Detection methods and clinical significance of the eight items of surgical infection
Department of Infectious Diseases, Air Force General Hospital (100036) Zhou Ping
The eight surgical infection tests are mandatory preoperative tests in all hospitals, including: five serum markers of hepatitis B virus (hepatitis B surface antigen (HBsAg), hepatitis B surface antibody (anti-HBs), hepatitis B e antigen (HBeAg), hepatitis B e antibody (anti-HBe), hepatitis B core antibody (anti-HBc), hepatitis C virus antibody (anti-HCV), HIV antigen antibody (anti-HIV), and syphilis serum-specific antibody (anti-HCV). HCV), antibodies to HIV antigens (anti-HIV) and syphilis serum-specific antibodies (anti-TP). The aim is to prevent, reduce and avoid cross-infection and transmission of these viruses in the hospital during surgery as well as to prevent medical risks and medical disputes. In this paper, we briefly introduce the testing methods and clinical significance of the eight items of surgical infection in our hospital as follows. Zhou Ping, Department of Infection Medicine, Air Force General Hospital
I. Detection methods.
At present, most domestic hospitals surgical infection eight detection methods are mainly three immunological methods: two enzyme immunoassay (EIA and ELISA) and chemiluminescence microparticle immunoassay (referred to as: chemiluminescence method). The advantages of the former: high specificity and sensitivity, lower cost; disadvantages: operation is more complex, time-consuming, only qualitative detection; the latter advantages: high specificity and sensitivity, easy to operate, rapid, quantitative (such as: HbsAg and anti-HBs)/semi-quantitative analysis; disadvantages: detection costs are higher.
II. Clinical significance.
(A) Clinical significance of the five hepatitis B items
HBsAg, anti-HBs, HBeAg, anti-HBe and anti-HBc five indicators, commonly known as “hepatitis B five” or “hepatitis B two and a half”. How to correctly analyze the clinical significance of these indicators is a problem that clinicians often encounter and find complicated.
1. Hepatitis B surface antigen (HBsAg)
HBsAg is the marker of HBV infection and is the first viral marker to appear in the body’s serum. the time of appearance of HBsAg is related to the route of HBV infection and the dose of infection. If HBsAg positive blood is transfused, HBsAg can be detected after 2 weeks, if detected by RIA method, HBsAg positive in serum can appear 6 days after vaccination; if the dose of infection is small, the time for HBsAg to appear positive can be 3 to 4 months, or even 6 months; generally, HBsAg positive can appear 4 to 6 weeks after HBV infection. (average about 4 weeks) before hepatitis symptoms and liver function abnormalities appear. The incubation period is about 2 months for blood-borne infections and about 3 months for oral infections.
The course of acute hepatitis B generally lasts 1-3 months, and 80% to 90% of patients can be clinically cured [1]. HBsAg positivity in the blood generally lasts 1-6 weeks and up to 20 weeks (14-148 days) in the longest cases; it disappears 1-4 weeks after the appearance of hepatitis symptoms or after the peak of serum transaminases If HBsAg positivity persists for more than 6 months and still does not turn negative, it is called persistent positivity or chronic carrier status; if it is acute hepatitis B, HBsAg positivity for more than 6 months is indicative of chronicity. The duration of HBsAg positivity and the proportion of acute hepatitis B chronicity are related to the age of the infected person, and the younger the age, the more likely it is to form a persistent infection or a chronic condition [2]. The younger the age, the greater the probability of forming persistent infection or chronicity of the disease; 80% of infants infected in the perinatal period will become carriers of HBsAg; about 30% of those infected in early childhood will become persistent HBsAg carriers, and the proportion of normal adults infected with HBV who form persistent infection may be less than 5%; about 35% to 50% of HBsAg-positive carriers in the general population of society are infected in the perinatal period from mother to child [ 3]. Recent studies have shown that after acute infection with HBV in adults, only 1% to 3% are chronic and the vast majority are cured. 129 children under 15 years of age with true acute infection were followed for 2 to 24 months by Kaganov et al [2, 3], 115 were cured and the vast majority produced anti-HBs and 14 (under half a year of age) died from fulminant hepatitis with no chronicity seen. This indicates that the majority of acute hepatitis B has a good prognosis without chronicity. However, HBsAg conversion is very difficult in HBV chronic infections, with an annual negative HBsAg conversion rate of 0.8% in chronically infected patients with normal liver histology and 0.5% in those with histologically confirmed chronic hepatitis [4].
