchoscopy and tracheal, bronchial tuberculosis microscopic findings (see 3.5);
- An increase of tuberculosis pathology (see Appendix C)
- Added diagnosis of non-tuberculous mycobacterium tuberculosis (see E.2 in Appendix E);
- Added diagnostic features for tuberculosis in children (see 3.2.1 and 3.3.1).
This standard was drafted. China Center for Disease Control and Prevention, Capital Medical University, Beijing Chest Hospital, Capital Medical University North
Beijing Children's Hospital, the People's Liberation Army No. 309 Hospital.
The main drafters of this standard. Wang Lixia, into poetry, Zhou Lin, Zhao Yanlin, Gao Mengqiu, early Nai Hui, Zhou Xinhua, Wang Xiexiu, Zhao Shunying,
Tu Dehua, Lin Minggui, Li Liang, Li Qi, Li Ning, Wu Xueqiong, Liu Ergyong, Lai Yuji, Wang Shengfen, Wang Qian, Ma Yan.
This standard replaces the standards previously issued as follows.
- GB 15987-1995;
- WS 288-2008.
Diagnosis of tuberculosis
1 Scope
This standard specifies the basis for the diagnosis of tuberculosis, diagnostic principles, diagnosis and differential diagnosis.
This standard applies to all types of medical and health institutions at all levels and their medical staff on the diagnosis of tuberculosis.
2 Terms and definitions
The following terms and definitions apply to this document.
2.1
Pulmonary tuberculosis
Tuberculosis occurs in lung tissue, trachea, bronchi and pleura. Tuberculosis etiology see Appendix A.
2.2
Mycobacterium tuberculosis
Mycobacterium tuberculosis for short, is the pathogen of human tuberculosis. Mycobacterium tuberculosis is elongated or slightly curved shape, blunt bacilli at both ends,
Length 1μm ~ 4μm, width 0.3μm ~ 0.6μm.
3 diagnostic basis
3.1 Epidemiology history
History of exposure to tuberculosis patients.
3.2 Clinical manifestations
3.2.1 Symptoms
Cough, sputum ≥ 2 weeks, or bloody sputum or hemoptysis suspicious symptoms of tuberculosis.
Most of the slow onset of tuberculosis, some patients without obvious symptoms, only found in the chest imaging examination. As the disease progresses, can be out
Now cough, expectoration, sputum bloody or hemoptysis, some patients may have recurrent upper respiratory tract infection symptoms. Tuberculosis can also occur in the body
Symptoms such as night sweats, tiredness, intermittent or prolonged afternoon fever, loss of appetite, weight loss, etc., female patients may be accompanied by menstrual disorders or amenorrhea.
A small number of patients with sudden onset, there are high fever, some with varying degrees of dyspnea.
Lesions in the pleura may have irritating cough, chest pain and breathing difficulties and other symptoms.
Lesions occur in the trachea, bronchial irritation and more cough, longer duration, bronchial lymphatic fistula formation and break into the bronchial or
Bronchial stenosis, there may be wheezing or breathing difficulties.
A small number of patients may be associated with tuberculous hypersensitivity syndrome, including. erythema nodosum, herpetic conjunctivitis/keratitis and so on.
Children with tuberculosis can also show stunting, children with primary tuberculosis may be due to tracheal or bronchial lymph nodes swollen oppression trachea or bronchus
Tubal, or lymph node - bronchial fistula, wheezing symptoms often appear.
When combined with extrapulmonary tuberculosis, there may be the corresponding symptoms of organs involved.
3.2.2 signs
Early lung signs are not obvious, when the lesion is involved in a large range, the local percussion was dull, auscultation and tubular breath sounds can be heard, the combined flu
Dye or combined bronchiectasis, can be heard and wet rales.
