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Diphtheria is a serious bacterial infection caused by Corynebacterium diphtheriae. This highly contagious disease primarily affects the respiratory system, resulting in a thick grayish coating in the throat and tonsils, obstructing breathing and causing severe complications. Before the development of effective vaccines, diphtheria was a major public health concern, causing significant morbidity and mortality worldwide.
Diphtheria poses a significant threat to unvaccinated or inadequately vaccinated individuals, particularly children and adults in resource-limited settings. The World Health Organization (WHO) estimates that nearly 7,000 cases of diphtheria still occur globally each year. The disease is endemic in several countries, primarily in Asia, Africa, and parts of the former Soviet Union.
Clinical manifestations of diphtheria can vary, ranging from a mild upper respiratory tract infection to severe respiratory distress and systemic complications. The characteristic pseudomembrane formed in the throat can lead to airway obstruction, causing difficulty in breathing, asphyxia, and even death. Moreover, the toxin released by C. diphtheriae can spread through the bloodstream, damaging vital organs like the heart and nervous system, leading to potentially fatal outcomes if left untreated.
The mechanism of diphtheria revolves around the production and action of the diphtheria toxin (DT), which is produced by Corynebacterium diphtheriae infected with a specific type of bacteriophage. The ability of the bacterium to produce DT is determined by phage conversion, which occurs when the bacterium is infected by a particular phage. The tox gene, responsible for encoding the diphtheria toxin, becomes integrated into the bacterial genome.
The diphtheria toxin precursor is a protein with a molecular weight of 60 kDa. Proteases, such as trypsin, cleave the precursor to generate two peptide chains: fragment A (DT-A) and fragment B (DT-B), which are connected by a disulfide bond. DT-B acts as a recognition subunit that binds to the heparin-binding EGF-like growth factor (HB-EGF) on the surface of host cells, initiating receptor-mediated endocytosis.
Once inside the endosome, DT is split by a trypsin-like protease, releasing DT-A into the cytoplasm. DT-A exerts its toxic effects by inhibiting protein synthesis in the affected cell. It accomplishes this by catalyzing the ADP-ribosylation of the elongation factor EF-2, an essential protein involved in the translation step of protein synthesis. ADP-ribosylation involves transferring an ADP-ribose molecule from NAD+ to a modified histidine residue called diphthamide within the EF-2 protein. This modification prevents EF-2 from moving transfer RNA (tRNA) from the A-site to the P-site of the ribosome, effectively halting protein synthesis.
Figure 1. Mechanism of action of DT.
(Source: Sharma, N. C. et al., 2019)
The effects of diphtheria toxin can be counteracted by administering high doses of nicotinamide, a form of vitamin B3. Nicotinamide drives the reversal of ADP-ribosylation by serving as one of the reaction's end products.
The toxoid vaccine is a type of vaccine used to protect against diphtheria. It contains a modified form of the diphtheria toxin called a toxoid. The toxoid is created by treating the toxin with chemicals or heat to inactivate its toxic properties while retaining its ability to stimulate an immune response.
The toxoid vaccine works by stimulating the immune system to produce antibodies that specifically target the diphtheria toxin. These antibodies provide protection by neutralizing the toxin if a person is exposed to bacteria that cause diphtheria. Toxoid vaccines are typically administered as part of a combination vaccine, such as the DTaP or Tdap vaccine, which also provides protection against tetanus and pertussis (whooping cough). These combination vaccines are given in a series of doses, starting in infancy and continuing throughout childhood. Booster doses are recommended in adolescence and adulthood to ensure continued protection.
The toxoid vaccine is considered highly effective in preventing diphtheria. It has played a significant role in reducing the incidence of diphtheria worldwide. Vaccination has been a key factor in controlling and nearly eliminating the disease in many countries. The toxoid vaccine is generally safe, with a low risk of serious side effects. Common side effects may include pain or swelling at the injection site, mild fever, or fussiness in infants. Serious reactions are rare.
References
| Target | Cat. No. | Product Name | Expression System | Tag/Conjugate | Application | |
| C. diphtheriae toxin | DAGH042 | C. diphtheriae toxin | N/A | Unconjugated | N/A | Inquiry |
| DAG4060 | Recombinant C. diphtheriae Toxin (mutation CRM197) | P. fluorescens | Unconjugated | N/A | Inquiry | |
| C. diphtheriae | DAGC697 | Native C. diphtheriae Antigen | N/A | Unconjugated | Immunogen, WB, ELISA | Inquiry |
| C. diphtheriae Diphtheria Toxoid | DAG2689 | C. diphtheriae Diphtheria Toxoid | N/A | Unconjugated | ELISA | Inquiry |
| Nicotinamide | DWT114 | Nicotinamide (Vitamin B3) Standard solution | N/A | N/A | Inquiry | |
| DAG3371 | Nicotinamide [BSA] | N/A | BSA | IHC, ICC | Inquiry |
| Target | Cat. No. | Product Name | Size | Species Reactivity | Application | Detection Sample | |
| Diphtheria toxin | DEIA1776 | Human Anti-Diphtheria Toxoid IgG ELISA Kit | 96T | Human | Quantitative | Serum or plasma | Inquiry |
| HB-EGF | DEIA5439 | Human HBEGF(Proheparin-binding EGF-like growth factor) ELISA Kit | 96T | Human | Quantitative | Serum, plasma, tissue homogenates and other biological fluids. | Inquiry |
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