HBsAg positivity indicates HBV infection, and its infection status has two conditions: ① complete viral replication and infectious. In this case, other viral replication indicators are also positive, such as HBeAg, HBVDNA, HBVDNA-P and Pre-S1, S2, etc.; (2) no complete viral replication, not infectious; HBVDNA integration into the host cell genome, the genes expressing other viral proteins are lost, only HBsAg expression without complete virus formation [2]. Clinically, HBsAg positivity is seen in the latent and acute phases of patients with acute hepatitis B; chronic hepatitis B, in asymptomatic carriers; in the serum of some patients with cirrhosis and liver cancer and in the plasma of HBV-infected hepatocytes.
Positive HBsAg generally indicates the presence of HBV infection in the organism, but negative does not completely exclude HBV infection. The reasons for this are: (i) HBsAg may be missed due to very low levels of HBV and HBsAg, the detection method is not sensitive enough, or false negatives may occur due to reagent quality and handling problems; (ii) S gene mutations cause impairment in the expression and secretion of HBsAg, and HBsAg cannot be measured in the serum or is rare despite the presence of HBV in the body [5,6]; (iii) HBsAg expressed after S gene mutations cannot be measured by some reagents now widely by some of the reagents now widely used [7,8]. The latter two, although HBsAg negative, are often accompanied by positivity for other markers of HBV infection such as HBeAg, anti-HBe and anti-HBc. Even if truly negative, HBV infection cannot be completely ruled out because in 8% of patients with hepatitis B, HBsAg has turned negative before the onset of symptoms; if anti-HBs or anti-HBe appears positive 2 to 9 months after the onset of the disease, the diagnosis of acute hepatitis B can still be made [9]. In fulminant hepatitis B, often anti-HBs appears early while HBsAg is negative; acute hepatitis B can occur after transfusion of HBsAg-negative but anti-HBc-positive blood. The presence of HBVDNA in the serum of certain HBsAg-negative hepatitis patients and blood donors can be further confirmed using PCR techniques [10].
When analyzing the positive HBsAg results, several points should be noted: ① The severity of the hepatitis or infected person’s disease cannot be judged by the level of HBsAg titer. Because the titer of HBsAg in the serum of HBV-infected patients often fluctuates, there is no direct relationship between its titer and the disease. The titer of HBsAg cannot be used to determine the type of hepatitis. HBsAg itself does not contain viral nucleic acid and is not infectious, but HBsAg positive serum, regardless of its titer, may contain infectious doses of viral particles. If HBVDNA is integrated into the host hepatocyte DNA, there are no free viral particles in the serum, and at this time HBsAg positive blood is not infectious. ④ HBsAg titer cannot be used as an indicator to evaluate or judge the effectiveness of clinical treatment of a drug. As mentioned earlier, HBsAg does not reflect the severity of the disease, nor does it contain the nucleic acid component of the virus, which itself often fluctuates, so there is no scientific basis for the rise or fall of HBsAg titer to indicate the effect of a drug [11].
2. hepatitis B surface antibody (anti-HBs)
Anti-HBs is a neutralizing antibody that provides protective immunity against HBV, neutralizing HBV infection and warding off reinfection. Most patients with self-limiting HBV infection have anti-HBs appear during the recovery period of acute infection. 80% of patients have anti-HBs appear within weeks to months after HBsAg disappears and clinical symptoms subside. the early appearance and titer of anti-HBs are related to repeated infections. The rate of anti-HBs positivity is highest in the recovery period of acute hepatitis B and low in all other types of hepatitis B. Generally speaking, anti-HBs positive serum is negative for HBsAg/anti-HBs-IgM and normal for ALT.