Lesions involving the trachea, bronchi, causing local stenosis, auscultation can be heard and fixed, limited wheezing, when caused by atelectasis,
Can be manifested tracheal displacement to the affected side, ipsilateral thoracic collapse, intercostal space narrowing, percussion for the voiced or real sound, auscultatory breath sounds weakened or disappeared.
Lesions involving the pleura, early in the affected side can be heard and pleural friction sound, with the increase of pleural effusion, ipsilateral thoracic full, intercostal space increased
Wide tracheal shift to the contralateral side, percussion was voiced to real sound, auscultatory breath sounds weakened to disappear. Pleural effusion may occur when effusion decreases or disappears
Thickening, adhesions, tracheal displacement to the affected side, ipsilateral thoracic collapse, intercostal space narrowing, respiratory movement is limited, percussion dullness, auscultation of breathing
Weak tone.
Primary pulmonary tuberculosis may be accompanied by superficial lymph nodes, disseminated hematogenous disseminated tuberculosis may be associated with hepatosplenomegaly, fundus choroid nodules, children with
May be accompanied by skin miliary rash.
3.3 chest imaging examination
3.3.1 Primary pulmonary tuberculosis
Primary pulmonary tuberculosis is mainly manifested as primary lesion and intrathoracic lymphadenopathy, or simple thoracic lymphadenopathy. Primary lung in children
Tuberculosis can also be manifested as empty, caseous pneumonia and bronchial tuberculosis caused by bronchial lymphatic fistula.
3.3.2 Hematogenous disseminated tuberculosis
Acute hematogenous disseminated tuberculosis showed uniform distribution of both lung size and density of the shadow of the miliary; subacute or chronic hematogenous spread
Pulmonary tuberculosis diffuse lesions, mostly located in the upper middle of the two lungs, different sizes, the density range, there may be integration. Children acute blood smear
Pulmonary tuberculosis is sometimes only manifested as ground glass-like shadow, infiltration of infants and young children around the miliary lesions obvious, fuzzy edge, easy to fusion.
3.3.3 secondary tuberculosis
Secondary pulmonary tuberculosis chest image performance varied. The main manifestations of light patches, nodules and cable shadow, or showed tuberculoma or isolated empty
Hole; severe cases can be manifested as lobar infiltration, cheese pneumonia, multiple cavity formation and bronchial disseminated; repeated extension of the progress of those who may have lung
Damage, destruction of lung tissue volume reduction, multiple thick fibers inside its walls, secondary bronchiectasis, or associated with multiple calcifications, adjacent lung
Pull the door and mediastinum shift shift, thoracic collapse, pleural thickening adhesions, compensatory emphysema appears in other lung tissue and old and new bronchus
Disseminated lesions and so on.
3.3.4 trachea, bronchial tuberculosis
Trachea and bronchial tuberculosis mainly manifested as irregular tracheal or bronchial wall thickening, stenosis or obstruction, narrow bronchial distal lung group
Weave may appear secondary atelectasis or consolidation, bronchiectasis and other parts of the bronchial disseminated lesions.
3.3.5 Tuberculous pleurisy
Tuberculous pleurisy is divided into dry pleurisy and exudative pleurisy. Dry pleurisy is an early inflammatory response to the pleura, usually without noticeable
Imaging performance; exudative pleurisy mainly for pleural effusion, and pleural effusion can be manifested as a small amount or a large amount of free fluid, or there
Limited to any part of the chest fluid, slow absorption often associated with thickened pleural adhesions can also evolve into pleural tuberculosis and empyema.
3.4 laboratory tests
3.4.1 Bacteriological examination
Check the method in Appendix B. The test results are as follows.
a) smear microscopy positive;
b) Mycobacterium culture positive, strain identified as Mycobacterium tuberculosis complex.
3.4.2 Molecular Biology examination
Mycobacterium tuberculosis nucleic acid test positive.
3.4.3 tuberculosis pathology examination
Tuberculosis histopathological changes in Appendix C.
