Diphtheria toxoid IgG ELISA kit

Sample

Serum, plasma

Species Reactivity

Human

Detection Method

iELISA

Intended Use

This product is used for the qualitative in vitro detection of diphtheria toxoid IgG antibodies in human serum/plasma or whole blood samples.

Contents of Kit

1. Pre-coated plate: 12T×8, diphtheria toxoid antigen
2. Mouse anti-human IgG monoclonal antibody enzyme label: 10ml × 1 bottle, HRP enzyme-labeled mouse anti-human IgG monoclonal antibody, containing stabilizer and biological preservatives
3. Concentrated washing solution (20×): 30ml×1 bottle, 20 times concentrated phosphate buffer, containing NaCl, Tween-20
4. Sample diluent: 50ml×1 bottle, sodium citrate buffer, stabilizer, etc.
5. Negative control substance: 0.5ml×1 bottle, inactivated human anti-diphtheria toxoid IgG negative serum, stabilizer
6. Positive control substance: 0.5ml×1 bottle, inactivated human anti-diphtheria toxoid IgG positive serum, stabilizer
7. Substrate A: 5.0ml×1 bottle, the main component is carbamide peroxide
8. Substrate B: 5.0ml×1 bottle, the main component is TMB
9. Stop solution: 5.0ml×1 bottle, 0.5M H2SO4 solution
10. Ziplock bag: 1 serving
11. Parafilm: 3 sheets

Storage

1. Store refrigerated at 2-8°C and away from light. Freezing is prohibited. The validity period is 12 months.
2. Unused pre-coated boards should be immediately put into a ziplock bag with desiccant and sealed, and the storage time at 2-8°C should not exceed one week.
3. Any unused reagents of other components should be capped immediately and stored at 2-8°C. The storage time should not exceed one week.
4. Please refer to the product label for the production date and expiration date of the product.

Performance Characteristics

1. Compliance rate of positive reference products: 10 positive reference products from the company were tested, and the results were all positive.
2. Compliance rate of negative reference products: 10 corporate negative reference products were tested, and the results were all negative.

Precision

CV%＜15%

General Description

It is suitable for auxiliary diagnosis of diphtheria bacilli infection, detection of whether the level of anti-diphtheria toxoid IgG antibodies in normal or susceptible people reaches the full protective titer (0.1IU/ml), and detection of anti-diphtheria toxoid IgG antibody levels after vaccination with vaccines containing diphtheria toxoid components. Whether the immune success standard (0.1IU/ml) is reached.
Diphtheria is an acute upper respiratory tract infection caused by Gram-positive Corynebacterium diphtheriae. Bacterial toxins can cause the production of upper respiratory tract obstructive pseudomembranes or damage myocardium and other tissues, leading to illness and death. Historically, many countries have experienced diphtheria epidemics that mainly affected children. In countries where diphtheria is endemic, the disease mostly occurs as sporadic cases or small outbreaks. Although most B. diphtheriae infections are asymptomatic or clinically relatively mild, case fatality rates are high (>10%), even in recent outbreaks.
Diphtheria bacilli are elongated, rod-shaped, Gram-positive bacilli with 4 biotypes (severe, belfanti, mild, and intermediate). In addition to bacterial exotoxins, cell wall components such as O antigen and K antigen play an important role in the pathogenicity of diphtheria. The heat-stable O antigen is the same for all Corynebacterium species, while the heat-labile K antigen varies from strain to strain and can be used to identify strains. At the same time, K antigen is important for mucosal adhesion, and invasiveness is mediated by cord factors (toxic glycolipids). The most important virulence factor of B. diphtheriae is exotoxins, which are highly conserved polypeptides mediated by bacteriophages and encoded by bacterial chromosomes. The exotoxin has very low activity outside the host cell, but after adhesion and entry into the cell through the non-toxic fragment B, the toxic fragment A dissociates and kills the cell by inhibiting cellular protein synthesis. Diphtheria exotoxins can cause local and systemic cell death.
In most cases, infection in diphtheria-susceptible individuals only results in transient pharyngeal bacterial carriage without illness. Contamination from skin wounds can cause cutaneous diphtheria and, occasionally, mucosal infections outside the respiratory tract. Skin and mucosal lesions are important sources of infection and occasionally cause systemic pathological reactions. Symptoms of respiratory diphtheria generally appear after an incubation period of 1 to 5 days. The onset of the disease is slow and is characterized by moderate fever and mild exudative pharyngitis. In severe cases, so-called pseudomembranes gradually form in the larynx, which have a typical asymmetrical gray-white appearance and are tightly adherent to deeper tissues. Pseudomembranes can extend into the nasal cavity and larynx, causing airway obstruction. Laryngeal diphtheria sometimes occurs without pharyngeal symptoms and is an emergency that often requires tracheotomy. Exotoxins absorbed through mucosal (or skin) lesions can cause toxic damage to the myocardium, kidneys, nervous system and other organs.
Immunity against severe local disease and systemic disease relies primarily on the antitoxin antibody IgG, whereas type-specific protection against vector and mild local disease is the induction of antibodies against cell wall variant K antigens. Cellular immunity may also play a protective role. However, sometimes infection does not induce protective immunity. There is no protection at circulating antitoxin levels below 0.01 IU/ml, partial protection at 0.01 IU/ml, complete protection at ≥0.1 IU/ml, and antitoxin levels of 1.0 IU/ml are associated with long-term protective immunity. The antitoxin crosses the placenta and the newborn acquires passive immunity during the first few months of life.
At present, the main methods for detecting diphtheria toxoid-specific IgG antibodies include: Schick test, cell neutralization test, enzyme-linked immunoassay (ELISA), etc.