Anti-HBs positivity can be seen in: (1) recovery from hepatitis B; (2) patients with previous HBV infection; (3) after hepatitis B vaccination; (4) some fulminant hepatitis B; patients recovering from natural infection have double positive serum anti-HBs and anti-HBc, and because anti-HBc persists for a longer period of time (>8 to 10 years) and anti-HBs persists for a shorter period of time (6 months ～The single anti-HBs positive is rare (except for hepatitis B vaccination), and the single anti-HBs positive with low titer is mostly a false positive due to non-specific reaction [2].
Clinically, simultaneous positivity of HBsAg and anti-HBs can sometimes be encountered, a pattern reported abroad with an overall incidence of 32% in all types of hepatitis; 5.75% in China. It is seen in the following situations: (1) dynamic equilibrium phase of antigen and antibody; (2) false-positive anti-HBs; (3) dual infection with different HBsAg subtypes or reinfection with the same type of HBV; (4) abnormal immune function of the body, after mutation of the viral S gene, which obviously changes the antigenic structure of HBsAg, so that it cannot react with the neutralization of anti-HBs of the wild strain, resulting in the appearance of anti-HBs of the wild strain and HBsAg of the mutant strain persist simultaneously in the same body [12] cannot handle HBsAg; (5) previous infection with HBV-1 or hepatitis B vaccine recipients are reinfected with HBV-2 [2].
The protective effect of anti-HBs on the organism has differed in recent years, and some have found that accidental HBV infection in anti-HBs-positive medical personnel can occur in acute hepatitis B. Domestic Luo anti-first [13] applied PCR technique to detect 9 cases of anti-HBs-positive patients and 4 cases of HBVDNA-positive. The protective effect of anti-HBs on the organism may be related to different HBV subtypes of infection, and anti-HBs of the same subtype are protective only against the same subtype of HBV infection, while they are not protective or less protective against different subtypes of HBV infection. In addition, it may also be related to the concentration of effective anti-HBs in the blood being too low.
3. Hepatitis B e antigen (HBeAg)
HBeAg is a soluble component of hepatitis B core antigen, often present together with serum HBVDNA, DNA-P and Dane particles, and is a marker of HBV replication and infectiousness. Usually HBeAg appears 1 week later than HBsAg and disappears 2 weeks before HBsAg; if HBeAg remains positive for more than 10 weeks, it indicates that the disease may tend to be chronic. HBeAg positivity in serum is only seen in: acute hepatitis with positive HBsAg, chronic hepatitis, asymptomatic HBsAg carriers and some patients with cirrhosis and liver cancer. In chronic infections, the rate of HBeAg positivity decreases with age; the annual natural negative rate of HBeAg in chronic hepatitis B patients is 25.6%. Asymptomatic carriers are 9.3% [14].
Generally speaking, HBeAg positivity is only seen in HBsAg-positive sera; clinically, HBsAg negativity and HBeAg positivity can sometimes be seen for the following reasons: ① the method of detecting HBsAg is not sensitive enough; ② interference of rheumatoid factor in the serum, resulting in false positivity. ③ HBsAg has formed immune complexes with anti-HBs, so HBsAg cannot be measured. ④ After the disappearance of HBsAg and the appearance of anti-HBs, HBV remains in the serum, and HBsAg on the surface of its Dane particles is wrapped by anti-HBs, so that it is not detected. ⑤ Reagent quality and operation can also lead to false positives for HBeAg [1].