3.4.4 Immunological examination
3.4.4.1 Tuberculin skin test, moderately or strongly positive (see Appendix D).
3.4.4.2 γ-interferon release test positive.
3.4.4.3 Mycobacterium tuberculosis antibody positive.
3.5 bronchoscopy
Bronchoscopy can be directly observed tracheal and bronchial lesions, can also suction secretions, brush and biopsy.
4 diagnostic principles
The diagnosis of tuberculosis is based on etiology (including bacteriology, molecular biology), combined with epidemiological history, clinical manifestations, chest
Video, related auxiliary examination and differential diagnosis, make a comprehensive analysis to make a diagnosis. Pathogenic, pathological findings as a basis for diagnosis.
Diagnosis of tuberculosis in children, in addition to sputum etiology check, but also pay attention to the etiology of gastric juice examination.
5 diagnostic
5.1 suspected cases
Where one of the following items.
a) have any one of 3.3;
b) children under 5 years of age. with 3.2 at the same time have any of 3.1, 3.4.4.1, 3.4.4.2.
5.2 Clinical diagnosis of cases
The differential diagnosis of other lung diseases, in line with one of the following items.
a) Have any of 3.3 and 3.2;
b) Have any of 3.3 and 3.4.4.1;
c) have any one of 3.3 and 3.4.4.2;
d) have any of 3.3 and 3.4.4.3;
e) have any of the 3.3 and extrapulmonary histopathology confirmed as tuberculosis;
f) With 3.3.4 and 3.5 can be diagnosed as tracheobronchial tuberculosis;
g) With 3.3.5 and pleural effusion as exudate, adenosine deaminase increased, with 3.4.4.1, 3.4.4.2, 3.4.4.3 either
Article who can be diagnosed as tuberculous pleurisy;
h) Clinical diagnosis of tuberculosis in children should also have the following two.
1) Have any one of 3.3 and 3.2;
2) Have any of 3.4.4.1, 3.4.4.2.
5.3 confirmed cases
5.3.1 sputum smear-positive pulmonary tuberculosis diagnosis
Where one of the following items.
a) 2 sputum specimens smear acid-fast bacilli test in line with 3.4.1.a who;
b) 1 sputum smear specimens acid-fast bacilli in line with 3.4.1.a, also have any of the 3.3;
c) One sputum smear Acid-fast bacilli test in accordance with 3.4.1.a, and one sputum specimen Mycobacterium culture complying with 3.4.1.b.
5.3.2 Only Mycobacterium Isolates and Culture Positive pulmonary tuberculosis diagnosis
In line with any of 3.3, at least 2 copies of sputum smear negative and mycobacterial culture in line with 3.4.1.b who.
5.3.3 molecular biology test positive pulmonary tuberculosis diagnosis
Meet any one of 3.3 and 3.4.2.
5.3.4 Pulmonary histopathology Positive pulmonary tuberculosis diagnosis
3.4.3 meet.
5.3.5 trachea, bronchial tuberculosis diagnosis
Where one of the following items.
a) with 3.5 and trachea, bronchial pathological examination in line with 3.4.3;
b) have 3.5 and tracheal, bronchial secretions etiological examination, in line with 3.4.1.a or 3.4.1.b or 3.4.2.
5.3.6 Diagnosis of tuberculous pleurisy
Where one of the following items.
a) with 3.3 and pleural effusion or pleural pathology examination in line with 3.4.3;
b) have 3.3 and pleural effusion pathology, in line with 3.4.1.a or 3.4.1.b or 3.4.2.
6 differential diagnosis
Symptoms, signs and imaging findings of tuberculosis are similar to many chest diseases. In the diagnosis of tuberculosis, attention should be paid to other diseases
Do not (see E.1), including identification of non-tuberculous mycobacterium tuberculosis (see E.2). Identified non-TB Mycobacterium non-tuberculosis
Mycobacterium tuberculosis treatment.
AA
Appendix A.