4. hepatitis B e antibody (anti-HBe)
Anti-HBe appears after the negative HBeAg, and the appearance of anti-HBe indicates a decrease in infectivity. In the past, anti-HBe was considered to be an indicator of recovery of HBV infection or absence of infectiousness. In recent years, studies have found that anti-HBe positive sera may still be infectious, but they are far less infectious than HBeAg positive sera. The same results were observed in mother-to-child transmission studies: 80-100% of infants born to mothers who were both positive for HBsAg and HBeAg were infected with HBV; while HBsAg-positive sera were 10-2 to 10-5. HBV infection was found in 80-100% of infants born to mothers who were both positive for HBsAg and HBeAg, while only 3% of infants born to HBsAg-positive, anti-HBe positive mothers were infected with HBV. These results indicate that HBeAg-positive sera are significantly more infectious than anti-HBe positive sera; anti-HBe positive sera are also somewhat infectious [11].
In general, anti-HBe positive patients have lower levels of HBV replication in their sera and their disease tends to stabilize and recover, but a significant proportion of anti-HBe positive patients can still be seen clinically to have fluctuating disease or to be developing. The main reason for this is that HBV is not eliminated by anti-HBe positivity, and HBV still exists and replicates in the organism. One study showed that in chronic active hepatitis with anti-HBe positivity, HBVDNA was detected in the serum of 87% of patients using PCR technique [10]. Intrahepatic HBsAg and HBcAg assays and HBVDNA in situ hybridization studies revealed that 26.7% of anti-HBe positive chronic hepatitis patients had active HBV replication, 53.3% had incomplete replication and expression, and only 20% had a non-replicating state. Serological conversion of HBeAg to anti-HBe in chronic hepatitis B can be accompanied by an increase in ALT levels and a subsequent decrease in HBV replication levels, but it does not imply complete clearance of HBV [2, 10]. HBeAg can be detected in the serum of HBV carriers with normal liver histology, while patients with histologically confirmed presence of chronic active hepatitis can be positive for anti-HBe in their serum, indicating that HBeAg is not necessarily a marker of chronic hepatitis B activity, and anti-HBe cannot be used as an indicator of healthy carriage.
Anti-HBeAg is generally not positive at the same time as HBeAg, if there is a report of simultaneous detection, it may be due to different subtypes (e1, e2, e3) of infection; anti-HBeAg and HBeAg negative at the same time is also rare, this can be seen in: ① HBeAg and anti-HBe titers are too low, the sensitivity of the test method is not enough; ② at the time of detection, HBeAg is disappearing and the corresponding antibody has not yet (3) some HBsAg carriers have acquired immunodeficiency syndrome and are unable to form anti-HBe [15].
5. hepatitis B core antibody (anti-HBc)
Anti-HBc is an antibody that appears earlier in the HBV antibody system, and can be detected 3-5 weeks after the appearance of HBsAg in acute HBV infection and before the appearance of clinical symptoms, and has a high titer in the recovery period of hepatitis; the longer the time of HBsAg positivity, the higher the titer of anti-HBc [2, 9]. Clinically, anti-HBc is mostly detected by the competitive inhibition method as a total antibody, including IgG, IgM, IgA and IgE type anti-HBc, with anti-HBcIgM predominating in the early stage and lasting 6 to 18 weeks, and anti-HBcIgG predominating later, which can persist in the body for years or even decades [11]. Usually, highly potent anti-HBc, seen in acute and chronic hepatitis and HBsAg carriers, and indicates that HBV replication may still be active and the serum is infectious; low potency anti-HBc indicates previous HBV infection and is generally not infectious.
A single positive anti-HBc is a common pattern in the clinic, and its incidence varies from place to place with reports ranging from approximately 0.9 to 11.9%. For the explanation of this single positive anti-HBc, the US Centers for Disease Control states [16]: after excluding false-positive (suppression ≤ 70% is mostly false-positive) results of the test, there are several reasons: ① Early recovery from acute infection (window period). HBsAg decreases or disappears, while anti-HBs has not yet been produced, and anti-HBc is the only specific HBV indicator that can be detected. ② passively acquired anti-HBc. infants born to HBsAg carrier mothers, IgG type anti-HBc in the mother can be transferred to the infant via the placenta, such maternal anti-HBc can exist in the infant for more than one year; transfusion of anti-HBc-positive blood or blood products. (iii) Distant infection with disappearance of anti-HBs. Because anti-HBc can persist for more than 8 to 10 years, while anti-HBs only persists in the body for 6 months to 3 years. ④Distant infection with low levels of HBsAg. In recent years, it has been suggested that a single positive anti-HBc is a marker of hepatitis C virus (HCV) infection, and it is believed that HCV antigens have the same antigenic component as HBcAg. However, a prospective study by Hoyos et al. on non-A non-B hepatitis after blood transfusion in patients undergoing cardiac surgery did not support this view [17-19].
In conclusion, the five serum markers of hepatitis B virus, which are only antigenic substances expressed by HBV genes and the corresponding antibodies produced by these antigens stimulating the body, are not themselves nucleic acid components of the virus, and therefore are not infectious in themselves, but are only markers of HBV infection. Since a single positive HBVM can be seen in a variety of situations, and different combinations of different HBVM patterns have different clinical significance, when analyzing the clinical significance of the “Hepatitis B Five”, one cannot analyze one of the indicators in isolation and one-sidedly, but should refer to several other indicators, and sometimes also to HBVDNA. DNA-P, Pre-S1, S2 and other tests should also be combined with clinical analysis in order to make a correct judgment and accurate evaluation.
Simple judgment of the clinical significance of the five items of hepatitis B: in general, the five serum markers of hepatitis B, if the viral antigen markers (HBsAg/HBeAg) positive, indicating the presence of hepatitis B virus infection; antigen, antibody are negative, no viral infection; antigen negative, one or more antibody positive, indicating previous infection or recovery period, the virus has been cleared.
(ii) Hepatitis C virus antibodies (anti-HCV).
The incubation period after HCV infection is 21-84 days (average 50 days), and HCV RNA can be detected in the blood within 1-2 weeks after infection, with an average of 50 days of elevated serum ALT. The anti-HCV detection reagents have been continuously improved and now, they have been developed to the 3rd and 4th generation, and the sensitivity and specificity of the tests have been improved. Although the detection rate of antibodies has gradually improved, there are still shortcomings, such as the late appearance of antibodies during the course of the disease, with antibodies detected on average 12 weeks after infection and several weeks after ALT elevation. Anti-HCV can be detected in the serum of only 50%-70% of patients at the onset of symptoms, and up to 90% of patients after 3 months of infection. In some patients, antibodies do not appear due to immunodeficiency; antibodies also cannot distinguish between acute, chronic and previous infections, and antibody levels lack consistency with the disease; therefore, they also cannot be used as indicators for judging the severity, prognosis and treatment.
1.Testing method.
The test for detection of antibodies to hepatitis C virus was first registered with the U.S. Food and Drug Administration (FDA) in 1990, and since then, new versions of such tests and other FDA-approved anti-HCV tests have been widely used for clinical diagnosis and screening of asymptomatic patients. Currently, the following tests are commonly used in clinical practice.
(1), anti-HCV screening tests: enzyme immunoassays (HCV- EIA210; HCV- ELISA
310) and enhanced chemiluminescence immunoassay (CIA).
(2), anti-HCV paracrine test: recombinant immunoblotting assay (RIBA) – high specificity anti-HCV paracrine test result analysis and qualitative/quantitative detection of HCV RNA by PCR technique.
2. Clinical significance.
(1), Anti-HCV screening assay.
Positive results: current HCV infection, previous infection, false positives.
Negative results: no HCV infection, window period of HCV infection, trace HCV infection
(2), Recombinant Immunoblotting Assay (RIBA) – Highly specific anti-HCV paracentesis test.
Positive results: current HCV infection, previous infection.
Negative results: absence of HCV infection, window period of HCV infection, trace HCV infection.