(Informative)
Tuberculosis etiology
A.1 Mycobacterium tuberculosis morphology and staining characteristics
Mycobacterium tuberculosis slender slightly curved, clustered branched proliferation. Because of its cell wall contains a lot of lipids, not easy to color,
Nissl acid-resistant stain was red, sterile hair and flagella, do not form spores (cells), is now proven capsule. Single, double, or in clusters.
On artificial media, due to the different bacteria, strains and environmental conditions, there may be a variety of forms, such as approximately spherical, rod-shaped or filamentous. In electricity
Microscopic observation of its complex structure. the micro-capsule, the three-tier structure of the cell shell, cytoplasmic membrane, cytoplasm, body, ribosome and the intermediate nuclei
constitute.
The typical Mycobacterium tuberculosis morphology is slender slightly curved or straight, blunt bacilli at both ends, length 1 μm ~ 4 μm, width 0.3μm ~
0.6 μm, single scattered, sometimes X, Y-shaped or cords. Sputum specimens smear after acid-fast staining at 100 times the biological microscope can be
see.
Mycobacterium tuberculosis in vitro and in vivo by penicillin, cycloserine or lysozyme induced cell wall peptidoglycan synthesis, isoniazid
Affect the synthesis of mycolic acid, macrophages phagocytosis Mycobacterium tuberculosis lysozyme role can destroy peptidoglycan, can lead to it into L-type,
Granular or filamentous.
A.2 Mycobacterium tuberculosis culture characteristics
Mycobacterium tuberculosis is an obligate aerobic bacteria, high nutritional requirements, the optimum pH of 6.5 to 6.8 is appropriate, slow growth, the initial separation of nutrition
Rich medium. Roche solid medium commonly used, containing egg yolk, glycerol, potato, inorganic salts and malachite green. Malachite green can be suppressed
System of bacteria growth, easy separation and long-term culture. Yolk contains lipid growth factor that stimulates growth. According to the number of inoculation, usually 2 weeks ~ 4
Colonies can be seen weeks of growth. Colonies on solid medium were grayish-white, dry and granular, prominent uplift, rough surface shrinkage, cauliflower-like
Colonies. In liquid medium, a coarse wrinkled membrane forms on the liquid surface and the medium remains clear. If added Tween 80 in the medium, can make tuberculosis
Bacillus evenly dispersed growth, usually 1 week ~ 2 weeks to grow. Clinical specimen examination liquid culture several times higher than the positive rate of solid culture. bacteria
Body slender slightly curved bacilli, stained red by acid-fast staining. Particularly strong resistance to dry, acid and alkali have a strong resistance, easy to produce
Resistance mutations and L-type bacteria.
A.3 Mycobacterium tuberculosis biochemical characteristics
Mycobacterium tuberculosis does not ferment sugar, can produce catalase. Mycobacterium tuberculosis is generally thought of as human, cow-type, non-human
Island type. Human type and bovine fungi morphological similar to all have strong virulence in guinea pigs, but the pathogenicity of human-type bacteria in rabbits than bovine-type bacteria is weak. Human type
Mycobacterium tuberculosis can synthesize niacin, nitrate reduction, thiophene-2-carboxylic acid hydrazide resistance, Mycobacterium bovis do not have the above characteristics. Human type
And cow-type strains, neutral red test were positive, non-toxic strains, the neutral red-negative and loss of cord-like growth. Hot catalase test on the difference knot
Mycobacterium tuberculosis and non-TB Mycobacterium is of great significance. Mycobacterium tuberculosis most tentase test positive, and hot catalase test negative, non
Mycobacterium tuberculosis is positive in most of the two tests. Hot catalase test test method is to place the concentrated bacterial suspension heated to 68 ℃ water bath for 20 min,
Then add H2O2. Observe whether there is a bubble, bubble-positive. Bovine Mycobacterium tuberculosis can be used to drink non-sterile lead-bearing cow milk
Since the onset of intestinal tuberculosis infection. Under the microscope are acid-fast bacilli, slender slightly curved, sometimes see people fonts, Y-shaped branches, the growth of culture by biochemical tests
Can identify the type of bacteria.
A.4 Mycobacterium tuberculosis resistance
Mycobacterium tuberculosis is resistant to acids, alkalis, the natural environment and dryness but is sensitive to damp-heat, alcohol and ultraviolet light and to anti-tuberculosis drugs
Easy to produce drug resistance. Mycobacterium tuberculosis cell wall contains lipid, it is sensitive to ethanol. 75% alcohol 5 min ~ 30 min death,
Liquid heating 62 ℃ ~ 63 ℃, 30 min death. Mycobacterium tuberculosis is sensitive to ultraviolet light and can be killed by direct sunlight for 2 h to 7 h.
UV can be used for tuberculosis patients clothes, books and other disinfection.
Mycobacterium tuberculosis in the dry sputum can survive for 6 months to 8 months, easy to develop resistance to anti-tuberculosis drugs. Mycobacterium tuberculosis resistance
Force and the presence of organic matter in the environment are closely related, such as sputum can enhance the resistance of Mycobacterium tuberculosis. Because most disinfectants can make sputum
The protein coagulation, wrapped around the bacteria, so that bacteria are not easily killed. 5% carbolic acid can kill Mycobacterium tuberculosis 30 min after no sputum,
Need to sputum 24h; 5% to the Soviet Union without sputum 5 minutes to kill Mycobacterium tuberculosis, sputum when required 1 h ~ 2 h.
Mycobacterium tuberculosis is resistant to acid (3% HCl or 6% H2SO4) or base (4% NaOH) and is not affected for 15 min. Available in points
Used to deal with contaminated samples of bacteria and digested specimens of viscous material. Mycobacterium tuberculosis 1. 13,000 malachite green arrived
Resistance, added to the medium can inhibit the growth of bacteria. Mycobacterium tuberculosis streptomycin, isoniazid, rifampicin, cycloserine, ethambutol,
Kanamycin, aminosalicylic acid and other sensitive, but prone to long-term drug resistance.
A.5 Mycobacterium tuberculosis variability
Mycobacterium tuberculosis variability includes.
a) Variability of drug resistance. Mycobacterium tuberculosis is more susceptible to anti-tuberculosis drugs, resulting in more resistant strains and poor treatment
difficult.
b) Toxicity variation. toxic M. bovis is cultured in medium containing glycerol, bile and potato and passaged 230 times,
It took 13 years to obtain an attenuated live strain, BCG, which is currently widely used in the prevention of human tuberculosis.
A.6 Mycobacterium tuberculosis pathogenicity
Mycobacterium tuberculosis does not produce internal and external toxins. Its pathogenicity may be due to bacterial proliferation in the tissue cells caused by inflammation, bacteria into
The toxicity of metabolites and metabolites is related to the immune damage caused by the body components. Pathogenic substances and capsule, lipid and protein-related.
A.6.1 capsule
The main components of the capsule polysaccharides, some lipids and proteins. The role of Mycobacterium tuberculosis. ① capsule with phagocytic cells table
Surface complement receptor 3 (CR3) binding, contribute to the adhesion and invasion of Mycobacterium tuberculosis on the host cell; ② a variety of enzymes in the capsule can be reduced
Solution of macromolecules in the host tissue for the nutrition required for the invasion of M. tuberculosis; ③ capsule can prevent the host of harmful substances into
Mycobacterium tuberculosis, even small molecules such as NaOH is not easy to enter. Therefore, tuberculosis specimens digested with 4% NaOH, the general bacteria quickly kill,
However, M. tuberculosis can tolerate tens of minutes. After invade Mycobacterium tuberculosis capsule can inhibit phagosome and lysosome fusion.