The clinical significance of anti-HCV should be analyzed in combination with anti-HCV collateral tests (recombinant immunoblot test (RIBA) – analysis of highly specific anti-HCV collateral test results and qualitative/quantitative detection of HCV RNA by PCR technique) and liver function tests.
3. Common clinical types.
(1) Anti-HCV screening test (+) + RIBA (+) + HCV RNA (+) + ALT/AST (+): presenting infection, active hepatitis.
(2) Anti-HCV screening test (+) + RIBA (+) + HCV RNA (+) + ALT/AST (-): current infection, viral carriage; inactive hepatitis.
(3) Anti-HCV screening test (+) + RIBA (+) + HCV RNA (-) + ALT/AST (+) except for other causes: presenting infection, hepatitis activity.
(4) Anti-HCV screening test (+) + RIBA (+) + HCV RNA (-) + ALT/AST (-): previous infection; trace HCV carriage, requiring periodic re-testing.
(5) Anti-HCV screening test (+) + RIBA (-) + HCV RNA (-) + ALT/AST (+): false positive; other causes of liver function abnormalities.
(6) Anti-HCV screening test (+) + RIBA (-) + HCV RNA (-) + ALT/AST (-): false positive.
(7) Anti-HCV screening test (-) + RIBA (-) + HCV RNA (+) + ALT/AST (+): acute infection window; trace HCV infection; occult hepatitis.
(8) Anti-HCV screening assay (-) + RIBA (-) + HCV RNA (+) + ALT/AST (-): trace HCV infection carriage.
(9) Anti-HCV screening test (-) + RIBA (-) + HCV RNA (-) + ALT/AST (+): no HCV infection; other causes of liver function abnormalities
(10) Anti-HCV screening assay (-) + RIBA (-) + HCV RNA (-) + ALT/AST (-): not infected with HCV.
4. Clinical significance of qualitative/quantitative detection of HCV RNA by PCR technique.
(1), clear infection and viremia.
(2) Early diagnosis of anti-HCV-negative acute hepatitis.
(3) Diagnosis of anti-HCV-negative immunocompromised chronic hepatitis.
(4), Infants of chronically HCV-infected mothers to clarify mother-to-child transmission.
(5), clear treatment indication before antiviral therapy and evaluation of treatment effect after treatment.
(3), HIV antibody (anti-HIV) testing.
1, detection methods: so far, serological tests are still the main basis for HIV laboratory diagnosis. Serological tests, that is, HIV antibody testing, is a routine method for the diagnosis of HIV infection, divided into two steps: primary screening test and confirmatory test.
(1), HIV antibody screening test: including: enzyme-linked immunosorbent assay (ELISA), gelatin particle agglutination test (PA), immunochromatographic/permeation test, rapid detection test (RT), etc.
ELISA-anti-HIV test, is the earliest and most widely used test to detect HIV antibodies internationally. From the first generation in 1985 to the current fourth and fifth generation kits, the sensitivity and specificity have improved significantly, and the window period for HIV detection has been continuously shortened. Although the ELISA-anti-HIV test has high sensitivity and specificity, there are a small number of false negatives and false positives. False negatives mainly occur during the window period or late onset when the antibody titer decreases; false positives are mainly due to the effects of autoimmune disease, kidney disease, liver disease, vaccination, etc., but generally speaking, the titer of false positives is usually not high.
(2), HIV antibody confirmation test.
HIV antibody confirmation tests include: immunoblotting (Western Blot, WB); immunofluorescence assay (IFA); strip immunoassay (LIF); radioimmunoprecipitation assay (RIPA), etc. The commonly used confirmation test in China is the immunoblot method (WB), which is highly specific. HIV-specific antibody detection ELISA (high sensitivity), coupled with WB (high specificity), the diagnostic accuracy is greater than 99%, and the false-positive rate is about 0.00006%, resulting in almost zero chance of incorrect diagnosis.