A.6.2 Lipids
According to experimental studies, bacterial virulence may be related to its complex lipid composition, especially glycolipids is more important. ① cord-like factor. yes
A glycolipid that binds mycolic acid to trehalose. Bacteria are serpentine-like arrangement in liquid medium. This factor and Mycobacterium tuberculosis
Toxicity is closely related. It can damage the cell mitochondrial membrane, affecting cell respiration, inhibiting leukocyte migration and causing chronic granulomas. If from it
Bacteria, the bacteria lose their virulence. ② phospholipids. can promote mononuclear cell proliferation, and macrophages in the inflammatory lesions into epithelioid
Cells, thus forming tuberculosis nodules. ③ sulfatide (sulfatide). can inhibit the phagocytic phagosomes and lysosome binding, so that
Mycobacterium tuberculosis can survive long-term in phagocytes. ④ waxy D. is a peptide glycolipid and mycobacterial acid complex, available from toxic strains or
BCG raised with methanol, with adjuvant effect, can stimulate the body to produce delayed-type hypersensitivity.
A.6.3 Proteins
Antigenicity, combined with waxy D can make the body hypersensitivity, causing tissue necrosis and systemic poisoning symptoms, and in the formation of tuberculosis
Nodules play a role.
A.7 Mycobacterium tuberculosis immune response
Mycobacterium tuberculosis is an intracellular infection of bacteria, its immunity is mainly T cell-based cellular immunity. T cells can not directly and intracellular bacteria,
The first reaction with infected cells, leading to cell collapse, the release of Mycobacterium tuberculosis. Mycobacterium tuberculosis although the body can produce antibodies, but antibodies
Only contact with the release of bacteria play a supporting role.
A.7.1 Immune response
It has long been thought that in innate immunity macrophages are the major target cells for tuberculosis infection and also the earliest onset of anti-TB infection in the body
Used with the most representative cell populations. However, with further research, other cell populations found to play an important role in the development of tuberculosis infection,
Such as neutrophils, was first collected to the site of inflammation, oxygen-dependent bactericidal substances and extracellular capture mechanism to kill pathogenic microorganisms. and
And some researchers in the experimental animals infected with neutrophils, the results of mycobacterium growth increased; the other hand, before the experiment with the stimulation of neutral
The myeloid growth rate is reduced by the agent that proliferates the granulocytes. And later found defensins in neutrophils. However, the neutropenia
Cells not only have this protective effect on the body, some reports show that due to the different host sensitivity to Mycobacterium tuberculosis, neutral
The pathological damage of cells will be more than its protective effect. Cellular immune response against Mycobacterium tuberculosis, like other intracellular infectious bacteria, cells
Mediated immune responses are more important than antibody-mediated immune responses. So often think that the existence of intracellular tuberculosis can not be combined with antibodies, because
This humoral immune response has no protective effect on the body of tuberculosis infection. However, this is not the case, and the effect of antibodies on intracellular bacteria infections is increasing
The more researchers are paying attention to get a deeper understanding of the mechanism of tuberculosis immunity. In the anti-TB cellular immune response, mainly
The participating cells are CD4 + and CD8 + T cells. Mycobacterium tuberculosis in macrophages is presented to CD4 + T cells by MHC class II antigen,
Induced by early cytokines such as IL-12, IL-18 and other Th1-type cells. This CD4 + T cell is capable of producing large amounts of IFN-γ
And other cytokines, activate macrophages, accelerate phagocytosis and kill Mycobacterium tuberculosis. In addition, studies have shown that CD4 + T cells are also involved in the infection of the fine
Apoptosis of cells. Antigen-specific cytolytic CD4 + T cells kill Mycobacterium tuberculosis-phagocytic macrophages, in which cell lysis
The spread of bacteria, but the release of bacteria will be phagocytosed by other macrophages in the body, so the formation of a vicious circle; only
Regulating the balance between the ac...
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