2. Diagnosis of window period HIV infection.
Anti-HIV negative, not necessarily no infection, may be in the window period of viral infection, that is, from the body HIV virus infection to the production of antibodies during this period, the essence of the window period is the specific virus antibodies from none to have, from less to more transformation process, there are two factors that determine the length of the window period, one is the degree of antibody response of the body to viral infection, and the other is the sensitivity of the detection method. The average is usually 2 to 3 months (can be 1 to 9 months), but more than 95% of HIV-1 infected patients produce antibodies in less than 6 months. The methods used for diagnosis are.
(1), P24 antigen test.
After the body is infected with HIV, P24 antigen is an early pathogenic marker that can be detected in the serum, which can be detected about 2~3 weeks after infection and enters the peak of antigen around 1~2 months, then with the production of antibodies to form antigen-antibody complexes, due to the neutralization effect of antibodies, the concentration of P24 antigen decreases to a level that is difficult to detect. 100%.
(2), HIV RNA detection.
The use of molecular biology PCR technology can be qualitative and quantitative detection of HIV nucleic acid (HIV RNA), with high sensitivity and specificity, in the early detection and diagnosis of HIV infection is of great significance, and is also a good indicator for determining the effectiveness of clinical treatment and estimating prognosis, and is also the main basis for the development and adjustment of treatment plans. At present, the commonly used clinical nucleic acid detection methods: reverse transcription PCR (RT-PCR) and real-time fluorescence quantitative PCR.
(D) Syphilis serum-specific antibodies (anti-TP)
1, syphilis infection serological test.
Serum syphilis antibody test is an important method for clinical diagnosis of syphilis infection. 4-6 weeks after the entry of syphilis spirochetes into the body, the serum can produce non-specific antibodies against lipid-like antigens and specific antibodies against syphilis spirochete antigens. Based on the characteristics of the two types of antibodies produced by syphilis spirochetes after entering the body, serological tests are divided into two main categories.
(1) Non-syphilis spirochete antigen serological tests: including: ①Venereal disease research laboratory test (VDRL); ②Unheated serum reactin test ( USR); ③Rapid plasma reactin ring card test (RPR); ④Toluidine red unheated serum test (TRUST). At present, the most commonly used representative methods are RPR and TRUST . They are suitable for syphilis screening, efficacy observation, and examination of recurrence or reinfection.
(2) Syphilis spirochete antigen serological test: including: ① syphilis spirochete gelatin particle agglutination test (TPPA); ② syphilis spirochete hematocrit agglutination test (TPHA); ③ fluorescent syphilis spirochete antibody adsorption test (FTA-ABS); ④ syphilis spirochete enzyme-linked immunosorbent assay (TP-ELISA); ⑤ syphilis spirochete protein blot test (TP-WB), etc.
The detection method of syphilis serum-specific antibodies (anti-TP) in the eight items of our surgical infection is the syphilis spirochete enzyme-linked immunosorbent assay (TP-ELISA) in the syphilis spirochete antigen serological test.
2, the clinical significance of non-syphilis spirochete antigen serological test.
(1), positive may indicate: ① present infection; ② recurrence or reinfection; ③ biological false positive.
(2), clinical use for syphilis screening, anti-syphilis treatment efficacy observation.
3, the clinical significance of syphilis spirochete antigen serology test.
(1), positive indicates: ① present infection; ② previous infection.
(2), infected with syphilis, syphilis spirochete antibody positive for life, therefore, can not be used as an indicator to evaluate the effectiveness of treatment.
(3), can be used as a confirmatory test for non-syphilis spirochete antigen serological tests (such as RPR, etc.) for primary positive specimens.
4.Serological diagnosis of syphilis infection.
Non-syphilis spirochete antigen serological test (such as RPR, etc.) primary screening positive specimens need to confirm the test of syphilis spirochete antigen serological test, in order to exclude biological false positive; syphilis spirochete antigen serological test positive results, if you need to determine whether the current infection, or previous infection or recurrence, reinfection, or anti-syphilis efficacy evaluation need non-syphilis spirochete antigen serological test (such as RPR, etc.) to help.